Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0392674 (exhaustion)
 13,658 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of nisin on the proton motive force (delta p) generated by glucose-energized cells of the obligate putrefactive anaerobe Clostridium sporogenes PA 3679 was determined. The components of delta p, the transmembrane potential (delta psi) and the pH gradient (delta pH), were determined from the distributions of the lipophilic cation [3H]TPP+ ([3H]tetraphenylphosphonium bromide) and [14C]salicylic acid, respectively. The cells maintained a constant delta p of -111 mV, consisting of a delta pH of 0.4 to 1.0 pH units at an external pH of 5 to 7 and a delta psi of -60 to -88 mV. Nisin, carbonyl cyanide m-chlorophenylhydrazone (CCCP), and N,N'-dicyclohexylcarbodiimide (DCCD) at pH 6.0 elicited the complete release of preaccumulated [3H]tetraphenylphosphonium bromide and [14C]salicylic acid, with a concomitant depletion of delta psi and delta pH. Nisin and DCCD caused rapid drops in intracellular ATP levels from 1.2 to 0.01 and 0.06 nmol/mg of cells (dry weight), respectively. Cells exposed to nisin and DCCD lost the ability to form colonies, thus suggesting that delta psi and delta pH are necessary for cell viability. The data suggest that depletion of delta p and exhaustion of cellular ATP reserves are the basis for nisin inhibition of C. sporogenes PA 3679.
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PMID:Nisin dissipates the proton motive force of the obligate anaerobe Clostridium sporogenes PA 3679. 132 40

We have recently reported that acute intraperitoneal administration of pyridostigmine bromide to rats resulted in significant decrements in physical performance in the heat, adverse thermoregulatory effects, and exacerbated elevations in several indices of heat/exercise injury. Since it will be consumed orally as a prophylaxis for organophosphate poisoning, pyridostigmine was dissolved in the drinking water of rats. Consumption of pyridostigmine for 7 days (n = 34, 6.6 mg/day) resulted in a 23% (p less than 0.001) reduction of circulating cholinesterase when compared with a control group (n = 31) while ingestion for 14 days (n = 35, 8.9 mg/day) elicited a 39% (p less than 0.001) inhibition of circulating cholinesterase when compared to a second control group (n = 33). Water and food consumption, rate of weight gain, and overt behavior were unaffected by pyridostigmine consumption. When approximately half the animals in each group were exercised (9.14 m/min) in the heat (35 degrees C) to hyperthermic exhaustion (Tre = 42.5-43 degrees C, rats unable to right themselves), pyridostigmine consumption for 14 days effected a significantly (p less than 0.05) increased rate of weight loss, but no further effects on thermoregulation or performance were noted. Several minor increments were observed in clinical indices of heat/exercise injury in rats consuming pyridostigmine for 14 days. These data indicate that oral dosages of pyridostigmine can probably be titrated to levels of cholinesterase inhibition which are efficacious in prophylaxis against organophosphate toxicity without significant effects on selected physiologic and metabolic processes.
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PMID:Oral pyridostigmine administration in rats: effects on thermoregulation, clinical chemistry, and performance in the heat. 378 59

We have studied the structure of myosin heavy chain (MHC) in the pectoralis muscle of genetically dystrophic (Connecticut Strain) and White Leghorn chicks. MHC was alkylated with N-ethylmaleimide, purified by Sepharose-4B chromatography, and cleaved with cyanogen bromide. The MHC CNBr peptides were analyzed by one-dimensional and two-dimensional isoelectric focusing/sodium dodecyl sulfate gradient gels and by amino acid sequencing. Specific changes were detected in the gel patterns which could be correlated with the loss of muscle function as measured by the exhaustion score (the ability of chicks to rise from a reclining position) in three experimental groups (exhaustion scores: less than 3, 10-20, greater than 30). We have also examined the amino acid sequence of a 3-methyl-histidine-containing peptide which originates from the 20-kDa fragment of pectoralis muscle MHC in dystrophic chicks: Val-Leu-Asn-Ala-Ser-Ala-Ile-Pro-Glu-Gly-*Gln-Phe-*Ile-Asp-Ser-Lys-Lys- Ala-Ser-Leu-Gln-Lys-Leu-Gly-Ser-Ile-Asp-Val-(Asp, 3-methylhistidine, Gln). Comparison of the homologous MHC sequences shows two positions at which MHC from dystrophic chicks differs from that of the White Leghorn chicks *(Glu----Gln and Met----Ile). Thus, both the peptide map and sequence analyses demonstrate that in avian muscular dystrophy an abnormal pectoralis MHC is synthesized. It is not yet clear whether the "dystrophic" MHC is a variant MHC or if it arises from the abnormal expression of an earlier developmental form (embryonic or neonatal) of pectoralis muscle MHC.
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PMID:Structure of myosin heavy chain in avian muscular dystrophy. 399 78

