Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study is presented of the effect of a new native calcium antagonist foridon on the course of the disease central and peripheral hemodynamics, fatty metabolism, lipid peroxidation intensity, activity of ceruloplasmin and catalase, iron and chromium saturation of transferrin, content of cyclic nucleotides in thrombocytes, the state of cellular immunity and the number of circulating immune complex in 30 patients with advancing and stable exertion stenocardia (control--30 analogous patients treated by phynoptin and corinfar). It was established that foridon produced a positive effect on the intensity of the pain syndrome, hemodynamics, degree of lipid peroxidation, content of cyclic nucleotides and immune status of stenocardia patients.
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PMID:[The efficacy of foridon in treating stenocardia patients]. 180 58

L-656,224 (7-chloro-2-[(4-methoxyphenyl)methyl]-3-methyl-5-propyl-4-benzofuranol) was a potent inhibitor of leukotriene biosynthesis in intact rat and human leukocytes and CXBG mastocytoma cells (IC50 values, 18-240 nM) and of crude human leukocyte and highly purified porcine leukocyte 5-lipoxygenase (IC50 value, 4 X 10(-7) M). The selectivity of L-656,224 for 5-lipoxygenase was shown through the relative lack of activity of the compound on 12-lipoxygenase, 15-lipoxygenase, cyclooxygenase, catalase, and myeloperoxidase. The compound showed (i) oral activity against hyperalgesia induced in the rat paw by injection of yeast or platelet-activating factor, (ii) dyspnea in sensitized inbred rats induced by an aerosol of antigen, and (iii) bronchoconstriction induced by an aerosol of Ascaris in squirrel monkeys, suggesting a role for 5-lipoxygenase inhibitors in the treatment of asthma and peripheral pain.
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PMID:L-656,224 (7-chloro-2-[(4-methoxyphenyl)methyl]-3- methyl-5-propyl-4-benzofuranol): a novel, selective, orally active 5-lipoxygenase inhibitor. 283 37

Met5-enkephalin, tyr-gly-phe-met, is an endogenous pentapeptide, with morphine agonist activity. In this study, we demonstrated that met5-enkephalin was degraded with the release of tyrosine by resting human PMN, whereas it was degraded as well as oxidized to its sulfoxide derivative, met5-(O)-enkephalin, by phagocytosing PMN. PMN also degraded met5-(O)-enkephalin but to a lesser extent. Bacitracin at 1 gm/L inhibited the degradation and oxidation of met5-enkephalin without affecting the production of superoxide and viability of PMN. The oxidation of met5-enkephalin by phagocytosing PMN was inhibited by catalase or NaN3 but not by SOD. This suggests that the oxidation of met5-enkephalin by phagocytosing PMN was, at least in part, dependent on the MPO system (MPO-H2O2-halide). Using purified canine MPO, we further demonstrated that MPO-H2O2-CI- oxidized met5-enkephalin to met5-(O)-enkephalin. The MPO-mediated oxidation of met5-enkephalin was inhibited by methionine but not by methionine sulfoxide, tyrosine, glycine, or phenylalanine, confirming that it was the methionine moiety of met5-enkephalin which was oxidized. Since both the sulfoxide derivative and the degradation products met5-enkephalin have reduced opiate agonist activity, oxidation and degradation of met5-enkephalin by PMN may contribute to the pain at the site of inflammation. (J Lab Clin Med 99:418, 1982.)
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PMID:Degradation and oxidation of methionine enkephalin by human neutrophils. 627 80

