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Biomedical subjects

J Parmar

Publications and source records attributed to J Parmar.

14 recordsLinked to original sources
PubMed2006

Pre-operative radial arterial diameter predicts early failure of arteriovenous fistula (AVF) for haemodialysis.

INTRODUCTION: Long term patency of arteriovenous fistula (AVF) is relevant to the management of end stage renal failure (ESRF) patients on haemodialysis (HD). We evaluated the role of routine radial arterial duplex for imaging radial artery before AVF formation to investigate the relationaship between radial artery internal diameter (ID) and AVF patency. METHODS: 21 patients with ESRF were examined by duplex sonography before AVF formation, 1 day, 1 week, 4 week and 12 weeks post AVF formation. For assessment of AVF patency, patients were divided into 2 groups. Group-1, 11 patients with radial artery ID <1.5mm and Group-2, 10 patients with radial artery ID >1.5mm. Measurement of radial artery blood inflow rate was calculated from mean blood flow velocity and vessel diameter. All AVFs were constructed on the forearm using autologous veins. RESULTS: In Group-1, 5 patients (45%) showed immediate thrombosis of AVF graft. All patients in group-2 had patent AVF at 12 weeks. Pre-AVF formation radial artery blood inflow rate between two groups was not significantly different (p=0.06). Radial artery blood inflow rate was consistently and significantly higher in group-2 at all later time points with p value of <0.01 (Mann Whitney test). CONCLUSION: There was a high failure rate of AVF with radial artery ID of <1.5mm. In the presence of small radial arteries primary access AVF in the upper arm should be considered.

Arteriovenous Shunt, Surgical↗
PubMed2006

Plasma pooling to expedite bioequivalence estimation of rifampicin in fixed dose combinations.

Rifampicin has been found to be one of the most important antitubercular drugs; however, variable bioavailability of rifampicin in some fixed dose combinations (FDCs) as well as separate formulations has been reported in the literature. This resulted in proper evaluation of FDCs with standard protocol for bioequivalence trials. Earlier, plasma pooling as a rapid method for bioequivalence assessment of rifampicin in FDCs was proposed from our laboratory. Results obtained after pooled plasma sample analysis were compared with those from the individual plasma sample analysis. Case studies from our laboratories further validate and support the use of plasma pooling method as a faster and cost effective tool for bioequivalence assessment of rifampicin in FDCs, which will be useful in order to speed up the registration and approval of good quality FDCs.

Administration, Oral↗
PubMed2004

Hepatocellular carcinoma in association with cirrhosis in a patient with cystic fibrosis.

BACKGROUND: Cystic fibrosis liver disease (CFLD) occurs in 37% of patients with CF. To date and to the best of our knowledge, there has not been a documented case of hepatocellular carcinoma in association with cirrhosis and CF. CASE REPORT: A 32-year-old lady with cystic fibrosis (CF) presented for her annual review. She had been diagnosed with CFLD since early adolescence. A routine ultrasound of her liver revealed lesions consistent with hepatocellular carcinoma. This was confirmed on histology. She had no risk factors for hepatitis, and thorough investigation revealed no other cause for her chronic liver disease. She was also found to be pregnant at the time of diagnosis. Her tumour was considered too large for resection and liver transplantation and she was referred to a national centre for laser ablative therapy. CONCLUSION: It is our concern that with the increased life expectancy of patients with CF and the chronic nature of CFLD that this may be an increasingly recognised complication amongst the CF adult population. Therefore, we have changed our practice to more intense surveillance of patients with established CFLD to incorporate biannual ultrasound imaging of the hepatic system and yearly serum concentration measurements of alpha-fetoprotein.

Adult↗
PubMed2004

Fixed dose combinations for tuberculosis: Lessons learned from clinical, formulation and regulatory perspective.

