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)

Ischaemic lactate/ammonia tests, serum carnosinase and creatine kinase assays and percutaneous needle muscle biopsies were performed on 10 patients with chronic fatigue syndrome (CFS), and 10 with chronic alcohol misuse complaining of muscular symptoms. Basal serum lactate levels were significantly elevated in the alcohol misusers compared to the CFS patients, but all were within the reference range. Lactate profiles after ischaemic forearm exercise did not differ significantly for the two patient groups. In one patient previously diagnosed as having CFS, myoadenylate deaminase deficiency was identified on the basis of a flat ammonia response to ischaemia and absent muscle adenosine monophosphate deaminase activity. In addition, two further patients in the CFS group were subsequently shown to have other disorders: one had polymyositis and one had myopathy with mild type II fibre atrophy of unknown cause. Histomorphometric examination of muscle needle biopsy in the alcohol misusers showed features of chronic alcohol-induced skeletal myopathy in six patients and polymyositis in one patient. Type II fibre atrophy factors were significantly elevated in the alcohol group but were within the reference range in CFS patients. Dynamic tests of muscle function and muscle histology are valuable tools in excluding alternative pathology in CFS, whereas muscle histomorphometry is of the greatest value in the diagnosis of chronic alcoholic myopathy.
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PMID:Use of dynamic tests of muscle function and histomorphometry of quadriceps muscle biopsies in the investigation of patients with chronic alcohol misuse and chronic fatigue syndrome. 783 72

Autoimmune dysfunction of certain vasoactive neuropeptides (VNs) has been postulated as a contributing cause of sudden infant death syndrome (SIDS), chronic fatigue syndrome (CFS), Gulf War syndrome (GWS) and other fatigue-related disorders. This family of VNs includes pituitary adenylate cyclase activating polypeptide (PACAP), vasoactive intestinal peptide (VIP) and calcitonin gene related peptide (CGRP). The postulated mechanism is compromise of adenylate cyclase activation, a vital and unique step in cyclic AMP production from ATP, through autoimmune dysfunction of VNs, their receptors or their genes possibly involving cytosine-phosphate-guanine (CpG) fragments. CpG fragments are immunomodulatory dinucleotides serving as 'friend or foe' recognition systems to differentiate bacterial and viral (hypomethylated CpG) from mammalian (methylated CpG) DNA. However hypomethylation disorders affecting these fragments in mammals may convert them to dysfunctional states by promoting autoimmune inflammatory reactions. Epigenetic mechanisms acting on gene promoter regions may contribute to the development of VN autoimmune fatigue-related disorders through CpG fragments located in vital segments of VN/receptor genes by causing signalling defects with profound implications for VN function. Neurotransmitter dysfunction particularly glutamatergic transmission could also result with disruption of neuronal cellular biochemical functions such as ammonia regulation. Endosomal acidity and mitochondrial membrane potential modifiers such as chloroquine, together with immunoregulatory therapies, may have therapeutic implications in protecting against these apparent autoimmune disorders. This paper examines specific epigenetic and biochemical mechanisms possibly mediated by VN or receptor genes resulting in postulated VN autoimmune fatigue-related disorders. These mechanisms may have implications for treatment and prevention options for VN autoimmune disorders. VN autoimmune processes have implications for military medicine where radiological, chemical and biological agents may play an important role in pathogenesis.
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PMID:Does dysregulation of key epigenetic and biochemical pathways occur in postulated vasoactive neuropeptide autoimmune disorders? 1602 37

