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Biomedical subjects

M Patel

Publications and source records attributed to M Patel.

At least 307 records · Page 17Linked to original sources
PubMed1994

Localization of Locusta-DP in locust CNS and hemolymph satisfies initial hormonal criteria.

Locusta-diuretic peptide (Locusta-DP) is a potent stimulant of fluid secretion and cyclic AMP production by locust Malpighian tubules. In this study, a polyclonal antiserum raised to the C-terminus of Locusta-DP reveals a wide distribution of immunoreactive cell bodies and processes throughout the CNS, and endings in two important neurohemal release sites: the corpora cardiaca and the perivisceral organs. HPLC fractionation of CNS, neurohemal structures, and hemolymph reveals immunoreactive material that coelutes with synthetic Locusta-DP and stimulates cyclic AMP production by locust tubules. The identity of the immunoreactive and biologically active material is confirmed as authentic Locusta-DP by mass spectrometry.

Animals↗
PubMed1994

Consistent responses of the human vascular smooth muscle cell in culture: implications for restenosis.

PURPOSE: The mechanisms whereby restenoses occur at discrete sites within the vasculature remain uncertain. We have recently reported that vascular smooth muscle cells (VSMC) derived from patients with graft stenoses are resistant to growth inhibition by heparin. In this study, we have examined whether VSMC proliferation rates and responses to inhibition by heparin vary according to the individual or the anatomic site of origin. METHODS: Long saphenous veins from seven patients were divided into proximal, middle, and distal portions, and VSMC were cultured separately from each. VSMC proliferation in response to 15% fetal calf serum +/- 100 micrograms/ml heparin was measured by counting triplicate samples at 0, 3, 7, 10, and 14 days. This experiment was repeated from the second to the sixth passage (n = 6) and for artery and vein pairs derived from four additional patients. RESULTS: Differences between vein segment cultures of individual veins were found not to differ significantly from experimental error for either proliferation or heparin inhibition and were not altered by repeated passage (ANOVA). There were, however, significant differences in sensitivity to heparin inhibition between patients (p = 0.02) (ANOVA). There were no significant differences between paired samples of artery and vein for either proliferation or heparin inhibition (Mann-Whitney test). CONCLUSIONS: VSMC growth characteristics reflect the individual patient and are maintained in cell culture.

Analysis of Variance↗
PubMed1994

Pneumococcal soft-tissue infections: a problem deserving more recognition.

Streptococcus pneumoniae is an uncommonly recognized etiology of soft-tissue infections. Our experience suggests that pneumococci can cause serious infections of soft tissues, especially in patients with connective-tissue diseases. Systemic lupus erythematosus was an underlying condition in three of the six patients described in the present report.

Adolescent↗
PubMed1994

Growth inhibition of human vascular smooth muscle cells by fenofibrate: a possible therapy for restenosis.

OBJECTIVE: The aim was to assess the growth inhibitory effect of fibrates on human vascular smooth muscle cells. Restenosis is the most important factor limiting the long term success of invasive vascular interventions and there is as yet no effective preventive treatment. Platelet derived growth factor (PDGF) is considered to be an important growth promoting agent for vascular smooth muscle cells (VSMC) and fenofibric acid (a hypolipidaemic drug) has been reported to be a PDGF antagonist. METHODS: The effect of the fibrate drugs fenofibrate, clofibrate, bezafibrate, and gemfibrozil were examined on the proliferation of cultured human vascular smooth muscle cells derived from saphenous vein (n = 20) and graft stenoses (n = 7). RESULTS: Fenofibrate (100 microM) produced potent inhibition (48%) of VSMC proliferation at a concentration equivalent to that of its circulating metabolite fenofibric acid, but none of the other drugs produced any significant effect on growth. VSMC derived from graft stenoses were equally sensitive to inhibition as saphenous vein derived controls, in contrast to our previous work which reported that graft stenosis derived VSMC were resistant to growth inhibition by the physiological inhibitor heparin. The antiproliferative effect of fenofibrate was independent of inhibition of cellular cholesterol synthesis or toxicity. Fenofibrate inhibited VSMC growth induced by 15% fetal calf serum, PDGF, and basic fibroblast growth factor to a similar degree, indicating that it is not a specific PDGF antagonist. CONCLUSIONS: Fenofibrate is not a specific PDGF antagonist. Fenofibric acid, one of the principal metabolites of fenofibrate, did not produce any inhibition of growth, suggesting that oral administration of fenofibrate would not be efficacious. Fenofibrate is the first potent inhibitor to be described for VSMC derived from human myo-intimal hyperplastic lesions.

Bezafibrate↗
PubMed1994

Effect of calcium channel blockers on the growth of human vascular smooth muscle cells derived from saphenous vein and vascular graft stenoses.

