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Biomedical subjects

S Patel

Publications and source records attributed to S Patel.

At least 649 records · Page 36Linked to original sources
PubMed1988

Macrophage and lymphocyte subpopulations in magnifying endoscopic lesions of Crohn's disease.

Using dye staining and a magnifying colonoscope, small lesions in the rectum of patients with Crohn's disease (which had otherwise appeared normal on sigmoidoscopy) can be detected. Subpopulations of macrophages and lymphocytes in the abnormal and adjacent normal areas of the rectum were studied using a panel of monoclonal antibodies. There was a distinct increase in RFD9+ and 3G8+ macrophages in the abnormal areas compared with the normal. The CD4:CD8 ratio of lymphocytes in the two areas remained unchanged.

Antibodies, Monoclonal↗
PubMed1988

Interleukin 2 receptor expression by macrophages in inflammatory bowel disease.

The expression of interleukin 2 receptor by macrophages from normal and inflamed terminal ileum and colon has been studied by using two monoclonal antibodies. In tissue sections from normal ileum and colon, scattered positive lymphocytes and only occasional weakly positive macrophages were seen. In ileal and colonic Crohn's disease or ulcerative colitis many positive macrophages and lymphocytes were seen in the lamina propria. These findings were confirmed by staining cytospin preparations of isolated intestinal mononuclear cells. The isolated macrophages were able to phagocytose opsonized zymosan and the majority were able to undergo a respiratory burst when triggered with opsonized zymosan or phorbol myristate acetate (PMA), suggesting that they were activated. Stimulation with interferon-gamma or lipopolysaccharide did not increase the number of macrophages staining with the antibodies to the interleukin 2 receptor. Therefore we postulate that a large majority of the macrophages expressing interleukin 2 receptor in inflammatory bowel disease are a recently recruited population of cells.

Antibodies↗
PubMed1988

Tandem bypass: occipital artery to posterior inferior cerebellar artery side-to-side anastomosis and occipital artery to anterior inferior cerebellar artery end-to-side anastomosis--a case report.

A unique example of posterior fossa revascularization is presented. A tandem bypass was performed by anastomosing the midoccipital artery to the posterior inferior cerebellar artery in a side-to-side fashion followed by anastomosis of the distal occipital artery to the anterior inferior cerebellar artery in an end-to-side fashion. The operation was designed to revascularize two separate vascular territories that were isolated in a patient thought to have an extremely compromised posterior circulation. The patient is doing well and is asymptomatic 3 years postoperatively.

Brain Stem↗
PubMed1988

Is skeletal response to parathyroid hormone abnormal in experimental renal failure?

It is widely believed that skeletal resistance is the mechanism of impaired calcemic response to parathyroid hormone (PTH) in renal failure. The action of PTH not only involves skeletal mobilization of Ca, it may also stimulate intestinal absorption of Ca and renal conservation of Ca. We have examined each of these factors and studied the calcemic response to PTH in renal failure. PTH, 3 U/hr/100 gm, was infused for 5 hours in rats with renal failure 3 weeks after a five-sixths nephrectomy. In nonfasted animals, the post-PTH increments of total plasma Ca (0.71 +/- 0.06 mg/dl) and ionized Ca (0.37 +/- 0.06 mg/dl) of control sham-operated rats were significantly greater than those of rats with renal failure (plasma Ca 0.37 +/- 0.02 mg/dl and plasma ionized Ca 0.17 +/- 0.01 mg/dl both p less than 0.001). Urinary Ca excretion rate remained unchanged during PTH infusion despite the increase in plasma Ca. Plasma levels of calcitriol after PTH injection were higher in control rats (257 +/- 18 pg/ml) than in rats with renal failure (162 +/- 5 pg/ml, p less than 0.001). Pretreatment of rats with renal failure with 50 ng calcitriol intravenously corrected the abnormal calcemic response to PTH. To exclude the PTH effect on intestinal Ca absorption, PTH infusion was carried out in animals fasted for 18 hours. The post-PTH increments of Ca were no longer different between rats with renal failure (plasma Ca 0.37 +/- 0.04 mg/dl, plasma ionized Ca 0.20 +/- 0.01 mg/dl) and control rats (plasma Ca 0.37 +/- 0.03 mg/dl, plasma ionized Ca 0.19 +/- 0.01), suggesting that skeletal mobilization of Ca was similar between the two groups of animals. We conclude that lack of intestinal response to PTH rather than skeletal resistance was the mechanism of impaired calcemic response to PTH in this model of renal failure.

