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Biomedical subjects

P Mehta

Publications and source records attributed to P Mehta.

At least 199 records · Page 11Linked to original sources
PubMed1984

Improved response of patients refractory to random-donor platelet transfusions by intravenous gamma globulin.

Because of frequent unavailability of HLA-compatible platelets or their inefficiency in increasing platelet counts in patients requiring platelet transfusions, platelet refractoriness remains a major problem. Since human gamma globulin has been shown to interfere with the binding of platelet-reactive immunoglobulin G (IgG) to platelets in vitro, and since gamma globulin has proved effective in reversing destruction of platelets in idiopathic thrombocytopenic purpura, we decided to investigate intravenous gamma globulin as an adjunct to random-donor platelet transfusions. We studied three patients, one with acute T-cell leukemia, and two with aplastic anemia. When a total dose of 2 g/kg of body weight of intravenous gamma globulin was infused over five to six days in these patients, two of them showed a remarkable increment in platelet counts and improved hemostasis with random-donor platelet transfusions. We conclude that intravenous gamma globulin may be used in critical situations to improve the response of patients refractory to random-donor platelet transfusions.

Adult↗
PubMed1984

Activity of Carbetimer in a human tumor cloning system.

The antitumor activity of Carbetimer was tested against 171 patient's tumors in a human tumor cloning system. Sixty-seven tumor specimens had adequate growth to be considered evaluable. In 21 specimens survival of tumor colony forming units was less than or equal to 50% that in control plates. Antitumor effect was most impressive in carcinomas of the breast, ovary, and lung. This information will be useful in planning disease oriented Phase II trials.

Antineoplastic Agents↗
PubMed1984

Thromboxane release in coronary artery disease: spontaneous versus pacing-induced angina.

To determine thromboxane A2 release in coronary artery disease, we measured its stable metabolite thromboxane B2 by radioimmunoassay in 20 patients. In 15 patients with stable disease (last angina episode greater than 96 hours before study), coronary venous thromboxane B2 concentrations were lower than in aortic blood (mean 109 +/- 36 vs 194 +/- 40 pg/ml, p less than 0.001). In contrast, in five other patients with spontaneous angina, coronary venous thromboxane B2 concentrations were higher than aortic thromboxane B2 concentrations during the angina episode (mean 1716 +/- 316 vs 875 +/- 388 pg/ml, p less than 0.02). Plasma thromboxane B2 levels were in the normal range (mean 175 +/- 35 pg/ml) in patients with stable angina but significantly (p less than 0.02) higher in patients with spontaneous angina. With atrial pacing to the point of chest pain and/or ECG changes in patients with stable coronary artery disease, aortic thromboxane B2 concentrations increased in 10 of 13 patients (mean 283 +/- 70 pg/ml, p less than 0.02). Coronary venous thromboxane B2 concentrations increased in seven patients at peak pacing rates (mean 223 +/- 76 pg/ml) and in three other patients after termination of pacing. These data indicate that release of thromboxane A2 is much greater during spontaneous angina than with pacing stress in patients with coronary artery disease. Thromboxane A2 released during spontaneous or pacing-induced angina may modulate coronary and systemic vascular tone. Enhanced thromboxane A2 activity may either precede or follow myocardial ischemia and could be a factor in the initiation and propagation of the ischemic episode.

Adult↗
PubMed1984

Antimicrobial effect of chlorhexidine and povidone-iodine on vaginal bacteria.

