Search PubMed⌕ Search

Biomedical subjects

S Banerjee

Publications and source records attributed to S Banerjee.

At least 325 records · Page 18Linked to original sources
PubMed1996

Apobec-1 interacts with a 65-kDa complementing protein to edit apolipoprotein-B mRNA in vitro.

The editing of apolipoprotein-B (apoB) mRNA involves the deamination of cytidine at nucleotide 6666 to uridine. The catalytic subunit of the editing enzyme, apobec-1, is a cytidine deaminase that requires other unidentified proteins to edit apoB mRNA in vitro. We partially purified an activity from baboon kidney that functionally complements apobec-1. The complementing activity was protease-sensitive and micrococcal nuclease-resistant, had a native molecular mass of 65 +/- 10 kDa on size exclusion chromatography, and sedimented at 4.5 S in glycerol gradients. Purified recombinant His6-tagged apobec-1 immobilized on beads depleted >90% of the complementing activity from partially purified extracts. These beads edited apoB mRNA in vitro in the absence of exogenous apobec-1 or complementing activity. A functional holoenzyme containing apobec-1 and the complementing activity was eluted from the apobec-1-affinity resin using 0.5 M imidazole, whereas buffer containing 0.4 M KCl eluted only the complementing activity. The carboxyl-terminal 59 amino acids of apobec-1 were not required for interaction with the complementing activity in vitro. Our results demonstrate that the complementing protein interacts directly with apobec-1 in the absence of apoB mRNA.

APOBEC-1 Deaminase↗
PubMed1996

Randomised controlled trial of effect of intervention by psychogeriatric team on depression in frail elderly people at home.

OBJECTIVE: To investigate the efficacy of intervention by a psychogeriatric team in the treatment of depression in elderly disabled people receiving home care from their local authority. DESIGN: Randomised controlled trial with blind follow up six months after recruitment. SETTING: Community of south east London. SUBJECTS: 69 people aged 65 or over who received home care and were depressed according to criteria of the standardised automatic geriatric examination for computer assisted taxonomy (AGECAT). 33 were randomly allocated to an intervention group and 36 to a control group. INTERVENTION: Members of the intervention group received an individual package of care that was formulated by the community psychogeriatric team in their catchment area and implemented by a researcher working as a member of that team. The control group received normal general practitioner care. MAIN OUTCOME MEASURES: Recovery from depression (AGECAT case at recruitment but non-case at follow up). RESULTS: Data were analysed on an intention to treat basis. 19 (58%) of the intervention group recovered compared with only nine (25%) of the control group, a difference of 33% (95% confidence interval 10% to 55%). This powerful treatment effect persisted after controlling for possible confounders in logistic regression analysis, with members of the intervention group more likely than members of the control group to have recovered at follow up (odds ratio 9.0 (2.0 to 41.5)). This did not seem to be a simple effect of antidepressant prescription: use of antidepressants at follow up did not have a significant effect (multiply adjusted odds ratio 0.3 (0.0 to 1.9)). CONCLUSIONS: Depression is treatable in elderly people receiving home care. Therapeutic nihilism based on an assumed poor response to treatment in these socially isolated, disabled elderly people in the community is not supported.

Aged↗
PubMed1996

Immunity to the G1 globular domain of the cartilage proteoglycan aggrecan can induce inflammatory erosive polyarthritis and spondylitis in BALB/c mice but immunity to G1 is inhibited by covalently bound keratan sulfate in vitro and in vivo.

Earlier work from this laboratory showed that the human proteoglycan aggrecan from fetal cartilages can induce a CD4+ T cell-dependent inflammatory polyarthritis in BALB/c mice when injected after removal of chondroitin sulfate chains. Adult keratan sulfate (KS)-rich aggrecan does not possess this property. We found that two CD4+ T cell hybridomas (TH5 and TH14) isolated from arthritic mice recognize bovine calf aggrecan and the purified G1 domain of this molecule, which also contains a portion of the interglobular domain to which KS is bound. These hybridoma responses to G1 are enhanced by partial removal of KS by the endoglycosidase keratanase or by cyanogen bromide cleavage of core protein. KS removal results in increased cellular uptake by antigen-present cells in vitro. After removal of KS by keratanase, G1 alone can induce a severe erosive polyarthritis and spondylitis in BALB/c mice identifying it as an arthritogenic domain of aggrecan. The presence of KS prevents induction of arthritis presumably as a result of an impaired immune response as observed in vitro. These observations not only identify the arthritogenic properties of G1 but they also point to the importance of glycosylation and proteolysis in determining the arthritogenicity of aggrecan and fragments thereof.

Aggrecans↗
PubMed1996

Use of a DNA polymerase III bypass mutant of Escherichia coli, pcbA1, to isolate potentially useful mutations of a complex plasmid replicon.

