Gene/Protein Disease Symptom Drug Enzyme Compound
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 21,692 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The geometry of replicative form (RF) DNA synthesis of the H-1 parvovirus was studied with the electron microscope using formamide or aqueous variations of the Kleinschmidt spreading procedure. H-1 DNA was isolated from human or hamster cells infected with a temperature-sensitive mutant, ts1, which is deficient in progeny single-stranded DNA synthesis at the restrictive temperature (S.L. Rhode, 1976), thus minimizing possible confusion between RF and progeny DNA replicative intermediates (RIs). The purity of the isolated H-1 DNA, as determined by gel electrophoresis, ethidium bromide staining, autoadiography, and digestion with endo R-EcoRI, was high. H-1 RF DNA'S WERE LINEAR DOUBLE-STRANDED MOLECULES, 1.53 MUM IN LENGTH. H-1 RIs of RF DNA replication were double-stranded, Y-shaped molecules, with the same length as RF DNAs. The replication origin was localized no more than 0.15 genome lengths from one end of the RF DNA, with replication proceeding toward the other end at a uniform rate. Similar RF and RI molecules of dimer size were also observed. The length of H-1 single-stranded DNA extracted from purified virions was measured relative to that of phiX174 and it had a very similar contour length, so that the molecular weight of H-1 single-stranded DNA would be at least 1.48 X 10(6) to 1.59 X 10(6) (Berkowitz and Day, 1974).
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PMID:Replication process of the parvovirus H-1. VII. Electron microscopy of replicative-form DNA synthesis. 83 44

It is evident that much remains to be learned about the nasal passages and their responses to toxic materials. For the nose of both laboratory animals and humans, information is needed in the areas of anatomy, physiology, biochemistry, neurobiology, physiopathology, and oncology. This article briefly discussed toxic and neoplastic responses of the nasal passages, and identified a number of issues and questions that provide potentially valuable areas for further research. It was stated that: (1) Histopathologic examination of the nose could profit from the development of a good all-purpose fixative. (2) A consistent and appropriate classification of nasal passageways, epithelia, and other structures is needed to avoid further confusion. (3) A workable scheme for lesion mapping is needed for routine description of lesion distribution in the nasal passages in rodent toxicology studies. (4) Quantitative data are needed concerning regional substrate specificities and kinetics of nasal enzymes in animals and humans for a wide range of enzymes responsible for metabolism of xenobiotics. Moreover, the following questions should be addressed in the future: (1) What is the nature of the progenitor cells in the olfactory epithelium, basal cells alone, or basal and ductular cells? (2) What determines the resistance of regenerated rat olfactory epithelium to subsequent methyl bromide exposure? (3) Can this resistance phenomenon be demonstrated with other olfactory toxicants and in other species? (4) What influence do cage contaminant gases have on olfactory research in laboratories using rodents? The authors also believe that, despite the fact that nasal airflow has been a subject of investigation for many years, much remains to be learned about this complex process. It is expected that the application of computer technology to mathematical modeling of nasal airflow and regional gas uptake will yield significant new information for the understanding of mechanisms responsible for the distribution of upper respiratory tract lesions in animals and humans. The combination of models of regional uptake, wall flux rates, critical biochemical events, nasal blood flow, and other features of nasal physiology, and integration of these models with lower respiratory tract models, will provide valuable tools for investigations of nasal pathology and toxicology. It was also stressed that the effects of toxicants on olfactory function in humans deserve more attention since, in some past studies, it was suggested that the protection afforded by current TLVs against olfactory toxicity may be marginal. A simple and sensitive olfactometric test of general application for toxicology testing in animals remains to be validated.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Toxic and neoplastic responses in the nasal passages: future research needs. 195

Recent reports that peptides can frequently mimic epitopes on globular proteins are inconsistent with early studies demonstrating that antibodies to native globular proteins generally do not bind peptides. This discrepancy could result from current confusion of two different populations of antibodies in antisera: one reacting with peptides and denatured protein and the other reacting only with the native protein. To test this possibility, several hundred monoclonal antibodies to rat cytochrome c were examined by ELISA for binding the intact protein and cyanogen bromide-cleaved peptides. Inhibition by soluble native cytochrome c identified which antibodies were specific for the native protein. The vast majority of these antibodies did not bind the peptides, whereas most of the antibodies specific for denatured forms did bind them. The results are consistent with the idea that antibodies to denatured antigen are readily detected in solid-phase assays, where some antigen molecules denature as they attach to microtiter plates, and show that these antibodies are generally the ones that react with peptides. Thus, reevaluation of data suggesting that anti-native globular protein antibodies bind peptides is warranted.
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PMID:Antigenicity and native structure of globular proteins: low frequency of peptide reactive antibodies. 244 85