The antimicrobial potency of 4 per cent chlorhexidine gluconate was compared with that of 10 per cent povidone-iodine (1 per cent free iodine) on the vaginal bacteria of 150 premenopausal, non-pregnant women. From 30 of the women blood samples were taken before and at either 15, 30 or 60 minutes after vaginal cleansing with chlorhexidine for chlorhexidine analysis. Five minutes after applying either chlorhexidine or povidone-iodine almost 99 per cent of bacteria present on the lateral wall of the vagina were killed. Chlorhexidine was significantly more effective than povidone-iodine. Serosanguineous , mucoid or white-yellowish vaginal discharge did not alter the effectiveness of either antimicrobial agent. In contrast to povidone-iodine, vaginally applied chlorhexidine was not absorbed in measurable amounts (sensitivity of detection method: 0 X 1 mg/l) into the bloodstream. Chlorhexidine may therefore prove of value for treating vaginitis especially during pregnancy and also for combating microbes such as Group B streptococci which are potentially harmful to the newly-born child.

Absorption↗
PubMed1984

Platelet function and biosynthesis of prostacyclin and thromboxane A2 in whole blood after aspirin administration in human subjects.

Small doses of aspirin have been shown to inhibit platelet thromboxane A2 while sparing vascular prostacyclin synthesis. Because leukocytes generate prostacyclin and participate in thrombosis along with platelets, the effects of three different doses of aspirin (40, 325 and 650 mg) on platelet function as well as on endogenous biosynthesis of thromboxane A2 and prostacyclin in whole blood were examined. In normal volunteers given a single 40 mg dose of aspirin, platelet aggregation and adenosine triphosphate release were inhibited for 24 hours. In contrast, platelet function was inhibited for 4 to 7 days in volunteers given 325 or 650 mg of aspirin. Platelet and whole blood generation of thromboxane A2 was inhibited less than 60% by the 40 mg dose, but almost completely by both the 325 and 650 mg doses. Likewise, whole blood generation of prostacyclin was inhibited 70% by the 40 mg dose and over 90% by the larger doses. Inhibition of thromboxane A2 as well as of prostacyclin was evident for 4 days with the 40 mg dose and for 7 days with the larger doses. Decreases in whole blood thromboxane A2 and prostacyclin with any dose of aspirin were of similar magnitude. These data indicate that aspirin in doses of 40 to 650 mg inhibits platelet function and biosynthesis of thromboxane A2 and prostacyclin in whole blood in human beings in a dose-dependent fashion.

6-Ketoprostaglandin F1 alpha↗
PubMed1984

Potential role of platelets in the pathogenesis of tumor metastasis.

Platelet activity may be involved in tumor metastasis. The tumor cells, after detachment from the primary site, adhere to vascular endothelium at distant sites and proliferate. Platelets form aggregates with tumor cells in circulation, facilitating their adhesion to the vascular endothelium. Formation of platelet-tumor cell aggregates and their sequestration in various end-organs may result in thrombocytopenia. Certain tumor cell lines directly stimulate platelet activity, some by releasing platelet-aggregating material, a urea-extractable membrane component, others by release of cathepsin, and still others by undefined mechanisms. The direct effect of platelets on tumor cells may be of pathogenic significance. For example, platelet-derived factors stimulate growth of some tumors, whereas others increase vascular permeability and thus facilitate migration of tumor cells across the vessel wall. Lack of these platelet factors, as in thrombocytopenic animals, may indeed inhibit tumor metastasis. Arachidonic acid metabolism in platelets and the vessel walls may contribute to metastatic process. In particular, thromboxane A2 and prostacyclin generation capabilities appear to be important in modulating platelet-tumor cell deposition and growth. To alter the metastatic process, several preliminary trials of platelet-inhibitory agents have been performed. However, the results of these trials have been equivocal, perhaps related to nonspecific effects of these agents on arachidonic acid metabolism. Studies directed at specific pathways of platelet-vessel wall interaction on some tumors appear promising. These newer agents may be of therapeutic value in man.

Animals↗
PubMed1984

Decreased stabilization of prostacyclin activity in patients with bone tumors.