Vascular restenosis after invasive interventions is an important clinical problem for which no preventive pharmacologic therapy exists. Calcium channel blockers have been shown to inhibit myointimal hyperplasia in animal models of restenosis and in some small and flawed clinical coronary restenosis trials. We examined the inhibitory effect of amlodipine, verapamil, and diltiazem on the growth of cultured human vascular smooth muscle cells (VSMC) derived from saphenous vein (n = 20) and graft stenoses (n = 7), in 14-day proliferation assays and [methyl 3H]thymidine uptake studies. Amlodipine and verapamil produced significant inhibition (30%) of VSMC proliferation and DNA synthesis at 10 microM but not at 500 nM-1 microM. To our knowledge, this is the first study to examine the antiproliferative effect of calcium channel blockers in VSMC derived from human graft stenoses. Growth inhibition of VSMC from graft stenoses was not significantly different from that of control saphenous vein-derived cells. We conclude, therefore, that calcium channel blockers inhibit human VSMC proliferation in vitro, regardless of whether the cells were grown from graft stenoses or saphenous vein. However, the concentrations at which these calcium channel blockers elicit antiproliferative effects may not be attainable during therapeutic dosing in humans.

Amlodipine↗
PubMed1994

Flow characteristics of long spinal needles.

A 120 mm, 27-gauge needle has recently been introduced for subarachnoid anaesthesia when using a single-space, combined spinal-extradural technique. The flow characteristics of this needle were compared with those of a 120 mm, 26-gauge needle using a pressure monitor infusion pump. Surprisingly, the resistance to fluid flow of the 26-gauge needle was twice that of the 27-gauge needle. The results of this experiment were confirmed by the findings of a clinical study undertaken in 100 obstetric patients who required regional anaesthesia. The time taken from dural puncture to appearance of cerebrospinal fluid at the hub of the needle was on average three times greater with the 26-gauge needle.

Adult↗
PubMed1994

Inhibition of human vascular smooth muscle cell proliferation by lovastatin: the role of isoprenoid intermediates of cholesterol synthesis.

Restenosis remains the largest single obstacle to the long-term success of invasive vascular interventions. Lovastatin, an HMG-CoA reductase inhibitor, has been shown to reduce myointimal hyperplasia in animal models of restenosis and in one clinical coronary restenosis trial. We have assessed the effect of lovastatin on the growth of cultured human vascular smooth muscle cells derived from saphenous vein and vascular graft stenoses. Lovastatin (2 microM) inhibited proliferation over 14 days in saphenous vein (and graft stenoses) derived vascular smooth muscle cells by 42% and 32% respectively: this was not significantly different. Lovastatin (10 microM) reduced [methyl 3H]-thymidine uptake by 51% in saphenous vein-derived cells. These concentrations were significantly higher than those achieved in plasma during therapeutic dosage. Lovastatin-induced inhibition of vascular smooth muscle cell proliferation and [methyl 3H]-thymidine uptake was completely reversed by adding mevalonate (100 microM) but cholesterol (10-40 micrograms ml-1) had no effect. Isopentenyl adenine (25-50 microM) did not affect the inhibition of [methyl 3H]-thymidine uptake by lovastatin (10 microM), but farnesol (20 microM), another isoprenoid precursor of cholesterol synthesis, reversed the antiproliferative effect.

Adenine↗
PubMed1994

An examination of the 1990-91 famine in Sudan.

Shortly before and during the harvest of 1990, a series of warnings were issued by concerned international and UN agencies that Sudan would experience a very poor harvest followed by an acute food shortage over the period 1990-91. The 1990 harvest was estimated to be similar to that obtained in 1984. After the very poor harvest in 1984, Sudan experienced a major famine during which deaths may have numbered in the hundreds of thousands. There were fears that this experience might be repeated in 1990-91. By the time of the subsequent 1991 harvest, it was clear to all that a severe food crisis had been experienced. There were severe shortages of water and food and very high malnutrition rates of children were noted by UNICEF across a wide range of areas. Despite these adverse indications, starvation deaths were probably numbered in thousands, rather than hundreds of thousands. Famine mortality, which may include deaths from famine associated disease, was similarly low. The initial predictions, it now seems, may have over-estimated famine mortality almost one hundred times. Several potential explanations of the over-estimate are examined. These include prediction errors, government and donor responses to the drought such as food aid and immunization, and traditional community and household level coping strategies in times of food shortage.

Disasters↗
PubMed1994

Failure of CGS15943A to block the hypotensive action of agonists acting at the adenosine A3 receptor.

