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(1998).","npl_type":"a","external_id":["9463323","pmc1376892","10.1086/301716"],"record_lens_id":"033-867-393-453-229","lens_id":["092-346-371-426-162","033-867-393-453-229","146-135-828-704-116"],"sequence":28,"category":[],"us_category":[],"cited_phase":"APP","rel_claims":[]}},{"npl":{"num":18,"text":"van den Heuvel et al., \"The Oxidative Phosphorylation (OXPHOS) System: Nuclear Genes and Human Genetic Diseases,\" Bioessays 23:518-525 (2001).","npl_type":"a","external_id":["10.1002/bies.1071","11385631"],"record_lens_id":"026-618-464-052-879","lens_id":["103-986-738-807-379","026-618-464-052-879","122-006-804-621-47X"],"sequence":29,"category":[],"us_category":[],"cited_phase":"APP","rel_claims":[]}},{"npl":{"num":19,"text":"International Search Report mailed Oct. 29, 2007 (PCT/US07/12007).","npl_type":"a","external_id":[],"lens_id":[],"sequence":30,"category":[],"us_category":[],"cited_phase":"APP","rel_claims":[]}},{"npl":{"num":20,"text":"Cataldo et al., \"Abnormalities in mitochondrial structure in cells from patients with bipolar disorder,\" Am J Pathol. 177:575-85, 2010.","npl_type":"a","external_id":["10.2353/ajpath.2010.081068","20566748","pmc2913344"],"record_lens_id":"095-217-846-397-632","lens_id":["197-149-241-468-836","170-351-454-578-974","095-217-846-397-632"],"sequence":31,"category":[],"us_category":[],"cited_phase":"APP","rel_claims":[]}},{"npl":{"num":21,"text":"Kato et al., \"Comprehensive gene expression analysis in bipolar disorder,\" Can J Psychiatry. 52:763-71, 2007.","npl_type":"a","external_id":["10.1177/070674370705201203","18186176"],"record_lens_id":"033-395-623-033-527","lens_id":["053-072-270-139-631","033-395-623-033-527","105-902-780-022-50X"],"sequence":32,"category":[],"us_category":[],"cited_phase":"APP","rel_claims":[]}},{"npl":{"num":22,"text":"Zahn et al., \"Transcriptional profiling of aging in human muscle reveals a common aging signature,\" PLoS Genet. 2:e115, 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for invention","granted":true,"earliest_filing_date":"2007-05-18","grant_date":"2012-04-24","anticipated_term_date":"2029-06-19","discontinuation_date":"2020-10-05","has_disclaimer":false,"patent_status":"INACTIVE","publication_count":2,"has_spc":false,"has_grant_event":true,"has_entry_into_national_phase":false},"abstract":{"en":[{"text":"The invention features methods diagnostic of a psychotic disorder such as bipolar disorder or schizophrenia. The methods include obtaining a cell sample from a subject, subjecting a cell from the sample to stress (e.g., nutrient stress), and measuring nucleic acid or polypeptide expression in the cell, where an alteration in expression is indicative of the subject having or being at increased risk of developing a psychotic disorder. The invention also features prognostic monitoring methods for subjects having a psychotic disorder, useful in determining the progression of a psychotic disorder in a subject or the effectiveness of a therapy.","lang":"en","source":"USPTO_FULLTEXT","data_format":"ORIGINAL"}]},"abstract_lang":["en"],"has_abstract":true,"claim":{"en":[{"text":"1. A method for diagnosing bipolar disorder in a subject, said method comprising the steps: (a) obtaining a cell sample from said subject, wherein said sample is a blood sample; (b) subjecting a cell from said sample to stress; and (c) measuring the level of expression in said cell of at least three nuclear encoded mitochondrial energy metabolism nucleic acids or polypeptides, wherein a decrease in said level of expression, as compared to the expression in a cell that is subjected to said stress from a sample obtained from a control subject, is indicative of said subject having bipolar disorder, wherein at least three of said nucleic acids or polypeptides are selected from the group consisting of NADH dehydrogenase (ubiquinone) 1 alpha subcomplex, 5, 13 kDa (NDUFA5; Entrez Gene ID:4698); NADH dehydrogenase (ubiquinone) 1 alpha subcomplex, 6, 14 kDa (NDUFA6; Entrez Gene ID:4700); NADH dehydrogenase (ubiquinone) 1 beta subcomplex, 1, 7 kDa (NDUFB1; Entrez Gene ID: 4707); ubiquinol-cytochrome c reductase binding protein (UQCRB; Entrez Gene ID: 7381); ubiquinol-cytochrome c reductase core protein II (UQCRC2; Entrez Gene ID: 7385); ubiquinol-cytochrome c reductase hinge protein (UQCRH; Entrez Gene ID: 7388); cytochrome c oxidase subunit IV isoform 1 (COX4I1; Entrez Gene ID: 1327); cytochrome c oxidase subunit VIIa polypeptide 2 like (COX7A2L; Entrez Gene ID: 9167); cytochrome c oxidase subunit VIIc (COX7C; Entrez Gene ID: 1350); COX11 homolog, cytochrome c oxidase assembly protein (yeast) (COX11; Entrez Gene ID: 1353); COX15 homolog, cytochrome c oxidase assembly protein (yeast) (COX15: Entrez Gene ID: 1355); ATP synthase, H+ transporting, mitochondrial F0 complex, subunit C2 (subunit 9) (ATP5G2; Entrez Gene ID: 517); ATP synthase, H+ transporting, mitochondrial F0 complex, subunit G (ATP5L; Gene ID: 10632); ATP synthase, H+ transporting, mitochondrial F1 complex, O subunit (ATP5O; Entrez Gene ID No: 539); and ATP synthase, H+ transporting, mitochondrial F0 complex, subunit s (factor B) (ATP5S; Entrez Gene ID No: 27109).","lang":"en","source":"USPTO_FULLTEXT","data_format":"ORIGINAL"},{"text":"2. A method for diagnosing bipolar disorder in a subject, said method comprising the steps: (a) obtaining a cell sample from said subject, wherein said cell sample comprises a lymphocyte; (b) subjecting a cell from said sample to stress; and (c) measuring the level of expression in said cell of at least three nuclear encoded mitochondrial energy metabolism nucleic acids or polypeptides, wherein a decrease in said level of expression, as compared to the expression in a cell that is subjected to said stress from a sample obtained from a control subject, is indicative of said subject having bipolar disorder, wherein at least three of said nucleic acids or polypeptides are selected from the group consisting of NADH dehydrogenase (ubiquinone) 1 alpha subcomplex, 5, 13 kDa (NDUFA5; Entrez Gene ID:4698); NADH dehydrogenase (ubiquinone) 1 alpha subcomplex, 6, 14 kDa (NDUFA6; Entrez Gene ID:4700); NADH dehydrogenase (ubiquinone) 1 beta subcomplex, 1, 7 kDa (NDUFB1; Entrez Gene ID: 4707); ubiquinol-cytochrome c reductase binding protein (UQCRB; Entrez Gene ID: 7381); ubiquinol-cytochrome c reductase core protein II (UQCRC2; Entrez Gene ID: 7385); ubiquinol-cytochrome c reductase hinge protein (UQCRH; Entrez Gene ID: 7388); cytochrome c oxidase subunit IV isoform 1 (COX4I1; Entrez Gene ID: 1327); cytochrome c oxidase subunit VIIa polypeptide 2 like (COX7A2L; Entrez Gene ID: 9167); cytochrome c oxidase subunit VIIc (COX7C; Entrez Gene ID: 1350); COX11 homolog, cytochrome c oxidase assembly protein (yeast) (COX11; Entrez Gene ID: 1353); COX15 homolog, cytochrome c oxidase assembly protein (yeast) (COX15: Entrez Gene ID: 1355); ATP synthase, H+ transporting, mitochondrial F0 complex, subunit C2 (subunit 9) (ATP5G2; Entrez Gene ID: 517); ATP synthase, H+ transporting, mitochondrial F0 complex, subunit G (ATP5L; Gene ID: 10632); ATP synthase, H+ transporting, mitochondrial F1 complex, O subunit (ATP5O; Entrez Gene ID No: 539); and ATP synthase, H+ transporting, mitochondrial F0 complex, subunit s (factor B) (ATP5S; Entrez Gene ID No: 27109).","lang":"en","source":"USPTO_FULLTEXT","data_format":"ORIGINAL"},{"text":"3. A method for diagnosing bipolar disorder in a subject, said method comprising the steps: (a) obtaining a cell sample from said subject; (b) subjecting a cell from said sample to glucose stress; and (c) measuring the level of expression in said cell of at least three nuclear encoded mitochondrial energy metabolism nucleic acids or polypeptides, wherein a decrease in said level of expression, as compared to the expression in a cell that is subjected to said stress from a sample obtained from a control subject, is indicative of said subject having bipolar disorder, wherein at least three of said nucleic acids or polypeptides are selected from the group consisting of NADH dehydrogenase (ubiquinone) 1 alpha subcomplex, 5, 13 kDa (NDUFA5; Entrez Gene ID:4698); NADH dehydrogenase (ubiquinone) 1 alpha subcomplex, 6, 14 kDa (NDUFA6; Entrez Gene ID:4700); NADH dehydrogenase (ubiquinone) 1 beta subcomplex, 1, 7 kDa (NDUFB1; Entrez Gene ID: 4707); ubiquinol-cytochrome c reductase binding protein (UQCRB; Entrez Gene ID: 7381); ubiquinol-cytochrome c reductase core protein II (UQCRC2; Entrez Gene ID: 7385); ubiquinol-cytochrome c reductase hinge protein (UQCRH; Entrez Gene ID: 7388); cytochrome c oxidase subunit IV isoform 1 (COX4I1; Entrez Gene ID: 1327); cytochrome c oxidase subunit VIIa polypeptide 2 like (COX7A2L; Entrez Gene ID: 9167); cytochrome c oxidase subunit VIIc (COX7C; Entrez Gene ID: 1350); COX11 homolog, cytochrome c oxidase assembly protein (yeast) (COX11; Entrez Gene ID: 1353); COX15 homolog, cytochrome c oxidase assembly protein (yeast) (COX15: Entrez Gene ID: 1355); ATP synthase, H+ transporting, mitochondrial F0 complex, subunit C2 (subunit 9) (ATP5G2; Entrez Gene ID: 517); ATP synthase, H+ transporting, mitochondrial F0 complex, subunit G (ATP5L; Gene ID: 10632); ATP synthase, H+ transporting, mitochondrial F1 complex, O subunit (ATP5O; Entrez Gene ID No: 539); and ATP synthase, H+ transporting, mitochondrial F0 complex, subunit s (factor B) (ATP5S; Entrez Gene ID No: 27109).","lang":"en","source":"USPTO_FULLTEXT","data_format":"ORIGINAL"},{"text":"4. A method for diagnosing bipolar disorder in a subject, said method comprising the steps: (a) obtaining a lymphocyte from said subject; (b) culturing said lymphocyte under glucose stress; and (c) measuring the level of expression in said lymphocyte of at least 15 nuclear encoded mitochondrial energy metabolism nucleic acids, wherein said nucleic acids comprise ATP synthase, mitochondrial F1 complex, O subunit (ATP5O; Entrez Gene ID: 539); cytochrome c oxidase subunit IV isoform 1 (COX4I1; Entrez Gene ID: 1327); and ubiquinol-cytochrome c reductase binding protein (UQCRB; Entrez Gene ID: 7381) and wherein a decrease in said level of expression, as compared to the expression in a lymphocyte obtained from a control subject that is cultured under glucose stress, is indicative of said subject having bipolar disorder.","lang":"en","source":"USPTO_FULLTEXT","data_format":"ORIGINAL"},{"text":"5. A method for diagnosing bipolar disorder in a subject, said method comprising the steps: (a) obtaining a lymphocyte from said subject; (b) culturing said lymphocyte under glucose stress; and (c) measuring the level of expression in said lymphocyte of at least 15 nuclear encoded mitochondrial energy metabolism nucleic acids of claim 4 , wherein said nucleic acids comprise ATP synthase, mitochondrial F1 complex, O subunit (ATP5O; Entrez Gene ID: 539); cytochrome c oxidase subunit IV isoform 1 (COX4I1; Entrez Gene ID: 1327); ubiquinol-cytochrome c reductase binding protein (UQCRB; Entrez Gene ID: 7381); ATP synthase, H+ transporting, mitochondrial F0 complex, subunit s (factor B) (ATP5S; Entrez Gene ID: 27109); and ubiquinol-cytochrome c reductase core protein II (UQCRC2; Entrez Gene ID: 7385) and wherein a decrease in said level of expression, as compared to the expression in a lymphocyte obtained from a control subject that is cultured under glucose stress, is indicative of said subject having bipolar disorder.","lang":"en","source":"USPTO_FULLTEXT","data_format":"ORIGINAL"}]},"claim_lang":["en"],"has_claim":true,"description":{"en":{"text":"CROSS-REFERENCE TO RELATED APPLICATIONS This application claims benefit of U.S. Provisional Application No. 60/801,313, filed May 18, 2006, and U.S. Provisional Application No. 60/928,151, entitled “Methods for Diagnosis and Prognosis of Psychotic Disorders,” filed May 7, 2007, Inventor Christine Konradi. Each of these applications is hereby incorporated by reference. BACKGROUND OF THE INVENTION The invention relates to diagnostic and prognostic methods for psychotic disorders such as bipolar disorder, schizophrenia, and other disorders characterized by abnormal expression of metabolic genes. Psychotic disorders such as bipolar disorder (BPD) are among the top ten causes of disability worldwide. BPD, in particular, is responsible for a national annual economic burden of over $40 billion (estimated in 1991). While the etiology of BPD and other psychotic disorders such as schizophrenia remain largely unknown, recent findings point to a disturbed mitochondrial energy metabolism in such subjects. BPD causes dramatic mood swings, affects between 1 to 3% of the population in the US and is associated with high risk of suicide. In the case of BPD, recent studies have shown decreased hippocampal (HIP) and dorsolateral prefrontal cortex (PFC) levels of creatine kinase mRNA, as well as decreased levels of high-energy phosphates in the frontal and temporal lobes of BPD patients, providing support for the idea that mitochondrial energy metabolism plays an important role in the etiology of the disease. Previously, a down-regulation in nuclear mRNA coding for mitochondrial electron transport proteins in post-mortem hippocampal tissue from patients with BPD had been reported. BPD, along with other psychotic disorders such as schizophrenia, are diagnosed based on the course of symptoms and family history, but the etiology of such disorders remains elusive. Previously, no clinical tests existed to verify diagnosis. Thus, there is a need for improved diagnostic and prognostic techniques for psychotic disorders. SUMMARY OF THE INVENTION The present invention features methods for diagnosing subjects with a psychotic disorder and prognostic methods for monitoring the progression or improvement of a subject having a psychotic disorder. Accordingly, in a first aspect the invention features a method for diagnosing a psychotic disorder (e.g., bipolar disorder, schizophrenia, or any psychotic disorder described herein) or propensity thereto in a subject including the steps of (a) obtaining a cellular sample, for example, a fluid sample (e.g., a blood sample) or tissue sample, from the subject; (b) subjecting a cell from the sample to stress, for example, nutrient stress (e.g., glucose stress), oxygen stress, temperature stress, or osmotic stress; and (c) measuring expression in the cell of at least one (e.g., 2, 3, 4, 5, 7, 10, 15, 25, 50, or 100) nucleic acid(s) or polypeptide(s) listed in Table 3, FIGS. 1 A(I)- 1 A(IV), or FIGS. 6A-6D where an alteration (e.g., a decrease) in the expression as compared to the expression in a corresponding cell from a cell sample taken from a control subject is indicative of the subject having a psychotic disorder or propensity thereto. In one embodiment, the cell sample includes a lymphocyte. In another embodiment, step (b) subjecting includes culturing the cell. In a second aspect, the invention features, a method for diagnosing a psychotic