After demonstration of the pathophysiologic principles bronchial obstruction a review of the pharmacotherapeutic possibilities is presented. The main of therapeutics comprehends beta-2-receptor stimulants in combination with theophylline derivatives. Further therapeutic efforts with anticholinergic drugs (ipratropium bromide) preponderant in chronic bronchitis or intrinsic bronchial asthma respectively and with cromolyn sodium in extrinsic asthma are valuable. Glucocorticoids are allowed to be given only after exhaustion of all other modes of treatment, if possible as intermittent long term treatment. The stimulation of expectoration is an essential part of pharmacotherapy. The complex application of less specific methods of pharmacotherapy and physiotherapy belongs to the comprehensive treatment of patients. The threatening life asthmatic status demands the appropriate use of all possibilities of pharmacotherapy and intensive care if necessary.
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PMID:[Recent aspects of pharmacotherapy in obstructive airway diseases with special regard to bronchial asthma (author's transl)]. 611 Nov 62

trans-3,3'-Bis[alpha-(trimethylammonio)methyl]azobenzene bromide (BisQ) is a potent agonist of the acetylcholine receptor (AcChoR) of Electrophorus electricus. BisQ is highly constrained, suggesting that its structure is complementary to the combining site of the AcChoR when the latter is in its activated state. Antibodies produced in rabbits to a conjugate of bovine serum albumin and a derivative of BisQ mimicked the binding characteristics of the AcChoR with respect to the order of binding of a variety of agonists and to the preferred recognition of decamethonium ion (an agonist) over hexamethonium ion (an antagonist). Immunization of three rabbits with purified anti-BisQ yielded antisera having binding characteristics of anti-AcChoR in that, by complement fixation and enzyme immunoassay, crossreactions with receptor preparations from rat, Torpedo, and eel could be demonstrated in sera of all three rabbits immunized. Two of the three rabbits showed signs of muscle weakness similar to that seen after immunization with the AcChoR. One of the rabbits was injected intramuscularly with neostigmine and showed temporary improvement. Another showed post-tetanic exhaustion of hind-limb muscles after stimulation of the sciatic nerve at 50 Hz. Antibodies reactive with the AcChoR, therefore, were elicited by immunization with an antibody to a potent ligand of the AcChoR without the necessity of isolating the receptor itself. A similar mechanism may play a part in the etiology of at least some autoimmune diseases in which antibodies to various other receptors are involved.
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PMID:Anti-idiotypic route to anti-acetylcholine receptor antibodies and experimental myasthenia gravis. 618 15

Adult, male rats (300-325 g) were treated with pyridostigmine bromide (n = 22) or saline (n = 22) to quantitate the effects of cholinesterase inhibition (64%) on the ability to work (9.14 m/min, level treadmill) in the heat (35 degrees C). Pyridostigmine-treated rats had a mean endurance of 23 min, whereas saline-treated animals ran for nearly 35 min (P less than 0.001). Rates of rectal and skin temperature increments were significantly higher (P less than 0.001) in pyridostigmine-treated rats as were water losses (P less than 0.001). Exercise in the heat to hyperthermic exhaustion effected anticipated increments in circulating urea nitrogen, creatinine, lactate dehydrogenase, and potassium levels, whereas pyridostigmine pretreatment had additive effects on lactate and creatine kinase concentrations. Additionally, pyridostigmine elicited a significant (P less than 0.01) hyperglycemia before exercise, an effect noted also with other organophosphate simulants. We concluded that pyridostigmine-induced cholinesterase inhibition had a variety of debilitating effects during work in the heat.
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PMID:Effects of pyridostigmine on ability of rats to work in the heat. 672 66

As a symptom of an underlying condition, cough is one of the most common reasons patients see physicians. To the majority, a cough means that 'something is wrong' and it causes exhaustion and/or self-consciousness. Patients find these reasons as well as effects on lifestyle, fear of cancer and/or AIDS or tuberculosis to be the most troublesome concerns for which they seek medical attention. The treatment of cough can be divided into two main categories: (a) therapy that controls, prevents or eliminates cough (i.e. antitussive); and (b) therapy that makes cough more effective (i.e. protussive). Antitussive therapy can be either specific or nonspecific. Definitive or specific antitussive therapy depends on determining the aetiology or operant pathophysiological mechanism, and then initiating specific treatment. Since the cause of chronic cough can almost always be determined, it is possible to prescribe specific therapy that can be almost uniformly successful. Non-specific antitussive therapy is directed at the symptom; it is indicated when definitive therapy cannot be given. Practically speaking, the efficacy of nonspecific therapy must be evaluated in double-blind, placebo-controlled, randomised studies of pathological cough in humans. Such studies have demonstrated the efficacy of dextromethorphan, codeine and ipratropium bromide aerosol in patients with chronic bronchitis. While the preferred treatment for patients with cough due to angiotensin converting enzyme (ACE) inhibitor therapy is withdrawal of the offending drugs, it may be possible to ameliorate the cough by adding nifedipine, sulindac or indomethacin to the treatment regimen. The efficacy of protussive therapy has not been well documented. Although hypertonic saline aerosol and erdosteine in patients with bronchitis, and amiloride aerosol in patients with cystic fibrosis have been shown to improve mucus clearance, their clinical utility has not been adequately studied.
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PMID:Appropriate use of antitussives and protussives. A practical review. 769 10

