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Biomedical subjects

P Sen

Publications and source records attributed to P Sen.

At least 91 records · Page 5Linked to original sources
PubMed1990

Induction of chromosome breaks and sister chromatid exchanges in patients with Hodgkin's disease by two combination chemotherapy regimens of different leukemogenic potential.

The success of various combination chemotherapies in the treatment of cancer is compromised by their potential to cause secondary leukemia. Previous studies have suggested that the alkylating agents used in some regimens are the major etiological factor in these leukemias. In this study, we compared the abilities of two standard regimens used in the treatment of Hodgkin's disease to cause chromosome breaks and sister chromatid exchanges, the two most common types of chromosomal damage induced by alkylating agents. These regimens are MOPP [mechlorethamine-vincristine (Oncovin)-procarbazine-prednisone] and CVPP-ABDIC [cyclophosphamide-vinblastine-procarbazine-prednisone-doxorubicin (Adriamycin)-bleomycin-dacarbazine-1-(2-chloroethyl)-3-cyclohexyl-1- nitrosourea]. Our study demonstrated that (a) levels of spontaneous chromosome breaks and sister chromatid exchanges were low in untreated Hodgkin's disease patients; (b) significantly higher levels of these damages were induced in patients receiving eight cycles of CVPP-ABDIC, as compared with their pretreatment levels; (c) significantly elevated levels of sister chromatid exchanges, but not chromosome breaks, were induced in patients receiving two cycles of MOPP; and (d) no differences in the effect of these two regimens on cell cycle kinetics were observed. Although MOPP therapy has been reported to have higher rates of secondary leukemia than CVPP-ABDIC, our studies show that eight cycles of CVPP-ABDIC are more potent than two cycles of MOPP in inducing chromosome damage in patients during treatments.

Adult↗
PubMed1990

A kinetic model for calcium distribution.

Models for the distribution of minerals in the body are of interest as they allow researchers to trace the effect of a dose on mineral levels in plasma, storage and other compartments. Limited models are available in the literature for tracing the distribution of a calcium dose through a short time period. We propose a more general kinetic model which includes both limited absorption through the gut and loss of calcium via excretion. This new method has the advantages of giving reasonable results over moderate time periods, and allowing the extrapolation of calcium levels in extracellular fluid and storage. We fit the model to published data in order to obtain typical parameter values. These values are then used to analyze the implications of the model regarding the effect of calcium dose on calcium levels in various compartments.

Animals↗
PubMed1990

Possible prostaglandin-dopamine interactions during experimental gastric ulcer formation.

The effects of dopamine (DA) agonists and antagonists were investigated on indomethacin--and restraint stress (6 hr at RT)--induced gastric ulcer formation in rats. The DA-agonists, apomorphine and bromocryptine (both at 5 mg/kg) significantly attenuated the frequency and severity of gastric mucosal lesions in both experimental models. The DA-antagonist, haloperidol (0.05 and 1.0 mg/kg) aggravated the gastric ulcerogenesis of both indomethacin and stress, the effects with the lower dose being statistically significant. Haloperidol (0.05 mg/kg) also prevented the cytoprotective effects of apomorphine on indomethacin-ulcers. The atypical DA-antagonist, sulpiride (10 and 50 mg/kg), however, showed differential dose- and model-specific effects. Whereas, the lower dose attenuated indomethacin-ulcers, the higher dose (50 mg/kg) tended to aggravate this phenomenon. The trend of results were reversed in the restraint stress model. Indomethacin (1 mg/kg) aggravated stress-ulcers, an effect which was also appreciably neutralised by apomorphine (5 mg/kg) pretreatment. These results are discussed in light of possible prostaglandin-DA interactions during such experimental gastric pathology.

Animals↗
PubMed1989

Biochemical and pharmacological evidence for central cholinergic regulation of shock-induced aggression in rats.

Acetylcholinesterase (AChE) activity was estimated in brain and heart homogenates and plasma of 'aggressive' and 'nonaggressive' rats. Brain homogenates of 'nonaggressive' rats hydrolyzed significantly more substrate when compared to the 'aggressive' rats. Such differences were not seen in the heart homogenates or plasma of these two groups of rats. Acute DFP (0.1, 0.3 and 1.0 mg/kg) attenuated shock-induced aggression (SIA) 2 hr after treatment but facilitated SIA 24 hr and 48 hr after drug administration. Long-term DFP (0.3 mg/kg x 10 days), on the other hand, induced a significant enhancement in the SIA score, whereas atropine (1.0 and 5.0 mg/kg) produced a dose-related attenuation of the same. Pretreatment of rats with atropine (5 mg/kg) antagonized the long-term DFP-induced facilitation of SIA. These results are discussed in the light of an inhibitory central cholinergic mechanism in the regulation of SIA.