disorder (e.g., bipolar disorder, schizophrenia, or any psychotic disorder described herein) or propensity thereto in a subject, including the steps of (a) obtaining a cell sample, for example, a fluid sample (e.g., a blood sample) or tissue sample, from the subject; (b) subjecting a cell from the sample to stress, for example, nutrient stress (e.g., glucose stress), oxygen stress, temperature stress, or osmotic stress; and (c) measuring the level of expression in the cell of at least one (e.g., 2, 3, 4, 5, 7, 10, 15, 25, 50, or 100) mitochondrial energy metabolism nucleic acid(s) or polypeptide(s), where an alteration (e.g., a decrease) in the level of expression as compared to the expression in a cell from a sample obtained from a control subject is indicative of the subject having a psychotic disorder or propensity thereto. In one embodiment, the cell sample includes a lymphocyte. In another embodiment, step (b) subjecting includes culturing the cell. The invention also features prognostic methods for monitoring a psychotic disorder (e.g., bipolar disorder, schizophrenia, or any psychotic disorder described herein) in a subject having the disorder. The method including the steps of (a) obtaining a cell sample from the subject; (b) subjecting a cell from the sample to stress, for example, nutrient stress (e.g., glucose stress), oxygen stress, temperature stress, or osmotic stress; (c) measuring the level of expression in the cell of (i) at least one (e.g., 2, 3, 4, 5, 7, 10, 15, 25, 50, or 100) mitochondrial energy metabolism nucleic acid(s) or polypeptide(s) or (ii) at least one (e.g., 2, 3, 4, 5, 7, 10, 15, 25, 50, or 100) nucleic acid(s) or polypeptide(s) from in Table 3, FIGS. 1 A(I)- 1 (A)(IV), or FIGS. 6A-6D ; and (d) repeating steps (a)-(c) within five years, two years, or one year (e.g., within 6 months, 3 months, 2 months, one month, two weeks, or one week), thereby providing a second measurement of expression, where an alteration in the second measurement as compared to the level measured in step (c) is indicative of the progression of the psychotic disorder in the subject. The method may further include, between steps (c) and (d), a step of administering a therapy such as an anti-psychotic (e.g., those described herein) to the subject (e.g., where the therapy was not administered to the subject within two years, one year, or six months (e.g., within 6 months, 3 months, 2 months, one month, two weeks, or one week) prior to performing step (a))). By “subject” is meant either a human or non-human mammal. By “control subject” is meant a subject that does not have a psychotic disorder. By “stress,” in the context of stressing cells, is meant any condition resulting in a physiological strain on the cells as compared to standard cell culture conditions, as are known in the art. In some embodiments, these conditions include a reduced concentration of an essential nutrient (e.g., decreased glucose or sucrose concentrations), either increased or decreased oxygen conditions (e.g., as described herein), either increased or decreased temperature (e.g., as described herein), or either increased or decreased osmolarity (e.g., as described herein). By “biological sample” is meant any sample of biological origin or containing, or potentially containing, biological particles. In certain embodiments, biological samples are cellular samples. By “blood component” is meant any component of whole blood, including host red blood cells, white blood cells (e.g., lymphocytes), and platelets. Blood components also include the components of plasma, e.g., proteins, lipids, nucleic acids, and carbohydrates. By “cellular sample” is meant a sample containing cells or components thereof. Such samples include tissue samples (e.g., samples taken by biopsy from any organ or tissue in the body) and naturally occurring fluids (e.g., blood, lymph, cerebrospinal fluid, urine, cervical lavage, and water samples), portions of such fluids, and fluids into which cells have been introduced (e.g., culture media, and liquefied tissue samples). The term also includes a lysate. Any means for obtaining such a sample may be employed in the methods of the invention; the means by which the sample is obtaining is not critical to the invention. By “alteration in expression” is meant a change in expression level of a nucleic acid or polypeptide. This difference may be either an increase or a decrease in expression when compared to a control or baseline (e.g., a previous measurement). In certain embodiments, the increase or decrease is at least 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or 100%. An increase may further be at least 125%, 150%, 200%, 300%, or 500%. By “psychotic disorder” is meant a mental disorder characterized by psychosis which may involve cognitive problems, delusions, or hallucinations. Psychotic disorders include, without limitation, bipolar disorder, schizophrenia, schizoaffective disorder, schizophreniform disorder, shared psychotic disorder, and brief psychotic disorder. By “a bipolar disorder” is meant a mood or affective disorder characterized by pathological mood swings from mania to depression. The diagnostic criteria for a bipolar disorder (e.g., bipolar I: mania and depression; bipolar II: hypomania and depression; bipolar III: cyclothymic disorders; bipolar IV: hypomania or mania precipitated by antidepressant drugs; bipolar V: depressed patient with bipolar relatives; and bipolar VI: mania without depression) are known to the skilled artisan, and are described in the Diagnostic and Statistical Manual of Mental Disorders, DSM - IV, 1994, American Psychiatric Association. By “schizophrenia” is meant a severe brain disorder characterized by unusual thoughts or perceptions that include hallucinations, delusions, and thought disorder. Other symptoms may include a loss or a decrease in the ability to initiate plans, speak, express emotion, or find pleasure in everyday life. Schizophrenia may include cognitive deficits such as problems with attention, memory, and the ability to plan and organize. By “nuclear encoded mitochondrial energy metabolism nucleic acid molecule” is meant a polynucleotide, or fragment thereof, that naturally occurs in the nucleus and encodes a polypeptide that localizes to the mitochondria or that functions in mitochondrial energy metabolism. By “nuclear encoded mitochondrial energy metabolism polypeptide” is meant a protein, or fragment thereof, that functions in mitochondrial energy metabolism and is encoded by a nucleic acid molecule that naturally occurs in the cell nucleus. In some embodiments, the polypeptide functions in oxidative phosphorylation. Specifically excluded by this definition are mitochondrial genome encoded polypeptides. By “antipsychotic” is meant any pharmaceutical therapy capable of reducing or treating at least one symptom of a psychotic disorder. Antipsychotic include, without limitation, acetophenazine maleate, chlorpromazine hydrochloride, chlorprothixene, chlorprothixene hydrochloride, clozapine, fluphenazine decanoate, fluphenazine enathate, fluphenazine hydrochloride, haloperidol decanoate, haloperidol, haloperidol lactate, lithium carbonate, lithium citrate, loxapine hydrochloride, loxapine succinate, mesoridazine besylate, molindone hydrochloride, perphenazine, pimozide, proclorperazine maleate, proclorperazine, proclorperazine edisylate, promazine hydrochloride, risperidone, thioridazine, thioridazine hydrochloride, thiothixene, thiothixene hydrochloride, and trifluoperazine hydrochloride. Other features and advantages of the invention will be apparent from the following Detailed Description, the drawings, and the claims. BRIEF DESCRIPTION OF THE DRAWINGS The patent or application file contains at least one drawing executed in color. Copies of this patent or patent application publication with color drawing(s) will be provided by the Office upon request and payment of the necessary fee. FIGS. 1 A(I) through 1 D(IV) show the differential effects on expression of electron transport chain genes in lymphocytes taken from BPD patients as compared to controls cultured under normal and low glucose (stress) conditions. FIGS. 1 A(I) through 1 A(IV) show probe sets of the electron transport chain with a p<0.05 in low glucose BPD over controls (FIG. 1 A(I)), normal glucose BPD over controls (FIG. 1 A(II)), low over normal glucose controls (FIG. 1 A(III)), and low over normal glucose BPD (FIG. 1 A(IV)). FIG. 1 A(I) shows that seventeen transcripts were downregulated and none were upregulated. FIG. 1 A(II) shows that two transcripts (NADH dehydrogenase Fe—S protein 2 and COX VIIa 2 like) were downregulated and three transcripts (NADH dehydrogenase 1 alpha 5, COX IV-1 (213758_at), and COX VIIa 2) were upregulated. FIG. 1 A(III) shows eight transcripts were upregulated and none were downregulated. FIG. 1 A(IV) shows that six transcripts were downregulated and none were upregulated. Red indicates up-regulation, blue indicates down-regulation, and yellow indicates that no criteria were met. FIGS. 1 B(I) through 1 B(IV) show comparisons of regulated electron transport transcripts to all regulated transcripts (n=9399 non-redundant probe sets) in low glucose BPD over controls (FIG. 1 B(I)), normal glucose BPD over controls (FIG. 1 B(II)), low over normal glucose controls (FIG. 1 B(III)), and low over normal glucose BPD (FIG. 1 B(IV)). Redundant probe sets were masked; transcripts had to be present in at least 50% of all samples. FIGS. 1 C(I) through 1 C(IV) show that, of all probe sets on the array that were expressed in at least 50% of all samples (n14245), 114 coded for proteins involved in the electron transport chain. Expression levels of each individual probe set were compared between low glucose BPD and low glucose controls (FIG. 1 C(I)), normal glucose BPD and normal glucose controls (FIG. 1 C(II)), low and normal glucose controls (FIG. 1 C(III)) and low and normal glucose BPD ((FIG. 1 C(IV)). The solid green line marks equal regulation, the dashed red line shows the actual average regulation of all transcripts. FIGS. 1 D(I) through 1 D(IV) show real-time Q-rt-PCR analysis for low glucose BPD (n=15) versus controls (n=14; FIG. 1 D(I)), high glucose BPD (n=16) versus controls (n=15; FIG. 1 D(II)), high glucose versus low glucose controls (FIG. 1 D(III)), and high glucose versus low glucose BPD (FIG. 1 D(IV)). Four genes were used in the Q-rt-PCR verification: OSCP subunit of ATP synthase (ANOVA: p=0.006); ATP synthase subunit c (ANOVA: p=ns); ATP synthase subunit g (ANOVA: p=0.04); and cytochrome c oxidase IV isoform 1 (ANOVA: p=0.06). For each set, the averages of all four genes (ANOVA p<0.01) are also shown. Factorial ANOVA5 and Fisher's post hoc protected t-tests; *p≦0.05; **p≦0.01. FIG. 2 is a table showing sample information for BPD and normal control (NC) subjects used to generate the results described above. The following abbreviations are used in FIG. 2 : GL (low glucose-gene arrays); GN (normal glucose-gene arrays), PL (low glucose-Q-rt-PCR), PN (normal glucose-Q-rt-PCR), F (fresh lymphocytes); Li (lithium), VA (valproic acid), APD (antipsychotic drugs), AD (antidepressants), AC (anticonvulsants), w (white), a (Asian), m (male), and f (female). FIGS. 3A-3C show results in fresh, uncultured lymphocytes. FIG. 3A shows probe sets of the electron transport chain with a p<0.05 in BPD over controls in fresh lymphocytes. One transcript (NADH dehydrogenase 1 beta 7) was upregulated (indicated in red), and the six remaining transcripts were down-regulated (indicated in blue). FIG. 3B shows comparisons of regulated electron transport transcripts to all regulated transcripts (n=9399 non-redundant probe sets); BPD over controls in fresh lymphocytes. Redundant probe sets were masked; transcripts had to be present in at least 50% of all samples. FIG. 3C shows expression levels of the same 114 probe sets shown in FIG. 1 , which are compared between BPD and controls in fresh lymphocytes. The Enzo-IVT kit (Enzo Biochem, Farmingdale, N.Y.) was used for biotinylation, which is less efficient than the kits we used for cultured lymphocytes, and thus yielded lower gene expression intensities. FIGS. 4A-4E are graphs showing ANOVA data for BPD subjects to test for effects of Li ( FIG. 4A ), VPA ( FIG. 4B ), antiepileptics ( FIG. 4C ), antipsychotics ( FIG. 4D ), and antidepressants ( FIG. 4E ). Tables show ANOVA5 for samples grouped by glucose concentration (low versus normal), and ANOVA5 for interactions with drugs. Error bars represent a 95% confidence interval. FIG. 5 is a set of graphs showing pairwise comparison of 13 bipolar disorder (BPD) lymphocyte samples in normal and low-glucose medium (left) as well as 7 normal control (NC) lymphocyte samples in normal and low-glucose medium (right). Analysis of variance filtering (factorial analysis of variance, glucose concentration×treatment) was used to select electron transport transcripts with high variations between the groups. Fifteen transcripts survived the filtering and their logarithm-transformed values were averaged for each paired sample (n=13 for BPD; n=7 for NCs). Bipolar disorder lymphocytes showed a down-regulation of these transcripts under low-glucose stress (P≦0.003, paired t test), whereas NC lymphocytes showed an up-regulation of these transcripts (P≦0.02, paired t test). Dashed line indicates pair; solid line, average of group. FIGS. 6A-6E show individual B-cell and T-cell markers that were regulated in the comparison between low glucose for bipolar disorder lymphocytes and low glucose for normal control lymphocytes ( FIG. 6A ), normal glucose for bipolar disorder lymphocytes and normal glucose for control lymphocytes ( FIG. 6B ), low and normal glucose for normal control lymphocytes ( FIG. 6C ), and low and normal glucose for bipolar disorder lymphocytes ( FIG. 6D ). FIG. 6E shows P values of 1-way and factorial analyses (glucose level×treatment); shading indicates that the analysis of variance did not reach significance in both the 1-way and factorial analyses. FIGS. 7A-7D are graphs showing regulation of the entire group of 54 B-cell markers. Expression levels of each individual probe set were compared between low glucose for bipolar disorder lymphocytes and low glucose for normal control lymphocytes ( FIG. 7A ), normal glucose for bipolar disorder lymphocytes and normal glucose for normal control lymphocytes ( FIG. 7B ), low and normal glucose for normal control lymphocytes ( FIG. 7C ), and low and normal glucose for bipolar disorder lymphocytes ( FIG. 7D ). Solid line indicates equal regulation; dashed line, actual average regulation of all transcripts. See Table 9 for all GeneID numbers. FIGS. 8A-8D are graphs showing regulation of the entire group of 77 T-cell markers. Expression levels of each individual probe set were compared between low glucose for bipolar disorder lymphocytes and low glucose for normal control