The essential replicon region of plasmid pCU1 has, within 1.2 kb, two origins of replication that can function in the absence of Escherichia coli DNA polymerase I and one that requires this polymerase. To isolate mutants in the replicon pathway that uses the PolI-dependent origin in the presence of the two other origins, we examined the feasibility of exploiting E. coli strains carrying a polymerase c bypass mutation (pcbA) and which can survive and form colonies with the polymerase activity of polC inactivated at 42 degrees C. The selection scheme that is described was successful and resulted in the isolation of a mutant replicon that is not maintained at 42 degrees C in a PcbA-PolC+tsPolA+ strain. Nucleotide sequencing indentified the mutated region to be within the origin (OriV) that was known to be polA-dependent. Electron microscopy of mutant plasmid molecules replicating in a Pcb+ strain confirmed that OriV is inactivated.

Base Sequence↗
PubMed1996

Technetium-99m radiolabeled ouabagenin-cysteine conjugate: biological evaluation in animal models.

Two ouabagenin-cysteine conjugates were synthesized by condensing 3-beta monochloroacetyl and 3-beta, 11-alpha dichloroacetyl ouabagenin with cysteine. The resulting ligands were radiolabeled with technetium-99m (99mTc) to furnish a single homogenous 99mTc chelate in each case with good stability. The animal experiments with these 99mTc-labeled conjugates established the superiority of guinea pig over rat and rabbit as an animal model, as previously observed for other tritiated or radioidinated cardiac glycosides or aglycones. In biodistribution experiments in guinea pig, these 99mTc chelates showed a favorable heart to liver (and other nontarget organ) uptake ratio, comparable to that of recently reported 125I-digoxigenin iodohistamine-3-oxime. The low heart to blood ratio in animal experiments with ouabagenin derivatives could be attributed to the absence of 3-beta sugar residues in these molecules, which is in agreement with the previous observation reported in connection with radioiodinated digoxin and digoxigenin derivatives.

Animals↗
PubMed1996

Genetic toxicology of four commonly used benzodiazepines: a review.

Benzodiazepines are a group of drugs which have been extensively used for their activities as an anti-anxiety, sedative, muscle relaxant and anti-convulsant. Benzodiazepines at present are the most commonly prescribed drugs. Some of these drugs are teratogenic and also carcinogenic in experimental animals. The wide human exposure to this group of drugs throughout the world is of great concern for human health. In the present review, we have attempted to evaluate and update the mutagenic and genotoxic effects of four of the most commonly used benzodiazepines, i.e., chlordiazepoxide (CDZ), diazepam (DZ), nitrazepam (NZ) and oxazepam (OZ) based on available literature.

Animals↗
PubMed1996

Anomalies in hepatobiliary excretion of technetium-99m-MAG3 preparations.

Technetium-99m-MAG3 is accepted as a renal tubular function agent. However, sporadic liver and gall bladder visualisation during its clinical use is clearly a disadvantage. HPLC-purified 99mTc-MAG3 samples exhibited appreciable hepatobiliary uptake (7%), and an elevated level of such uptake was observed in unpurified kit preparations, which was stated to be associated with the excretory property of the radiolabeled kit impurities. To verify this we attempted to quantitate the hepatobiliary uptake of the kit preparations with that of its radiolabeled components. The contribution of each component toward hepatobiliary uptake of the sample was calculated from their abundance in the chelate mixture and the individual biodistribution of the isolated components. However, the anticipated hepatobiliary uptake of different preparations of 99mTc-MAG3 calculated in this way was always lower than that of the experimental value determined directly. Further work is needed to explain the anomaly.

Animals↗
PubMed1996

Sucralfate suppresses Helicobacter pylori infection and reduces gastric acid secretion by 50% in patients with duodenal ulcer.

BACKGROUND & AIMS: The mechanism(s) by which sucralfate heals duodenal ulcers remains unclear. The aim of this study was to determine the effect of sucralfate on Helicobacter pylori infection and on the accompanying hypersecretion of gastric acid the infection induces in patients with duodenal ulcer. METHODS: Basal and gastrin-releasing peptide (GRP) stimulated gastrin release and acid secretion. H. pylori density, gastric urease activity, and severity of gastritis were studied in patients with duodenal ulcer who were positive for H. pylori before, during, and after 4 weeks' treatment with sucralfate (2 g twice daily). RESULTS: The density of H. pylori decreased by 70% during sucralfate treatment and returned to the pretreatment level after discontinuation of therapy. This suppression of H. pylori infection was accompanied by an 80% decrease in gastric urease activity. GRP-stimulated plasma gastrin concentrations, GRP-stimulated acid output, and basal acid output all decreased by approximately 50% during sucralfate therapy and returned to pretreatment levels after treatment was discontinued. CONCLUSIONS: These findings indicate that sucralfate markedly suppresses H. pylori infection and the accompanying hypersecretion of acid the infection induces in patients with duodenal ulcer. These effects are likely to be important mechanisms by which the drug promotes duodenal ulcer healing.

Adult↗