Tumor metastasis is mediated in part by platelet activation. Since prostacyclin regulates platelet activity, we examined stabilization of bioactivity of exogenous prostacyclin in plasma of patients with malignant bone tumors. Bioactivity of prostacyclin (platelet aggregation inhibition) incubated in patient plasma was found to be significantly less compared to that in normal plasma. In addition, the duration of bioactivity of prostacyclin was considerably less in plasma of patients with bone tumors. These preliminary data indicate decreased prostacyclin activity in plasma of patients with malignant bone tumors, which may be a mechanism of platelet-tumor cell aggregate formation and subsequent evolution of metastasis.

Adolescent↗
PubMed1984

Biochemical and ultrastructural integrity of the saphenous vein conduit during coronary artery bypass grafting. Preliminary results of the effect of papaverine.

Factors associated with early and late graft patency related to aorta-coronary artery bypass grafting with a reversed segment of saphenous vein are clinically important. The present investigation examines the biochemical and electron microscopic integrity of this venous conduit intraoperatively with regard to pharmacologic manipulation with papaverine. Portions of saphenous vein were analyzed in 22 patients undergoing coronary artery bypass operations. Levels of a stable derivative of prostacyclin, 6-keto-PGF1 alpha, were measured by radioimmunoassay. Scanning as well as transmission electron microscopy was also performed. In particular, the efficacy of local vein treatment with papaverine, a phosphodiesterase inhibitor, was evaluated. We found that levels of 6-keto-PGF1 alpha in venous effluent showed a biphasic response with initial elevation followed by a relative depression after papaverine exposure. There were no such changes observed in veins subjected to a balanced electrolyte solution (Plasma-Lyte). In addition, levels of the platelet-inhibitory substance 6-keto-PGF1 alpha in venous tissue were less in papaverine-treated veins than those found in veins treated only with the balanced electrolyte solution (Plasma-Lyte). Furthermore, evidence for ultrastructural damage was also somewhat greater in the papaverine-treated group. An alternative method of dilating the saphenous vein after harvesting, which involves the creation of the proximal aorta-coronary anastomosis first and gentle finger manipulation subsequently, appeared to minimize venous injury. Under present clinical conditions, it appears that some amount of injury is inevitable during harvesting and suturing of the human saphenous vein during coronary bypass grafting.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Arterial prostacyclin generation is decreased in patients with malignant bone tumors.

Arterial production of PGI2 was measured in patients with malignant bone tumors and compared to that in arteries from subjects with benign bone tumors and others without tumor. Arteries from all study subjects exhibited spontaneous and arachidonate-induced PGI2 release. Arterial production of PGI2 as measured by 6-keto-PGF1 alpha was in the normal range in patients with benign tumors. In contrast, arteries from patients with malignant tumors had lower PGI2 release. Deficient arterial PGI2 production in patients with malignant tumor was present both at rest and upon stimulation of blood vessels with arachidonate. Decreased PGI2 generation could relate to tumor attachment to the endothelium, penetration of the vessel walls and subsequent metastasis.

Bone Neoplasms↗
PubMed1983

Effects of verapamil on platelet aggregation, ATP release and thromboxane generation.

We examined the effects of verapamil on platelet function. Verapamil (0.5 micrograms/ml) in this study inhibited platelet aggregation induced by threshold amounts of ADP, AA, and epinephrine. With higher concentrations of aggregating stimuli, verapamil caused a dose-dependent inhibition of aggregation. Verapamil reduced the extent of epinephrine-induced primary wave, but not that by ADP. Ristocetin-induced aggregation was not affected at any concentration of verapamil. Platelet ATP release induced by AA and ADP was also inhibited. In vitro platelet TXA2 generation was inhibited by verapamil in concentrations lower than those required for inhibition of aggregation.

Adenosine Triphosphate↗
PubMed1983

Legionella micdadei (Pittsburgh pneumonia agent). Two infections with unusual clinical features.