Ammonia (NH(3)) emission from livestock manures used in agriculture reduces N uptake by crops and negatively impacts air quality. This laboratory study was conducted to evaluate NH(3)emission from different livestock manures applied to two soils: Candler fins sand (CFS; light-textured soil, pH 6.8 and field capacity soil water content of 70 g kg(-1)) from Lake Alfred, Florida and Ogeechee loamy sand (OLS; medium-textured soil, pH 5.2 and field capacity soil water content of 140 g kg(-1)) from Savannah, Georgia. Poultry litter (PL) collected from a poultry farm near Douglas, Georgia, and fresh solid separate of swine manure (SM) collected from a farm near Clinton, North Carolina were used. Each of the soil was weighed in 100 g sub samples and amended with either PL or SM at rates equivalent to either 0, 2.24, 5.60, 11.20, or 22.40 Mg ha(-1) in 1L Mason jars and incubated in the laboratory at field capacity soil water content for 19 days to monitor NH(3) volatilization. Results indicated a greater NH(3) loss from soils amended with SM compared to that with PL. The cumulative NH(3)volatilization loss over 19 days ranged from 4 to 27% and 14 to 32% of total N applied as PL and SM, respectively. Volatilization of NH(3) was greater from light-textured CFS than that from medium-textured OLS. Volatilization loss increased with increasing rates of manure application. Ammonia volatilization was lower at night time than that during the day time. Differences in major factors such as soil water content, temperature, soil type and live stock manure type influenced the diurnal variation in volatilization loss of NH(3) from soils. A significant portion (> 50%) of cumulative NH(3) emission over 19 d occurred during the first 5-7 d following the application of livestock manures. Results of this study demonstrate that application of low rates of livestock manure (< or = 5.60 Mg ha(-1)) is recommended to minimize NH(3) emissions.
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PMID:Ammonia volatilization loss from surface applied livestock manure. 1928 Apr 86

A series of in vitro studies were carried out to determine i) the effects of enzyme and formaldehyde treatment on the degradation characteristics of carbohydrate and protein sources and on the synchronicity of these processes, and ii) the effects of synchronizing carbohydrate and protein supply on rumen fermentation and microbial protein synthesis (MPS) in in vitro experiments. Untreated corn (C) and enzyme-treated corn (EC) were combined with soy bean meal with (ES) and without (S) enzyme treatment or formaldehyde treatment (FS). Six experimental feeds (CS, CES, CFS, ECS, ECES and ECFS) with different synchrony indices were prepared. Highly synchronous diets had the greatest dry matter (DM) digestibility when untreated corn was used. However, the degree of synchronicity did not influence DM digestibility when EC was mixed with various soybean meals. At time points of 12 h and 24 h of incubation, EC-containing diets showed lower ammonia-N concentrations than those of C-containing diets, irrespective of the degree of synchronicity, indicating that more efficient utilization of ammonia-N for MPS was achieved by ruminal microorganisms when EC was offered as a carbohydrate source. Within C-containing treatments, the purine base concentration increased as the diets were more synchronized. This effect was not observed when EC was offered. There were significant effects on VFA concentration of both C and S treatments and their interactions. Similar to purine concentrations, total VFA production and individual VFA concentration in the groups containing EC as an energy source was higher than those of other groups (CS, CES and CFS). The results of the present study suggested that the availability of energy or the protein source are the most limiting factors for rumen fermentation and MPS, rather than the degree of synchronicity.
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PMID:Effects of synchronicity of carbohydrate and protein degradation on rumen fermentation characteristics and microbial protein synthesis. 2504 98

The human gut microbiome impacts human brain health in numerous ways: (1) Structural bacterial components such as lipopolysaccharides provide low-grade tonic stimulation of the innate immune system. Excessive stimulation due to bacterial dysbiosis, small intestinal bacterial overgrowth, or increased intestinal permeability may produce systemic and/or central nervous system inflammation. (2) Bacterial proteins may cross-react with human antigens to stimulate dysfunctional responses of the adaptive immune system. (3) Bacterial enzymes may produce neurotoxic metabolites such as D-lactic acid and ammonia. Even beneficial metabolites such as short-chain fatty acids may exert neurotoxicity. (4) Gut microbes can produce hormones and neurotransmitters that are identical to those produced by humans. Bacterial receptors for these hormones influence microbial growth and virulence. (5) Gut bacteria directly stimulate afferent neurons of the enteric nervous system to send signals to the brain via the vagus nerve. Through these varied mechanisms, gut microbes shape the architecture of sleep and stress reactivity of the hypothalamic-pituitary-adrenal axis. They influence memory, mood, and cognition and are clinically and therapeutically relevant to a range of disorders, including alcoholism, chronic fatigue syndrome, fibromyalgia, and restless legs syndrome. Their role in multiple sclerosis and the neurologic manifestations of celiac disease is being studied. Nutritional tools for altering the gut microbiome therapeutically include changes in diet, probiotics, and prebiotics.
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PMID:The gut microbiome and the brain. 2540 18