Authors studies impedance, stapedius reflex thresholds and stapedius muscle exhaustion on 31 ears of 16 MG patients. Investigations were carried out using GSI 33 computer-assisted middle ear analyzator. Stapedius reflex threshold values were increased in 93% of patients. Stapedius exhaustion was observed in 71% of patients. After the administration of the reversible cholinesterase inhibitor Mestinon (60 mg pyridostigmin bromide), reflex threshold decreased and exhaustion occurred in only 50% of cases. Authors review the literature in context with the audiometric diagnostics of MG and also recommend the use of these methods in more complicated ocular and bulbar cases of MG.
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PMID:The diagnostic value of stapedius reflex and stapedius reflex exhaustion in myasthenia gravis. 1078 53

A number of studies in western countries have shown that respiratory and physical rehabilitation of patients with chronic obstructive pulmonary disease (COPD) only has a minimal effect on respiratory function but can significantly improve physical capacity. The aim of our study was to apply these methods to patients in Kinshasa, Democratic Republic of Congo. We treated 38 patients (20 women) who had bronchial asthma (n=14) or COPD (n=24). These ambulatory patients were treated in two different hospitals in Kinshasa, the university hospital and the general hospital, three times per week for twelve weeks. The patients were treated with kinestherapy and inhaled bronchodilator drugs (salbutamol, and/or ipratropium bromide with a boreal nebulizer) as well as bronchial hygiene and performed breathing exercises on a Bodyguard Ergometer 990 with walking, running and climbing steps until exhaustion. After the rehabilitation program FEV1 increased from 1.37 +/- 0.62 (50% expected) to 1.54 +/- 0.69 (56% expected) (p<0.01). The same trend was observed for walking distance (from 644 +/- 459 m to 1213 +/- 569 m, p<0.001) and for maximal power developed on the cycloergometer (from 45 +/- 20 w to 73 +/- 37 w, p<0.001). In contrast, the maximal work load performed during climbing steps (from 106 +/- 44 w to 115 +/- 23 w) did not improve significantly. COPD patients improved their FEV1 significantly compared with asthma patients. Our study show that pulmonary rehabilitaion increase the level of spontaneous physical activity. The pulmonary rehabilitation program changes the quality of life of COPD patients who are able to move about better for longer periods of time, have a longer walking distance, and improved physical activity level.
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PMID:[Respiratory rehabilitation in patients with bronchial asthma and chronic obstructive pulmonary disease (COPD) in Kinshasa]. 1141 4

Although long-acting inhaled beta 2-agonists improve various outcome measures in COPD, no double-blind study has yet shown a significant effect of these drugs on exercise capacity. In a randomized, double-blind, placebo-controlled, crossover study, patients received formoterol (4, 5, 9, or 18 micrograms b.i.d. via Turbuhaler), ipratropium bromide (80 micrograms t.i.d. via pMDI with spacer), or placebo for 1 week. Main endpoint was time to exhaustion (TTE) in an incremental cycle ergometer test. Secondary endpoints were Borg dyspnoea score during exercise, lung function, and adverse events. Thirty-four patients with COPD were included, mean age 64.8 years, FEV1 55.6% predicted, reversibility 6.1% predicted. All doses of formoterol, and ipratropium significantly improved TTE, FEV1, FEF25-75%, FRC, IVC, RV and sGAW compared with placebo. A negative dose-response relationship was observed with formoterol. Ipratropium increased time to exhaustion more compared with formoterol, 18 micrograms, but not with formoterol, 4.5 and 9 micrograms. No changes in Borg score were found. There was no difference in the adverse event profile between treatments. In conclusion, 1 week of treatment with formoterol and ipratropium significantly improved exercise capacity and lung function compared with placebo. However, a negative dose-response relation for formoterol was unexpected and needs further investigation.
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PMID:Effects of formoterol (Oxis Turbuhaler) and ipratropium on exercise capacity in patients with COPD. 1219 35


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