lymphocytes ( FIG. 8A ), normal glucose for bipolar disorder lymphocytes and normal glucose for normal control lymphocytes ( FIG. 8B ), low and normal glucose for normal control lymphocytes ( FIG. 8C ), and low and normal glucose for bipolar disorder lymphocytes (FIG. D). Solid line indicates equal regulation; dashed line, actual average regulation of all transcripts. See Table 9 for all GeneID numbers. DETAILED DESCRIPTION Previous work has identified numerous changes in expression levels of genes in the brains of subjects suffering from bipolar disorder as compared to normal control subjects. While such changes in expression provide a basis for developing diagnostic and prognostic assays for psychotic disorders such as BPD or schizophrenia, one of the challenges in developing a convenient and flexible assay has been identifying whether corresponding expression changes take place in non-neuronal as well as neuronal tissues. As outlined below, we have observed differential gene expression in lymphocytes of individuals diagnosed with BPD as compared to normal controls when the lymphocytes are subjected to stress. In particular, we identified genes involved in mitochondrial function as being differentially regulated in lymphocytes from BPD patients. Based on this discovery, the present invention features diagnostic and prognostic methods that include taking a cell sample from a patient, subjecting the cell from the sample to stress, followed by determining nucleic acid or polypeptide expression in the sample, where an alteration (e.g., a decrease) in expression (e.g., in the nucleic acids or polypeptides identified herein or nucleic acids or polypeptides involved in mitochondrial function) in a cell from the subject as compared to expression in a cell from a control subject indicates that the subject either has or has an increased propensity toward developing a psychotic disorder such as BPD or schizophrenia. Psychotic Disorders The diagnostic methods of the invention can be used with any psychotic disorder, including bipolar disorder (BPD) and schizophrenia. Other exemplary psychotic disorders include schizoaffective disorder, schizophreniform disorder, shared psychotic disorder, and brief psychotic disorder. As different psychotic disorders (e.g., BPD and schizophrenia) often share symptoms and a given patient may be diagnosed differently by different physicians or at different institutions, the diagnostic methods of the invention can accordingly be used with any psychotic disorder. Identification of Differentially Regulated Genes in Psychotic Disorders Previous work has identified genes differentially regulated in hippocampal tissue taken from deceased subjects with a bipolar disorder or schizophrenia (“diseased subjects”), as compared to tissue taken from deceased subjects free of mental illness (“control subjects”) (see U.S. patent application publication 2004/0248286, hereby incorporated by reference). Briefly, RNA from the hippocampal tissue was prepared, and expression levels of transcripts from diseased subjects was compared to that of control subjects. Differential expression of forty-three genes shown in Table 1 below between subjects with bipolar disorder as compared to control subjects were observed. TABLE 1Decreased Gene Expression in Bipolar Disorder (p < 0.01)GeneMap LocationfoldP valuePres %Mitochondrial1ATP synthase, mitochondrial F0 complex, subunit c, isoform 32q31.1−1.630.00061002VDAC1 pseudogene, porin protein, isoform 1X−1.410.0007943Ubiquinone-binding protein5q31.1−1.370.00111004ATP synthase, mitochondrial F0 complex, subunit d17q25−1.670.00111005Mitochondrial ribosomal protein L33q21-q23−1.460.00111006Cytochrome c oxidase subunit VIIbXq13.2−1.580.00131007ATP synthase, mitochondrial F0 complex, subunit f, isoform 27q11.21−1.480.00161008Dynamin 1-like12p12.1−1.660.0016689Voltage-dependent anion channel 2; porin10q22−1.400.001810010Cytochrome c oxidase subunit VIIa polypeptide 2 (liver)6q12−1.420.002110011ATP synthase, mitochondrial F1 complex, O subunit (OSCP)21q22.11−1.530.002510012Voltage-dependent anion channel 1; porin5q31−1.490.002910013Single-stranded DNA binding protein7q34−1.440.00309414Fumarate hydratase1q42.1−1.470.003610015Solute carrier family 25, member 44q35−1.530.003810016ATP synthase, mitochondrial F1 complex, gamma polypeptide 110q22-q23−1.460.004510017NADH dehydrogenase (ubiquinone) 1, alpha/beta subcomplex, 1, 8 kDa16p11.2−1.450.0053100183-oxoacid CoA transferase5p13−1.620.0089100Energy metabolism19UDP-glucose pyrophosphorylase 22p14-p13−1.440.001910020ATPase, lysosomal 70 kDa, V1 subunit A, isoform 13q13.31−1.540.00438921ATPase, lysosomal 34 kDa, V1 subunit D14−1.470.0056100Protein degradation22Sec61 gamma7p14.1−1.390.000910023Proteasome (prosome, macropain) 26S subunit, ATPase, 614q22.1−1.490.002110024Protein-L-isoaspartate (D-aspartate) O-methyltransferase6q24-q25−1.750.006510025F-box only protein 96p12.3-p11.2−1.680.0077100Neurotransmission26Somatostatin3q28−2.780.00628427Glutamic acid decarboxylase 672q31−1.800.0090100Structural proteins28Actin related protein 2/3 complex, subunit 3, 21 kDa12q24−1.490.000410029Beta-tubulin, beta2−1.470.001910030Actin-related protein 2 homolog (yeast)2p14−1.500.0022100Others31Macrophage migration inhibitory factor (MIF)−1.350.000710032Rho guanine nucleotide exchange factor (GEF) 42q22−1.390.001210033FSHD region gene 14q35−1.420.001410034Eukaryotic translation initiation factor 3 subunit 1119q13.2−1.530.002110035Ataxin-10 (spinocerebellar ataxia type 10 protein)22q13.31−1.670.002910036UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 611q12.1−1.500.003710037Contactin 1; glycoprotein gp13512q11-q12−1.770.00466338Endosulfine alpha, a regulator of beta-cell K(ATP) channels1q21.1−1.500.004810039Tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein8q23.1−1.540.006710040Chromosome 1 open reading frame 15; KIAA0479 protein1q25−1.670.00749441Arg protein tyrosine kinase binding protein−1.510.00767342Fk506-Binding Protein, Alt. Splice 2−1.470.00788443Glutamic-oxaloacetic transaminase 1, soluble (aspartate aminotransferase 1)10q24.1-q25.1−1.610.0084100 Eighteen of the genes (42%) identified above encode mitochondrial proteins, including subunits of the membrane-bound respiratory enzyme complexes that carry out oxidative phosphorylation in the mitochondrial inner membrane. The changes in gene expression observed in hippocampi from patients with bipolar disorder included a decrease in expression of one gene encoding a component of mitochondrial respiratory complex I, NADH dehydrogenase; a decrease in one gene encoding a component of complex IV, cytochrome c oxidase; and a decrease in five genes encoding components of complex V, ATP synthases. Functional descriptions of each of the genes in Table 1 are described in Table 2 below. TABLE 2Function of Down Regulated Genes (p < 0.01)TitleAccession No.LocalizationFunctiontyrosine 3-M86400cyoplasmicactivates tyrosine and tryptophan hydroxylases in themonooxygenase/tryptophan 5-presence of ca(2+)/calmodulin-dependent protein kinase ii,monooxygenase activationand strongly activates protein kinase c. is probably aprotein, zeta polypeptide;multifunctional regulator of the cell signaling processesHuman phospholipase A2mediated by both kinases. activates the adp-ribosyltransferase (exos) activity of bacterial origineukaryotic translation initiationAB019392binds to the 40s ribosome and promotes the binding offactor 3 subunit 11methionyl-trnai and mrna (by similarity)VDAC1 pseudogene (voltage-AJ002428mitochondrialdependent anion channelouter membrane(VDAC) of the outermitochondrial membrane);porin protein, isoform 1contactin 1; glycoprotein gp135Z21488peripheralmediates cell surface interactions during nervous systemplasmadevelopment. in association with cntnap1 seems to play amembrane;role in the formation of paranodal axo-glial junctions inattached to themyelinated peripheral nerves and may have a role in themembrane by asignaling between axons and myelinating glial cellsgpi-anchorchromosome 1 open readingAB007948cytoplasmicThis gene product belongs to the nicotinamideframe 15; KIAA0479 protein;mononucleotide adenylyltransferase (NMNAT) enzymenicotinamide mononucleotidefamily, members of which catalyze an essential step in NADadenylyltransferase 2(NADP) biosynthetic pathway.fumarate hydrataseU59309mitochondrialtricarboxylic acid cyclesolute carrier family 25J02966mitochondrialcatalyzes the exchange of adp and atp across the(mitochondrial carrier; adenineinner membranemitochondrial inner membranenucleotide translocator),member 4UDP-GlcNAc:betaGal beta-1,3-AF029893type iican initiate the synthesis or the elongation of the linear poly-N-membranen-acetyllactosaminoglycansacetylglucosaminyltransferaseprotein. golgi.6; i-beta-1,3-N-acetylglucosaminyltransferaseHomo sapiens beta 2; beta-X02344tubulinATPase, H+ transporting,AA877795lysosomalvacuolar ATPaselysosomal 34 kDa, V1 subunit D(V-ATPase), a multisubunit enzyme that mediatesacidification ofeukaryotic intracellular organelles.low molecular massAI540957mitochondrialcomponent of the ubiquinol-cytochrome c reductase complexubiquinone-binding proteininner membrane(complex iii or cytochrome b-c1 complex),(9.5 kD); ubiquinol-cytochromec reductase complexubiquinone-binding proteinATP synthase, H+ transporting,U09813mitochondrialATP synthase, H+ transportingmitochondrial F0 complex,inner membranesubunit c (subunit 9) isoform 3ATPase, H+ transporting,L09235vacuolarcatalytic subunit of the peripheral v1 complex of vacuolarlysosomal 70 kDa, V1 subunitatpase. v-atpase vacuolar atpase is responsible for acidifyingA, isoform 1a variety of intracellular compartments in eukaryotic cellsNADH dehydrogenaseAC002400mitochondrialcomplex i is composed of about 30 different subunits(ubiquinone) 1, alpha/betainner membranesubcomplex, 1, 8 kDaglutamic-oxaloaceticM37400cyoplasmicl-aspartate + 2-oxoglutarate = oxaloacetate + l-glutamatetransaminase 1, soluble(aspartate aminotransferase 1)ARP2 actin-related protein 2AF006082cytoskeletonpart of a complex implicated in the control of actinhomolog (yeast); one of sevenpolymerization in cellssubunits of the Arp2/3 proteincomplex; actin-related protein.ATP synthase, H+ transporting,AF087135mitochondrialthis is one of the chains of the nonenzymatic componentmitochondrial F0 complex,inner membrane(cf(0) subunit) of the mitochondrial atpase complex.subunit dactin related protein 2/3AI525393cytoplasmicpart of a complex implicated in the control of actincomplex, subunit 3, 21 kDapolymerization in cellsIdentification of ArgBP1, an ArgX95677cytoskeletonArg protein tyrosine kinase binding proteinprotein tyrosine kinase bindingprotein that is the humanhomologue of a CNS-specificXenopus geneRho guanine nucleotideAB029035exchange factor (GEF) 4cytochrome c oxidase subunitN50520mitochondrialVIIbinner membraneATP synthase, H+ transporting,X83218mitochondrialmitochondrial F1 complex, Oinner membranesubunit (oligomycin sensitivityconferring protein)glutamate decarboxylase 1M81883(brain, 67 kDa)UDP-glucoseU27460cyoplasmicplays a central role as a glucosyl donor in cellular metabolicpyrophosphorylase 2pathwaysvoltage-dependent anionL08666mitochondrialforms a channel through the mitochondrial outer membranechannel 2; porin, mitochondrialouter membranethat allows diffusion of small hydrophilic molecules. thechannel adopts an open conformation at low or zeromembrane potential and a closed conformation at potentialsabove 30-40 mv. the open state has a weak anion selectivitywhereas the closed state is cation-selectivemitochondrial ribosomal proteinX06323mitochondrialbelongs to the l3p family of ribosomal proteinsL3protein-L-isoaspartate (D-D25547cyoplasmiccatalyzes the methyl esterification of l-isoaspartyl and d-aspartate) O-methyltransferaseaspartyl residues in peptides and proteins that result fromspontaneous decomposition of normal l-aspartyl and l-asparaginyl residues. it plays a role in the repair and/ordegradation of damaged proteinssomatostatinJ00306secretedsomatostatin inhibits the release of somatotropinsingle-stranded DNA bindingAA768912mitochondrialthis protein binds preferentially and cooperatively to ss-dna.proteinprobably involved in mitochondrial dna replicationFSHD region gene 1L76159deleted in facioscapulohumeral muscular dystrophyF-box only protein 9AL031178probably recognizes and binds to some phosphorylatedproteins and promotes their ubiquitination anddegradation; The F-box proteins constitute one of the foursubunits ofthe ubiquitin protein ligase complex called SCFsendosulfine alpha, a regulatorX99906endogenous ligand for sulfonylurea receptor. by inhibitingof beta-cell K(ATP) channelssulfonylurea from binding to the receptor, it reduces k(atp)channel currents and thereby stimulates insulin secretionSec61 gamma; necessary forAF054184ERnecessary for protein translocation in the endoplasmicprotein translocation in thereticulumendoplasmic reticulumlike mouse brain protein E46;AL050282defects in sca10 are the cause of spinocerebellar ataxia typeataxin-10 (spinocerebellar10ataxia type 10 protein)ATP synthase, H+ transporting,D16562mitochondrialmitochondrial F1 complex,inner membranegamma polypeptide 1ATP synthase, H+ transporting,AF047436mitochondrialmitochondrial F0 complex,inner membranesubunit f, isoform 2voltage-dependent anionL06132mitochondrialPorin;channel 1; Outer membrane;outer membranePorin; Mitochondrion3-oxoacid CoA transferase;U62961mitochondrialkey enzyme for ketone body catabolism. transfers the coaMitochondrion; Transferasematrixmoiety from succinate to acetoacetate. formation of theenzyme-coa intermediate proceeds via an unstableanhydride species formed between the carboxylate groups ofthe enzyme and substratedynamin 1-like; This proteinAF000430mitochondrialThis proteinestablishes mitochondrialmatrixestablishes mitochondrial morphology through a role inmorphology through a role inCytoplasmdistributingdistributing mitochondrialmitochondrial tubules throughout the cytoplasm.tubules throughout thecytoplasm.cytochrome c oxidase subunitNM_001865mitochondrialcomplex IVVIIa polypeptide 2 (liver)inner membranemacrophage migrationL19686inhibitory factor (MIF)proteasome (prosome,D78275cytoplasmic andinvolved in the atp-dependent degradation of ubiquitinatedmacropain) 26S subunit,nuclearproteinsATPase, 6Fk506-Binding Protein, Alt.X52220Splice 2 Using a different statistical threshold (p<0.02), an additional two hundred sixty three genes were identified that are differentially expressed in patients having a bipolar disorder. Table 3 provides an inclusive list of the three hundred six genes identified as regulated in patients having bipolar disorder (p level<0.02; fold induction>1.2), their Genebank accession numbers, fold change, and p value. TABLE 4Function of Differentially Expressed Genes (p < 0.02)Gene DescriptionAccession #Fold ChangeP valuethymosin, beta 10M92383−1.310.01063Cluster Incl. S81916: phosphoglycerate kinase {alternatively