The usual initial life-threatening effect of injury is hypovolemic shock. In the hierarchical physiologic response to hypovolemia, perfusion of peripheral tissues is sacrificed early and restored late. But the usual hemodynamic and metabolic measurements of blood pressure, urine output, and base deficit are not reliable indices of peripheral perfusion. Although the Clark electrode can quantitate tissue oxygen pressure and thereby serve as an index of perfusion, its use is compromised by several technical deficiencies. Recently, an optical method (optode) using fluorescent technology has been developed for measurement of oxygen tension in subcutaneous tissue (P sgO2). Our studies compared this device with the Clark electrode in the laboratory and tested its value in both animal and clinical studies of hypovolemic shock. The results of these several studies demonstrated that: (1) the new oximeter tracked a rapid fall or rapid rise of oxygen tension between room air (150 mm Hg) and 0 mm Hg ( a glucose oxidase/catalase solution) as well as the Clark electrode without encountering its technical problems; (2) with an acute hemorrhage to 20% of base line, the PsgO2 was found to decline rapidly in parallel with the decline of mean arterial pressure (MAP). Although the MAP rapidly returned to normal after immediate complete return of all shed blood, the PsgO2 did not reach normal levels for at least 2 hours, suggesting persistent peripheral vasoconstriction. (3) Studies in progress suggest that between 35 and 78% of trauma patients (n = 18) adequately resuscitated for hypovolemia b customary criteria have a decreased level of PsgO2 for as long as 60 hours after resuscitation for injury. If care is taken to prevent other causes of catecholamine induced vasoconstriction such as pain, fear, cold, and arterial hypoxia, these several results suggest that a certain number of injured patients are inadequately resuscitated despite the return to normal of conventional hemodynamic measurements. The serial analysis of PsgO2 may assist in managing patients and promote better understanding of the responses to injury.
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PMID:Subcutaneous tissue oxygen pressure: a reliable index of peripheral perfusion in humans after injury. 860 91

The radioactive and thermal effects of radon hot spring were biochemically compared under a sauna room or hot spring conditions with a similar chemical component, using the parameters that are closely involved in the clinic for radon therapy. The results showed that the radon and thermal therapy enhanced the antioxidation functions, such as the activities of superoxide dismutase (SOD) and catalase, which inhibit lipid peroxidation and total cholesterol produced in the body. Moreover the therapy enhanced concanavalin A (ConA)-induced mitogen response and increased the percentage of CD4 positive cells, which is the marker of helper T cells, and decreased the percentage of CD8 positive cells, which is the common marker of killer T cells and suppressor T cells, in the white blood cell differentiation antigen (CD8/CD4) assay. Furthermore, the therapy increased the levels of alpha atrial natriuretic polypeptide (alpha ANP), beta endorphin, adrenocorticotropic hormone (ACTH), insulin and glucose-6-phosphate dehydrogenase (G-6-PDH), and it decreased the vasopression level. The results were on the whole larger in the radon group than in the thermal group. The findings suggest that radon therapy contributes more to the prevention of life-style-related diseases related to peroxidation reactions and immune suppression than to thermal therapy. Moreover, these indicate what may be a part of the mechanism for the alleviation of hypertension, osteoarthritis (pain), and diabetes mellitus brought about more by radon therapy than by thermal therapy.
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PMID:Biochemical comparison between radon effects and thermal effects on humans in radon hot spring therapy. 1513 94

A 53-year-old, male patient presented with pain in the middle area of the back of his left foot. The painful area was associated with a reddish dome-shaped swelling of 24 by 18 mm which had ulcerated in the center part. Histopathologically, the cutaneous lesion consisted of an ulcer surrounded by abscess and granuloma and numerous acid-fast organisms were observed. Subsequently, the area just below the left inguinal area developed redness and swelling approaching the size of a quail egg. The patient responded favorably with rifampicin, levofloxacin, and minocycline therapy. The patient was immunodeficient, but negative for HIV-1 and HIV-2 antibodies and the etiology of his immunodeficient state is unclear. Skin tissues or pus were cultured at 37 degrees C on 2% Ogawa and BBL MGIT. Acid-fast organisms were recovered on MGIT within 4 to 12 days, while 2% Ogawa medium failed to recover acid-fast bacteria. Using growth from the positive MGIT tube as inoculum, MycoBroth, 7H9 broth, 7H11.2% Ogawa supplemented with or without iron complexes, and blood agar were inoculated and cultured at 30 and 37 degrees C. Growth at 30 and 37 degrees C was seen with MycoBroth, 7H9, hemin (60 microM) or ferric ammonium citrate (15 mg/ml) supplemented 7H11 and blood agar as well as 7H11 supplemented with factor X. Growth at 30 degrees C only was observed for ferric ammonium citrate supplemented 7H9 and 2% Ogawa. Generally, growth at 30 degrees C was better than that at 37 degrees C in all media. No growth at either temperature was observed with hemin or factor X supplemented 2% Ogawa. With respect to the biochemical characterization, the isolate was negative for niacin, nitrate reduction, urease, arylsulfatase, Tween 80 hydrolysis, catalase, 68 degrees C catalase, acid phosphatase, and tellurite reduction, while strongly positive for neutral red test. Sequencing of the 16S rRNA gene showed the isolate to be consistent with Mycobacterium haemophilum. Based on the composite characterization, the isolate was identified as M. haemophilum. This is the second case report of M. haemophilum infection in Japan in the literature.
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PMID:[Bacteriological features of Mycobacterium haemophilum isolated from skin lesions in an immunodeficient patient]. 1521 60