Animals↗
PubMed1987

Ethanol stimulates prostacyclin biosynthesis by human neutrophils and potentiates anti-platelet aggregatory effects of prostacyclin.

Previous reports on the direct effects of ethanol on human platelet aggregation function have been inconsistent. Ethanol ingestion produces vasodilation and raises intracellular cyclic AMP concentrations, effects similar to those of prostacyclin. We, therefore, hypothesized that ethanol may influence biosynthesis and/or bioactivity of prostacyclin. In our experiments, ethanol in concentrations up to 400 mg% had no consistent inhibitory effect on platelet aggregation in response to epinephrine, ADP, or combination of subthreshold concentrations of epinephrine plus ADP. However, ethanol in concentrations as low as 10 mg% potentiated the platelet aggregation inhibitory effects of prostacyclin. In addition, ethanol (20 mg%) decreased formation of thromboxane A2 in whole blood by 41% and stimulated formation of prostacyclin by 160% (both P less than 0.01). Additional studies using isolated human cells demonstrated synthesis of prostacyclin by neutrophils in the presence of platelets, and this neutrophil prostacyclin formation was enhanced in the presence of ethanol. These effects of alcohol in concentrations achieved after moderate intake may relate to the hemodynamic, biochemical, and cardioprotective effects of ethanol.

Drug Synergism↗
PubMed1987

The intracellular fate of vitellogenin in Xenopus oocytes is determined by its extracellular concentration during endocytosis.

We have investigated the effects of ligand concentration on the intracellular behavior of the yolk protein precursor vitellogenin in Xenopus oocytes. After internalization by receptor-mediated endocytosis, vitellogenin is delivered to a final storage compartment in mature, high density (1.23 g/ml sucrose) yolk platelets by a biphasic transport pathway. The first phase consists of a relatively rapid increase in the density of ligand-containing organelles to 1.21 g/ml, a region of the sucrose gradient containing a subpopulation of light yolk platelets and lysosomal enzyme activity. The second and rate-limiting phase in vitellogenin transport is the appearance of ligand in mature yolk platelets. The first phase of transport is accompanied by cleavage of vitellogenin into the mature yolk proteins. The majority of the light yolk platelets are not converted into heavy platelets when vitellogenin is absent from the medium for 24 h, indicating that they are a relatively stable organelle which does not mature into heavy platelets during this time period. The progress of vitellogenin through both phases of transport exhibits a concentration dependence, with much slower rates of density increase and lack of appearance in heavy yolk platelets at subsaturating ligand levels. The majority of vitellogenin entering oocytes at low ligand concentrations remains for at least 60 min in a low density endocytic compartment which is accessible to a second pulse of ligand. Vitellogenin-colloidal gold tracer studies indicate that this low density compartment is composed primarily of multivesicular bodies. Low concentrations of vitellogenin residing in this compartment for 4 h are no longer accessible to newly internalized ligand, suggesting that movement into an organelle incapable of fusing with endosomes has occurred.

Animals↗
PubMed1987

Reduction of stress/catecholamine-induced cardiac necrosis by beta 1-selective blockade.

