Characterization of ribonucleoprotein particles & protein synthesis in chloroplasts.
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Biomedical subjects
Publications and source records attributed to S Biswas.
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Human placental lactogen (HPL), alpha-fetoprotein, prolactin and growth hormones were assayed simultaneously twice weekly in 21 women from 4--16 weeks' gestation. Mean levels were established from 15 of the women for comparison with one woman with a twin pregnancy, two who aborted and three who received progestogen supplements. There was wide interpatient variation in all hormone levels excepting HPL. The mean levels of all except growth hormone showed an upward trend. Mean growth hormone levels were higher initially but remained within a 2--4 ng/ml range throughout. In the twin pregnancy, only HPL and alpha-fetoprotein levels were significantly raised. HPL was detected in one of the two women who aborted, whereas growth hormone was initially extremely high, falling precipitously prior to abortion in both women. Treatment with progestogen supplements did not appear to influence any of the hormones measured. This study suggests that serial estimations of HPL appear to be the most cost-effective guide to early fetal well-being of the four hormones measured.
Neuroblastoma is associated with chromosomal aberrations of 1p and 1q in a majority of cases. Some nonrandom secondary changes were observed in this study. The role of these changes in the development and progression of neuroblastoma is examined. Chromosomal analysis was performed on 33 children with neuroblastoma using fine needle aspiration cultures. Metaphases were observed in 57.5% of cases. 86.6% showed the involvement of chromosome 1. Double minutes and unidentifiable markers was also observed. The most frequent secondary changes included add(4)(q35), add(11)(p13), add(14)(q32), add(16)(q12). add(17)(p13), add(19)(q12) and add(21)(q22). Minority of cases showed deletions and translocations. Ploidy pattern ranged from diploid to hypotetraploid. The present study substantiates aberration of chromosome 1 in the form of deletions, additions, duplications and iso-chromosome with some notable secondary abnormalities.
Cytogenetic analyses of fine-needle aspiration samples were performed on five cases of which three were alveolar rhabdomyosarcomas (RMS), one was embryonal RMS and one was RMS of mixed alveolar and embryonal histology. Three cases of alveolar RMS and one case of embryonal RMS showed t(2;13). A del(1)(p11) in a mixed alveolar and embryonal RMS was observed without the presence of t(2;13). add(17)(q25) was present in one of the alveolar RMS along with a t(2;13). Modal number of chromosome in the five cases ranged from hyperdiploid to hypertetraploid. Clinical, cytological, histopathological and cytogenetic findings are correlated. The role of additional abnormalities is discussed with a review of appropriate literature.
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Endogenous opioid peptides and opiates like morphine produce their pharmacological effects through the membrane bound opioid receptors. These receptors belong to a superfamily of G-protein-coupled receptors, all of which possess seven membrane-spanning regions. Structure-activity relationship studies of opioids opened up new avenues for the pharmacological characterization of the opioid receptors. As a further advancement in this direction, molecular cloning has led to the identification of three different types of opioid receptors -- OP1 (delta), OP2 (kappa) and OP3 (mu) -- thereby supporting the results of earlier pharmacological studies which postulated their existence. The three opioid receptors are highly homologous. Consequent to the development of highly specific and selective agonists and antagonists, it was proposed that the three types of opioid receptors could be further categorized into different subtypes. However, the molecular biology data generated so far do not support the presence of the various subtypes of the three well-characterized opioid receptors. Recent strides towards the advancement of our knowledge relating to the molecular biology of these receptors have been reviewed in this article.
Blood samples collected from individuals belonging to malaria endemic areas were assayed for antigen-specific circulating immune complexes in polyethylene glycol precipitates of serum by enzyme immunoassay. Sera were tested from patients with acute P. vivax and P. falciparum infections, from clinically immune individuals and also from healthy normals. Circulating immune complexes (CICs) containing immunoglobulin G and M isotypes were found to be abundant in individuals with ongoing and past infections and also in clinically immune donors. In patients with acute infection but without any past history of malaria, CICs of IgM type were found to be significantly higher. Demonstration of antigen/antibody specific CICs could be a useful indicator of active, ongoing and recent/past infection, also of the status of immune responses of individuals belonging to various endemic areas.
