Physician and nurse awareness of drug-use-review activities.
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British Columbia↗
Biomedical subjects
S Gupta
Publications and source records attributed to S Gupta.
Emptying of the intrathoracic stomach with and without pyloroplasty.
By radioisotope technique, we studied the emptying function of the vagotomized intrathoracic stomach after esophagectomy for carcinoma of the esophagus in 24 patients, and compared it with the preoperative emptying function. The patients were randomized into a control group (no pyloroplasty) and a study group (pyloroplasty). Gastric emptying was delayed in both groups, postoperatively; however, the delay was greater in the control group than in the study group. Therefore, vagotomy delays the emptying of the thoracic stomach, and this delay is not completely corrected by pyloroplasty.
Esophageal Neoplasms↗
Axillopopliteal bypass grafting: indications, late results, and determinants of long-term patency.
In the last 12 years we have performed 55 axillopopliteal bypass graftings with 6 mm polytetrafluoroethylene grafts for limb salvage in 50 patients who were at high risk for limb loss. Indications for this procedure were (1) severe atherosclerotic disease of the common, superficial, and deep femoral arteries (33 cases); (2) failed aortofemoral bypass grafting with sufficient fibrosis or disease progression in the deep femoral artery (five cases); (3) insufficient hemodynamic and clinical improvement after axillofemoral bypass grafting (10 cases); and (4) sepsis in the groin from a previously infected graft (seven cases). The 30-day operative mortality rate was 8%, and the 5-year cumulative patient survival rate was 40%. Overall 1-, 3-, and 5-year cumulative primary graft patency rates were 58%, 45%, and 40%, respectively. Comparable limb salvage rates were 83%, 68%, and 58%. Repeat operations increased 5-year patency rates from 40% to 59% (p less than 0.05). Three-year patency rate for grafts placed in the presence of poor angiographic runoff in one vessel was 62% and for good angiographic runoff (two to three vessels) it was 57% (NS). Grafts to the above-knee popliteal artery had a patency rate of 67% at 3 years, whereas for grafts that crossed the knee joint it was 51% (NS). Three-year patency rate for 24 straight axillopopliteal grafts was 42%, and for 31 sequential axillofemoral-popliteal grafts it was 74% (p less than 0.05). These results show that axillopopliteal bypass grafting is justified when other standard operations are not possible in patients who are in imminent danger of limb loss, and that every possible effort should be made to use the common or deep femoral artery as part of a sequential axillofemoral-popliteal procedure.
Aged↗
Clinicopathological studies of carcinoma oesophagus with special reference to changes in surrounding epithelium.
A total 17 cases of carcinoma oesophagus were studied in a period of 2 years. Ten patients (58.82%) were males and rest were females. Maximum cases (64.70%) were seen in 5th and 6th decades. Majority of the patients belonged to low socio-economic group (47.05%) followed by middle socio-economic group (41.17%). Dysphagia was present in all cases, followed by weight loss 52.94% and other symptoms. Cancer was equally distributed in middle third and lower third of the oesophagus (41.18% in each group) only in 3 cases it was in upper third of the oesophagus. Histologically 70.5% tumours were squamous cell carcinoma, 17.64% were adenocarcinoma and 11.76% were undifferentiated carcinoma. Surrounding epithelium in 17.64 per cent cases showed chronic oesophagitis, 4 cases (23.52%) showed acanthosis and dysplasia, and two cases revealed carcinoma in situ. Hence findings of oesophagitis, acanthosis, dysplasia, carcinoma in situ suggest that oesophagitis and acanthosis may be considered as precancerous lesions.
Adenocarcinoma↗
Characterization of lymphoid tumors induced by a recombinant murine retrovirus carrying the avian v-myc oncogene. Identification of novel (B-lymphoid) tumors in the thymus.