spliced} [human,S81916−1.460.019787phosphoglycerate kinase deficient patient with episodes of muscl, mRNA PartialMutant, 307 nt] /cds = (0, 143)//ug = Hs.169313 /len = 307muscle specific geneAB019392−1.530.002077reticulon 4AB020693−1.280.013635voltage-dependent anion channel 1 pseudogeneAJ002428−1.410.000727p21 (CDKN1A)-activated kinase 3AF068864−1.530.016696p21 (CDKN1A)-activated kinase 3AF068864−1.550.014761similar to S. pombe dim1+AF023612−1.230.006959guanine nucleotide binding protein (G protein), alpha 13L220751.490.018088tubulin, beta, 2X02344−1.470.001895tubulin, beta, 2X02344−1.410.003694D-dopachrome tautomeraseAF012434−1.230.013399Cluster Incl. AL050065: Homo sapiens mRNA; cDNA DKFZp566M043 (from cloneAL0500651.270.000158DKFZp566M043) /cds = UNKNOWN /gb = AL050065 /gi = 4884295 /ug = Hs.212587/len = 1568keratin, hair, acidic, 3BX826341.240.012361tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, zetaU28964−1.390.007862polypeptideribosomal protein S7Z25749−1.220.017676KIAA0316 gene productAB002314−1.370.013021fibroblast growth factor 9 (glia-activating factor)D14838−1.290.014416Cluster Incl. X95677: H. sapiens mRNA for ArgBPIB protein /cds = (134, 1033)X95677−1.50.004338/gb = X95677 /gi = 1491701 /ug = Hs.169237 /len = 2374KIAA1032 proteinAB028955−1.450.004604tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, betaX57346−1.340.016325polypeptidepyruvate kinase, muscleM26252−1.220.012184dentatorubral-pallidoluysian atrophy (atrophin-1)U47924−1.340.005434DNA segment on chromosome 6(unique) 2654 expressed sequenceY18504−1.210.016847EGF-like-domain, multiple 4AB011541−1.30.008183acylphosphatase 2, muscle typeX84195−1.340.004579tachykinin, precursor 1 (substance K, substance P, neurokinin 1, neurokinin 2,U37529−3.120.011804neuromedin L, neurokinin alpha, neuropeptide K, neuropeptide gamma)ribosomal protein L10aAL022721−1.280.017343gamma-aminobutyric acid (GABA) A receptor, alpha 2S62907−1.40.007998potassium inwardly-rectifying channel, subfamily J, member 6U52153−1.370.018175GNAS complex locusX04409−1.230.015949GNAS complex locusX04409−1.280.004268somatostatinAI636761−2.740.006587RAD51-like 3 ( S. cerevisiae )AF0349561.320.011514guanine nucleotide binding protein (G protein), beta 5AF017656−1.360.007348KIAA0377 gene productAB002375−1.220.014708ribonuclease H1AF039652−1.280.008304neuropeptide YAI198311−1.840.017551NADH dehydrogenase (ubiquinone) 1 beta subcomplex, 1 (7 kD, MNLL)AI345944−1.390.004675FSHD region gene 1L76159−1.420.001405Cluster Incl. AA780435: ae93d06.s1 Homo sapiens cDNA, 3 end /clone = 1020491AA7804351.250.015387/clone_end = 3 /gb = AA780435 /gi = 2839766 /ug = Hs.204446 /len = 451T-box, brain, 1U492501.240.014785desmocollin 2X568071.220.005732amyloid beta (A4) precursor protein-binding, family A, member 2 (X11-like)AF047348−1.320.007039Cluster Incl. AL050204: Homo sapiens mRNA; cDNA DKFZp586F1223 (from cloneAL0502041.240.015298DKFZp586F1223) /cds = UNKNOWN /gb = AL050204 /gi = 4884443 /ug = Hs.28540/len = 1634chloride intracellular channel 2Y126961.210.003863chemokine (C-X3-C) receptor 1U20350−2.420.017113Cluster Incl. AI659108: tu08c09.x1 Homo sapiens cDNA, 3 end /clone = IMAGE-AI659108−1.280.0166052250448 /clone_end = 3 /gb = AI659108 /gi = 4762678 /ug = Hs.99093 /len = 492DKFZP566B183 proteinAL050272−1.580.019681v-myb myeloblastosis viral oncogene homolog (avian)M136661.230.004209contactin 1Z21488−1.790.004286chromosome 1 open reading frame 15AB007948−1.790.006118sortilin-related receptor, L(DLR class) A repeats-containingY08110−1.340.010094down-regulator of transcription 1, TBP-binding (negative cofactor 2)M97388−1.240.003746vesicle-associated soluble NSF attachment protein receptor (v-SNARE; homolog ofAF060902−1.280.003184S. cerevisiae VTI1)neuronal proteinW28770−1.660.011113putatative 28 kDa proteinL48692−1.360.019003Cluster Incl. AL109702: Homo sapiens mRNA full length insert cDNA cloneAL109702−1.230.007009EUROIMAGE 42138 /cds = UNKNOWN /gb = AL109702 /gi = 5689811 /ug = Hs.19720/len = 1869ubiquitin-conjugating enzyme E2M (UBC12 homolog, yeast)AF075599−1.220.001561kinesin family member 3BAB002357−1.320.006715eukaryotic translation elongation factor 1 alpha 2X70940−1.340.015877RNA 3′-terminal phosphate cyclaseY11651−1.280.01692proline-rich Gla (G-carboxyglutamic acid) polypeptide 1AF0092421.220.019808necdin homolog (mouse)U35139−1.410.014012src family associated phosphoprotein 2AF051323−1.370.006528excision repair cross-complementing rodent repair deficiency, complementation groupM13194−1.210.0034251 (includes overlapping antisense sequence)Rho guanine nucleotide exchange factor (GEF) 4AB029035−1.390.001221U6 snRNA-associated Sm-like protein LSm7AA121509−1.320.010447glutamate decarboxylase 1 (brain, 67 kD)M81883−1.840.008965paraneoplastic antigen MA2AB020690−1.390.018583programmed cell death 6AF035606−1.330.004502cytoplasmic FMRP interacting protein 2L47738−1.220.01979ATP synthase, H+ transporting, mitochondrial F1 complex, delta subunitAI436567−1.270.002319transcription elongation factor A (SII)-like 1M99701−1.20.016432Cluster Incl. AL049321: Homo sapiens mRNA; cDNA DKFZp564D156 (from cloneAL0493211.270.019168DKFZp564D156) /cds = UNKNOWN /gb = AL049321 /gi = 4500094 /ug = Hs.9927/len = 1440NADH dehydrogenase (ubiquinone) Fe—S protein 4 (18 kD) (NADH-coenzyme QAA203303−1.420.009172reductase)chromosome 14 open reading frame 2AF054175−1.320.002134NADH dehydrogenase (ubiquinone) 1 beta subcomplex, 3 (12 kD, B12)AA203354−1.360.008742Cluster Incl. AL031178: Human DNA sequence from clone 341E18 on chromosomeAL031178−1.680.0076846p11.2-12.3. Contains a Serine/Threonine Protein Kinase gene (presumptive isologof a Rat gene) and a novel alternatively spliced gene. Contains a putative CpG island,ESTs and GSSsCluster Incl. N98670: yy66d08.r1 Homo sapiens cDNA, 5 end /clone = IMAGE-278511N98670−1.270.008167/clone_end = 5 /gb = N98670 /gi = 1270092 /ug = Hs.111632 /len = 574endosulfine alphaAI658639−1.30.010107endosulfine alphaX99906−1.550.001717microsomal glutathione S-transferase 3AF026977−1.390.001451proteasome (prosome, macropain) subunit, beta type, 7D38048−1.280.004323non-metastatic cells 1, protein (NM23A) expressed inAL038662−1.650.008898DR1-associated protein 1 (negative cofactor 2 alpha)AI991040−1.280.002766ADP-ribosylation factor 3M74491−1.210.012197methionine-tRNA synthetaseX94754−1.20.004773HMT1 hnRNP methyltransferase-like 1 ( S. cerevisiae )X99209−1.210.018481glypican 3U504101.230.005816putative breast adenocarcinoma marker (32 kD)AF042384−1.210.009768KIAA0935 proteinAB023152−1.240.009612microtubule-associated proteins 1A/1B light chain 3W28807−1.270.002703cytochrome c oxidase subunit VbM19961−1.290.003535like mouse brain protein E46AL050282−1.670.002917P311 proteinU30521−1.30.017844nuclear receptor co-repressor 1AF044209−1.210.010503cullin 1U58087−1.310.002505peroxiredoxin 2L19185−1.310.007342nascent-polypeptide-associated complex alpha polypeptideAF054187−1.240.013613polymerase (RNA) II (DNA directed) polypeptide B (140 kD)X63563−1.30.005797proteasome (prosome, macropain) 26S subunit, non-ATPase, 4U51007−1.220.010387protein phosphatase 3 (formerly 2B), catalytic subunit, beta isoform (calcineurin AM29551−1.450.013912beta)ATPase, Ca++ transporting, cardiac muscle, slow twitch 2M23115−1.40.011465KIAA0090 proteinD420441.210.01314ATP synthase, H+ transporting, mitochondrial F1 complex, alpha subunit, isoform 1,D14710−1.380.001708cardiac musclealdolase C, fructose-bisphosphateAF054987−1.290.01524isocitrate dehydrogenase 3 (NAD+) betaAA522698−1.260.004632ATP synthase, H+ transporting, mitochondrial F1 complex, gamma polypeptide 1D16562−1.460.004519ATP synthase, H+ transporting, mitochondrial F0 complex, subunit f, isoform 2AF047436−1.480.001591dynactin 3 (p22)W26651−1.250.014741solute carrier family 25 (mitochondrial carrier; adenine nucleotide translocator),J03592−1.280.008112member 6transcriptional activator of the c-fos promoterD54318−1.410.004007transcriptional activator of the c-fos promoterU49857−1.360.013221serologically defined breast cancer antigen 84AF091085−1.240.004593glutamic-oxaloacetic transaminase 2, mitochondrial (aspartate aminotransferase 2)M22632−1.260.019781RNA binding motif protein 8AAL049219−1.220.00522isoleucine-tRNA synthetaseU04953−1.320.01167cytochrome c oxidase subunit VIbT57872−1.290.005962glycogeninU31525−1.250.019465melanoma antigen, family D, 1W26633−1.410.0057743-oxoacid CoA transferaseU62961−1.620.008802dynamin 1-likeAF000430−1.660.001584phosphoglycerate mutase 1 (brain)J04173−1.230.013865cytochrome c oxidase subunit VaM22760−1.40.00763leucine-rich PPR-motif containingM92439−1.310.015861cytochrome c oxidase subunit VIIa polypeptide 2 (liver)AA978033−1.420.00198ATX1 antioxidant protein 1 homolog (yeast)U70660−1.230.009151v-Ki-ras2 Kirsten rat sarcoma 2 viral oncogene homologL00049−1.360.006442eukaryotic translation initiation factor 3, subunit 2 (beta, 36 kD)U39067−1.210.014181NADH dehydrogenase (ubiquinone) 1 beta subcomplex, 8 (19 kD, ASHI)AI541050−1.220.011804solute carrier family 25 (mitochondrial carrier; adenine nucleotide translocator),J02966−1.530.003831member 4translocase of inner mitochondrial membrane 17 homolog A (yeast)X97544−1.260.001239chromogranin B (secretogranin 1)Y00064−2.090.011271lactate dehydrogenase BX13794−1.210.003571ATPase, H+ transporting lysosomal (vacuolar proton pump), member MAA877795−1.350.009456glutathione peroxidase 4 (phospholipid hydroperoxidase)X71973−1.230.013006low molecular mass ubiquinone-binding protein (9.5 kD)AI540957−1.370.00106palmitoyl-protein thioesterase 1 (ceroid-lipofuscinosis, neuronal 1, infantile)U44772−1.390.00881nardilysin (N-arginine dibasic convertase)X93209−1.210.011077ATP synthase, H+ transporting, mitochondrial F0 complex, subunit c (subunit 9)U09813−1.630.000557isoform 3ceroid-lipofuscinosis, neuronal 3, juvenile (Batten, Spielmeyer-Vogt disease)AC002544−1.240.006393CGI-51 proteinAL035398−1.260.001213seryl-tRNA synthetaseX91257−1.40.008777melanoma antigen, family D, 2Z98046−1.230.007847ATPase, H+ transporting, lysosomal (vacuolar proton pump), alpha polypeptide,L09235−1.540.0043370 kD, isoform 1NADH dehydrogenase (ubiquinone) Fe—S protein 3 (30 kD) (NADH-coenzyme QAF067139−1.340.001686reductase)golgi associated, gamma adaptin ear containing, ARF binding protein 2AC002400−1.450.005359GDP dissociation inhibitor 2Y13286−1.310.01581Ras-related GTP-binding proteinU41654−1.390.009322meningioma expressed antigen 5 (hyaluronidase)AB014579−1.260.011112Cluster Incl. AF055023: Homo sapiens clone 24723 mRNA sequenceAF0550231.260.004067/cds = UNKNOWN /gb = AF055023 /gi = 3005751 /ug = Hs.58220 /len = 1834glutamic-oxaloacetic transaminase 1, soluble (aspartate aminotransferase 1)M37400−1.610.008363COP9 (constitutive photomorphogenic, Arabidopsis, homolog) subunit 3AF031647−1.260.009059ribosomal protein L3AL022326−1.380.010345amyloid beta precursor protein binding protein 1, 59 kDU50939−1.260.005884ARP2 actin-related protein 2 homolog (yeast)AF006082−1.50.002224succinate dehydrogenase complex, subunit B, iron sulfur (lp)U17886−1.230.005271ATP synthase, H+ transporting, mitochondrial F0 complex, subunit dAF087135−1.670.001078Cluster Incl. AA527880: nh86h10.s1 Homo sapiens cDNA, 3 end /clone = IMAGE-AA527880−1.230.011144965443 /clone_end = 3 /gb = AA527880 /gi = 2269949 /ug = Hs.661 /len = 568actin related protein 2/3 complex, subunit 3 (21 kD)AI525393−1.490.000404polymerase (RNA) II (DNA directed) polypeptide L (7.6 kD)N24355−1.240.000766voltage-dependent anion channel 3AF038962−1.30.009254ubiquinol-cytochrome c reductase hinge proteinAA526497−1.370.002659ATP synthase, H+ transporting, mitochondrial F0 complex, subunit F6AA845575−1.390.003637proteasome (prosome, macropain) subunit, alpha type, 6X59417−1.370.003532dynactin 1 (p150, glued homolog, Drosophila)AF086947−1.230.016308protein tyrosine phosphatase, receptor type, N polypeptide 2U81561−1.410.019536cytochrome c oxidase subunit VIcW51774−1.430.003852NADH dehydrogenase (ubiquinone) 1 alpha subcomplex, 1 (7.5 kD, MWFE)N47307−1.340.004606tubulin-specific chaperone cU61234−1.240.003964low density lipoprotein-related protein-associated protein 1 (alpha-2-macroglobulinM63959−1.20.013075receptor-associated protein 1)glyoxalase ID13315−1.320.012924glycyl-tRNA synthetaseU09510−1.270.012995glycyl-tRNA synthetaseU09510−1.320.011219aldo-keto reductase family 1, member B1 (aldose reductase)X15414−1.350.004964nucleolar and coiled-body phosphprotein 1D21262−1.240.002917cytochrome c oxidase subunit VIIbN50520−1.560.001375coatomer protein complex, subunit alphaU24105−1.320.01774ATP synthase, H+ transporting, mitochondrial F1 complex, O subunit (oligomycinX83218−1.480.001619sensitivity conferring protein)dynein, cytoplasmic, heavy polypeptide 1AB002323−1.280.012195uncharacterized bone marrow protein BM036AI057607−1.260.005077farnesyl diphosphate synthase (farnesyl pyrophosphate synthetase,D14697−1.320.016932dimethylallyltranstransferase, geranyltranstransferase)NADH dehydrogenase (ubiquinone) flavoprotein 1 (51 kD)AF053070−1.250.012356ATPase, H+ transporting, lysosomal (vacuolar proton pump) 31 kDX76228−1.40.010499UDP-glucose pyrophosphorylase 2U27460−1.440.001884ATPase, vacuolar, 14 kDD49400−1.270.001322inner membrane protein, mitochondrial (mitofilin)L42572−1.220.017318DEAD/H (Asp-Glu-Ala-Asp/His) box polypeptide 1X70649−1.370.005672uroporphyrinogen decarboxylaseAF104421−1.290.005848complement component 1, q subcomponent binding proteinM69039−1.330.00363solute carrier family 25 (mitochondrial carrier; phosphate carrier), member 3X60036−1.350.008737Cluster Incl. L08666: Homo sapiens porin (por) mRNA, complete cds and truncatedL08666−1.350.010491cds /cds = UNKNOWN /gb = L08666 /gi = 190199 /ug = Hs.78902 /len = 1464mitochondrial ribosomal protein L3X06323−1.430.000177protein-L-isoaspartate (D-aspartate) O-methyltransferaseD25547−1.750.006481proteasome (prosome, macropain) 26S subunit, ATPase, 5AF035309−1.230.010559IK cytokine, down-regulator of HLA IIAJ005579−1.250.00818hepatitis B virus x-interacting protein (9.6 kD)AF029890−1.30.009123NADH dehydrogenase (ubiquinone) Fe—S protein 5 (15 kD) (NADH-coenzyme QAI541336−1.270.012446reductase)ATP synthase, H+ transporting, mitochondrial F0 complex, subunit c (subunit 9),X69907−1.280.004027isoform 1cytochrome c oxidase subunit VIIIAI525665−1.220.003607chromobox homolog 3 (HP1 gamma homolog, Drosophila)AI740522−1.260.003802proteasome (prosome, macropain) subunit, alpha type, 1M64992−1.310.017706Cluster Incl. U66042: Human clone 191B7 placenta expressed mRNA fromU66042−1.20.002954chromosome X /cds = UNKNOWN /gb = U66042 /gi = 1519267 /ug = Hs.82171 /len = 1327glutathione synthetaseU34683−1.230.014357peroxiredoxin 4U25182−1.280.014485Sjogren syndrome antigen B (autoantigen La)X69804−1.220.01958hypothetical protein MGC10715AL049650−1.220.016112peptidylglycine alpha-amidating monooxygenaseM37721−1.390.016292dynactin 2 (p50)U50733−1.230.013766single-stranded DNA-binding protein 1AA768912−1.420.003143single-stranded DNA-binding