Rhesus monkeys were inoculated intravenously with 1 x 10(4) P. knowlesi infected erythrocytes. After about three days prepatency, peripheral smears were found positive and the animals were cured with chloroquine phosphate when parasitaemia reached about 15-25 per cent. The monkeys were repeatedly exposed with three bouts of infection. The first and second bouts were cured but after the third challenge, all 10 monkeys showed a longer prepatent period, lower parasitaemia and then self-recovery. Sera were collected in different phases of infection to assess immune responses. Antimalarial IgG and IgM responses were measured by ELISA. The presence of IgM antibody was associated with every bout of infection. With repeated infections until self-recovery, a substantial amount of IgG was found in circulation. A significant level of schizont-infected cell agglutination antibody was also detected in the animals after survival from challenge infection. Antigen-specific circulating immune complexes, both of IgG and IgM types, appeared in various phases of infection, but their appearance did not coincide with the acquired immune responses of the animals. During the self-recovery phase, almost all monkeys had an elevated level of serum C3 and C4.
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BACKGROUND: [corrected] The spread of drug resistance in Plasmodium falciparum has made the situation essential to look into new effective therapeutic agents like antibiotics. Azithromycin is a potential, chemotherapeutic agent which possesses antimalarial activity and favourable pharmacokinetic properties. It is an azalide microbiocide derived semi-synthetically from macrolide erythromycin. Like other antibiotics, the azalide azithromycin has ability to inhibit protein synthesis on 70S ribosomes. SETTINGS: Experimental study. SUBJECTS AND METHODS: The parasiticidal profile was studied in five chloroquine sensitive and five chloroquine resistant P. falciparum isolates obtained from various places of India. The antimalarial activity was evaluated in P. falciparum schizont maturation by short term culture for 24 hours and by exposing the parasites to the drug for 96 hours. Parasites synchronized at ring stage were put for culture with various concentrations of azithromycin dihydrate (0.01-40 micro/ml). RESULTS: At highest concentration (40 micro/ml), parasite growth was inhibited totally in all 10 isolates. Antimalarial activity at 96 hours was greater than at 24 hours in both chloroquine sensitive and resistant parasites, which may indicate that the inhibition of parasite growth may occur at clinically achievable concentration of the drug when parasites were exposed for several asexual cycles. CONCLUSION: Azithromycin shows a potential for eventual use alone or in combination in the treatment of chloroquine sensitive and resistant P. falciparum malaria.
Due to increasing trend in chloroquine resistance, the antifolate (sulpha-pyrimethamine combination) drugs are gaining more importance in the treatment of uncomplicated falciparum malaria. The efficacy of sulpha-pyrimethamine combinations in the treatment is compromised by the development of resistance in parasite. The occurrence of mutations at active sites in Plasmodium falciparum gene sequences coding for dihydrofolate reductase (DHFR) and dihydropteroate synthetase (DHPS) confer resistance to pyrimethamine and sulphadoxine. This study presents the characterization of a P. falciparum sample from a patient who did not respond to standard doses of a pyrimethamine/sulpha regimen. Although parasitaemia fell rapidly, the infection had not resolved six days later as because the response to treatment selected resistant sub-population. The in vitro drug sensitivity assays demonstrated resistance to pyrimethamine, sulphadoxine and cycloguanil; while polymerase chain reaction (PCR) and restriction digest based methods indicated that at known drug resistant loci the isolate had a genotype of DHFR Val-16 and Thr-108 previously only associated with cycloguanil resistance. As per the published reports this type of paired mutations in natural isolates are rare. It is of considerable interest to carry out studies on alleles on alleles of this gene in relation to resistance at epidemiological level.