Lymphoid tumors induced by a recombinant murine retrovirus carrying the v-myc oncogene of avian MC29 virus were characterized. The Moloney murine leukemia virus myc oncogene (M-MuLV (myc], carried by an amphotropic MuLV helper, induced tumors in NIH Swiss and NFS/N mice after a relatively long latency (8 to 24 wk). Tumor masses appeared in the thymus, spleen, and lymph nodes. Flow cytometry of the tumor cells indicated that approximately 50% were positive for Thy 1.2. Most of these tumors also expressed one or more other cell surface markers of thymocytes and mature T cells (CD4, CD8). Southern blot hybridization revealed genomic rearrangements for the TCR beta genes. The TCR beta analysis suggested that the M-MuLV(myc)-induced Thy 1.2+ tumors were derived from somewhat less mature cells than tumors induced by M-MuLV, which is a classical non-acute retrovirus lacking an oncogene. The remainder of the M-MuLV(myc)-induced tumors were Thy 1.2-, but they were positive for Ly-5 (B220) and also for MAC-2. The Thy 1.2- tumors were characteristically located in the thymus. However, they were negative for TCR beta gene rearrangements. Some, but not all, of the Thy 1.2- tumors contained rearrangements for Ig genes. Additionally, they typically expressed mRNA specific for B but not for T cells. Thus, these thymic tumors had characteristics of the B cell lineage. Tumor transplantation experiments demonstrated that the Thy 1.2- tumor cells could reestablish in the thymus and spleen of irradiated hosts, and low level expression of the Thy 1 molecule was observed in the thymus but not the spleen on the first passage. After serial passage, one Thy 1- tumor altered its cell surface phenotype to Thy 1low B220-.
Animals↗
Germ cell tumors in Indian children.
The present paper is a retrospective study of one hundred and thirty five germ cell tumors seen in children at the University Hospital, Varanasi during a period of 21 years. These tumors constituted 7.5% of all solid tumors in the pediatric age group. Histologically 89 tumors (65.9%) were benign and 46 (34.1%) were malignant. Eighty percent of ovarian and all the testicular germ cell tumors were malignant. Thirty per cent of the tumors were located in the sacrococcyx. The ovaries were the next common site. There were 80 girls, 53 boys, and 2 cases in which the sex was not recorded. The predominance amongst girls was mainly due to the more frequent involvement of ovaries as compared to the testes. Twenty nine of the children were in the first year of life. The factors probably responsible for the higher incidence of malignancy, the differences in anatomic location, and the sex distribution in comparison to other reports have been examined and discussed.
Adolescent↗
Correction of altered plasma membrane potentials. A possible mechanism of cyclosporin A and verapamil reversal of pleiotropic drug resistance in neoplasia.
We have recently shown that cyclosporin A (CsA) reverses pleiotropic drug resistance in human acute lymphatic leukemia in vitro and daunorubicin resistance in Ehrlich ascites tumor in vivo. In the present study we examined the mechanisms by which CsA might reverse pleiotropic drug resistance relative to changes in cellular plasma membrane potentials and intracellular calcium ([Ca2+]i). Membrane potentials were measured with DIOC5 dye flow-cytometrically and [Ca2+]i levels with Quin 2 dye spectrofluorimetrically. All pleiotropic (PDR) drug-resistant tumor sublines had decreased membrane potentials (membrane depolarized) compared with their corresponding drug-sensitive parental tumors. In comparison, the membrane potentials of a control antimetabolite-resistant acute leukemia cell line were unchanged. The basal levels of [Ca2+]i in the PDR sublines were variable compared with those of parental drug-sensitive cell lines. Incubation of all PDR tumor sublines with CsA or verapamil resulted in the restoration of membrane potentials to that characteristic of the corresponding drug-sensitive parental tumor. Cyclosporin A produced variable changes in the levels of [Ca2+]i. These data suggest that alteration of membrane potentials is one of the mechanisms responsible for pleiotropic drug resistance in malignancy and show that this alteration is corrected by CsA and verapamil.
Animals↗
Lipopolysaccharide-induced murine B cell proliferation: a role of protein kinase C.
Lipopolysaccharide (LPS)-induced murine B cell proliferation was blocked by 1-(5-isoquinoline-sulfonyl)-2-methylpiperazine dihydrochloride (H7), an inhibitor of protein kinase C (PKC), in a dose- and time-dependent manner. The maximum inhibition of B cell proliferation was observed when H7 was added at the initiation of cultures. H7-induced inhibition was prolonged and irreversible. Furthermore, pretreatment of B cells with phorbol myristate acetate ester, a process that degrades membrane-associated PKC, rendered them unresponsive to LPS. These data strongly suggest that the activation of PKC is one of the mechanisms of LPS-induced murine B cell proliferation.