Hydrogen peroxide is an oxidising agent that is used in a number of household products, including general-purpose disinfectants, chlorine-free bleaches, fabric stain removers, contact lens disinfectants and hair dyes, and it is a component of some tooth whitening products. In industry, the principal use of hydrogen peroxide is as a bleaching agent in the manufacture of paper and pulp. Hydrogen peroxide has been employed medicinally for wound irrigation and for the sterilisation of ophthalmic and endoscopic instruments. Hydrogen peroxide causes toxicity via three main mechanisms: corrosive damage, oxygen gas formation and lipid peroxidation. Concentrated hydrogen peroxide is caustic and exposure may result in local tissue damage. Ingestion of concentrated (>35%) hydrogen peroxide can also result in the generation of substantial volumes of oxygen. Where the amount of oxygen evolved exceeds its maximum solubility in blood, venous or arterial gas embolism may occur. The mechanism of CNS damage is thought to be arterial gas embolisation with subsequent brain infarction. Rapid generation of oxygen in closed body cavities can also cause mechanical distension and there is potential for the rupture of the hollow viscus secondary to oxygen liberation. In addition, intravascular foaming following absorption can seriously impede right ventricular output and produce complete loss of cardiac output. Hydrogen peroxide can also exert a direct cytotoxic effect via lipid peroxidation. Ingestion of hydrogen peroxide may cause irritation of the gastrointestinal tract with nausea, vomiting, haematemesis and foaming at the mouth; the foam may obstruct the respiratory tract or result in pulmonary aspiration. Painful gastric distension and belching may be caused by the liberation of large volumes of oxygen in the stomach. Blistering of the mucosae and oropharyngeal burns are common following ingestion of concentrated solutions, and laryngospasm and haemorrhagic gastritis have been reported. Sinus tachycardia, lethargy, confusion, coma, convulsions, stridor, sub-epiglottic narrowing, apnoea, cyanosis and cardiorespiratory arrest may ensue within minutes of ingestion. Oxygen gas embolism may produce multiple cerebral infarctions. Although most inhalational exposures cause little more than coughing and transient dyspnoea, inhalation of highly concentrated solutions of hydrogen peroxide can cause severe irritation and inflammation of mucous membranes, with coughing and dyspnoea. Shock, coma and convulsions may ensue and pulmonary oedema may occur up to 24-72 hours post exposure. Severe toxicity has resulted from the use of hydrogen peroxide solutions to irrigate wounds within closed body cavities or under pressure as oxygen gas embolism has resulted. Inflammation, blistering and severe skin damage may follow dermal contact. Ocular exposure to 3% solutions may cause immediate stinging, irritation, lacrimation and blurred vision, but severe injury is unlikely. Exposure to more concentrated hydrogen peroxide solutions (>10%) may result in ulceration or perforation of the cornea. Gut decontamination is not indicated following ingestion, due to the rapid decomposition of hydrogen peroxide by catalase to oxygen and water. If gastric distension is painful, a gastric tube should be passed to release gas. Early aggressive airway management is critical in patients who have ingested concentrated hydrogen peroxide, as respiratory failure and arrest appear to be the proximate cause of death. Endoscopy should be considered if there is persistent vomiting, haematemesis, significant oral burns, severe abdominal pain, dysphagia or stridor. Corticosteroids in high dosage have been recommended if laryngeal and pulmonary oedema supervene, but their value is unproven. Endotracheal intubation, or rarely, tracheostomy may be required for life-threatening laryngeal oedema. Contaminated skin should be washed with copious amounts of water. Skin lesions should be treated as thermal burns; surgery may be required for deep burns. In the case of eye exposure, the affected eye(s) shod eye(s) should be irrigated immediately and thoroughly with water or 0.9% saline for at least 10-15 minutes. Instillation of a local anaesthetic may reduce discomfort and assist more thorough decontamination.
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PMID:Hydrogen peroxide poisoning. 1529 93

