Gene/Protein Disease Symptom Drug Enzyme Compound
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The possibility that prolonged heat exposure resulting in a failure of central thermoregulatory mechanism may induce cellular damage in brain was examined in young rats. Children exposed to Indian summer heat can develop sudden pathophysiological symptoms. Subjection of young animals to similar acute systemic heat exposure at 38 degrees C (relative humidity, 46%) for 4 h resulted in a profound hyperthermia, and behavioral stress symptoms e.g. salivation and prostration. Subsequent morphological examination of the brain tissue revealed profound cellular changes. In the cerebral cortex, dark neurons, swollen astrocytes, and expanded white and gray matter were quite frequent. At the ultrastructural level, collapse of microvessels, perivascular edema, vacuolation and damage to postsynaptic membrane was very common. Thus, profound hyperthermia can induce cellular changes by some direct or indirect (e.g. neurochemical) mechanism.
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PMID:Acute heat exposure causes cellular alteration in cerebral cortex of young rats. 176 59

Rocastine [AHR-11325, 2-[2-(dimethylamino)ethyl]-2,3-dihydro-4-methylpyrido-[3,2-f]-1,4- oxazepine-5(4H)-thione (E)-2-butenedioate)] is a rapid-acting, potent, nonsedating antihistamine. In guinea pigs challenged with a lethal dose of histamine, rocastine is as effective [based on 1 hr. oral, protective dose (PD50S)] as brompheniramine, chlorpheniramine, pyrilamine, and promethazine and superior to astemizole, diphenhydramine, terfenadine, and oxatomide. Rocastine has a faster onset of action than does terfenadine; rocastine being as effective with a 15 min pretreatment time (PD50 = 0.13 mg/kg) as it is with a 1 hr pretreatment time (PD50 = 0.12 mg/kg), while the 15 min PD50 of terfenadine (PD50 = 44.0 mg/kg) is 22 times greater than the 1 hr PD50 (PD50 = 1.93 mg/kg). Against aerosolized histamine, rocastine was 7.12 x, 2.63 x, and equipotent to pyrilamine in preventing histamine-induced prostration at pretreatment times of 1,3, and 6 hr, respectively. Rocastine protected guinea pigs from collapse induced by aerosolized antigen; rocastine was approximately 36 x more potent (based on 1 hr PD50) than diphenhydramine and as potent as oxatomide and terfenadine. Rocastine did not alter the EEG of cats at doses in vast excess (150x) of its antihistaminic dose nor did it potentiate yohimbine toxicity in mice. Further, rocastine possesses no anticholinergic, antiadrenergic, or antiserotonergic properties in vitro. Rocastine is a selective, nonsedating, H1-antagonist with a rapid onset of action.
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PMID:Rocastine (AHR-11325), a rapid acting, nonsedating antihistamine. 257 Dec 44

Clinical signs and lesions of levamisole toxicosis include: nausea, vomiting, increased salivation, frequent urination and defecation, colic, dizziness, headache, muscle tremors, ataxia, anxiety, hyperesthesia with irritability, clonic convulsions, depression, rapid respiration, dyspnea, prostration, collapse, hemorrhages in the subepicardium and thalamus, enteritis, hepatic degeneration and necrosis, and splenic congestion. Most of these signs and lesions are similar to those observed in nicotine poisoning. Levamisole causes vasopressor and panting effects which are blocked by ganglionic blocking agents hexamethonium and mecamylamine but are not blocked by atropine. The vasopressor effect of levamisole is blocked by alpha-adrenergic antagonists phentolamine and dibenamine; however, the respiratory effect of levamisole is not affected by these alpha-adrenergic antagonists. Repeated IV injections of levamisole cause a tachyphylactic response. With levamisole-induced tachyphylaxis, the effects of other ganglionic stimulants dimethylpiperazinium and nicotine are also abolished. Levamisole causes an electroencephalographic arousal which is antagonized by atropine sulfate and mecamylamine. There is also a structural similarity of levamisole to nicotine. These studies suggest that levamisole is a nicotine-like compound. Possible treatment of levamisole poisoning is discussed. Drug interactions of levamisole with organophosphates and anthelmintics, eg, pyrantel, methyridine, and diethylcarbamazine, are also discussed.
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PMID:Toxicity and drug interactions of levamisole. 721 95