Worldwide, tuberculosis (TB) remains one of the most important communicable diseases in terms of morbidity and mortality. Its control requires multi-drug therapy for at least six months, which could lead to patient non-compliance, failure of therapy and ultimately resulting in the emergence of drug resistance. Fixed dose combinations (FDCs) in TB therapy reduce the number of tablets to be consumed and thereby increase patient compliance with recommended treatment regimens. Thus, FDCs play a significant role in preventing the emergence of drug resistance and successful treatment. However, the quality of FDCs with respect to variable bioavailability and their registration requirements are major hurdles to their implementation in national TB control programs. It is anticipated that a large global market for FDCs will encourage large-scale production and increased competition, which in turn will result in FDCs at affordable prices. The Global Drug Facility (GDF), established by the World Health Organization (WHO), aims to ensure universal uninterrupted access to quality TB drugs for implementation of directly observed treatment short-course (DOTS) in resource-poor countries. In this program, four FDCs were accepted as the drugs of first choice because of their obvious advantages in controlling TB. This demands the necessity of addressing quality and registration requirements of FDCs systematically. In light of this current knowledge on anti-TB FDCs, their dosage, combinations, available clinical studies and the experiences with TB therapy has been discussed in this article, which should serve as lessons for selection of appropriate FDCs for other diseases such as malaria and AIDS.

Antitubercular Agents↗
PubMed2000

Radiation-induced cell cycle delays and p53 status of early passage melanoma cell lines.

Cell cultures exposed to DNA-damaging agents such as gamma radiation respond by arresting at cell cycle checkpoints, and the p53 tumor suppressor protein is strongly implicated in this behavior. We have investigated the TP53 status and cell cycle response to ionizing radiation of a series of early passage cell lines (designated NZM1 to NZM15) previously developed from patients with metastatic melanoma. The TP53 status of each of the cell lines was determined by single-strand conformation polymorphism and DNA sequence analysis. The majority of the lines appeared to have a wild-type TP53 gene sequence, consistent with published studies. Two lines (NZM4 and NZM7.2) were found to have an identical T-->C transition mutation in nucleotide 721 (exon 7) of the coding region. NZM7.2 (mutant) and NZM7.4 (wild-type) were clonally derived from the same line (NZM7). The existence of radiation-induced cell cycle arrest in G and/or G2M phase was determined 16 h after irradiation (6.3 Gy) by DNA staining and flow cytometric analysis. The mitotic inhibitor paclitaxel was used as a reference compound, with or without irradiation, to assess the efficiency of radiation-induced cell cycle arrest. G1 phase arrest was associated only with the presence of the wild-type TP53 gene, but the efficiency of induced arrest varied among the cell lines and the period of G phase arrest appeared to be short. A significant difference (P < 0.002) was also found between the efficiency of induction of G2 phase arrest and the presence of wild-type TP53 gene. The results provide evidence that although the melanoma cell lines generally had an intact TP53 gene, the efficiency of p53-mediated cycle arrest might be deficient and contribute to the resistance of this tumor to treatment.

Adult↗
PubMed1992

Coronary artery endothelial cell and smooth muscle dysfunction after global myocardial ischemia.

We hypothesized that coronary artery endothelial cell function and smooth muscle function are modified by global myocardial ischemia and used bradykinin-induced secretion of endothelium-derived relaxing factor as a marker of endothelial cell function. Bradykinin and sodium nitroprusside together determined maximum smooth muscle relaxation. Potassium chloride-induced contraction determined smooth muscle contractility. Endothelium-mediated smooth muscle relaxation expressed as a ratio of total coronary smooth muscle relaxation before and after ischemia quantified endothelial cell function. The effect of global normothermic ischemia on in situ coronary arteries from 7 swine hearts was studied. Coronary arterial rings taken from 0 to 220 minutes of ischemia at 20-minute intervals were studied in vitro. The data revealed unexpected tolerance of endothelium-mediated relaxation to ischemia. Endothelium-derived relaxing factor function was maintained to 160 minutes and smooth muscle function, to 120 minutes of ischemia. Coronary artery dysfunction seen in other studies after less ischemia may be the result of injury introduced during reperfusion, may be the consequence of myocardial injury, or may be due to events operative at the level of small arterioles.