protein 1AA768912−1.30.014364eukaryotic translation initiation factor 4BX55733−1.20.014218GCN5 general control of amino-acid synthesis 5-like 1 (yeast)AI525379−1.370.001552nitrogen fixation cluster-likeU47101−1.290.018877Sec61 gammaAF054184−1.390.000911transcription elongation factor B (SIII), polypeptide 2 (18 kD, elongin B)AI857469−1.250.004063ectonucleoside triphosphate diphosphohydrolase 6 (putative function)AL035252−1.240.00585cutaneous T-cell lymphoma-associated tumor antigen se20-4; differentially expressedAB015345−1.280.010929nucleolar TGF-beta1 target protein (DENTT)SET translocation (myeloid leukemia-associated)M93651−1.270.007058voltage-dependent anion channel 1L06132−1.490.00374NADH dehydrogenase (ubiquinone) 1 alpha subcomplex, 2 (8 kD, B8)AF047185−1.270.002062eukaryotic translation elongation factor 1 epsilon 1AF054186−1.330.017208hypothetical proteinH15872−1.270.011372Cluster Incl. AI382123: te30a09.x1 Homo sapiens cDNA, 3 end /clone = IMAGE-AI382123−1.430.012272087416 /clone_end = 3 /gb = AI382123 /gi = 4194904 /ug = Hs.182919 /len = 857SWI/SNF related, matrix associated, actin dependent regulator of chromatin,D26155−1.360.002574subfamily a, member 2KIAA0447 gene productAB007916−1.220.018871JTV1 geneU24169−1.230.01197thyroid hormone receptor interactor 3L40410−1.310.007183KIAA1049 proteinAB028972−1.370.003695integral membrane protein 2BAA477898−1.320.008173lactate dehydrogenase AX02152−1.370.009983protein phosphatase 1, regulatory subunit 7Z50749−1.360.001411adaptor-related protein complex 1, sigma 2 subunitAF091077−1.380.015644Cluster Incl. AA203545: zx59a05.r1 Homo sapiens cDNA, 5 end /clone = IMAGE-AA203545−1.290.018083446768 /clone_end = 5 /gb = AA203545 /gi = 1799271 /ug = Hs.56876 /len = 568emopamil binding protein (sterol isomerase)Z37986−1.20.013307fumarate hydrataseU59309−1.470.003497protein translocation complex betaAA083129−1.210.009925proteasome (prosome, macropain) 26S subunit, non-ATPase, 8D38047−1.30.014744regulator of G-protein signalling 10AF045229−1.30.002964UDP-GlcNAc: betaGal beta-1,3-N-acetylglucosaminyltransferase 6AF029893−1.50.003738proteasome (prosome, macropain) subunit, beta type, 4D26600−1.390.004463ras-related C3 botulinum toxin substrate 1 (rho family, small GTP binding proteinM29870−1.260.012621Rac1)APEX nuclease (multifunctional DNA repair enzyme)M80261−1.20.007584S-phase kinase-associated protein 1A (p19A)U33760−1.420.002275non-metastatic cells 1, protein (NM23A) expressed inX73066−1.230.010548RAN, member RAS oncogene familyM31469−1.40.007467COP9 (constitutive photomorphogenic, Arabidopsis, homolog) subunit 5U65928−1.380.002999platelet-derived growth factor receptor, alpha polypeptideM215741.270.007996mitogen-activated protein kinase 10U07620−1.210.00607neural precursor cell expressed, developmentally down-regulated 8D23662−1.230.011055Ras homolog enriched in brain 2D78132−1.20.004309ubiquitin-conjugating enzyme E2N (UBC13 homolog, yeast)D83004−1.330.003258RAP1, GTP-GDP dissociation stimulator 1X63465−1.540.009557Melanoma-associated antigen recognised by cytotoxic T lymphocytesU19796−1.220.010698U50535 /FEATURE = /DEFINITION = HSU50535 Human BRCA2 region, mRNAU505351.230.009684sequence CG006protein tyrosine phosphatase, receptor type, AM34668−1.250.015648heat shock protein 75U12595−1.310.005772proteasome (prosome, macropain) subunit, alpha type, 2D00760−1.30.008858proteasome (prosome, macropain) subunit, alpha type, 3D00762−1.390.012143somatostatinJ00306−1.310.012147transcription elongation factor B (SIII), polypeptide 1 (15 kD, elongin C)L34587−1.320.00108replication protein A1 (70 kD)M63488−1.250.01319X14675 /FEATURE = cds /DEFINITION = HSBCR3C Human bcr-abl mRNA 5 fragmentX146751.270.011268(clone 3c)retinoblastoma binding protein 4X74262−1.210.013161proteasome (prosome, macropain) subunit, beta type, 3D26598−1.240.000943proteasome (prosome, macropain) subunit, beta type, 2D26599−1.310.005831proteasome (prosome, macropain) subunit, beta type, 4D26600−1.330.001273proteasome (prosome, macropain) 26S subunit, non-ATPase, 8D38047−1.30.004844proteasome (prosome, macropain) subunit, beta type, 7D38048−1.350.002867proteasome (prosome, macropain) 26S subunit, non-ATPase, 1D44466−1.360.001895tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, zetaM86400−1.470.010563polypeptidecyclin-dependent kinase 5X66364−1.270.017644proteasome (prosome, macropain) 26S subunit, non-ATPase, 11AB003102−1.360.005788neuregulin 1L122601.210.009292histidine triad nucleotide binding proteinU51004−1.290.009004proteasome (prosome, macropain) 26S subunit, ATPase, 6D78275−1.490.002007Fk506-Binding Protein, Alt. Splice 2X52220−1.320.013334glycosylphosphatidylinositol specific phospholipase D1L117021.20.000988macrophage migration inhibitory factor (glycosylation-inhibiting factor)L19686−1.360.000667FK506 binding protein 1A (12 kD)M34539−1.250.008632ubiquitin carrier proteinM91670−1.280.014471glutathione-S-transferase like; glutathione transferase omegaU90313−1.30.015862v-crk sarcoma virus CT10 oncogene homolog (avian)D10656−1.240.018048GDP dissociation inhibitor 2D13988−1.240.008673protease, serine, 11 (IGF binding)D87258−1.210.019954proteasome (prosome, macropain) 26S subunit, ATPase, 1L02426−1.210.010531RAB5A, member RAS oncogene familyM28215−1.240.013948proteasome (prosome, macropain) 26S subunit, ATPase, 3M34079−1.260.001283polymerase (RNA) II (DNA directed) polypeptide L (7.6 kD)U37690−1.270.000267tubulin, beta, 4U47634−1.380.008012tubulin, beta, 5X00734−1.370.008912casein kinase 2, beta polypeptideX57152−1.240.013439dynamin 1-likeAF000430−1.30.009226basic transcription factor 3X53280−1.20.017502tubulin, alpha 1 (testis specific)X06956−1.670.011897microtubule-associated protein tauJ03778−1.310.002685ubiquinol-cytochrome c reductase core protein IL16842−1.40.004071H2A histone family, member OL19779−1.220.012995calcium/calmodulin-dependent protein kinase IL41816−1.290.007763S-adenosylmethionine decarboxylase 1M21154−1.280.019389protein kinase, cAMP-dependent, regulatory, type I, alpha (tissue specific extinguisherM33336−1.30.0125611)protein kinase, cAMP-dependent, regulatory, type I, alpha (tissue specific extinguisherM33336−1.330.0136021)IK cytokine, down-regulator of HLA IIS74221−1.230.012642ubiquitin-conjugating enzyme E2L 3S81003−1.290.011308aconitase 2, mitochondrialU87939−1.260.011241 Expression of any polynucleotide, the corresponding polypeptide, or any combination thereof identified in Tables 1, 2, or 3, in FIGS. 1 A(I)- 1 A(IV), or in FIGS. 6A-6D may be used as the basis for diagnostic or prognostic assays of the invention. Further, as many of the genes identified herein are involved in mitochondrial energy metabolism, expression of any gene whose polypeptide product is localized to the mitochondria and involved in energy metabolism may be used in the diagnostic and prognostic methods of the invention. Stressing Cells The diagnostic methods of the invention feature a step of stressing cells in a sample taken from a subject. Any technique for stressing cells known in the art may be used; such techniques include nutrient stress, oxygen stress, temperature stress, osmotic stress, or a combination thereof. Nutrient stress can be achieved by subjecting cells to a lower availability of a vital nutrient such as glucose or sucrose as compared to standard cell culture conditions. For example, in the lymphocyte culture using RPMI-1640 media described herein, glucose is normally present at 2 g/l. Here, glucose depravation can accordingly be provided by culturing cells at reduced glucose concentrations (e.g., less than 2, 1.5, 1, 0.75, 0.5, 0.25, 0.1, or 0.05 g/l glucose). Nutrient stress, in any cell culture media system, can be achieved by a similar reduction of a vital nutrient. Oxygen stress can be induced by either increasing or decreasing the oxygen available to cultured cells (e.g., pO 2 is generally 10-80 mm in normal tissues). Oxygen stress can be induced by decreasing the pO 2 to an amount lower than is normally observed, e.g., less than 40, 30, 20, 10, 5, 2, or 1 mm pO 2 or increasing the pO 2 above the normal levels, e.g., greater than 80, 90, 100, 110, 120, 130, 150, 170 mm pO 2 . In another example, standard culture conditions typically include a 5% CO 2 :20% O 2 :75% N 2 atmosphere. By altering oxygen concentration, e.g., cultured in a reduced oxygen environment, where oxygen levels are less than 19%, 15%, 10%, 5%, 2%, or 1%, or in an increased oxygen environment, e.g., at least 21%, 23%, 25%, 28%, 30%, or 35% oxygen, the cells can be stressed. Stress can also be induced by culturing cells at increased or decreased temperature. Typically, cells are cultured at 37° C. Low temperature stress can be induced by culturing at a temperature less than 35, 34, 32, 30, 28, 25, 22, or 20° C. Increased temperatures can involve culturing cells at, e.g., at least 39, 40, 42, 44, 46, 48, or 50° C. Stress can also be induced by culturing cells at altered osmolarity, either by increasing or decreasing salt levels as compared to control samples. The salt which is increased or decreased will depend on the particular type of cell being cultured and the culture medium being used. Any biologically compatible salt known in the art can be added or any salt normally found in culture media can be removed to generate osmotic stress. In one example, using a lymphocyte culture as described below which employs RPMI-1640 media, the concentration of sodium chloride, which is normally 6 g/l, can be increased (e.g., at least 7, 8, 9, 10, 12, 15, or 20 g/l) or decreased (e.g., less than 5.5, 5, 4, 3, 2, 1, 0.5, 0.25 g/l) to produce osmotic stress. An appropriate duration of a stress depends on the severity of the particular stress employed, and can be determined by one of skill in the art. Typically, the stress can be employed for at least 6, 12, 18, or 24 hours or at least 2, 3, 5, 6, 7, 10, 14, or 21 days. If multiple stresses are simultaneously employed (e.g., nutrient and temperature stress), either the length or severity of each individual stress required for diagnosis of a psychotic disorder can be reduced. Measuring Gene or Protein Expression Expression levels of particular nucleic acids or polypeptides can be correlated with a particular disease state, and thus are useful in diagnosis. Expression levels can be measured using any technique known in the art. The skilled artisan will understand that the particular method employed for measuring expression is not critical to the invention. In one embodiment, a patient having a psychotic disorder (e.g., BPD or schizophrenia) will show an alteration in the expression of at least one of the nucleic acids listed in Table 1, Table 3, in FIGS. 1 A(I)- 1 A(IV), or in FIGS. 6A-6D . In another embodiment, a patient having a psychotic disorder will have a particular expression profile that includes significantly decreased expression of two or more nuclear encoded mitochondrial metabolism nucleic acid molecules or proteasome associated nucleic acid molecules (e.g., those listed in Table 1, Table 3, in FIGS. 1 A(I)- 1 A(IV), or in FIGS. 6A-6D ) as compared to a normal control. Alterations in gene expression are detected using methods known to the skilled artisan and described herein. In one embodiment, oligonucleotides or longer fragments derived from any of the nucleic acid sequences described herein (e.g., those listed in Table 1, Table 3, in FIGS. 1 A(I)- 1 A(IV), or in FIGS. 6A-6D ) may be used as targets in a microarray. The microarray is used to assay the expression level of large numbers of genes simultaneously and to identify genetic variants, mutations, and polymorphisms. Such information can be used to diagnose a psychotic disorder (e.g., BPD or schizophrenia). In another embodiment, an alteration in the expression of a nucleic acid sequence described herein (e.g., those listed in Table 1, Table 3, in FIGS. 1 A(I)- 1 A(IV), or in FIGS. 6A-6D ) is detected using real-time quantitative PCR (Q-rt-PCR) to detect changes in gene expression. Q-rt-PCR methods are known in the art and are described herein. In another embodiment, an antibody that specifically binds a polypeptides encoded by a nucleic acid described herein (e.g., listed in Table 1, Table 3, in FIGS. 1 A(I)- 1 A(IV), or in FIGS. 6A-6D ) may be used for the diagnosis of a psychotic disorder (e.g., BPD or schizophrenia). A variety of protocols for measuring an alteration in the expression of such polypeptides are known, including immunological methods (such as ELISAs and RIAs), and provide a basis for diagnosing a psychotic disorder (e.g., BPD or schizophrenia). Again, a decrease in the level of the polypeptide is diagnostic of a patient having a psychotic disorder (e.g., BPD or schizophrenia). In yet another embodiment, hybridization with PCR probes that are capable of detecting at least one of the polynucleotide sequences listed in Table 1, Table 3, in FIGS. 1 A(I)- 1 A(IV), or in FIGS. 6A-6D , including genomic sequences, or closely related molecules, can be used to hybridize to a nucleic acid sequence derived from a patient having a psychotic disorder (e.g., BPD or schizophrenia). The specificity of the probe, whether it is made from a highly specific region, e.g., the 5′ regulatory region, or from a less specific region, e.g., a conserved motif, and the stringency of the hybridization or amplification (maximal, high, intermediate, or low), determine whether the probe hybridizes to a naturally occurring sequence, allelic variants, or other related sequences. Hybridization techniques can be used to identify mutations indicative of a psychotic disorder in genes listed in Table 1, Table 3, in FIGS. 1 A(I)- 1 A(IV), or in FIGS. 6A-6D , or may be used to monitor expression levels of these genes (for example, by Northern analysis (Ausubel et al., Current Protocols in Molecular Biology , Wiley Interscience, New York, 1997)). In yet another approach, humans can be diagnosed for a propensity to develop a psychotic disorder (e.g., BPD or schizophrenia) by direct analysis of the sequence of at least one of the nucleic acids listed in Table 1 or Table 3. Quantitative Real Time PCR Q-rt-PCR can be performed using any method known in the art. In one embodiment, cDNA was synthesized from 1 μg of total RNA with the Invitrogen SuperScript First-Strand Synthesis System for Q-rt-PCR (Invitrogen, Calif.), using oligo dT as the primer. A primer set for each gene was designed with the help of Primer 3 (available from the Massachusetts Institute of Technology, Cambridge, Mass.). Amplicons were designed to be between 100 and 200 base pairs in length. Melt curve analysis and polyacrylamide gel electrophoresis were used to confirm the specificity of each primer pair. The real-time Q-rt-PCR reaction was performed in the MJ RESEARCH DNA ENGINE OPTICON (MJ Research, Waltham, Mass.; Opticon Monitor Data Analysis Software v 1.4), with the DyNAmo SYBR Green Q-rt-PCR Kit (Finnzymes, Finland), according to the company protocol, in 25 μl volume, with 2.5 μl of 1:5 diluted cDNA samples and 0.3 μM primers. PCR cycling conditions were as follows: initially, samples were heated at 95° C. for 10 minutes, followed by 49 cycles of 94° C. for 30 seconds, 55° C. for 30 seconds, 72° C. for 30 seconds. Data were collected between 72° C. and 79° C., depending on amplicon melting temperature. A melt curve analysis was performed at the end of each Q-rt-PCR experiment. Dilution curves were generated for each primer in every experiment by diluting cDNA from a control sample 1:3 twice, yielding a dilution series of 1.00, 0.333, and 0.111. The log of the dilution value was plotted against the cycle threshold (CT) value. Blanks were run with each dilution curve to control for cross contamination. Dilution curves, blanks, and samples were run in duplicate. Reported values were normalized to the average of three internal standards, which are not regulated in the gene array analysis or in the Q-rt-PCR analysis (see Table 5). TABLE 5Entrez GeneID Numbers and Primer Sequences of Genes ChosenRespiratoyEntrezChainGeneIDGenes of InterestComplexNo.Forward SequenceReverse SequenceCytochrome c oxidaseIV1327CGAGCAATTTCCACCTCTGTCAGGAGGCCTTCTCCTTCTCIV-1 (COX4I1)(SEQ ID NO: 1)(SEQ ID NO: 8)ATP synthase, F0,V517TGGGATTGGAACTGTGTTTGTCACATGGCAAAGAGGATGAc2 (ATP5G2)(SEQ ID NO: 2)(SEQ ID NO: 9)ATP synthase, F0,V10632TGTTGTTGGACCATGTGTGAGCGGGCTAAACAGACGTGTAg (ATP5L)(SEQ ID NO: 3)(SEQ ID NO: 10)ATP synthase, F1,V539CTGAAGGAACCCAAAGTGGGAAAAGGCAGAAACGACTCCO (OSCP)(SEQ ID NO: 4)(SEQ ID NO: 11)Control genesGlyceraldehyde-3-phos-NA2597CTCCCATTCTTCCACCTTTGGTCCACCACCCTGTTGCTphate dehydrogenase(SEQ ID NO: 5)(SEQ ID NO: 12)(GAPDH)Keratin 10NA3858GGGCGAGTCTTCATCTAAGGAATGGTCTGTGTGAAGGGAGA(SEQ ID NO: 6)(SEQ ID NO: 13)Integral membraneNA9452CATTCGTGAGGATGACAACACAGCAACAAGTCCAGGTAAGCprotein 2A (ITM2A)(SEQ ID NO: 7)(SEQ ID NO: 14)Abbreviation: NA, not applicable.