1. Adenosine receptor agonists were evaluated for their activity at the putative adenosine A3 receptor which mediates a 'xanthine-resistant' hypotensive response in the anaesthetized rat. The compounds tested were: the A1/A3 receptor agonist, N-[2-(4-aminophenyl)ethyl]adenosine (APNEA), the non-selective adenosine receptor agonist, 5'-N-ethylcarboxamidoadenosine (NECA), the adenosine A1 receptor-selective agonists, N-[(1S,trans)-2-hydroxycyclopentyl]adenosine (GR79236) and N6-cyclopentyl adenosine (CPA), the A2a receptor-selective agonists, 2-[[2-[4-(2-carboxyethyl) phenyl] ethyl] amino]-N- ethylcarboxamidoadenosine (CGS21680) and 2-phenylaminoadenosine (CV1808), and the moderately A2b selective agonist, N-[(2-methylphenyl)methyl]adenosine (metrifudil). 2. In confirmation of literature findings, APNEA (1-1000 nmol kg-1) induced hypotension and bradycardia; the hypotension was not blocked by pretreatment with the xanthine antagonist, 8-P-sulphophenyltheophylline (8-sPT; 40 mg kg-1, i.v.), whereas the bradycardia was attenuated. The non-xanthine antagonist, 9-fluoro-2-(2-furyl)-5,6-dihydro [1,2,4]triazolo[1,5-c]- quinazin-5-imine (CGS15943A; 3 mg kg-1 i.v.), also attenuated the bradycardia without affecting the hypotension. 3. The adenosine A1 receptor-selective agonists, GR79236 and CPA, both produced dose-dependent falls in blood pressure and heart rate which were antagonized by 8-sPT (40 mg kg-1) and CGS15943A (3 mg kg-1). 4. The adenosine A2a receptor-selective agonists, CGS21680 and CV1808, produced only a hypotensive response which was antagonized by 8-sPT (40 mg kg-1) and to a much greater extent by CGS15943A (3 mg kg-1), consistent with the response being mediated solely by A2a receptors. 5. The modestly A2b receptor-selective agonist, metrifudil, produced a dose-dependent fall in blood pressure and at higher doses a fall in heart rate. The hypotension induced by metrifudil was not antagonized by either 8-sPT (40 mg kg-1) or CGS15943A (3 mg kg-1) even though the bradycardia was abolished, suggesting that this agonist activates the putative A3 receptor.6. The non-selective adenosine receptor agonist, NECA, produced a hypotension and bradycardia that was attenuated by 8-sPT (40 mg kg-1), confirming previous work. The non-xanthine antagonist,CGS15943A (3 mg kg-'), also attenuated the hypotension and bradycardia. The bradycardia was blocked to a much greater extent, suggesting that NECA may therefore induce hypotension partly by activating the putative A3 receptor.7. In conclusion, we have confirmed that the putative A3 receptor mediating hypotension in the anaesthetized rat is not blocked by 8-sPT, and further shown that it is not blocked by CGS15943A. The A2a agonists CGS21680 and CV1808 showed no discernible activity at the A3 receptor, whereas APNEA,NECA, CPA and metrifudil appear to activate this receptor. The adenosine A1 receptor agonist,GR79236, shows considerable selectivity for the A1 receptor but may activate the A3 receptor at high doses.

Adenosine↗
PubMed1994

Central retinal artery occlusion from carotid dissection diagnosed by cervical computed tomography.

BACKGROUND: Carotid dissection may lead to many different types of neurological deficits, both transient and permanent. CASE DESCRIPTION: We present a patient with an isolated central retinal artery occlusion who was found to have an ipsilateral carotid dissection by neck computed tomographic scan, later confirmed by angiography. CONCLUSIONS: This is the first reported case of carotid dissection causing central retinal artery occlusion without any other neurological deficits. It demonstrates the diagnostic usefulness of computed tomographic imaging in such cases.

Adult↗
PubMed1994

Hemodynamic effects of manual hyperinflation in critically ill mechanically ventilated patients.

SUBJECT OBJECTIVE: To assess the hemodynamic effects of manual lung hyperinflation in mechanically ventilated patients and to measure the different inspiratory pressures and tidal volumes generated by different operators. DESIGN: Measurements of aortic blood flow (by esophageal Doppler ultrasonography), systemic blood pressure, tidal volumes (by respirometry), and inspiratory pressures in the ventilator circuit were measured on the ventilator, during six intended manual hyperinflations (tidal volume > 150% that delivered by ventilator) using a 2-L rebreathing bag, and at 1, 5, 10, and 15 min after reconnection to the ventilator. SETTING: Intensive care unit. PATIENTS: Eighteen mechanically ventilated patients with normovolemia and stable circulatory status were assessed on a total of 20 occasions. INTERVENTIONS: Patients were disconnected from the ventilator to enable six manual hyperinflations to be given. Measurements were made before and at 5-min intervals until no further hemodynamic changes were seen. MEASUREMENTS AND RESULTS: Hyperinflation (50% increase in tidal volume) was achieved only in 10 of 20 studies. Large variations were seen in percentage change in peak inspiratory pressure (-30% to +250%) and tidal volume (-33% to +127%) generated. Falls in cardiac output correlated to the increase in tidal volume but not to the increase in peak inspiratory pressure and took up to 15 min to recover to baseline values. Changes in cardiac output were independent of lung compliance and concurrent vasoactive drug support. No consistent change was noted in either blood pressure or heart rate. CONCLUSIONS: Lung hyperinflation is frequently not achieved by the manual technique. Significant changes in cardiac output can occur and appear to be related to the tidal volume rather than pressure generated.

Adult↗