114 haemodynamically stable patients with acute head injury were randomised, double-blind, to either placebo or atenolol given intravenously (10 mg every 6 h) for 3 days then orally (100 mg daily) for a further 4 days. Both groups were equally stressed as shown by raised arterial noradrenaline levels. In patients receiving placebo, but not in those receiving atenolol, there was a significant (p less than 0.01) positive correlation between arterial noradrenaline and levels of the myocardial isoenzyme of creatine kinase (CKMB). 30% of the placebo group compared with 7.4% of the atenolol group (p less than 0.05) showed CKMB levels greater than 3% of total creatine kinase (compatible with myocardial damage). CKMB levels greater than 6% of total creatine kinase (compatible with acute myocardial infarction) were present in 16.7% of patients receiving placebo but in no patients receiving atenolol (p = 0.053). Atenolol appeared to reduce significantly the likelihood of supraventricular tachycardia and ST-segment and T-wave changes and prevented cardiac necrosis seen at necropsy.

Adolescent↗
PubMed1987

Neurotransmission in the pedunculopontine nucleus and pilocarpine-induced motor limbic seizures in rats.

Systemic injection of the cholinergic agonist, pilocarpine (380 mg/kg, i.p.) initiates a sequence of events leading to motor limbic seizure activity. Focal injection of the excitatory amino acid antagonist, 2-amino-7-phosphonoheptanoic acid (50 pmol-1 nmol) into the pedunculopontine nucleus (PPN), prior to pilocarpine injection, results in a powerful anticonvulsant action. The GABA agonist, muscimol (25-50 pmol) also afforded protection against pilocarpine-evoked convulsions when injected focally into the PPN. The results suggest that an overall inhibition of PPN output neurons is required for anticonvulsant action.

2-Amino-5-phosphonovalerate↗
PubMed1987

Role of plasminogen, plasmin, and plasminogen activators in the migration of fibroblasts into plasma clots.

Human diploid fibroblasts were seeded onto or into plasma clots and different aspects of cell adhesion and migration were measured. The roles of plasminogen activators and plasmin were studied by either the removal of plasminogen from plasma prior to clotting or by the addition of 10 mM epsilon-aminocaproic acid, which brings about an inhibition of plasmin in this system. When cells were seeded onto the surface of plasma clots, rates of attachment, spreading, and migration were unaffected by plasminogen depletion or plasmin inhibition. In contrast, when cells were seeded into plasma clots, then, although the rates of cells spreading were unaffected, cell migration was abolished by plasminogen depletion or by plasmin inhibition. When cells were seeded onto the surface of plasma clots and the rate of migration into the clots was measured, there was an absolute requirement for plasmin activity; while fibroblasts migrated rapidly into the fibrin lattice of control clots, in the case of plasminogen-depleted clots, cells failed to penetrate the lattice. Focussing through a plasma clot revealed that fibroblasts do not migrate through the fibrin lattice but instead, localized areas of fibrinolysis are generated and cells migrate over the surface of the area of lysis.

Aminocaproic Acid↗
PubMed1987

The role of saccular afferents in vertical optokinetic nystagmus in primates. A study in relation to optokinetic nystagmus in microgravity.

After bilateral sacculectomies, the squirrel monkey's vertical optokinetic nystagmus showed a gain increase of slow-phase down-nystagmus and a gain decrease of the slow-phase up-nystagmus. The nystagmus beating field of the former shifted upward but that of the latter did not change clearly. These results are in general agreement with the findings in man during the recent shuttle flight and indicate the functional linkage of saccular afferents to the vertical optokinetic nystagmus.

Afferent Pathways↗
PubMed1987

ICMR task force study on hormonal contraception. Transfer of levonorgestrel (LNG) administered through different drug delivery systems from the maternal circulation into the newborn infant's circulation via breast milk.