Acetylcholinesterase↗
PubMed1989

Cooperative binding of Agrobacterium tumefaciens VirE2 protein to single-stranded DNA.

The VirE2 protein of Agrobacterium tumefaciens Ti plasmid pTiA6 is a single-stranded-DNA-binding protein. Density gradient centrifugation studies showed that it exists as a tetramer in solution. Monomeric VirE2 active in DNA binding could also be obtained by using a different protein isolation procedure. VirE2 was found to be thermolabile; brief incubation at 37 degrees C abolished its DNA-binding activity. It was insensitive to the sulfhydryl-specific reagent N-ethylmaleimide. Removal of the carboxy-terminal 37 residues of the 533-residue VirE2 polypeptide led to complete loss of DNA-binding activity; however, chimeric fusion proteins containing up to 125 residues of the VirE2 C terminus were inactive in DNA binding. In nuclease protection studies, VirE2 protected single-stranded DNA against degradation by DNase I. Analysis of the DNA-VirE2 complex by electron microscopy demonstrated that VirE2 coats a single-stranded DNA molecule and that the binding of VirE2 to its substrate is cooperative.

Bacterial Proteins↗
PubMed1989

Effect of beta-adrenoceptor antagonists and some related drugs on maximal electroshock seizures in mice.

(+/-) Propranolol (1-50 mg/kg), (+) propranolol (50 mg/kg) and pindolol (10-50 mg/kg) exhibited significant protective effects against MES (maximum electroshock seizures), whereas, timolol (1 mg/kg), the propranolol analog, UM-272 (1 and 10 mg/kg), and the beta-agonist, terbutaline (1 and 10 mg/kg) were ineffective. Cholinergic agents, physostigmine (0.01-1.0 mg/kg), and atropine (1 and 10 mg/kg), the serotonin antagonist, cyproheptadine (0.05 mg/kg), and the prostaglandin synthesis inhibitor, indomethacin (10 mg/kg), were also without effect on the MES extensor phase. Further, pretreatment of mice with terbutaline, atropine, cyproheptadine or indomethacin did not influence the anti-MES effect of propranolol to any significant extent. The results indicate that the observed anticonvulsant effects of beta-adrenoceptor antagonists are unrelated to noradrenergic or other central neurotransmitter systems and that a non-specific mechanism, probably a membrane stabilizing effect is involved.

Adrenergic beta-Antagonists↗
PubMed1989

Unusual presentation: testicular seminoma.

A case of seminoma is described in a patient with HIV infection. The tumor presented atypically with no lymphocytic infiltrates within the stroma. HIV infection has been reported to be associated with an increased incidence of Kaposi's sarcoma, non-Hodgkin's lymphomas, oropharyngeal carcinoma and pancreatic carcinoma.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Heterogeneity in chromosome damage and repair rates after bleomycin in ataxia telangiectasia cells.

Cells derived from patients with ataxia telangiectasia (AT) are known to be exceptionally sensitive to ionizing radiation and chemotherapeutic agents such as bleomycin (BLM), neocarzinostatin, and etoposide. This increased sensitivity is manifested by high chromosome aberration frequencies after treatment. In order to probe the underlying basis for this phenomenon, the technique of premature chromosome condensation was used to determine whether the increased chromosome damage observed after bleomycin treatment is due to increased initial chromosome damage or to a decreased capability of these cells to repair chromosome damage. Five AT cell lines were brought to quiescence and treated with BLM, and initial chromosome damage and repair rates were determined in the G1 prematurely condensed chromosomes. AT cells exhibited increased aberration frequencies compared to normal human fibroblasts immediately after BLM treatment. The five AT cell lines were heterogeneous in the fast component of chromosome break repair, varying from a nearly normal fast repair component in one cell line to a nearly defunct fast repair component in two other AT cell lines. Thus, while the AT cell lines were heterogeneous in the basis for their chromosome breakage sensitivity, all AT cell lines tested showed increased residual chromosome damage after BLM treatment while still in the quiescent phase.

Ataxia Telangiectasia↗
PubMed1988

Chromosomal alterations in cell lines derived from mouse rhabdomyosarcomas induced by crystalline nickel sulfide.