Methyl bromide has been widely used in Japan to fumigate grains and wood. One death and 3 cases of hospitalization resulted from exposure to methyl bromide at place of residence. These 4 cases were not employed and were members of one family living above a warehouse, the ground level of this building was a warehouse where herbs were stored and the second floor was their living area. On the 13th of May 1978 at 7:00 p.m., the herbs were fumigated with methyl bromide gas. The fumigator used 15 kg of methyl bromide (2 cylinders), a quantity far greater than usual. It is assumed that the concentration in the warehouse was between 10,000-15,000 ppm. Early in the morning on the 16th of May (3 days later), one of the family members, a 12-year-old girl, developed severe convulsions, and later 2 others also had severe convulsions, while the other suffered from marked mental confusion. The serum or plasma bromide ion level ranged from 280 to 600 ppm. The results of the clinical laboratory test showed that GOT exceeded the normal level in 3 out of the 4 cases. Moreover, LDH activity was above the normal range in 3 cases and CPK activity was increased in all the cases.
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PMID:[Cases of severe methyl bromide poisoning residing above a warehouse]. 338 89

A 30-year-old male drug abuser developed ophthalmoplegia, bulbar paralysis, and limb weakness responsive to edrophonium. However, potentiation of a low-amplitude evoked muscle action potential was produced with repetitive nerve stimulation at 10 Hz, and the clinical and electrophysiological data suggested the diagnosis of botulism. The source of botulism type B toxin was a clinically obscure cyst produced by subcutaneous infiltration of cocaine two weeks prior to the onset of symptoms. The patient improved with chronic administration of pyridostigmine bromide and plasmapheresis. Wound botulism may be underdiagnosed because of confusion with inflammatory neuropathy or myasthenia gravis. Neuromuscular transmission studies in patients with acute craniosomatic paralysis can prevent such oversights.
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PMID:Descending paralysis resulting from occult wound botulism. 648 40

We report on a patient with bromide intoxication, presenting with confusion, disorientation, and auditory and visual hallucinations after taking a sedative medication containing bromide (mixture menopause; 15 ml containing 1 g potassium bromide) for 1 month. Blood chemistry showed a high chloride level (176 mEq/l) and a negative anion gap (-60 mEq/l). The spurious hyperchloremia was due to interference of chloride ion determination by the ion-selective electrode method with a high level of bromide in serum: 352 mg/dl (44 mEq/l). In this case the only striking abnormality which alerted the physician to the possibility of halide intoxication was the negative anion gap. Hence, a negative anion gap is an important clue which leads to the diagnosis of halide intoxication.
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PMID:A negative anion gap as a clue to diagnose bromide intoxication. 775 65

Light-sensitive channels encoded by the Drosophila transient receptor potential-like gene (trpl) are activated in situ by an unknown mechanism requiring activation of Gq and phospholipase C (PLC). Recent studies have variously concluded that heterologously expressed TRPL channels are activated by direct Gq-protein interaction, InsP3 or Ca2+. In an attempt to resolve this confusion we have explored the mechanism of activation of TRPL channels co-expressed with a PLC-specific muscarinic receptor in a Drosophila cell line (S2 cells). Simultaneous whole-cell recordings and ratiometric Indo-1 Ca2+ measurements indicated that agonist (CCh)-induced activation of TRPL channels was not always associated with a rise in Ca2+. Internal perfusion with BAPTA (10 mM) reduced, but did not block, the response to agonist. In most cases, releasing caged Ca2+ facilitated the level of spontaneous channel activity, but similar concentrations (200-500 nM) could also inhibit TRPL activity. Releasing caged InsP3 invariably released Ca2+ from internal stores but had only a minor influence on TRPL activity and none at all when Ca2+ release was buffered with BAPTA. Caged InsP3 also failed to activate any light-sensitive channels in situ in Drosophila photoreceptors. Two phospholipase C inhibitors (U-73122 4 microM and bromo-phenacyl bromide 50 microM) reduced both spontaneous and agonist-induced TRPL activity in S2 cells. The results suggest that, as in situ, TRPL activation involves G-protein and PLC; that Ca2+ can both facilitate and in some cases inhibit TRPL channels, but that neither Ca2+ nor InsP3 is the primary activator of the channel.
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PMID:Activation of heterologously expressed Drosophila TRPL channels: Ca2+ is not required and InsP3 is not sufficient. 988 70