*For array data, see FIGS. 1A(1)-1A(4). Microarray Analysis The methods of the invention can employ microarrays for determining expression of nucleic acids or polypeptides. Such techniques are known in the art and are described in US 2004/0248286. Any appropriate array technology known in the art can be used in the diagnostic and prognostic methods of the invention. Monitoring a Subject with a Psychotic Disorder In addition to diagnostic methods, the invention also features methods for monitoring the progression of a psychotic disorder in a subject. Such methods include obtaining a cell sample from the subject, subjecting a cell from the sample to stress, and measuring the expression of a polypeptide or polynucleotide in the cell. A second measurement of expression is subsequently performed using the same steps following a time interval (e.g., at least 1, 2, 5, 7, 14, or 28 days, or at least 1, 2, 3, 4, 5, 6, 8, 10, 12, or 24 months). The two measurements are then compared, where a change in expression is indicative of disease progression or improvement. In one example, an increase in a gene associated with mitochondrial function or electron transport is taken as an indication of the severity of the disorder decreasing. Such monitoring methods can be performed in conjunction with administration of a therapy (e.g., pharmaceutical therapy such as those described herein) to the subject and, thus, can be used to determine if a particular therapy is having the desired effect on gene expression, which can be indicative of the severity of the psychotic disorder. In one example, the first measurement is taken prior to commencement of a therapy. Therapy is begun following the first measurement, and a second measurement is performed six months following the commencement of therapy. A change in the second measurement as compared to the first measurement can thus be taken as indication of the effectiveness of the therapy. The following example is intended to illustrate, rather than limit, the invention. Example 1 Differential Gene Expression in Lymphocytes from BPD Patients We isolated lymphocytes from 20-30 ml of blood taken from normal controls and patients diagnosed with BPD according to the criteria of DSM IV ( DSM - IV, Diagnostic and Statistical Manual of Mental Disorder , Fourth Ed., American Psychiatric Association, Washington, D.C., 1994). The Structured Clinical Interview for DSM IV Axis I Disorders and the Brief Psychiatric Rating Scale were used to verify diagnoses. For specifics on test subjects see FIG. 2 . Lymphocytes were separated by centrifugation using Histopaque columns (Sigma-Aldrich, St. Louis, Mo.) and split into three batches. One batch was directly subjected to gene expression microarray analysis or alternatively, frozen at −80° C., whereas two batches were washed three times and cultured in either regular RPMI-1640 medium or low glucose RPMI-1640 medium (50% normal glucose content; 1 g/l) for a period of 5 days. The cultured cells were optionally frozen at −80° C. Cells were harvested; RNA was extracted (RNagents kit: Promega, Madison, Wis.), and cDNA was synthesized from 0.5 ng RNA and biotinylated RNA synthesized from cDNA (MessageAmp 11-96 kit; Ambion, Austin, Tex.). Biotinylated RNA was fragmented and hybridized to the HG-U133A 2.0 array (Affymetrix, Santa Clara, Calif.) overnight at 45° C. and stained on a washing station with two rounds of streptavidin-phycoerythrin (Molecular Probes, Eugene, Ore.) separated by a round of biotinylated antistreptavidin antibody (Vector Laboratories, Burlingame, Calif.). The fresh-frozen lymphocytes were worked up in one batch for gene array experiments. All of the cultured lymphocytes were worked up together in a separate batch with an improved protocol developed during the course of this project, for which the amount of input RNA could be lowered from 4 μg to 1 μg. Because of the small sample sizes and the variable amount of lymphocytes yielded from individual probands, a number of samples did not yield enough mRNA for gene array analysis ( FIG. 2 ). The number of samples per group ranged from 10 to 17. Gene expression levels were calculated with the RMA algorithm (Irizarry et al., Biostatistics 4:249-264, 2003) and compared using the comparison analysis of the dChip program, which computes P values based on the t distribution, with the degrees of freedom set according to the Welch-modified 2-sample t. test. Only samples that met quality control criteria provided by the GeneChip Operating Software (Affymetrix) and DNA-Chip Analyzer (dChip 2006) (Li and Wong, Proc. Natl. Acad. Sci. USA 98:31-36, 2001) were incorporated into the analysis ( FIG. 2 ) (mean±SD noise, 0.9±0.1; mean±SD percentage present call, 56.2%±1.7%; mean±SD 3′-5′ glyceraldehyde-3-phosphate dehydrogenase ratio, 1.4±0.4; mean±SD 3′-5′ β-actin ratio, 1.6±0.8; mean±SD percentage of array outliers, 0.16%±0.22%; mean±SD percentage of single outliers, 0.046%±0.043%; no significant differences were observed between groups). All genes differently expressed between two groups (p<0.05; >50% ‘present’ call; four groups: (I) low glucose: BPD over control; (II) normal glucose: BPD over control; (III) control: low over normal glucose; (IV) BPD: low over normal glucose) were subjected to a classification analysis using the Gene Ontology database gene product attributes (GO), calculated with the dChip software. Multiples of same transcripts were masked for classification analyses. Similar results were obtained with log 2-transformed and natural scale data. Analysis of variance filtering was carried out in using dChip software. Permuted and adjusted P values for mitochondrial genes were obtained with the MAPPFinder program (Doniger et al., Genome Biol. 4:R7, 2003). We used 271 groupings (MAPPs) of individual genes for this analysis, grouped in a manner that avoided duplication of the same genes in independent groups. MAPPFinder calculates a nonparametric statistic based on 2000 permutations of the data, randomizing the gene associations for each sample to generate a distribution of z scores for each MAPP, which are then used to assign permuted P values. In addition, the Westfall-Young adjustment, which calculates the family wise error rate for each sample and accounts for multiple testing, is used for multiple testing. This adjustment gives the adjusted P value. Fisher exact test was used to examine the statistical difference between the percentage of regulation of mitochondrial transcripts vs. the percentage of regulation of all of the transcripts. Families of genes, such as genes of the mitochondrial respiratory chain or genes specific for B or T cells, were compared between NC and BPD samples with 2-tailed, paired t tests using the natural expression values. For example, for the mitochondrial respiratory chain, the expression level of each of the 114 individual transcripts in an experimental group was divided by the average expression level of each transcript in all of the groups. False discovery rates were calculated in the dChip program by estimating the empirical false discovery rate for a group of genes (i.e., the 114 mitochondrial transcripts) using 2000 random permutations. In the comparison of control and BPD lymphocytes in low glucose medium, the GO categories that had more hits for downregulated genes than would be expected by chance included ‘mitochondrion’ (p=0), ‘cytochrome-c oxidase activity’ (p=0.0007), ‘mitochondrial electron transport chain’ (p=0.001) and ‘ubiquinol-cytochrome-c reductase activity’ (p=0.0001). Further analyses revealed that 18 probe sets of electron transport transcripts, out of 114 on the array (see Table 7 for GenBank and Entrez Gene number of all 114 transcripts), were significantly lower expressed in BPD lymphocytes under glucose deprivation (FIG. 1 A(I)), while none were expressed at higher levels. The 18 probe sets represented 15 individual mRNA transcripts, composing 19% of all electron transport probe sets on the array (35/114 probe sets were duplicate probe sets), while on average only 8.2% of probe sets were lower in BPD lymphocytes under glucose deprivation (FIG. 1 B(I)). This difference was significant in Fisher exact test. Furthermore, the entire group of electron transport transcripts was shifted significantly in BPD toward lower expression levels (FIG. 1 C(I) and Table 6). TABLE 6Statistics for the Entire Group of Mitochondrial RespiratoryChain TranscriptsP Value for 2-Tailed,Paired t Test ofUp-regulationDown-regulationComparisonExpression % Values*FDR, %†FDR, %†Low glucose, NC‡ vs BPD§<.001≦6Not calculableNormal glucose, NC‡ vs BPD§0.21≦33≦50BPD, normal‡ vs low§ glucose0.62Not calculable≦17NC, normal‡ vs low§ glucose<.001≦12Not calculableFresh lymphocytes, NC‡ vs BPD§0.05≦100≦17Abbreviations:BPD, bipolar disorder;FDR, false discovery rate;NC, normal control.*Values are for genes of the mitochondrial respiratory chain (for GeneID numbers, see eTable 1 [http://www.archgenpsychiatry.com]). For percentage expression values, the expression level of each of the 114 individual transcripts in an experimental group was divided by the average expression level of this transcript in all of the groups.†The FDRs were calculated in the dChip program (http://biosun1.harvard.edu/complab/dchip) by estimating the empirical FDR using 2000 random permutations.‡Baseline group.§Experimental group. No differences between BPD and control lymphocytes were observed either under normal glucose concentrations (FIGS. 1 A(II), 1 B(II), 1 C(II)), or in fresh, uncultured lymphocytes ( FIGS. 3A-3C ). The difference in the expression level of electron transport transcripts between BPD and control subjects seems to be caused by a different molecular response to glucose deprivation. While control subjects showed an upregulation of these transcripts in response to energy stress (FIGS. 1 A(III), 1 B(III), 1 C(III)), BPD subjects have a tendency to downregulate these transcripts (FIGS. 1 A(IV), 1 B(IV), 1 C(IV)). Upregulated transcripts in control lymphocytes in low glucose medium, compared to control lymphocytes in normal glucose medium, had significant hits in the GO categories of ‘mitochondrion’ (p=0.002) and ‘cytochrome-c oxidase activity’ (p=0.002), while downregulated transcripts in BPD lymphocytes in low glucose medium, compared to BPD lymphocytes in normal glucose medium, had a significant hit in the GO category of ‘mitochondrion’ (p=0.01). While the entire group of electron transport transcripts was significantly shifted toward upregulation in the control lymphocytes under glucose deprivation stress (FIG. 1 C(III)), no significant shift toward downregulation was observed in the BPD lymphocytes under energy stress (FIG. 1 C(IV)). Regulation trends were verified with real-time quantitative PCR (Q-rt-PCR; FIGS. 1 D(I) to 1 D(IV)), carried out as previously described (C. Konradi et al., Arch. Sen. Psychiatry 61:300-308, 2004, MacDonald et al., Biol. Psychiatry 57:1041-1051, 2005). All values were normalized to an average of three internal control genes: integral membrane protein 2A (accession number: NM — 004867), glyceraldehyde-3-phosphate dehydrogenase (GeneID-2597), and Keratin 10 (accession number NM — 000421). Control genes were not regulated. Four electron-transport transcripts that were used to verify the gene array data replicated the major patterns observed in the gene array analysis (FIGS. 1 D(I)- 1 D(IV)), although the levels of difference seen in the gene expression microarray study are at the threshold of detectability for Q-rt-PCR. When the analysis was limited to paired samples (n=13 for subjects with BPD, n=7 for NCs; see FIG. 2 for pairs), 15 transcripts showed high between-group variability as determined in a factorial analysis of variance (Table 8). These 15 transcripts were averaged and plotted ( FIG. 5 ). In BPD lymphocytes, these transcripts were down-regulated under low-glucose stress (P≦0.003, paired t test), whereas in NC lymphocytes, these transcripts were up-regulated (P≦0.02, paired t test). In the paired samples, a comparison of NC and BPD lymphocyte mRNA expression levels in low glucose showed that 17 transcripts were expressed significantly lower in BPD lymphocytes, similar to the larger sample. Finally, no significant relationship between electron transfer transcript expression and medication was found when mitochondrial expression levels obtained in the gene arrays were plotted against drug treatment in a hierarchical cluster analysis or when analyses of variance were calculated (each group of drug compared with absence of that drug in low and normal glucose) using qPCR data (data not shown). TABLE 7All Nuclear Transcripts of the Mitochondrial Respiratory Chain Used for Analysis in FIGS. 1-4low glucose:normal glucose:BPD/controlBPD/controlfoldfoldGBLocusLinkAffymetrixchangep-valuechangep-valuegeneAccession #IDprobe set ID(natural)(log 2)(natural)(log 2)Complex INADH dehydrogenase 1NM_0045414694202298_at−1.000.943−1.010.750alpha, 1, 7.5 kDaNADH dehydrogenase 1BC0036744695209224_s_at−1.060.3201.170.040alpha, 