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
Serum lactic dehydrogenase isoenzymes alteration in carcinoma cervix uteri.
Serum LDH-isoenzyme studies revealed that in carcinoma cervix, the principal activity was confined to LDH-2 and LDH-3 with a significant rise in LDH-2 fraction when compared with the control values (P less than 0.001). Radiotherapy caused significant lowering of LDH-2 and LDH-3 (P less than 0.001 in each case). There was no relation of LDH-isoenzyme distribution in different clinical stages and morphological distribution within the tumor. Further, LDH-2 and LDH-3 were found to be lowered significantly in good and moderate clinical radiation response (CRR) groups (P less than 0.001 in each case) but in poor CRR group no significant change in LDH-2 and LDH-3 was observed following radiotherapy. LDH-isoenzyme determination in carcinoma cervix is very helpful in assessing the treatment response following radiotherapy and thus may be an important prognostic parameter.
Female↗
Vasoactive intestinal polypeptide inhibits the expression of the MHC class II antigens on astrocytes.
The brain has been traditionally viewed as an immunologically privileged site. However, recent findings suggest that the brain is in fact equipped with its own immune circuitry. Astrocytes and microglia have been considered the most likely candidates to assume the role of intracerebral antigen presenting cells (APC). Using the techniques of immunofluorescence cytochemistry and flow cytometric analysis, we observed that vasoactive intestinal polypeptide (VIP) can significantly inhibit gamma-interferon (IFN-gamma)-induced Ia expression on astrocytes derived from newborn Lewis rats. Further, we analyzed a number of neuropeptides and transmitters for their ability to exert a similar inhibitory modulation on IFN-gamma induced Ia expression or for the ability to induce or augment Ia expression on rat astrocytes. Our results showed that only norepinephrine (NE), a major brain neurotransmitter, and VIP, a ubiquitous brain peptide, have the ability to inhibit Ia expression on Lewis rat astrocyte cultures. Alternately, we report that cholecystokinin (CCK), a brain/gut peptide, has the ability to induce Ia on about 5-10% of the cells analyzed. These findings suggest that endogenous brain substances have the ability to modulate intracerebral immune responses by regulating the expression of Ia on astrocytes.
Animals↗
Norepinephrine inhibits gamma-interferon-induced MHC class II (Ia) antigen expression on cultured brain astrocytes.
Recent evidence that astrocytes can be induced to express the class II major histocompatability (MHC) antigens suggests that these cells may be involved in the development of intracerebral immune responses. The principal inducer of MHC class II antigen (Ia) expression is a soluble lymphokine, gamma-interferon (gamma-IFN). Normally astrocytes do not express significant levels of Ia antigens despite the fact that agents such as gamma-IFN may be present in the central nervous system (CNS). Here we report that a major neurotransmitter, norepinephrine (NE), inhibits, in a dose-response fashion, the ability of gamma-IFN to induce Ia antigen expression on cultured astrocytes derived from newborn BALB/c mice. This finding may indicate that the brain contains inhibitory modulators that serve to prevent the up-regulation of intracerebral immune responsiveness.
Animals↗
Acquired immunodeficiency syndrome-associated renal disease in children.
Five children with acquired immunodeficiency syndrome (AIDS) and clinically significant renal disease had detailed pathologic examination of renal tissue (biopsy specimens, autopsy specimens, or both). All patients had proteinuria, hypoalbuminemia, and edema; one patient had persistent azotemia. In two cases, renal disease was the first manifestation of human immunodeficiency virus (HIV) infection. All patients had progressive renal disease, and four of the five died. Pathologic studies revealed focal glomerulosclerosis and mesangial proliferative glomerulonephritis with deposits of immunoglobulins and complement demonstrated by immunofluorescence and electron microscopy. Characteristic tubuloreticular structures were also demonstrated in the glomerular endothelial or epithelial cells in two cases. Renal disease is part of the multisystem involvement in children with AIDS. The pathogenesis of renal disease is not known, but circulating immune complexes are known to occur in children with HIV infection and may be involved.