To investigate complaints of Gulf War veterans, epidemiologic, case-control and animal modeling studies were performed. Looking for OPIDP variants, our epidemiologic project studied 249 Naval Reserve construction battalion (CB24) men. Extensive surveys were drawn for symptoms and exposures. An existing test (PAI) was used for neuropsychologic. Using FACTOR, LOGISTIC and FREQ in 6.07 SAS, symptom clusters were sought with high eigenvalues from orthogonally rotated two-stage factor analysis. After factor loadings and Kaiser measure for sampling adequacy (0.82), three major and three minor symptom clusters were identified. Internally consistent by Cronbach's coefficient, these were labeled syndromes: (1) impaired cognition; (2) confusion-ataxia; (3) arthro-myo-neuropathy; (4) phobia-apraxia; (5) fever-adenopathy; and (6) weakness-incontinence. Syndrome variants identified 63 patients (63/249, 25%) with 91 syndromes. With pyridostigmine bromide as the drug in these drug-chemical exposures, syndrome chemicals were: (1) pesticide-containing flea and tick collars (P < 0.001); (2) alarms from chemical weapons attacks (P < 0.001), being in a sector later found to have nerve agent exposure (P < 0.04); and (3) insect repellent (DEET) (P < 0.001). From CB24, 23 cases, 10 deployed and 10 non-deployed controls were studied. Auditory evoked potentials showed dysfunction (P < 0.02), nystagmic velocity on rotation testing, asymmetry on saccadic velocity (P < 0.04), somatosensory evoked potentials both sides (right P < 0.03, left P < 0.005) and synstagmic velocity after caloric stimulation bilaterally (P-range, 0.02-0.04). Brain dysfunction was shown on the Halstead Impairment Index (P < 0.01), General Neuropsychological Deficit Scale (P < 0.03) and Trail Making part B (P < 0.03). Butylcholinesterase phenotypes did not trend for inherent abnormalities. Parallel hen studies at Duke University established similar drug-chemical delayed neurotoxicity. These investigations lend credibility that sublethal exposures to drug-chemical combinations caused delayed-onset neurotoxic variants.
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PMID:Epidemiological association in US veterans between Gulf War illness and exposures to anticholinesterases. 1002 6

More than 2200 subjects were enrolled in the MorphiDex (MS:DM) development program, with a 1:1 (weight:weight) ratio of morphine sulfate (MS) to dextromethorphan hydrobromide (DM). Of the 1400 subjects exposed to MorphiDex, more than 350 subjects were treated for at least 6 months, and over 200 subjects were treated for a year or longer. The clinical population comprised an approximately equal number of men (46.2%) and women (53.8%), ranging in age from 16 to 96 years, and mostly Caucasian (91.8%). The most frequent (54.8%) daily dose of MorphiDex for subjects enrolled in the clinical program was 120 mg or less. Slow DM metabolizers took significantly lower daily doses of MorphiDex than rapid metabolizers without a significant difference in the incidence of adverse events. Plasma bromide concentrations were low and showed a wide margin of safety for both slow and rapid DM metabolizers. There were no clinically significant treatment-related changes in clinical laboratory tests, neurological examinations, or vital signs. The most common adverse events seen in the multiple dose controlled studies were nausea, dizziness, vomiting, somnolence, constipation, confusion, asthenia, headache, and pruritus. With long-term treatment, the prevalence of adverse events was greatest during the first month of MorphiDex exposure and then decreased over time. The incidence of constipation remained fairly constant over time.
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PMID:Long-term safety of MorphiDex. 1068 40

A 75-year-old man was admitted to our hospital with disorientation and progression of speech disturbance and gait disturbance. He had been given a diagnosis of cervical spondylosis about four years previously, and gait disturbance and numbness in his extremities have been gradually increasing. Hyperchloremia and a careful history taking, which led to the discovery of habitual use of an analgesic containing bromvalerylurea, suggested bromism. A high level of bromide in serum yielded a diagnosis of bromism. Disorientation and speech disturbance were treated and improved by infusion diuresis. Gait disturbance only partly improved. There is a possibility that not only cervical spondylosis, but also chronic bromvalerylurea intoxication, may have contributed to the neurological disturbance resulting in gait disturbance and numbness. Bromvalerylurea, which is contained in many commercially available analgesics, should be noted as a possible cause of neurological disturbance.
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PMID:[A case of chronic bromvalerylurea intoxication due to habitual use of commercially available nonsteroidal anti-inflammatory drugs presenting an indefinite hyperchloremia]. 1160 23


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