Prior studies have shown a preferential decondensation (or fragmentation) of the heterochromatic long arm of the X chromosome of Chinese hamster ovary cells when treated with carcinogenic crystalline NiS particles (crNiS). In this report, we show that the heterochromatic regions of mouse chromosomes are also more frequently involved in aberrations than euchromatic regions, although the heterochromatin in mouse cells is restricted to centromeric regions. We also present the karyotypic analyses of four cell lines derived from tumors induced by leg muscle injections of crystalline nickel sulfide which have been analyzed to determine whether heterochromatic chromosomal regions are preferentially altered in the transformed genotypes. Common to all cell lines was the presence of minichromosomes, which are acrocentric chromosomes smaller than chromosome 19, normally the smallest chromosome of the mouse karyotype. The minichromosomes were present in a majority of cells of each line although the morphology of this extra chromosome varied significantly among the cell lines. C-banding revealed the presence of centromeric DNA and thus these minichromosomes may be the result of chromosome breaks at or near the centromere. In three of the four lines a marker chromosome could be identified as a rearrangement between two chromosomes. In the fourth cell line a rearranged chromosome was present in only 15% of the cells and was not studied in detail. One of the three major marker chromosomes resulted from a centromeric fusion of chromosome 4 while another appeared to be an interchange involving the centromere of chromosome 2 and possibly the telomeric region of chromosome 17.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Modulation of humoral immune responses by endogenous opioids.

The effects of opioid agonists and antagonists were investigated on humoral immune mechanisms in mice and rats. Opioid agonists like morphine, Leu-enkephalin, and Met-enkephalin, enhanced antigen-induced histamine release from mixed peritoneal cells of rats in vitro; this enhancement was effectively antagonized by naloxone, an opioid antagonist. Naloxone, per se, decreased anaphylactic mortality in doses of 10 mg/kg, while it increased mortality in a dose of 1 mg/kg. Reduced IgE antibody titer, measured by passive cutaneous anaphylaxis, decreased hemagglutination titer to sheep red blood cells, blocked histamine release from mixed peritoneal cells of rats in vitro induced by antigen, but had no significant effect when histamine release was induced by compound 48/80. Thus, it appears that endogenous opioids are involved in humoral immune responses.

Anaphylaxis↗
PubMed1988

Effect of a segregated-care system on patients' length of stay in intensive care.

The Internal Medicine Residency Program of the Raritan Bay Medical Center's Perth Amboy Division was changed in July 1987 from a full continuity-of-care system to a unit-isolation one. The authors compared patients' data from the first two months of the academic years 1986-87 and 1987-88 and were unable to observe any impact of the change on length of stay in intensive care. However, informal interviews with the house staff members indicated that the change had a positive impact on their education, because of their closer observation of the pathophysiology of individual disease states and greater enjoyment of the time spent in critical care.

Adolescent↗
PubMed1988

Assessment of cardiac function in patients with the acquired immunodeficiency syndrome.

We have assessed right and left ventricular function by multigated radionuclide ventriculography in 12 consecutive patients with acquired immunodeficiency syndrome (AIDS) grouped according to the CDC classification system for HIV infection. Results were correlated with clinical, electrocardiographic and echocardiographic findings. Clinical examination and chest x-ray films showed no evidence of acute cardiac or pulmonary pathology. Five patients had evidence of ventricular dysfunction by radionuclide ventriculography along with significant ECG abnormalities. Three patients had abnormal ECG findings with normal ejection fractions. Echocardiography showed no evidence of significant valvulopathy or pericardial disease except for one patient with fibrinous strands associated with the pericardium. Decreased ejection fractions did not correlate with disease classification, risk group or survival. This study suggests that a major percentage of AIDS patients have some evidence of cardiac abnormalities. We conclude that abnormal ECG findings in an AIDS patient should alert the clinician to possible underlying ventricular dysfunction.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Endogenous opioids and immune responses: an experimental study.

Possible involvement of endogenous opioids in humoral immune responses has been explored in the experimental animals. Opioid agonists like morphine and leu-enkephalin significantly enhanced antigen-induced histamine release from the peritoneal mast cells of sensitised rats in vitro; this was effectively antagonised by naloxone. Naloxone itself inhibited antigen-induced histamine release. Animals were effectively protected against anaphylactic shock by naloxone which also antagonised morphine-induced increase in anaphylactic mortality. Naloxone reduced haemagglutination titre to sheep red blood cells and IgE antibody titre as measured by passive cutaneous anaphylaxis. Thus, endogenous opioids appear to be involved in the mediation of humoral immune responses. They seem to act at various steps in the immune mechanism viz (i) antibody production and (ii) release of mediators of hypersensitivity reactions.

Anaphylaxis↗