Acquired Immunodeficiency Syndrome↗
Ascorbic acid levels in the proglottides of four species of cestode parasites of mammals and birds in relation to their sexual maturity.
Ascorbic acid levels were found to be closely related to different stages of growth and maturity of Avitellina centripunctata, Moniezia expansa, and Stilesia globipunctata from goats and sheep and of Raillietina echinobothrida from fowl. The ascorbic acid level in avian parasites was higher than that in mammalian. The level was highest in immature proglottides and lowest in gravid proglottides.
Animals↗
Norepinephrine inhibits gamma-interferon-induced major histocompatibility class II (Ia) antigen expression on cultured astrocytes via beta-2-adrenergic signal transduction mechanisms.
The astrocyte is now recognized as a facultative immunocompetent antigen-presenting cell that can initiate intracerebral immune responses. However, despite the presence of activated T lymphocytes and their associated lymphokines within the central nervous system, there is a paucity in the expression of the major histocompatibility (MHC) antigens on normal neural tissue. These membrane-localized glycoproteins are required for the process of antigen presentation and, therefore, for the initiation of immune responses. To date, little is understood regarding the nature of inhibitory mechanisms that might be responsible for maintaining the brain as an immunoprivileged site. In this study we found that norepinephrine, a major brain transmitter, significantly inhibited gamma interferon-induced MHC class II antigen expression on astrocytes derived from neonatal Lewis rats. We show that this inhibition can be attenuated by the addition of a beta-adrenergic antagonist, propranolol, but not by the addition of a beta 1-selective antagonist, atenolol, or by an alpha-adrenergic antagonist, phentolamine. Furthermore, it was found that a similar inhibition could be achieved by the addition of either dibutyryl-cAMP or dipyridimole, a phosphodiesterase inhibitor. Therefore, it seems that norepinephrine-mediated inhibition of MHC class II antigen expression on astrocytes works through beta 2-adrenergic signal transduction pathways. Taken together, these in vitro results suggest that the brain contains inhibitory factors that may play a pivotal role in the regulation of intracerebral immune responses by modulating the expression of MHC antigens on astrocytes.
Animals↗
Impaired neutrophil function in patients with AIDS or AIDS-related complex: a comprehensive evaluation.
We measured the neutrophil function of 6 patients with AIDS and Kaposi's sarcoma (KS); 22 patients with AIDS-related complex (ARC); and 28 healthy, heterosexual controls. Neutrophils from patients with ARC showed significantly less chemotaxis (P less than or equal to .025) than did those from patients with AIDS and KS or from controls. Serum from patients with AIDS and KS or with ARC significantly (P less than or equal to .05) inhibited chemotaxis of neutrophils from controls; heat treatment of the serum abolished this inhibitory effect. Bacterial killing by neutrophils from patients with AIDS and KS or with ARC was also significantly (P less than or equal to .05) less than for neutrophils from controls, as was neutrophil phagocytosis binding of Candida albicans (P less than or equal to .05). Expression of OKM1 antigen was increased in the patients studied. Enzyme degranulation, adherence, and aggregation were also examined. The defects found in neutrophil function are selective and may be important in the increased susceptibility of patients with human immunodeficiency virus infection to bacterial and fungal infections.
AIDS-Related Complex↗
Failure of ketoconazole as anti-androgen therapy in nonresectable primary hepatocellular carcinoma.
Lacking a treatment for nonresectable hepatocellular carcinoma (HCC), we have utilized the androgen antagonist properties of ketoconazole in treating eight patients, seven men and one woman, with HCC, which, in view of a higher prevalence of HCC in men, seems to be androgen dependent. Response to treatment was determined by grading symptoms, serum alphafetoprotein, alteration in tumor size, and duration of survival. No patient had any significant side-effects from ketoconazole. No symptomatic improvement occurred, percent tumor size increased from 38.6 +/- 12, mean +/- SEM, to 44.4 +/- 12, and mean survival in six patients who were followed until death was less than 8 weeks from diagnosis. Anti-androgenic therapy with ketoconazole was not effective in any of these patients.
Adult↗
Modulation of glucocorticoid receptor from development to aging.
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Aging↗
Unique two-stage intervention to modify prescribing trends.
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British Columbia↗