The symptoms of severe malaria and their contribution to mortality were assessed in 290 children in northern Ghana. Common symptoms were severe anemia (55%), prostration (33%), respiratory distress (23%), convulsions (20%), and impaired consciousness (19%). Age influenced this pattern. The fatality rate was 11.2%. In multivariate analysis, circulatory collapse, impaired consciousness, hypoglycemia, and malnutrition independently predicted death. Children with severe malaria by the current World Health Organization (WHO) classification, but not by the previous one (1990), showed relatively mild clinical manifestations and a low case fatality rate (3.2%). In hospitalized children with severe malaria in northern Ghana, severe anemia is the leading manifestation, but itself does not contribute to mortality. In this region, malnutrition and circulatory collapse were important predictors of fatal malaria. The current WHO criteria serve well in identifying life-threatening disease, but also include rather mild cases that may complicate the allocation of immediate care in settings with limited resources.
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PMID:Manifestation and outcome of severe malaria in children in northern Ghana. 1530 5

Plasmodium falciparum serine repeat antigen (SERA5) is a promising asexual blood stage malaria candidate vaccine. However, there is a paucity of information about natural immune responses to SERA5 in children from malaria-endemic regions. We undertook a hospital-based case-control study of severe malaria in Apac District, Northern Uganda, in children 6-59 months of age. The commonest symptoms observed in children with severe malaria (SM) were respiratory distress (53.4%) and prostration (40.4%) followed by circulatory collapse (7.4%), severe anemia (Hb < 5 g/dL, 7.0%), and seizures (2.6%). None of the SM children had impaired consciousness, coma, or cerebral malaria. We measured serum IgG antibodies using a recombinant construct of SERA5 (SE36) in enzyme-linked immunosorbent assays. High titers of IgG anti-SE36 were associated with protection against severe malaria in children under 5 years old.
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PMID:High titers of IgG antibodies against Plasmodium falciparum serine repeat antigen 5 (SERA5) are associated with protection against severe malaria in Ugandan children. 1647 69

A definite intoxication develops as a result of a closed intestinal loop and toxic material accumulates in the closed loops. Much evidence has been submitted to show that this loop poison causes the intoxication observed after producing a closed intestinal loop. Sufficient evidence has been presented to prove that the essential poison is present in these closed intestinal loops, and usually in concentrated form. Chemical study of the contents of closed intestinal loops shows that a single substance or group of substances possesses toxic properties. This resists autolysis and pancreatic and ereptic digestion. It is thrown out of solution by five volumes of alcohol or by half saturation with ammonium sulphate. It is readily soluble in water and is not injured by boiling. It is not removed by dialysis. The method of isolation excludes practically all substances except primary proteoses. The characteristic resistance to digestive enzymes suggests a heteroproteose. Proteose intoxication in dogs gives a picture identical with that described after poisoning with intestinal loop fluid: early salivation and vomiting, followed by diarrhea and prostration, fall in temperature and blood pressure, and finally death in collapse. Autopsy shows essentially a splanchnic paralysis and remarkable engorgement of liver and spleen, but especially of the mucosa of the duodenum and small intestine. The blood shows great concentration due to loss of fluid and may remain incoagulable because of an excess production of antithrombin. Proteoses escaping from the blood are excreted in the urine. This toxic proteose concerned in intestinal obstruction has not yet been isolated in the urine, but may be excreted by the kidneys. This probably explains the clinical improvement and lessened intoxication noted after transfusion. Experimental evidence points to a primary proteose as the essential poison concerned in the intoxication of closed intestinal loops and intestinal obstruction.
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PMID:INTESTINAL OBSTRUCTION : V. PROTEOSE INTOXICATION. 1986 66

Shenfu injection is developed by improving dosage form of ancient prescription "Shenfu Tang" and is mainly derived from extracts of both traditional Chinese medicine red ginseng and prepared lateral root of monkshood with polysorbate 80 as auxiliary material. Shenfu injection may be administered through intramuscular injection, intravenous drip or intravenous injection. It produces good effects in restoring Yang and rescuing patients from collapse, tonifying Qi and preventing exhaustion. It is mainly used to treat not only syncope and prostration resulting from sudden Yang collapse (infectious, hemorrhagic and water depletion shock etc), but also pavor, palpitation, dyspnea with cough, stomachache, diarrhea and arthralgia etc caused by deficiency of Yang (deficiency of vital energy). Research group has audited the monitored hospitals and has carried out postmarketing study of Shenfu solution from many aspects including literature review, spontaneous reporting system (SRS) and hospital information system (HIS) data analysis etc. A summary is shown below.
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PMID:[Research and practice about risk control of shenfu injection]. 2553 12