Animals↗
PubMed1991

Inotropic stimulation and oxygen consumption in a canine model of dilated cardiomyopathy.

Inotropic support for the dilated, failing ventricle results in complex hemodynamic changes affecting preload, afterload, contractility, and heart rate, each of which affects myocardial oxygen consumption. Appreciation of a hierarchy of hemodynamic determinants of myocardial oxygen consumption may be helpful to the clinician trying to balance oxygen demands and hemodynamic performance. We tested the hypothesis that epinephrine alters the hierarchy of hemodynamic determinants of myocardial oxygen consumption in a canine model of dilated cardiomyopathy created by rapid ventricular pacing. Dogs (n = 10) were instrumented to record left ventricular pressure and dimension, and a modified right heart bypass preparation was used to control left ventricular workload. Coronary sinus effluent was quantitatively collected and analyzed for oxygen content and used to calculate myocardial oxygen consumption. Epinephrine administration significantly increased myocardial oxygen consumption in the empty, beating heart; however, when the relationships of multiple determinants of left ventricular work and load were compared before and after epinephrine administration, no oxygen wasting effect was observed. Using multivariate linear regression analysis, a hierarchy of hemodynamic determinants of myocardial oxygen consumption was created. In the untreated heart, stroke work and cardiac output were the primary hemodynamic determinants of oxygen consumption; epinephrine significantly altered the determinants such that wall stress became the dominant hemodynamic determinant of myocardial oxygen consumption. Focused manipulation of wall stress in the treated, failing heart may limit the potentially deleterious effects of inotropic stimulation in this setting.

Adenine Nucleotides↗
PubMed1990

Effect of magnesium ions on red cell membrane properties.

Spectrin forms aggregates in solution when incubated at relatively high concentrations (several millimolar) of divalent cations. According to the evidence of electron microscopy, aggregates of globular appearance and rather uniform size are cooperatively formed from spectrin dimers, no intermediate structures being seen. Inter-dimer chemical cross-linking of spectrin in intact red cell membranes is enhanced if magnesium ions at a concentration of 0.5 mM or more are present. On the other hand, the elimination of magnesium from the interior of intact cells causes no significant change in shear elastic modulus, measured by micropipette assays, nor is there any dependence of membrane filtration rate on intracellular free magnesium concentration in the range 0-1 mM. Magnesium-depleted cells are, however, converted into echinocytes within a short period, in which control cells, exposed to ionophore and external magnesium ions, remain completely discoid. Magnesium-depleted cells also undergo structural changes on heating below the temperature at which vesiculation sets in. These reveal themselves by the transformation of the cells to a unique characteristic shape, by grossly reduced filtrability, and by extensive agglutination of the cells when treated with a bifunctional reagent. Magnesium ions thus regulate the stability, but not to any measurable extent the gross elasticity, of the red cell membrane.

Cross-Linking Reagents↗
PubMed1990

Effects of deficiencies of glycophorins C and D on the physical properties of the red cell.

Red cells of the rare Leach phenotype lack the membrane glycophorins C and D, and a proportion of the red cells are elliptocytes. Judging from tests on suspensions of red cell ghosts sheared rotationally in an ektacytometer, it has previously been suggested that these membranes are relatively fragile and poorly deformable. We have carried out analyses of individual red cells to investigate possible factors which underlie the physical changes in these glycophorin-deficient cells. Micropipette analysis of the red cell membrane showed that the rigidity and viscosity were normal, both for elliptocytes and discocytes, for three donors deficient in glycophorins C and D. Red cell transit times through 5 microns pores, measured electronically for 2000 individual cells, showed no differences from controls. It was confirmed that the index of deformation obtained using an ektacytometer was reduced, but our results suggest that this arises from shape rather than membrane changes. The elliptocytes were found to have a lower volume and surface area than discocytes from the same donor (measured by micropipette aspiration of single red cells), and were rarely found in less dense red cell fractions. No reticulocytes were found to be elliptical. These data suggest that the elliptocytes are older red cells, and are formed from red cells which are initially released into the circulation with normal shape. Their elongated shape might arise from permanent distortion of the unstable membrane by shear forces in the circulation.

