Further studies on normal and dystrophic human skeletal muscle in tissue culture.
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Biomedical subjects
Publications and source records attributed to B Singh.
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Cellular lesions in the metathoracic ganglion of P. americana following insecticide treatment have been examined. Treatment of the isolated ganglia with dieldrin (10 microM) and bioresmethrin (5 microM) induced mitochondrial damage in the neuropile and nerve cell bodies. The mitochondria in treated nerve cells were swollen with broken cristae and devoid of normal morphological appearance. Following in vivo treatment of cockroaches with these insecticides, this type of mitochondrial damage was observed even at the onset of poisoning. In the prostrate cockroaches, however, the mitochondrial swelling was accompanied by the accumulation of electron dense granules. In addition, the neuropiles of insecticide-treated ganglia contained secondary lysosomes which increased in size and number with the progress of poisoning and showed signs of depletion of synaptic vesicles. The action of dieldrin upon the ultrastructure was completely abolished by pretreatment of ganglia with 10 mM Mg2+. On the other hand, pretreatment of ganglia with tetrodotoxin and pentobarbital-sodium had very little effect on the action of dieldrin though these compounds blocked the action of bioresmethrin. The results of this study suggest that cellular lesions in the insect CNS, caused by dieldrin, are due to an enhanced uptake of calcium into nerve terminals which may occur independent of membrane depolarization. The effects of bioresmethrin upon the ultrastructure of the CNS are apparently mediated by nerve excitation and membrane depolarization. It is concluded that treatment of intact cockroaches with dieldrin and bioresmethrin initiates catabolic processes in the nerve cells leading to cellular lesions which are indicative of neuronal degeneration.
Glial cell damage in the central nervous system of P. americana following insecticide treatment has been studied. Treatment of isolated metathoracic ganglia with 10 microM dieldrin caused an increase in the electron opacity of the inner and outer glial cells without effecting such a change in the structure of glial cells in the ventral connectives. Glial cells in the ganglia and ventral connectives treated with 5 microM bioresmethrin were found to be swollen and even more electron lucent than the control cells. In the prostrate cockroaches (24 hr after the treatment) the action of bioresmethrin and dieldrin upon peripheral glial cells was identical. Both insecticides caused vacuolation and darkening of outer glial cells; their effects extended to include glial cells in the ventral connectives. At the onset of poisoning, 20-30 min following the application of dieldrin, outer glial cells exhibited slight increase in electron opacity while the inner glial cells showed increase in lysosomal activity. The observed action of dieldrin upon the ultrastructure of glial cells was prevented by pretreatment of the nervous tissue with 10 mM Mg2+. Though tetrodotoxin and sodium-pentobarbital had very little effect upon the action of dieldrin, these drugs blocked bioresmethrin-induced alterations in the fine structure of glial cells. The results of this study suggest that alterations in the ultrastructure of insect neuroglia following treatment with insecticides tested in this study are probably due to perturbations in the neural element of the nervous system.
Three hundred 18-day-old male chicks (Arbor Acre) were divided into five groups of 60 each and given high-protein (42.28%), high-calcium (3.37%), urea-containing (5%), vitamin-A-deficient, or control diets to study the effect of nutritional imbalances on the development of nephritis and related biochemical changes over 15 weeks. The first four diets increased the levels of glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, uric acid, and nonprotein nitrogen in serum. Blood urea was increased by only the urea diet. Hypoglycemia and a decrease in hepatic glucose-6-phosphatase were also observed in chicks fed the first four diets. The vitamin-A-deficient diet resulted in a depletion of vitamin A in the liver and kidneys. These changes were directly correlated with the prolonged feeding of experimental diets and also with the severity of nephritis and degenerative changes in various organs. It was concluded that increasing the intake of nitrogen or calcium in order to increase production may in fact have the opposite effect, leading to degenerative changes in various tissues and to nephritis.
Young laying hens were infected with Coxiella burnetii to study egg transmission, clinical and serologic responses, excretion of the agent in feces, and its persistence in internal organs. No clinical symptoms were noticed. The birds developed good titers in a capillary agglutination test by 13 days postinfection (DPI), which peaked at 30 DPI and therafter declined gradually, becoming negative in some birds around 90 DPI. In vivo and in vitro egg transmission of the agent could not be demonstrated. C. burnetii was recovered at 90 DPI from spleen and liver but not from kidney and ovary.
In 14,891 necropsies performed on domestic poultry during January 1976 to October 1977, two cases of skeletal abnormalities were found. One was a tarsometatarsal spur in an adult female chicken, and the other was a crossed-beak associated with microphthalmia.
In vivo administration of isatin (200 mg/kg) significantly lowered the activity of rat kidney alkaline phosphatase after 5 hr but enhanced the activity of rat duodenal and jejunal enzyme after 2 and 5 hr (P less than 0.01). The increased activity of the duodenal and jejunal alkaline phosphatase might be due to the induction of the enzyme by isatin.
Rats and guinea pigs were exposed to 0.5 ppm ozone, 10 mg/m3 sulfuric acid mist, or their combination for 6 hrs/day, 5 days/week for six months. Exposure-related microscopic alterations were seen in the lungs of guinea pigs exposed to ozone alone or in combination with sulfuric acid mist. No other microscopic lesions were present in either rats or guinea pigs. No biologically meaningful synergistic effects were noted in animals exposed to the combination of ozone and sulfuric mist.
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The efficacy and electrophysiologic effects of adenosine and verapamil in termination of paroxysmal supraventricular tachycardia (SVT) were compared in 18 patients (age 18-48 years, mean 33 +/- 9 years) with recurrent sustained and inducible SVT. Ten patients had atrioventricular nodal reentrant tachycardia (AVNRT) and 8 had atrioventricular reentrant tachycardia involving a retrograde accessory pathway (cycle length of SVT 280-360 msec; mean 315 +/- 20 msec). Each patient served as his own control. After induction of SVT, adenosine was administered first (6 mg i.v. bolus). If the tachycardia was not terminated, a bolus of 12 mg was given. Ten minutes later, verapamil (5 mg i.v. over 30 sec) was administered after reinduction of SVT. If the tachycardia was not terminated, a 5 mg dose was repeated every 5 minutes upto 20 mg. Adenosine terminated the SVT in 16 cases (6 mg - 7 patients, 12 mg - 9 patients). Verapamil was effective in 11 patients (5 mg - 6 patients, 10 mg - 4 patients, 15 mg - 1 patient, 20 mg - nil). The overall efficacy of adenosine (89%) was significantly greater than that of verapamil (61%; p < 0.05). Adenosine terminated the tachycardia more quickly than verapamil (mean 24 +/- 11 sec versus 142 +/- 40 sec; p < 0.01). Termination of tachycardia by both drugs was related to antegrade block of the atrioventricular node in all patients except one with AVNRT in whom adenosine blocked the retrograde fast pathway. Ventricular premature beats were seen transiently in 5 patients following adenosine. Transient side effects such as flushing, burning and chest pain were frequently observed with adenosine and correlated with the termination of tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)
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