2, 8 kDaNADH dehydrogenase 1NM_0045424696218563_at−1.010.908−1.000.968alpha, 3, 9 kDaNADH dehydrogenase 1NM_0024894697217773_s_at−1.030.3891.020.600alpha, 4, 9 kDaNADH dehydrogenase 1NM_0050004698201304_at−1.150.035−1.080.043alpha, 5, 13 kDaNADH dehydrogenase 1AK0222094698215850_s_at−1.060.527−1.060.149alpha, 5, 13 kDaNADH dehydrogenase 1BC0027724700202000_at−1.100.025−1.060.340alpha, 6, 14 kDaNADH dehydrogenase 1BC0027724700202001_s_at−1.010.8281.050.222alpha, 6, 14 kDaNADH dehydrogenase 1NM_0050014701202785_at−1.050.610−1.020.705alpha, 7, 14.5 kDaNADH dehydrogenase 1NM_0142224702218160_at−1.040.4841.010.832alpha, 8, 19 kDaNADH dehydrogenase 1AF0506414704208969_at−1.010.970−1.010.628alpha, 9, 39 kDaNADH dehydrogenase 1NM_0045444705217860_at−1.010.8861.020.727alpha, 10, 42 kDaNADH dehydrogenase 1NM_01601351103204125_at−1.020.6671.080.086alpha, assembly factor 1NADH dehydrogenase 1NM_0045454707206790_s_at−1.090.011−1.040.472beta, 1, 7 kDaNADH dehydrogenase 1NM_0045464708218200_s_at1.020.6151.020.577beta, 2, 8 kDaNADH dehydrogenase 1NM_0045464708218201_at−1.020.7431.030.225beta, 2, 8 kDaNADH dehydrogenase 1NM_0024914709203371_s_at−1.050.223−1.000.942beta, 3, 12 kDaNADH dehydrogenase 1NM_0045474710218226_s_at−1.030.305−1.020.515beta, 4, 15 kDaNADH dehydrogenase 1NM_0024924711203621_at−1.050.1151.020.495beta, 5, 16 kDaNADH dehydrogenase 1NM_0024934712203613_s_at−1.050.172−1.010.776beta, 6, 17 kDaNADH dehydrogenase 1NM_0041464713202839_s_at1.000.860−1.080.054beta, 7, 18 kDaNADH dehydrogenase 1M333744713211407_at1.020.5971.020.567beta, 7, 18 kDaNADH dehydrogenase 1NM_0050044714201226_at−1.020.6891.020.548beta, 8, 19 kDaNADH dehydrogenase 1NM_0050044714201227_s_at−1.050.3391.000.987beta, 8, 19 kDaNADH dehydrogenase 1AA7230574714214241_at1.140.360−1.010.863beta, 8, 19 kDaNADH dehydrogenase 1NM_01905654539218320_s_at−1.070.1951.050.225beta, 11, 17.3 kDaNADH dehydrogenase 1,NM_0050034706202077_at−1.040.3101.000.890alpha/beta, 1, 8 kDaNADH dehydrogenase 1,NM_0024944717203478_at−1.080.073−1.010.703unknown, 1, 6 kDaNADH dehydrogenase 1,NM_0045494718218101_s_at−1.060.2151.020.789unknown, 2, 14.5 kDaNADH dehydrogenaseNM_0050064719203039_s_at−1.050.234−1.040.433Fe—S protein 1, 75 kDaNADH dehydrogenaseNM_0045504720201966_at−1.010.543−1.120.183Fe—S protein 2, 49 kDaNADH dehydrogenaseNM_0045514722201740_at−1.010.7691.020.435Fe—S protein 3, 30 kDaNADH dehydrogenaseBC0052704724209303_at−1.080.083−1.000.983Fe—S protein 4, 18 kDaNADH dehydrogenaseNM_0045524725201757_at−1.060.197−1.030.285Fe—S protein 5, 15 kDaNADH dehydrogenaseNM_0045534726203606_at−1.020.7681.020.742Fe—S protein 6, 13 kDaNADH dehydrogenaseBC005954374291211752_s_at−1.020.713−1.050.189Fe—S protein 7, 20 kDaNADH dehydrogenaseNM_0024964728203189_s_at−1.030.384−1.000.980Fe—S protein 8, 23 kDaNADH dehydrogenaseNM_0024964728203190_at−1.030.300−1.010.660Fe—S protein 8, 23 kDaNADH dehydrogenaseAF0921314723208714_at1.020.5651.040.389flavoprotein 1, 51 kDaNADH dehydrogenaseNM_0210744729202941_at1.030.458−1.030.609flavoprotein 2, 24 kDaComplex IIsuccinate dehydrogenaseNM_0041686389201093_x_at1.040.3411.010.819complex, A, flavoprotein (Fp)succinate dehydrogenaseAI348006255812, 6389222021_x_at−1.020.579−1.030.498complex, A, flavoprotein (Fp)succinate dehydrogenaseNM_0030006390202675_at1.030.4911.000.900complex, B, iron sulfur (Ip)succinate dehydrogenaseAW2941076390214166_at1.020.8721.070.178complex, B, iron sulfur (Ip)succinate dehydrogenaseNM_0030016391202004_x_at1.020.742−1.120.099complex, C, 15 kDasuccinate dehydrogenaseBG1105326391215088_s_at−1.050.2761.040.326complex, C, 15 kDasuccinate dehydrogenaseAF0805796391216591_s_at−1.150.437−1.160.431complex, C, 15 kDasuccinate dehydrogenaseNM_0030026392202026_at−1.040.3401.100.070complex, DComplex IIIubiquinol-cytochrome cNM_0062947381205849_s_at−1.060.0581.020.386reductase binding proteinubiquinol-cytochrome cBC0052307381209065_at−1.200.0001.070.290reductase binding proteinubiquinol-cytochrome cM267007381209066_x_at−1.060.0261.010.692reductase binding proteinubiquinol-cytochrome cNM_01338729796218190_s_at−1.020.670−1.010.828reductase complex (7.2 kD)ubiquinol-cytochrome cNM_0033657384201903_at1.070.214−1.070.118reductase core protein Iubiquinol-cytochrome cNM_0033667385200883_at−1.090.036−1.040.562reductase core protein IIubiquinol-cytochrome cAV7273817385212600_s_at−1.070.073−1.050.327reductase core protein IIubiquinol-cytochrome cNM_0060047388202233_s_at−1.090.0261.010.853reductase hinge proteinubiquinol-cytochrome cNM_00683010975202090_s_at−1.060.1661.030.432reductase, 6.4 kDaubiquinol-cytochrome cBC0006497386208909_at−1.010.560−1.040.159reductase, Rieske iron-sulfur 1Complex IVcytochrome c oxidase IVAA8549661327200086_s_at−1.080.0001.010.722cytochrome c oxidase IVNM_0018611327202698_x_at−1.050.010−1.040.104cytochrome c oxidase IVAW3375101327213758_at−1.030.7331.130.014cytochrome c oxidase VaNM_0042559377203663_s_at−1.000.982−1.020.705cytochrome c oxidase VbNM_0018621329202343_x_at1.010.752−1.020.517cytochrome c oxidase VbBC0062291329211025_x_at−1.020.855−1.030.529cytochrome c oxidase VbAI5573121329213735_s_at−1.040.5681.010.839cytochrome c oxidase VbAI5573121329213736_at−1.250.1921.070.694cytochrome c oxidase VIa 1NM_0043731337200925_at1.000.8641.020.558cytochrome c oxidase VIa 2NM_0052051339206353_at1.010.749−1.030.625cytochrome c oxidase VibNM_0018631340201441_at−1.030.558−1.010.7541 (ubiquitous)cytochrome c oxidase VIcNM_0043741345201754_at−1.060.098−1.030.383cytochrome c oxidase VIIaNM_0018651347201597_at−1.020.6841.110.0182 (liver)cytochrome c oxidase VIIaNM_0047189167201256_at−1.080.014−1.050.0412 likecytochrome c oxidase VIIbNM_0018661349202110_at−1.000.9631.050.271cytochrome c oxidase VIIcNM_0018671350201134_x_at−1.050.136−1.010.774cytochrome c oxidase VIIcAA3827021350213846_at−1.090.159−1.010.822cytochrome c oxidase VIIcAF0421651350217491_x_at−1.070.0191.010.753cytochrome c oxidase 8ANM_0040741351201119_s_at1.010.8031.030.335(ubiquitous)cytochrome c, somaticBC00529954205208905_at−1.030.567−1.000.980cytochrome c-1NM_0019161537201066_at1.070.1551.020.491COX10 homologNM_0013031352203858_s_at1.000.9901.030.564COX11 homologNM_0043751353203551_s_at−1.150.132−1.000.938COX11 homologBC0058951353211727_s_at−1.120.0111.030.588COX15 homologNM_0043761355219547_at−1.040.3911.060.130COX15 homologBC0023821355221550_at−1.150.036−1.020.946Complex VATP synthaseAW11860891647213057_at1.090.1591.090.091mitochondrial F1 complexassembly factor 2ATP synthaseAF07058491647214330_at1.030.5541.020.617mitochondrial F1 complexassembly factor 2ATP synthase, alpha, ,AI587323498213738_s_at−1.030.150−1.010.689cardiac muscleATP synthase, bBC005960515211755_s_at−1.010.693−1.020.479ATP synthase, betaNM_001686506201322_at1.030.266−1.020.572ATP synthase, c (subunit 9)AL080089516208972_s_at−1.010.9011.020.792ATP synthase, c (subunitD13119517208764_s_at−1.070.0451.000.9709) isoform 2ATP synthase, c (subunitNM_001689518207507_s_at−1.020.731−1.010.9219) isoform 3ATP synthase, c (subunitNM_001689518207508_at−1.000.9291.010.7959) isoform 3ATP synthase, dAF06173510476210149_s_at−1.050.286−1.010.727ATP synthase, deltaNM_001687513203926_x_at1.010.8971.020.734ATP synthase, deltaBE798517513213041_s_at1.050.4011.060.285ATP synthase, eNM_007100521207335_x_at−1.080.144−1.010.887ATP synthase, eBC003679521209492_x_at−1.050.311−1.020.507ATP synthase, epsilonNM_006886514217801_at−1.060.0681.060.102ATP synthase, f, isoform 2NM_0048899551202961_s_at−1.000.967−1.040.377ATP synthase, F6NM_001685522202325_s_at−1.040.3811.020.513ATP synthase, gNM_00647610632207573_x_at−1.030.3731.020.655ATP synthase, gAA91767210632208745_at−1.140.0011.030.537ATP synthase, gAF07065510632208746_x_at−1.040.2291.000.931ATP synthase, gAL05027710632210453_x_at−1.040.2521.000.984ATP synthase, gamma 1NM_005174509205711_x_at−1.000.892−1.050.061ATP synthase, gamma 1BC000931509208870_x_at1.010.718−1.030.182ATP synthase, gamma 1AV711183509213366_x_at−1.020.650−1.030.213ATP synthase, gamma 1BG232034509214132_at−1.120.4281.050.404ATP synthase, ONM_001697539200818_at−1.090.001−1.040.286(oligomycin sensitivityconferring protein)ATP synthase, OS77356539216954_x_at−1.160.0011.010.738(oligomycin sensitivityconferring protein)ATP synthase, s (factor B)NM_01568427109206992_s_at−1.080.079−1.090.093ATP synthase, s (factor B)NM_01568427109206993_at−1.150.0141.080.222ATP synthase, s (factor B)AW19588227109213995_at−1.110.0981.030.559Abbreviations: ATP, adenosine triphosphate; BPD, bipolar disorder; COX, cytochrome c oxidase; Fe—S, iron-sulfur; ID, identification; NADH, reduced nicotinamide adenine dinucleotide; NC, normal control.*Boldface type indicates statistical significance. TABLE 8Fifteen Mitochondrial Transcripts Used for Paired ComparisonsBPD: normalNC: normalANOVA (diagnosis ×versus lowversus lowglucoseLocusglucoseglucoseconcentration)LinkfoldfoldFgeneIDprobe setchangep-valuechangep-valuestatisticp-valueComplex INADH dehydrogenase 14698201304_at−1.150.0171.250.05613.00.001alpha, 5, 13 kDaNADH dehydrogenase 14707206790_s_at−1.040.1771.070.0806.90.012beta, 1, 7 kDaComplex IIsuccinate6392202026_at−1.090.0741.070.2055.00.032dehydrogenase, DComplex IIIubiquinol-cyt c reductase7381205849_s_at−1.040.1161.070.0827.60.009binding proteinubiquinol-cyt c reductase7381209065_at−1.090.0681.180.03111.40.002binding proteinubiquinol-cyt c reductase7384201903_at1.070.134−1.110.1735.30.027core protein IComplex IVCOX 111353211727_s_at−1.040.4521.140.0075.40.026COX IV-11327200086_s_at−1.010.7901.110.0367.60.009COX VIIa-1 (muscle)1346204570_at1.120.079−1.110.1715.40.026COX VIIa-2 (liver)1347201597_at−1.060.1041.10.0817.30.010COX VIIc1350217491_x_at−1.020.5001.080.0675.40.026Complex VATP synthase, F010632208745_at−1.050.2321.110.0307.10.011complex, gATP synthase, F027109206993_at−1.120.0321.020.7805.90.020complex, s (factor B)ATP synthase, F1514217801_at−1.10.0011.070.11514.60.001complex, epsilon subunitATP synthase, F1539216954_x_at−1.070.0421.160.0216.40.016complex, O (OSCP)Abbreviations: ANOVA, analysis of variance; ATP, adenosine triphosphate; BPD, bipolar disorder; COX, cytochrome c oxidase; cyt c, cytochrome c; ID, identification; NADH, reduced nicotinamide adenine dinucleotide; NC, normal control; OSCP, oligomycin sensitivity-conferring protein.*Boldface type indicates statistical significance. To determine whether a shift between B and T cells had taken place in any of the comparisons, the expression levels of 54 B-cell-specific transcripts and 77 T-cell-specific transcripts were examined ( FIGS. 6A-6E , 7 A- 7 D, and 8 A- 8 E; Table 9) for transcripts). The percentage of individually regulated genes did not surpass the chance expectations in any of the comparisons ( FIGS. 6A-6E ; see FIGS. 1 B(I)- 1 B(IV) for chance expectations), and the group of B-cell-specific ( FIGS. 7A-7D ) and T-cell-specific ( FIGS. 8A-8D ) transcripts was not significantly shifted. In addition, five marker genes for natural killer lymphocytes and five marker genes for monocytes were unchanged in all of the comparisons. Sixteen marker genes for granulocytes were examined as well; however, most were under the detection limit and none were affected by any condition. TABLE 9Transcripts Specific for B and T Cells Used for Analysis in FIGS. 6-8Affymetrix probe setgeneGB Accession #GeneIDIDB-Cell MarkersB-cell CLL/lymphoma 10AF0822838915205263_atB-cell CLL/lymphoma 11A (zincAF08021653335210347_s_atfinger protein)B-cell CLL/lymphoma 11A (zincNM_01801453335219497_s_atfinger protein)B-cell CLL/lymphoma 11A (zincNM_01801453335219498_s_atfinger protein)B-cell CLL/lymphoma 11B (zincNM_02289864919219528_s_atfinger protein)B-cell CLL/lymphoma 2M13994596203684_s_atB-cell CLL/lymphoma 2NM_000633596203685_atB-cell CLL/lymphoma 3NM_005178602204908_s_atB-cell CLL/lymphoma 6 (zinc fingerNM_001706604203140_atprotein 51)B-cell CLL/lymphoma 6 (zinc fingerS67779604215990_s_atprotein 51)B-cell CLL/lymphoma 7ANM_020993605203795_s_atB-cell CLL/lymphoma 7ANM_020993605203796_s_atB-cell CLL/lymphoma 7BNM_0017079275202518_atB-cell CLL/lymphoma 7CNM_0047659274219072_atB-cell CLL/lymphoma 9NM_004326607204129_atB-cell linkerNM_01331429760207655_s_atB-cell receptor-associated proteinNM_01884455973205084_at29B-cell receptor-associated proteinAL58368755973217657_at29B-cell receptor-associated proteinAI39396055973217662_x_at29B-cell receptor-associated proteinNM_00574510134200837_at31B-cell scaffold protein with ankyrinNM_01793555024219667_s_atrepeats 1B-cell translocation gene 1, anti-AL535380694200920_s_atproliferativeB-cell translocation gene 1, anti-NM_001731694200921_s_atproliferativecardiotrophin-like cytokine factor 1NM_01324623529219500_atCD19 antigenNM_001770930206398_s_atCD22 antigenNM_0017714099, 933204581_atCD40 antigen (TNF receptorNM_001250958205153_s_atsuperfamily member 5)CD40 antigen (TNF receptorBF664114958215346_atsuperfamily member 5)CD40 antigen (TNF receptorX6059295835150_atsuperfamily member 5)CD48 antigen (B-cell membraneNM_001778962204118_atprotein)CD80 antigen (CD28 antigen ligandNM_005191941207176_s_at1, B7-1 antigen)CD83 antigen (activated BNM_0042339308204440_atlymphocytes, immunoglobulin)CD86 antigen (CD28 antigen ligandBG236280942205685_at2, B7-2 antigen)CD86 antigen (CD28 antigen ligandNM_006889942205686_s_at2, B7-2 antigen)CD86 antigen (CD28 antigen ligandL25259942210895_s_at2, B7-2 antigen)interleukin 4 receptorNM_0004183566203233_atmembrane-spanning 4-domains,BC002807931210356_x_atsubfamily A, member 1membrane-spanning 4-domains,X12530931217418_x_atsubfamily A, member 1musculin (activated B-cell factor-1)AF0601549242209928_s_atPaired box gene 5 (B-cell lineageBF5106925079221969_atspecific activator)pre-B-cell colony enhancing factor 1NM_00574610135217738_atpre-B-cell colony enhancing factor 1NM_00574610135217739_s_atPre-B-cell leukemia transcriptionBF9679985087212151_atfactor 1pre-B-cell leukemia transcriptionBE3977155089202875_s_atfactor 2pre-B-cell leukemia transcriptionNM_0025865089202876_s_atfactor 2pre-B-cell leukemia transcriptionBC0031115089211096_atfactor 2pre-B-cell leukemia transcriptionBC0031115089211097_s_atfactor 2pre-B-cell leukemia transcriptionNM_0061955090204082_atfactor 3pre-B-cell leukemia transcriptionNM_02052457326207838_x_atfactor interacting protein 1pre-B-cell leukemia transcriptionBF34426557326212259_s_atfactor interacting protein 1Pre-B-cell leukemia transcriptionAI34854557326214176_s_atfactor interacting protein 1pre-B-cell leukemia transcriptionAI93516257326214177_s_atfactor interacting protein 1prohibitin 2NM_00727311331201600_attumor necrosis factor receptorNM_001192608206641_atsuperfamily, member 17T-cell MarkersCD2 antigen (p50), sheep red bloodNM_001767914205831_atcell receptorCD28 antigen (Tp44)NM_006139940206545_atCD28 antigen (Tp44)AF222341940211856_x_atCD28 antigen (Tp44)AF222343940211861_x_atCD3Z antigen, zeta polypeptideJ04132919210031_at(TiT3 complex)CD4 antigen (p55)U47924920203547_atCD5 antigen (p56-62)NM_014207921206485_atCD6 antigenNM_006725923208602_x_atCD6 antigenU66145923211893_x_atCD6 