Search PubMed⌕ Search

Biomedical subjects

R Biswas

Publications and source records attributed to R Biswas.

At least 73 records · Page 4Linked to original sources
PubMed1993

Characteristics of a membrane-associated antilactogen binding site for tamoxifen.

The antilactogen binding site (ALBS) is a membrane associated protein to which tamoxifen (TAM) and related non-steroidal antiestrogens, but not estrogen, bind. It is through this site that TAM inhibits lactogen binding to the prolactin (Prl) receptor and subsequent Prl induced growth and differentiation in target tissues. Binding of lactogens to the Prl receptor is inhibited by TAM or 4-hydroxy-TAM at 4 degrees C as well as room temperature, thus suggesting that the ALBS is not an enzyme. TAM acts by inhibiting the binding of lactogens to the receptor rather than promoting dissociation of the hormone-receptor complex. Lactogens bind to mammary gland membranes with an Kd of 4.3-8.2 x 10(-10) M. In the presence of 10(-7) M TAM the affinity decreased to a Kd of 0.8-1.6 x 10(-9) M. Binding of 3H-TAM to mammary gland membranes was effectively inhibited by an anti-Prl receptor antibody, thus suggesting a close relationship between the Prl receptor and the ALBS. Separate affinity purification of the ALBS and the Prl receptor resulted in peak fractions demonstrating specific binding activity for both TAM and lactogenic hormones. Re-isolation of the affinity purified Prl receptor on a TAM-Sepharose affinity resin again resulted in co-elution of both binding activities. The isolates from both affinity resins contained primarily a single band with an apparent molecular mass of 90 kDa. This band was precipitated with the anti-Prl receptor antibody and specifically bound the affinity label ring-3H-TAM aziridine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Altered prolactin response of the lymphocytes of tumor-bearing mice.

Interaction of prolactin and glucocorticoid on thymocytes and splenocytes of normal and tumor-bearing mice with reference to their mitogen-responsive blastogenesis has been studied. Prolactin alone had little or no mitogenic effect on thymocytes and splenocytes of normal mice but it was co-stimulatory, with ConA, in inducing blastogenesis in normal splenocytes. Thymocytes and splenocytes of tumor-bearing mice responded differently to prolactin. Hormone alone inhibited growth of thymocytes but at certain concentrations stimulated splenocytes. When cultured with prolactin and ConA, the thymocytes of tumor hosts responded with increased proliferation compared to that induced by ConA alone. Glucocorticoid suppressed ConA-induced lymphocyte proliferation in both normal and tumor-bearing mice. Prolactin reversed the inhibitory effect of glucocorticoid in normal mice but failed to abrogate inhibition in tumor hosts. Altered responsiveness of lymphocytes of tumor hosts to prolactin was not a function of circulating prolactin, as the serum prolactin level was similar in normal and tumor-bearing mice. Prolactin, however, could not reverse estradiol-induced suppression of lymphocyte proliferation. The lactogenic hormone, but not somatogenic hormones, altered the glucocorticoid inhibition of lymphocyte growth.

Animals↗
PubMed1992

Hepatitis C virus replication during acute infection in the chimpanzee.

The events following experimental infection of 2 chimpanzees with the H strain of hepatitis C virus (HCV) were studied by quantitating the levels of HCV RNA in liver and serum. Serum and liver samples were tested every 1-3 weeks for up to 32 weeks. The genomic and antigenomic strands of HCV RNA were individually detected in liver and serum by strand-specific reverse transcription followed by polymerase chain reaction (PCR) using nested primers specific for the 5' noncoding region of the HCV genome and were quantitated by end-point dilution of the nucleic acid extract. Both genomic and antigenomic strands were detected in liver and serum within 1 week after inoculation and approximately 1 week before the development of elevated levels of alanine aminotransferase (ALT) activity. Changes in levels of antigenomic strand paralleled those of the genomic strand in both serum and liver. Titers of HCV RNA in serum and liver generally correlated with changes in ALT levels.

Acute Disease↗
PubMed1991

[Serologic and genomic markers of the hepatitis C virus in transfusion recipients with non-A, non-B hepatitis].