Elasticity↗
PubMed1990

Procoagulant activity in whole blood from patients with breast and colorectal cancer.

Whole blood procoagulant activity was determined by measuring the endotoxin-induced shortening of the celite-activated whole blood recalcification time in patients with breast cancer (n = 29), colorectal cancer (n = 18), benign breast disease (n = 26), benign colorectal disease (n = 10), normal volunteers (n = 17) and surgical in-patients with non-malignant and non-inflammatory conditions (n = 18). Using this method, patients with breast and colorectal cancer produced significantly more procoagulant activity than normal controls (P less than 0.001), surgical in-patients (P less than 0.005) and patients with benign breast (P less than 0.001) and benign colorectal (P = 0.05) disease respectively. The difference between subjects classified as 'cancer' or 'non-cancer' was highly significant (P less than 0.0001). There were no significant differences in total white cell or absolute monocyte counts between subject groups, and in individual patients, there was no correlation between these parameters and the procoagulant activity. It is concluded that the activated whole blood recalcification time is a more reproducible way of measuring whole blood procoagulant activity than the original technique, and that using this method, patients with cancer show higher procoagulant activity than corresponding benign controls.

Adult↗
PubMed1989

Alteration of the mechanical properties of sickle cells by repetitive deoxygenation: role of calcium and the effects of calcium blockers.

The formation of dense, poorly deformable sickle cells was studied by subjecting pre-separated, less dense cells to repeated deoxygenation and reoxygenation for 15 h. In the presence of Ca (2 mmol/l), this process caused the number of irreversible sickled cells to increase five-fold, mean cell haemoglobin concentration to increase by 13% and cellular potassium to decrease by 22%. Also, red cell filterability through 5 microns filter pores was greatly worsened. These effects decreased but were not totally abolished when the extracellular Ca concentration was lowered to zero or 0.01 mmol/l. If a high K medium was used (135 mmol/l), cell swelling rather than shrinkage occurred. Swelling also occurred if ouabain was added to the incubation. The Ca-channel blockers nitrendipine and nisoldipine had different effects. Nitrendipine, in the range 10(-7) - 10(-5) mol/l, was partially protective against all the induced changes, but nisoldipine was not protective at 10(-8) or 10(-6) mol/l. Thus, deterioration in the properties of sickle cells appears to be linked to Ca-dependent potassium loss during repeated sickling and is inhibited by nitrendipine.

Anemia, Sickle Cell↗
PubMed1984

In vitro and in vivo cytotoxic activity of native and ricin conjugated monoclonal antibodies to HBs antigen for Alexander primary liver cell carcinoma cells and tumours.

In in vitro and in vivo systems, native or ricin conjugated monoclonal anti-HBs, are capable of inhibiting or slowing the growth of Alexander primary hepatocellular carcinoma cells. Failure of the immune response to this component of the hepatitis B virus may be one permissive factor in the development of some primary liver cell carcinoma in chronic HBV carriers.

Animals↗
PubMedDate not supplied

Abdominal actinomycosis.

Four cases of abdominal actinomycosis managed during a two year period at Ndola Central Hospital are reported with a review of relevant literature. Difficulties associated in diagnosing this form of the disease are stressed. It is suggested that a limited form of surgery in combination with parenteral penicillin therapy is usually effective in the management of abdominal actinomycosis.

Abdomen↗