Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015674 (chronic fatigue syndrome)
 2,978 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

BACKGROUND: Chronic fatigue syndrome (CFS) has no diagnostic clinical signs or diagnostic laboratory abnormalities and it is unclear if it represents a single illness. The CFS research case definition recommends stratifying subjects by co-morbid conditions, fatigue level and duration, or functional impairment. But to date, this analysis approach has not yielded any further insight into CFS pathogenesis. This study used the integration of peripheral blood gene expression results with epidemiologic and clinical data to determine whether CFS is a single or heterogeneous illness. RESULTS: CFS subjects were grouped by several clinical and epidemiological variables thought to be important in defining the illness. Statistical tests and cluster analysis were used to distinguish CFS subjects and identify differentially expressed genes. These genes were identified only when CFS subjects were grouped according to illness onset and the majority of genes were involved in pathways of purine and pyrimidine metabolism, glycolysis, oxidative phosphorylation, and glucose metabolism. CONCLUSION: These results provide a physiologic basis that suggests CFS is a heterogeneous illness. The differentially expressed genes imply fundamental metabolic perturbations that will be further investigated and illustrates the power of microarray technology for furthering our understanding CFS.
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PMID:Integration of gene expression, clinical, and epidemiologic data to characterize Chronic Fatigue Syndrome. 1464 39

A metabolomics approach was used to explore the effects of Panax quinquefolius (PQ) and Acorus gramineus (AG) on learning and memory in rats with diabetic-induced cognitive impairment. Thirty Wistar rats were divided into three groups, namely the normal-group, model-group, and Panax quinquefolius-Acorus gramineus-group (PQ-AG-group, 1.80g/kg/d). Diabetes was induced by intraperitoneal injection of streptozotocin (STZ, 65mg/kg). Cerebrospinal fluid (CSF) was collected via cisterna magna puncture, and the Morris water maze method was used to evaluate learning and memory in rats after 11 weeks of PQ-AG treatment. Metabolic profiling of CFS samples wasperformed by using UPLC-Q-TOF-MS. Compared to the normal-group, the escape latency of the Morris water mazewas significantly prolonged in model-group rats after 12 weeks (p<0.01). Compared with the model-group, however, the escape latency was significantly shortened in PQ-AG-group rats (p<0.05). In multivariate statistical analysis, we identified 33 potential biomarkers, and six biomarkers were alteredby PQ-AG. These biomarkers were involved in the metabolism of pyrimidine; nicotinate and nicotinamide; glycine, serine, and threonine; and ascorbate and aldarate. Taken collectively, our results indicate that PQ-AG can attenuate diabetic-induced cognitive impairment by affecting a variety of metabolic pathways. Our results provide an experimental basis for studying the mechanism of action of PQ-AG.
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PMID:Metabolomics study of cerebrospinal fluid from diabetic rats with cognitive impairment simultaneously treated with Panax quinquefolius and Acorus gramineus. 3327 56