BACKGROUND: The exclusion of donors with antibodies against the c-100 protein of the hepatitis C virus (HCV) has permitted a considerable reduction in post transfusional (PTH) non A non B hepatitis in those receiving transfusions. However, the risk has not been completely eliminated and there is evidence that some HCV carriers do not present detectable antibodies against protein c-100. In these cases a new diagnostic methodology, named polymerase chain reaction (PCR), permits the detection of the viral genome. METHODS: One hundred fifty eight prospective transfusion recipients were studied. Nineteen (12%) developed non A non B PTH criteria. The presence of anti c-100 and the viral genome were investigated by PCR in 17 of the patients. RESULTS: Nine of the 17 receptors (53%) with non A non B PTH presented antibodies against the HCV. In all patients and in two seronegative patients genomic sequences of HCV were detected by PCR. CONCLUSIONS: By a combination of genomic (PCR) and serological technique, 11 of the 17 transfusion recipients (64%) with non A non B PTH demonstrated evidence of HCV infection. In two cases the infection was seronegative. Although the HCV appeared to be the principal agent of the non A non B PTH in this study it could not be recognized in a third of the recipients who developed non A non B PTH.

Adult↗
PubMed1991

Tamoxifen inhibition of prolactin action in the mouse mammary gland.

Binding of lactogenic hormones to particulate and solubilized microsomal membranes isolated from mammary glands of lactating mice is inhibited by direct addition of 10(-10) M or greater concentrations of triphenylethylene antiestrogens [i.e. tamoxifen (TAM), 4-hydroxy-tamoxifen, and Nafoxidine] to the binding assays. Estradiol and other antiestrogens such as BPEA (-2-(4-tert-butyl-phenoxy) ethyl diethylamine hydrochloride, LY117018, and LY 156758 do not have this effect. The triphenylethylene antiestrogens bind to the membrane-associated antiestrogen binding sites (AEBS). Effectiveness of binding to the AEBS parallels the effectiveness of inhibition of the lactogen binding. The effect is selective in that binding of epidermal growth factor and insulin to these same membranes is unaffected by the antiestrogens. Binding of PRL to membranes prepared from the livers of the lactating mice is also unaffected. Both the PRL receptor and AEBS are primarily localized to the microsomal membrane fraction of cells. Maximal inhibition of PRL binding by TAM is observed in the light microsomes that contain plasma membranes. In addition to inhibition of PRL binding, TAM also prevents the PRL-induced accumulation of caseins by cultured mouse mammary explants. Thus it appears that the triphenylethylene antiestrogens, acting through the AEBS, act as antilactogens in the normal mammary gland.

Animals↗
PubMed1990

Binding of opioids to human MCF-7 breast cancer cells and their effects on growth.

The well characterized human breast cancer cell line, MCF-7, has been shown to possess membrane receptors for various opioid ligands, and these compounds have been shown to modulate the growth of the cells in culture. Using specific radioligands for the receptor types, we were able to demonstrate that the MCF-7 cells possess multiple opioid receptor types. Relatively high-affinity-binding sites are present for the mu- and kappa-specific ligands, while lower affinity sites are present for the delta-agonist. Opioid ligands specific for the different receptor types significantly inhibited the growth of the MCF-7 cells in a dose-dependent manner when grown in the presence of 10% fetal bovine serum. This inhibitory effect was reversed by the simultaneous administration of the opioid receptor antagonist, naloxone. However, the opioid effect appears to be restricted to the hormonally responsive fraction of the MCF-7 cell growth. Cells grown in the presence of charcoal-stripped fetal bovine serum are refractory to the effects of the opioids unless the media is supplemented with estradiol. The data presented here suggest an important regulatory role for opioids in the growth and development of human breast cancers.

Breast Neoplasms↗
PubMed1989

Antiestrogen inhibition of prolactin-induced growth of the Nb2 rat lymphoma cell line.

The rat lymphoma cell line Nb2 is highly prolactin responsive in terms of growth. Estrogens are without effect in these cells that lack the estrogen receptor. The growth stimulation by lactogenic hormones is effectively inhibited by antiestrogens, such as tamoxifen and nafoxidine, at concentrations as low as 10(-10) M. The growth inhibition is partially reversed by replacement of the antiestrogens by prolactin. Nb2 cells contain estrogen-noncompetitive specific antiestrogen binding sites on their membranes that bind tamoxifen with an average Kd of 3.1 X 10(-10) M. Addition of antiestrogens to the binding reaction inhibits lactogenic hormone binding to membrane-bound receptors. The order of affinities of various antiestrogens (tamoxifen, nafoxidine, 2-(4-tert-butyl-phenoxy)ethyl diethylamine hydrochloride, and LY117018) for the antiestrogen binding sites parallels the order of their potencies as growth and lactogen binding inhibitors. These data suggest that antiestrogens, possibly acting through the antiestrogen binding sites, may function as antilactogens.

Animals↗