Co-trimoxazole in the treatment of malaria in psoriatics.
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Biomedical subjects
Publications and source records attributed to A Chopra.
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A study of eleven patients presenting with neurological complications following acute viral conjunctivitis, mostly haemorrhagic, is reported and the literature reviewed. A Guillain-Barre syndrome-like profile was seen in six patients while the remaining had features of radiculomyelitis. Besides asymmetrical neurological deficits, protein cell reaction and residual muscle wasting, the occurrence of dysautonomias was the striking feature noted in the patients with a Guillain-Barre syndrome-like profile. The dysautonomic features included fatal paroxysmal hypertensive and hypotensive crises in one patient and self limiting tachycardias, episodic profuse sweating, abnormal expiration-inspiration ratio and valsalva ratio in four patients. High antibody titers to EV-70 virus were seen in five patients. A follow up of one and a half year revealed poor neurologic recovery in patients with radiculomyelitis as compared to good functional recovery in others. The importance of early recognition and appropriate treatment of dysautonomias is emphasised. The probable aetiopathogenesis of the neurological complications including dysautonomias is discussed.
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In HeLa cells two different types of mutants resistant to the cardiac glycoside ouabain (OuaR mutants) or erythrophleum alkaloid cassaine (CasR mutants) have been obtained. One type of mutants resistant to these compounds (designated as group A) are highly resistant (between 50 and 2000-fold) to various cardiac glycosides and their genins such as ouabain, oleandrin, digitoxin, digitoxigenin, strophanthidin, convallatoxin, gitoxin, gitoxigenin, gitaloxin, bufalin, and digoxigenin, but exhibit no cross-resistance to SC4453, a digoxin analog which contains a pyridazine ring in place of the lactone ring in the C-17 position. The second type of mutants (group B) exhibit cross-resistance to all of the cardiac glycosides including SC4453, but their level of resistance is at least 5-10-fold less than that of group A mutants. Interestingly, both groups of mutants exhibited similar degree of cross-resistance towards digoxin and actodigin (AY22241), indicating some differences in their behavior from other cardiac glycosides. Both classes of mutants exhibit no cross-resistance to a wide variety of other structurally and functionally related compounds, e.g. sanguinarine nitrate, ethacrynic acid, penicillic acid, veratridine, harmaline hydrochloride, 5,5'-diphenylhydantoin, quindonium bromide, methyl quinolizinum bromide, estradiol 17 beta-acetate, 21-acetoxy-pregnenolone, vanadium pentoxide, digitonin, and adriamycin, indicating that the genetic lesions in both groups of mutants are specific for cardiac glycosides. This inference is supported by the observation that both group A and B mutants show reduced binding of [3H]ouabain. In group A mutants, a part of the Na+/K+-ATPase activity is highly resistant to inhibition by ouabain, indicating that the genetic lesion in these mutants directly affects Na+/K+-ATPase. In contrast, the Na+/K+-ATPase from the group B mutants showed similar resistance towards ouabain and SC4453 as observed for the parental HeLa cells, indicating that these mutants are affected in a cellular component, other than Na+/K+-ATPase, which is involved in the interaction of cardiac glycosides with the cells. The lack of cross-resistance of the group A mutants to SC4453 and normal sensitivity of their Na+/K+-ATPase to this compound provides strong evidence that the mechanism of interaction of SC4453 with Na+/K+-ATPase differs from that of other cardiac glycosides.
In Chinese hamster ovary cells, stable mutants exhibiting specific resistance or collateral sensitivity towards the various microtubule inhibitors podophyllotoxin, colchicine, griseofulvin, taxol, nocodazole, vinblastine, and maytansine have been isolated. A number of independent mutants selected for resistance to podophyllotoxin and colchicine contain electrophoretically altered forms of two proteins, P1 and P2, of relative molecular masses of approximately 63 000 and 69 000, respectively. The proteins P1 and P2 have been shown to be microtubule related by a number of different genetic and biochemical criteria and are among the major proteins of Chinese hamster ovary cells, being present in approximately equimolar amounts with tubulin. In addition, a griseofulvin-resistant mutant contains a novel mutation (presumably nonsense) which reduces the relative molecular mass of a protein, P5 (relative mass congruent to 200 000), by about 20 000. Specific antibodies to protein P1 have been raised and cross-reactivity studies show that a similar protein is also present in cells from all vertebrate species examined, viz. man, monkey, mouse, Chinese hamster, Syrian hamster, and chicken. Immunofluorescence studies with anti-P1 and anti-tubulin antibodies show that, in interphase cells from various species, the P1 antibody reacts specifically with mitochondria whose overall cellular distribution is strikingly similar to the distribution of microtubules. The mitochondrial localization of the microtubule-related protein P1 provides strong suggestive evidence regarding the existence of a chemical and functional linkage between these two structures, with protein P1 playing an important role in this linkage. Some implication of these results are discussed and it is suggested that mitochondria play an important role in the dynamics of microtubules.
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We report an interesting case of generalized papular and nodular lesions with central keratinous plugs and severe hyperkeratotic-acanthotic histopathology with arthritis in a 19-year-old male patient who had suffered from a similar disease 2 years earlier. Papules and nodules erupted a few days after the arthritis and this was noticed during both episodes. On healing, nodules fell spontaneously leaving behind insignificant hyperpigmented scars.
So far, reviews that have appeared on fungal lipids present data mainly on the lipid composition of these organisms and the influence of lipids on their physiology. These reviews provide little information about the enzymes of lipid metabolism in these organisms and it is assumed, by most workers, that lipid synthesis in all fungi takes place as in Saccharomyces cervesiae, the only fungus in which the complete pathways of phospholipid biosynthesis have been worked out. During the last few years, literature has accumulated on lipid metabolic enzymes of other fungi, as investigators became increasingly interested in this area of research. The present review, after an introduction, will be divided into different sections and each section will deal, comparatively, with various aspects of fungal lipid metabolism and physiology. This review will, therefore, bring out the differences or similarities of lipid metabolism in diverse fungal species.
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