The aim of the study was to investigate clinical efficacy of the medical complex Galavit in patients with acute phase of duodenal ulcer (DU) in. The subjects were 60 DU patients aged 32 +/- 2 years with ulcerous defects of 0.4 to 1.3 cm in diameter. In patients receiving Galavit, pain was coped with by Mann-Whitney method in 2.5 +/- 0.2 days, p < 0.001; in the control group--in 5.7 +/- 0.1 days. In the Galavit group the ulcers healed in 11.3 +/- 0.2 days, p < 0.001; in the control group--17.8 +/- 0.3 days; in 4 cases (13.3%) the ulcerous defects healed with forming of rough scars. Galavit elevated T-lymphocyte rate from 53.1 +/- 0.6% to 65.1 +/- 0.2%, p < 0.001; T-helper inductor level--from 27.8 +/- 0.2% to 38.5 +/- 0.3%, p < 0.001; cytotoxic T-lymphocyte level--from 18.5 +/- 0.5% to 27.3 +/- 0.3%, p < 0.001; B-lymphocyte level--from 12.3 +/- 0.2% to 19.1 +/- 0.1%, p < 0.001. The therapy significantly lowered malonic aldehyde level by 23.5%, trienoic conjugate level--by 61.6%; superoxide dismutase level rose 1.6 times, catalase level--1.4 times, glutathion reductase level--from 19.03 +/- 1.17 to 27.01 +/- 1.24 optical density units/mg, p < 0.001. The study did not find any significant changes in the immune status and lipid peroxidative/antioxidative system of patients receiving basic therapy. The results show that Galavit has anti-inflammatory effect, improves immune status and anti-oxidative protection. It is appropriate to administer Galavit as a component of DU basic therapy. The results show that Galavit has anti-inflammatory effect, improves immune status and anti-oxidative protection. It is appropriate to administer Galavit as a component of DU basic therapy.
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PMID:[Efficacy of galavit in patients with duodenal ulcer]. 1621 70

Nerve growth factor (NGF) regulates the nociceptive properties of a subset of small diameter sensory neurons by increasing the expression of the heat-sensing transient receptor potential (TRP) channel, TRPV1. This action involves activation of the tyrosine kinase receptor (Trk) A/p38 MAPK pathway. Recent studies indicate that activation of TrkA promotes superoxide generation via NADPH oxidase. In this study, we determined whether the NADPH oxidase pathway is involved in NGF-stimulated TRPV1 expression using a rat pheochromocytoma 12 line and rat dorsal root ganglion neurons. Treatment of these cells with NGF (100 ng/mL) increased TRPV1 protein expression (approx. twofold) but not mRNA. This increase was mimicked by H(2)O(2) and attenuated by catalase and inhibitors of NADPH oxidase. NGF stimulated NADPH oxidase activity, while 24 h exposure further increased expression of the Rac1 and gp91(phox) subunits of the holoenzyme. Inhibition of NADPH oxidase by transient transfection of a dominant negative Rac1 mutant (RacN17) plasmid blocked NGF-stimulated TRPV1 protein expression, while expression of a constitutively active Rac1 increased basal and NGF-stimulated TRPV1 levels. Inhibition of NADPH oxidase activity also attenuated NGF-dependent p38 MAPK activation. We conclude that the Rac1/NADPH oxidase pathway regulates p38 activation and TRPV1 expression which aids in the maintenance of peripheral neuron integrity and pain perception.
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PMID:Essential role of Rac1/NADPH oxidase in nerve growth factor induction of TRPV1 expression. 1628 57

Oxidative stress is an important pathophysiological mechanism of many neurological diseases. Reactive oxygen and nitrogen species have been cited as molecules involved in the nociceptive process. In this study, rats were submitted to sciatic nerve transection (SNT) for induction of neuropathic pain, and enzyme activities of SOD and catalase as well as lipid peroxidation (LPO) were measured in the lumbosacral spinal cord. The results show that LPO was not changed after SNT. SOD activity was reduced 7 days after SNT, while the change in catalase activity occurred on the third and seventh days in both sham and SNT animals. Hyperalgesia in SNT group was detected at the same points in time. These results suggest that SNT was not a strong enough stimulus to deplete all antioxidant content in the spinal cord, since increase in LPO was not detected. However, the role of oxidative stress in nociception can not be excluded.
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PMID:Neuropathic pain modifies antioxidant activity in rat spinal cord. 1677 Jul 31


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