The transfer of levonorgestrel (LNG) from the maternal plasma via breast milk to the infant was studied in 38 fully lactating and breast-feeding women at 4-6 weeks postpartum, for a duration of 28 days. These volunteers were provided with LNG contraceptive treatment delivered through three, different routes of drug delivery system: (i) intrauterine devices impregnated with LNG (LNG-IUD); (ii) subdermal implant (Norplant (R)-2); and (iii) minipills (LNG 30 micrograms daily). On the first day after either the LNG-IUD (n = 14 women) or Norplant (R)-2 (n = 14 women) insertion, the maternal blood and breast milk samples were collected at 2, 4 and 8 hourly intervals. This was followed by daily collection of these samples as well as infant's blood from days 2 to 4 and thereafter on days 7, 14 and 28. For infant's blood samples from LNG minipill users (n = 10 women), only a single 4-hour sample was collected on the first day and no samples were collected on days 3 and 4. The rest of the schedule for collection of maternal blood and breast milk as well as infant's blood samples were the same in minipill users as for the other two treatment groups. The study revealed a lower LNG percentage transfer from maternal sera to breast milk--11.8 +/- 2, 7 +/- 2 and 8 +/- 1 and relatively higher percentage LNG transfer from breast milk to infant's sera--75 +/- 17, 68 +/- 20 and 32 +/- 3, in LNG-IUD, Norplant (R)-2 and minipill users, respectively. Therefore, LNG contraceptive steroid is transferred into the infant's circulation, the biological significance of which remains to be established.

Administration, Oral↗
PubMed1987

Multivesicular bodies play a key role in vitellogenin endocytosis by Xenopus oocytes.

A combination of electron microscopic tracers and subcellular fractionation has been used to examine the endocytic pathway of the yolk protein precursor, vitellogenin (VG), in Xenopus oocytes. VG was adsorbed to colloidal gold, and the organelles traversed by newly internalized ligand were examined at various time intervals after endocytosis. VG-Au enters oocytes via coated pits and vesicles and then appears rapidly in tubular endosomes and multivesicular bodies (MVBs). MVBs play a central role in VG processing for storage; the large majority of newly internalized VG enters this compartment, remaining there for up to several hours. Condensation of VG into crystalline bodies begins in MVBs, and continues with growth of the crystals until typical platelets are formed. When oocytes are exposed to high [VG], MVBs containing large amounts of internalized VG are morphologically indistinguishable from the primordial yolk platelets described earlier (Dumont, 1978). The use of VG-Au particles of two sizes demonstrates that gold particles in early MVBs were generally associated with the limiting membrane of these organelles, while older MVB compartments have gold particles well separated from the limiting membranes, suggesting that dissociation of VG from its receptor occurs in this compartment. Newly internalized ligand preferentially forms a new MVB, rather than fusing and mixing with previously formed MVBs. Progressive yolk protein condensation gradually transforms MVBs into yolk platelets over a period of several hours. Analysis of 125I-VG-Au behavior after sucrose gradient fractionation of oocytes allowed correlation of biochemical compartments with those observed in the electron microscope. MVBs containing yolk in progressive stages of condensation were found at densities from 1.16 up to 1.21 g/cc. The final, rate-limiting step in VG transport is a shift of ligand from light (1.21 g/cc) to heavy (1.23 g/cc) platelet compartments (Wall and Meleka, 1985). The morphological correlate of this process is movement of VG-Au from small (less than 3-4 microns diameter) to large (greater than 4 microns diameter) platelets.

Animals↗
PubMed1987

Analysis of the brain regions involved in myoclonus produced by intracerebral picrotoxin.

Picrotoxin caused myoclonic jerking of the opposite forelimb when applied to the striatum and the cortical surface of rat brain. Intrastriatal picrotoxin increased [3H]2-deoxyglucose uptake by the ipsilateral frontal cortex, thalamus and subthalamic nucleus. Electrolyte and ibotenic acid lesions made in the globus pallidus prevented striatally evoked myoclonus without affecting the movements elicited from the cortex. Electrolytic lesions in the subthalamic nucleus and thalamus affected striatally evoked myoclonus more than the cortically elicited response. It is concluded that striato-pallidal-thalamic-cortical circuitry is responsible for striatally evoked myoclonus.

Animals↗