antigenU66146923211900_x_atCD6 antigenAW134823923213958_atCD69 antigen (p60, early T-cellL07555969209795_atactivation antigen)CD8 antigen, alpha polypeptideAW006735925205758_at(p32)cutaneous T-cell lymphoma-NM_02266364693220957_atassociated antigen 1expressed in T-cells andAB02069423197212106_ateosinophils in atopic dermatitisexpressed in T-cells andAB02069423197212108_ateosinophils in atopic dermatitisfrequently rearranged in advancedNM_00547910023219889_atT-cell lymphomasfrequently rearranged in advancedAB04511823401209864_atT-cell lymphomas 2granulysinNM_00643310578205495_s_atgranulysinM852761057837145_athuman T-cell leukemia virusNM_0021583344206708_atenhancer factorIL2-inducible T-cell kinaseD137203702211339_s_atinducible T-cell co-stimulatorAB02313529851210439_atinducible T-cell co-stimulator ligandAL35569023308211197_s_atmal, T-cell differentiation proteinNM_0023714118204777_s_atmature T-cell proliferation 1NM_0142214515205106_atmature T-cell proliferation 1BC0026004515210212_x_atmature T-cell proliferation 1Z244594515216862_s_atpre T-cell antigen receptor alphaU36759171558211252_x_atpre T-cell antigen receptor alphaAL035587171558215492_x_atRearranged T-cell receptor alphaAE000659217412_atchain mRNA, variable regionsirtuin (silent mating typeNM_01653951548219613_s_atinformation regulation 2 homolog) 6T cell receptor alpha constantM1295928755209670_atT cell receptor alpha locusL347036955211902_x_atT cell receptor alpha locusAW8735446955215769_atT cell receptor alpha locusX610706955217056_atT cell receptor alpha locusAE0006596955217394_atT cell receptor alpha locusAW96643428517, 28663,215524_x_at28738, 28755,348035, 6955T cell receptor alpha locusM1556528517, 28663,210972_x_at28738, 28755, 6955T cell receptor alpha locusM1242328755, 6955209671_x_atT cell receptor alpha locus, T cellX725016955, 6964216191_s_atreceptor delta locusT cell receptor alpha variable 20BF97676428663215796_atT cell receptor associatedAJ24008550852217147_s_attransmembrane adaptor 1T cell receptor beta constant 1M1556428568, 28639210915_x_atT cell receptor gamma constant 2M308946967211144_x_atT cell receptor gamma constant 2M16768442532, 442670,209813_x_at445347, 6967, 6983T cell receptor gamma constant 2M13231442532, 442670,215806_x_at445347, 6967, 6983T cell receptor gamma constant 2M27331442532, 442670,216920_s_at445347, 6967, 6983T cell receptor V alpha geneAA284903216133_atsegment V-alpha-w23, cloneIGRa01T cell receptor V alpha geneAE000659217397_atsegment V-alpha-w24, cloneIGRa02Tax1 (human T-cell leukemia virusAF0908918887200976_s_attype I) binding protein 1Tax1 (human T-cell leukemia virusAF0908918887200977_s_attype I) binding protein 1Tax1 (human T-cell leukemia virusAI9354158887213786_attype I) binding protein 1Tax1 (human T-cell leukemia virusAF23499730851209154_attype I) binding protein 3Tax1 (human T-cell leukemia virusAK00132730851215459_attype I) binding protein 3Tax1 (human T-cell leukemia virusAK00132730851215464_s_attype I) binding protein 3T-cell acute lymphocytic leukemia 1NM_0031896886206283_s_atT-cell immunomodulatory proteinNM_03079081533221449_s_atT-cell leukemia translocation alteredNM_0221716988203054_s_atgeneT-cell leukemia/lymphoma 1ABC0035748115209995_s_atT-cell leukemia/lymphoma 1AX82240811539318_atT-cell lymphoma invasion andNM_0032537074206409_atmetastasis 1T-cell lymphoma invasion andU909027074213135_atmetastasis 1T-cell receptor active alpha-chain V-L34698211667_x_atregionT-cell receptor active alpha-chain V-AE000659217170_atregionT-cell receptor active beta-chainL48728216857_at(V10-D-J-C) mRNA, clone PL3.9T-cell receptor alpha chain (TCRA)X61079217063_x_atTCR V alpha 14.1/J alpha 32/CX61072216540_atalphatranscription factor 7 (T-cell specific,AW0273596932205254_x_atHMG-box)transcription factor 7 (T-cell specific,NM_0032026932205255_x_atHMG-box)transcription factor 7-like 2 (T-cellAI7030746934212761_atspecific, HMG-box)transcription factor 7-like 2 (T-cellAI3759166934212762_s_atspecific, HMG-box)transcription factor 7-like 2 (T-cellAV7214306934216035_x_atspecific, HMG-box)transcription factor 7-like 2 (T-cellAA6640116934216037_x_atspecific, HMG-box)transcription factor 7-like 2 (T-cellAJ2707706934216511_s_atspecific, HMG-box)TSPY-like 2NM_02211764061218012_atVac14 homologU2580155697216407_atAbbreviations:CLL, chronic lymphocytic leukemia;HMG, high-mobility group;ID, identification;IL2, interleukin 2;mRNA, messenger RNA;NA, not available;TNF, tumor necrosis factor;TSPY, testis-specific protein, Y-linked;Vac, vacuole morphology. Almost all BPD patients were on medication (see FIG. 2 ), thus raising the possibility of medication effects. This concern was alleviated by the fact that no single medication was present in more than 30% of all BPD patients, and medications ranged from lithium, to valproic acid (VA), anticonvulsants, antidepressants, and antipsychotics. We found no affiliation of electron transport transcript expression levels with medication ( FIGS. 4A-4E ). Therefore, if the data reflect a medication effect as opposed to an effect intrinsic to the disease, this effect must be common to all medications used to treat BPD and might represent a common therapeutic pathway. The likelihood for a medication effect is limited by the facts that (a) both the fresh (uncultured) lymphocytes and the normal glucose cultured lymphocytes showed no difference between controls and BPD, and (b) the lymphocytes in culture were washed three times before plating and then cultured for five days in the absence of any drugs. Thus, we believe that the differences observed between the BPD patients and controls is due to disease rather than due to medication. All patents, patent applications, and publications mentioned in this specification are herein incorporated by reference, to the same extent as if each independent patent, patent application, or publication was specifically and individually indicated to be incorporated by reference.","lang":"en","source":"USPTO_FULLTEXT","data_format":"ORIGINAL"}},"description_lang":["en"],"has_description":true,"has_docdb":true,"has_inpadoc":true,"has_full_text":true,"biblio_lang":"en"},"jurisdiction":"US","collections":[],"usersTags":[],"lensId":"175-002-565-987-646","publicationKey":"US_8163475_B2","displayKey":"US 8163475 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(a) obtaining a cell sample from said subject, wherein said sample is a blood sample;\n
(b) subjecting a cell from said sample to stress; and\n
(c) measuring the level of expression in said cell of at least three nuclear encoded mitochondrial energy metabolism nucleic acids or polypeptides, wherein a decrease in said level of expression, as compared to the expression in a cell that is subjected to said stress from a sample obtained from a control subject, is indicative of said subject having bipolar disorder, wherein at least three of said nucleic acids or polypeptides are selected from the group consisting of NADH dehydrogenase (ubiquinone) 1 alpha subcomplex, 5, 13 kDa (NDUFA5; Entrez Gene ID:4698); NADH dehydrogenase (ubiquinone) 1 alpha subcomplex, 6, 14 kDa (NDUFA6; Entrez Gene ID:4700); NADH dehydrogenase (ubiquinone) 1 beta subcomplex, 1, 7 kDa (NDUFB1; Entrez Gene ID: 4707); ubiquinol-cytochrome c reductase binding protein (UQCRB; Entrez Gene ID: 7381); ubiquinol-cytochrome c reductase core protein II (UQCRC2; Entrez Gene ID: 7385); ubiquinol-cytochrome c reductase hinge protein (UQCRH; Entrez Gene ID: 7388); cytochrome c oxidase subunit IV isoform 1 (COX4I1; Entrez Gene ID: 1327); cytochrome c oxidase subunit VIIa polypeptide 2 like (COX7A2L; Entrez Gene ID: 9167); cytochrome c oxidase subunit VIIc (COX7C; Entrez Gene ID: 1350); COX11 homolog, cytochrome c oxidase assembly protein (yeast) (COX11; Entrez Gene ID: 1353); COX15 homolog, cytochrome c oxidase assembly protein (yeast) (COX15: Entrez Gene ID: 1355); ATP synthase, H+ transporting, mitochondrial F0 complex, subunit C2 (subunit 9) (ATP5G2; Entrez Gene ID: 517); ATP synthase, H+ transporting, mitochondrial F0 complex, subunit G (ATP5L; Gene ID: 10632); ATP synthase, H+ transporting, mitochondrial F1 complex, O subunit (ATP5O; Entrez Gene ID No: 539); and ATP synthase, H+ transporting, mitochondrial F0 complex, subunit s (factor B) (ATP5S; Entrez Gene ID No: 27109)."],"number":1,"annotation":false,"title":false,"claim":true},{"lines":["A method for diagnosing bipolar disorder in a subject, said method comprising the steps:\n
(a) obtaining a cell sample from said subject, wherein said cell sample comprises a lymphocyte;\n
(b) subjecting a cell from said sample to stress; and\n
(c) measuring the level of expression in said cell of at least three nuclear encoded mitochondrial energy metabolism nucleic acids or polypeptides, wherein a decrease in said level of expression, as compared to the expression in a cell that is subjected to said stress from a sample obtained from a control subject, is indicative of said subject having bipolar disorder, wherein at least three of said nucleic acids or polypeptides are selected from the group consisting of NADH dehydrogenase (ubiquinone) 1 alpha subcomplex, 5, 13 kDa (NDUFA5; Entrez Gene ID:4698); NADH dehydrogenase (ubiquinone) 1 alpha subcomplex, 6, 14 kDa (NDUFA6; Entrez Gene ID:4700); NADH dehydrogenase (ubiquinone) 1 beta subcomplex, 1, 7 kDa (NDUFB1; Entrez Gene ID: 4707); ubiquinol-cytochrome c reductase binding protein (UQCRB; Entrez Gene ID: 7381); ubiquinol-cytochrome c reductase core protein II (UQCRC2; Entrez Gene ID: 7385); ubiquinol-cytochrome c reductase hinge protein (UQCRH; Entrez Gene ID: 7388); cytochrome c oxidase subunit IV isoform 1 (COX4I1; Entrez Gene ID: 1327); cytochrome c oxidase subunit VIIa polypeptide 2 like (COX7A2L; Entrez Gene ID: 9167); cytochrome c oxidase subunit VIIc (COX7C; Entrez Gene ID: 1350); COX11 homolog, cytochrome c oxidase assembly protein (yeast) (COX11; Entrez Gene ID: 1353); COX15 homolog, cytochrome c oxidase assembly protein (yeast) (COX15: Entrez Gene ID: 1355); ATP synthase, H+ transporting, mitochondrial F0 complex, subunit C2 (subunit 9) (ATP5G2; Entrez Gene ID: 517); ATP synthase, H+ transporting, mitochondrial F0 complex, subunit G (ATP5L; Gene ID: 10632); ATP synthase, H+ transporting, mitochondrial F1 complex, O subunit (ATP5O; Entrez Gene ID No: 539); and ATP synthase, H+ transporting, mitochondrial F0 complex, subunit s (factor B) (ATP5S; Entrez Gene ID No: 27109)."],"number":2,"annotation":false,"title":false,"claim":true},{"lines":["A method for diagnosing bipolar disorder in a subject, said method comprising the steps:\n
(a) obtaining a cell sample from said subject;\n
(b) subjecting a cell from said sample to glucose stress; and\n
(c) measuring the level of expression in said cell of at least three nuclear encoded mitochondrial energy metabolism nucleic acids or polypeptides, wherein a decrease in said level of expression, as compared to the expression in a cell that is subjected to said stress from a sample obtained from a control subject, is indicative of said subject having bipolar disorder, wherein at least three of said nucleic acids or polypeptides are selected from the group consisting of NADH dehydrogenase (ubiquinone) 1 alpha subcomplex, 5, 13 kDa (NDUFA5; Entrez Gene ID:4698); NADH dehydrogenase (ubiquinone) 1 alpha subcomplex, 6, 14 kDa (NDUFA6; Entrez Gene ID:4700); NADH dehydrogenase (ubiquinone) 1 beta subcomplex, 1, 7 kDa (NDUFB1; Entrez Gene ID: 4707); ubiquinol-cytochrome c reductase binding protein (UQCRB; Entrez Gene ID: 7381); ubiquinol-cytochrome c reductase core protein II (UQCRC2; Entrez Gene ID: 7385); ubiquinol-cytochrome c reductase hinge protein (UQCRH; Entrez Gene ID: 7388); cytochrome c oxidase subunit IV isoform 1 (COX4I1; Entrez Gene ID: 1327); cytochrome c oxidase subunit VIIa polypeptide 2 like (COX7A2L; Entrez Gene ID: 9167); cytochrome c oxidase subunit VIIc (COX7C; Entrez Gene ID: 1350); COX11 homolog, cytochrome c oxidase assembly protein (yeast) (COX11; Entrez Gene ID: 1353); COX15 homolog, cytochrome c oxidase assembly protein (yeast) (COX15: Entrez Gene ID: 1355); ATP synthase, H+ transporting, mitochondrial F0 complex, subunit C2 (subunit 9) (ATP5G2; Entrez Gene ID: 517); ATP synthase, H+ transporting, mitochondrial F0 complex, subunit G (ATP5L; Gene ID: 10632); ATP synthase, H+ transporting, mitochondrial F1 complex, O subunit (ATP5O; Entrez Gene ID No: 539); and ATP synthase, H+ transporting, mitochondrial F0 complex, subunit s (factor B) (ATP5S; Entrez Gene ID No: 27109)."],"number":3,"annotation":false,"title":false,"claim":true},{"lines":["A method for diagnosing bipolar disorder in a subject, said method comprising the steps:\n
(a) obtaining a lymphocyte from said subject;\n
(b) culturing said lymphocyte under glucose stress; and\n
(c) measuring the level of expression in said lymphocyte of at least 15 nuclear encoded mitochondrial energy metabolism nucleic acids, wherein said nucleic acids comprise ATP synthase, mitochondrial F1 complex, O subunit (ATP5O; Entrez Gene ID: 539); cytochrome c oxidase subunit IV isoform 1 (COX4I1; Entrez Gene ID: 1327); and ubiquinol-cytochrome c reductase binding protein (UQCRB; Entrez Gene ID: 7381) and wherein a decrease in said level of expression, as compared to the expression in a lymphocyte obtained from a control subject that is cultured under glucose stress, is indicative of said subject having bipolar disorder."],"number":4,"annotation":false,"title":false,"claim":true},{"lines":["A method for diagnosing bipolar disorder in a subject, said method comprising the steps:\n
(a) obtaining a lymphocyte from said subject;\n
(b) culturing said lymphocyte under glucose stress; and\n
(c) measuring the level of expression in said lymphocyte of at least 15 nuclear encoded mitochondrial energy metabolism nucleic acids of claim 4, wherein said nucleic acids comprise ATP synthase, mitochondrial F1 complex, O subunit (ATP5O; Entrez Gene ID: 539); cytochrome c oxidase subunit IV isoform 1 (COX4I1; Entrez Gene ID: 1327); ubiquinol-cytochrome c reductase binding protein (UQCRB; Entrez Gene ID: 7381); ATP synthase, H+ transporting, mitochondrial F0 complex, subunit s (factor B) (ATP5S; Entrez Gene ID: 27109); and ubiquinol-cytochrome c reductase core protein II (UQCRC2; Entrez Gene ID: 7385) and wherein a decrease in said level of expression, as compared to the expression in a lymphocyte obtained from a control subject that is cultured under glucose stress, is indicative of said subject having bipolar disorder."],"number":5,"annotation":false,"title":false,"claim":true}]}},"filters":{"npl":[],"notNpl":[],"applicant":[],"notApplicant":[],"inventor":[],"notInventor":[],"owner":[],"notOwner":[],"tags":[],"dates":[],"types":[],"notTypes":[],"j":[],"notJ":[],"fj":[],"notFj":[],"classIpcr":[],"notClassIpcr":[],"classNat":[],"notClassNat":[],"classCpc":[],"notClassCpc":[],"so":[],"notSo":[],"sat":[]},"sequenceFilters":{"s":"SEQIDNO","d":"ASCENDING","p":0,"n":10,"sp":[],"si":[],"len":[],"t":[],"loc":[]}}