We describe herein the clinical features, diagnosis, and successful treatment of two patients with Legionella micdadei pneumonia, the Pittsburgh pneumonia agent. The rapid pulmonary cavitation and relapse of symptoms after a course of therapy in a renal transplant recipient, and the prolonged illness with hemorrhagic pleural fluid, splenomegaly, and multiple-organ dysfunction in a nonimmunocompromised host, illustrate the clinical spectrum of infections with this organism.

Adult↗
PubMed1983

Antimicrobial properties of some plant extracts against bacteria.

Plant extracts obtained from Feronia limonia (leaves) Xanthium strumarium (flowering twigs) and Glossocardia bosvellia (leaves) were tested for their antimicrobial properties against certain bacterial species. Feronia leaf extract was ineffective on Bacillus pumilus and X. campestris, Vibrio cholerae was found quite sensitive to this extract. The extract of X. strumarium showed an abnormality with V. cholerae, where the inhibition exceeded the control with established antibiotics. Similarly, G. bosvellia caused maximum inhibition in Bacillus mycoides.

Anti-Bacterial Agents↗
PubMed1983

The significance of platelet-vessel wall prostaglandin equilibrium during exercise-induced stress.

Alterations in platelet-generated thromboxane A2 (TXA2) and vessel wall-generated prostacyclin (PGI2) have been associated with myocardial ischemia. To examine TXA2-PGI2 equilibrium at rest and during exercise stress, we studied 13 normal subjects and 15 coronary artery disease patients. Plasma TXB2 and 6-keto-PGF1 alpha were measured as stable metabolites of TXA2 and PGI2, respectively, by radioimmunoassay. In normal subjects, plasma TXB2 levels increased 24% during exercise from 135 +/- 30 to 168 +/- 42 pg/ml (p = NS). Plasma 6-keto-PGF1 alpha levels increased 224% from 54 +/- 17 to 175 +/- 57 pg/ml (p less than 0.05). In coronary artery disease patients, although resting plasma TXB2 levels (mean 136 +/- 43 pg/ml) were comparable to levels in normal subjects, a greater increase (82%) occurred during exercise (mean 248 +/- 70 pg/ml; p less than 0.02 compared to resting levels). Resting plasma 6-keto-PGF1 alpha levels (mean 94 +/- 28 pg/ml) were also similar to normal subjects but increased only by 43% during exercise (mean 134 +/- 53 pg/ml; p = NS compared to resting levels). These data suggest that: in normal subjects TXA2 and PGI2 increase during exercise, PGI2 increasing more than TXA2, and although coronary disease patients have resting TXA2 and PGI2 levels in the normal range, TXA2 levels increase more than PGI2 levels during exercise. These observations may have a bearing on the mechanism of exercise-induced angina pectoris in certain coronary artery disease patients.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Statistical testing of an allometric centered model of craniofacial growth.

An allometric centered model of craniofacial growth was tested by several computer-assisted statistical methods on the pure longitudinal growth data of twenty-four close-bred female rats and on cross-sectional human cranial growth data. The study demonstrated that such a model was heuristic and, being incapable of exact definition, was deemed inappropriate for further use in modeling of craniofacial skeletal growth. The necessity for vigorous testing of any hypothesis concerning the modeling of craniofacial growth is stressed.

Adolescent↗
PubMed1983

Effect of different amounts of arachidonic acid on vessel wall-generated PGI2 and TXA2.

It has been suggested that low concentrations of AA may have vasoprotective and high concentrations vaso-damaging effects. To relate these effects to vascular generation of PGI2 and TXA2, we incubated human umbilical vein rings with AA (0, 0.01, 0.1, 1 and 2 mM) and examined the supernates for 6-keto-PGF1 alpha and TXB2. Low concentrations of AA (0.01 and 0.1 mM) caused preferential and maximal PGI2 release, whereas higher concentrations (1 and 2 mM) resulted in marked and preferential increase in TXA2 release. Disequilibrium in vascular PGI2 and TXA2 release towards the latter may relate to vaso-damaging effects of high concentrations of AA.

6-Ketoprostaglandin F1 alpha↗