BACKGROUND: Cholelithiasis produces diverse histopathological changes in gallbladder mucosa namely acute inflammation, chronic inflammation, glandular hyperplasia, granulomatous inflammation, cholesterosis, dysplasia, and carcinoma. Gallstones have different chemical composition. They may be cholesterol, pigment or mixed stones. The aim of this prospective study was to see if any correlation existed between the chemistry of gallstones and any particular histopathologic picture. METHODS: Between May 1997 and December 1997 we diagnosed and operated on 40 patients with cholelithiasis. Diagnosis was established by ultrasound. After operation gallstones were sent for chemical analysis to detect presence of calcium bilirubinate and cholesterol. Serial sections of gallbladder from fundus to neck were stained by haematoxylin and eosin, and studied. RESULTS: Out of 40 patients (n = 40) 29 were females and 11 were males. The mean age of our patients was 38 +/- 21 years with a median of 40 years. Median age of males was 48 years compared to 38 years for females. Twenty-eight patients had mixed stones, 8 had pigment stones and 4 had cholesterol stones. Out of 28 patients with mixed stones 14 had histological picture of chronic cholecystitis, 8 had granulomatous cholecystitis, 4 had adenomatous hyperplasia, 1 had dysplasia and 1 had carcinoma. All 8 patients having pigment gallstones had chronic cholecystitis. Out of 4 patients with cholesterol gallstones, 2 had chronic cholecystitis, 1 had adenomatous hyperplasia and 1 had cholesterosis. Gallbladder having pigment stones were devoid of Rokitansky-Aschoff sinuses. CONCLUSION: Adenomatous hyperplasia and Rokitansky-Aschoff sinuses were not seen in gallbladder containing pigment stones but seen in gallbladders containing mixed and cholesterol stones in our study. Cholesterol may be a more potent stimulus for glandular hyperplasia or glandular hyperplasia may responsible for formation of cholesterol rich stones.
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A retrospective study was done at the Leprosy Control Unit (LCU) in Durgapur of Burdwan district, West Bengal, to determine the relapse rate following multidrug therapy (MDT). A total of 1581 patients (1276 PB and 305 MB) completed MDT regimens during a period of 5 years as per WHO recommendations and National Leprosy Eradication Programme (NLEP) guidelines. The treated patients were kept under surveillance as per NLEP guidelines and searched for relapses. The results of MDT were compared with those of pre-MDT (monotherapy) era at the same centre (total: 405 patients; PB-373, MB-32) and also with those of the Leprosy Clinic in Gopalpur (only dapsone was given to a total of 189 patients, PB-167, MB-22). Following monotherapy, the relapse rate was 10.06% at the Gopalpur Leprosy Clinic and 12.4% at the Durgapur LCU during the 2 years (PB) and 5 years (MB) of surveillance, whereas following MDT no relapse case was encountered both in PB and MB cases during the surveillance periods recommended by WHO. The results of this study are comparable with those of other studies. Though a few studies showed relapses during long-term surveillance beyond the periods recommended by WHO, it is once again established that MDT can prevent relapse in leprosy.
BACKGROUND: Antifolate antimalarials like sulfadoxine-pyrimethamine are used as second-line treatment for Plasmodium falciparum malaria patients who fail to respond to chloroquine. The efficacy of the sulfa-pyrimethamine combination in the treatment is also compromised by the development of resistance in the parasite. Resistance to these drugs has been shown to encode with point mutations in dihydrofolate reductase and dihydropteroate synthetase genes. SETTINGS: An experimental study. MATERIAL AND METHODS: Forty clinical isolates collected from different geographical locations in India were used to assess the relationships between resistance to sulfadoxine-pyrimethamine (SP) and mutations in P. falciparum dihydrofolate reductase (DHFR) and dihydropteroate synthetase (DHPS). In vitro drug susceptibility and mutation-specific polymerase chain reaction (PCR) assays were also done. RESULTS: It was observed that a number of isolates possessed mutant genotypes and showed low sensitivity to SP in vitro. Of the 40 clinical isolates studied, 87.5% had DHFR and 15% had DHPS gene mutations. As observed from PCR results, 55( (22/40) presented double mutation of DHFR Arg-59 and Asn-108 and 32.5 % (13/40) had single mutant type allele of Asn-108. Of the 40 isolates, 10 % (4/40) presented doubly mutated forms of DHPS Phe-436 and Thr-613 and single mutant type allele Gly-581 was detected in 5 % (2/40) isolates. Parasites carrying double or single mutant forms of DHFR/DHPS showed elevated minimum inhibitory concentration (MIC) values of both pyrimethamine (760-6754 nM; r=0.69) and sulfadoxine (108 - 540 micro M; r=0.87) when compared to sensitive and resistant strains. CONCLUSION: Though there was a correlation between molecular techniques and in vitro drug sensitivity profiles, the relevance of these findings to the clinical efficacy of SP combination drugs needs to be established by controlled clinical trials.