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Biomedical subjects

S Rastogi

Publications and source records attributed to S Rastogi.

At least 73 records · Page 4Linked to original sources
PubMed1992

Glycaemia regulates the glucose transporter number in the plasma membrane of rat skeletal muscle.

The number of glucose transporters was measured in isolated membranes from diabetic-rat skeletal muscle to determine the role of circulating blood glucose levels in the control of glucose uptake into skeletal muscle. Three experimental groups of animals were investigated in the post-absorptive state: normoglycaemic/normoinsulinaemic, hyperglycaemic/normoinsulinaemic and hyperglycaemic/normoinsulinaemic made normoglycaemic/normoinsulinaemic by phlorizin treatment. Hyperglycaemia caused a reversible decrease in total transporter number, as measured by cytochalasin B binding, in both plasma membranes and internal membranes of skeletal muscle. Changes in GLUT4 glucose transporter protein mirrored changes in cytochalasin B binding in plasma membranes. However, there was no recovery of GLUT4 levels in intracellular membranes with correction of glycaemia. GLUT4 mRNA levels decreased with hyperglycaemia and recovered only partially with correction of glycaemia. Conversely, GLUT1 glucose transporters were only detectable in the plasma membranes; the levels of this protein varied directly with glycaemia, i.e. in the opposite direction to GLUT4 glucose transporters. This study demonstrates that hyperglycaemia, in the absence of hypoinsulinaemia, is capable of down-regulating the glucose transport system in skeletal muscle, the major site of peripheral resistance to insulin-stimulated glucose transport in diabetes. Furthermore, correction of hyperglycaemia causes a complete restoration of the transport system in the basal state (determined by the transporter number in the plasma membrane), but possibly only an incomplete recovery of the transport system's ability to respond to insulin (since there is no recovery of GLUT4 levels in the intracellular membrane insulin-responsive transporter pool). Finally, the effect of hyperglycaemia is specific for glucose transporter isoforms, with GLUT1 and GLUT4 proteins varying respectively in parallel and opposite directions to levels of glycaemia.

Animals↗
PubMed1991

Characterization of glucose transporter-enriched membranes from rat skeletal muscle: assessment of endothelial cell contamination and presence of sarcoplasmic reticulum and transverse tubules.

The subcellular origin of membranes from rat skeletal muscle that contain insulin-responsive glucose transporters was investigated. Rat skeletal muscle membranes were prepared by isopycnic centrifugation in sucrose gradients. In vivo insulin treatment increased the content of GLUT-4 glucose transporters in the 25% sucrose fraction (enriched in the plasma membrane marker 5'-nucleotidase) and decreased it in the 35% sucrose fraction (devoid of plasma membrane markers). The possibility of endothelial cell membrane contamination in these fractions was investigated using a mouse monoclonal antibody, MRC OX-43, raised against a cell surface protein specific to rat vascular endothelium. MRC OX-43 did not react with any of the muscle membrane fractions, but did recognize a protein of around 100 kDa in extracts of human endothelial cells and rat aorta. An antibody to the dihydropyridine receptor of skeletal muscle, IIC12, was used to determine the presence of transverse tubules in these fractions. IIC12 reacted positively with a 180-kDa protein in purified rat transverse tubules. In contrast, this antibody did not cross-react with the 25% or 35% sucrose fractions. The 25% sucrose fraction was devoid of calsequestrin and ryanodine receptor, cisternal sarcoplasmic reticulum markers. However, small amounts of these proteins were detected in the 35% sucrose fraction. The results suggest that the 25% sucrose fraction represents plasma membranes, while the 35% sucrose fraction is an insulin-sensitive intracellular fraction that contains, but is not enriched in, sarcoplasmic reticulum cisternae. The results further show that insulin-induced recruitment of GLUT-4 transporters in skeletal muscles can be demonstrated independently of GLUT-4 recruitment in endothelial cells.

Animals↗
PubMed1990

Exercise induces recruitment of the "insulin-responsive glucose transporter". Evidence for distinct intracellular insulin- and exercise-recruitable transporter pools in skeletal muscle.

Acute exercise, like insulin, increases D-glucose uptake into rat hind limb muscles. Here we examine the distribution of the muscle glucose transporters GLUT-4 and GLUT-1 in plasma membrane and intracellular membrane fractions of skeletal muscle prepared from control, exercised, and acutely insulin-treated rats. Immunoblotting with an anti-GLUT-4 polyclonal antibody showed that acute insulin treatment (by hind limb perfusion or in vivo injection) increased GLUT-4 transporters in a plasma membrane fraction and decreased them in an intracellular membrane fraction. Exercise also increased the GLUT-4 transporters in the plasma membrane, but in contrast to insulin, did not significantly decrease them in the intracellular fraction. Immunoblotting with anti-GLUT-1 antibody revealed that this transporter is largely localized in the plasma membrane. Neither insulin nor exercise significantly increased GLUT-1 transporters in the plasma membrane. The data show that GLUT-4 is an insulin-responsive glucose transporter in skeletal muscle and, furthermore, that GLUT-4 also responds to acute exercise. The results are consistent with recruitment of GLUT-4 glucose transporters to the plasma membrane from intracellular stores. Moreover, exercise-sensitive GLUT-4 transporters do not originate from the insulin-sensitive intracellular membrane fraction, suggesting the existence of distinct intracellular insulin- and exercise-recruitable GLUT-4 transporter pools.

Animals↗
PubMed1990

Allergic nephropathy associated with ciprofloxacin.

We report a case of ciprofloxacin-related allergic tubulointerstitial nephritis, which manifested as nonoliguric renal failure, eosinophilia, and eosinophiluria. Our patient responded to discontinuation of ciprofloxacin therapy and oral administration of a brief course of corticosteroids. Although rare, allergic tubulointerstitial nephritis apparently can be caused by ciprofloxacin therapy. Clinicians should be aware of this entity.

Acute Kidney Injury↗
PubMed1990

Influence of parathyroidectomy on liver glycogen in rats treated with carbon tetrachloride.

Carbon tetrachloride (CCl4) brings about a rise in cytosolic free calcium which may lead to glycogen mobilization. Therefore, glycogen and glucose-6-phosphatase (G-6-pase) levels in the liver of parathyroidectomized (PTX) rats following CCl4 treatment have been estimated. CCl4 depletes both glycogen and G-6-pase levels in the liver. PTX followed by CCl4 administration, however, fails to restore liver glycogen and G-6-pase levels. The results suggest that neither cytosolic Ca2+ nor phospholipase A2 mediation is needed for glycogen mobilization, however, glucocorticoid intervention might have a role in such mechanisms.

Animals↗
PubMed1989

Decrease in glucose transporter number in skeletal muscle of mildly diabetic (streptozotocin-treated) rats.

Diabetes is associated with a decrease in glucose uptake into muscle, the primary tissue responsible for whole body glucose uptake in the fed state. To study the basis of such a decrease we estimated the number of glucose transporters in skeletal muscle membranes from control and streptozotocin (STZ)-treated rats. Animals were injected with 65 mg STZ/kg and were clearly diabetic (hyperglycemic and glycosuric) at 1 week. After an overnight fast, animals were killed, and skeletal muscle from hind limbs were removed and used to prepare plasma membranes and internal membranes. The number of glucose transporters was determined by D-glucose-protectable equilibrium binding of [3H]cytochalasin-B. STZ-treated rats showed a 37% decrease in the number of glucose transporters per mg protein in crude membranes. The decrease was more pronounced in plasma membranes (average 50% decrease) than in the intracellular membranes (32% decrease). The reduction in the number of glucose transporters was specific, since it was not paralleled by changes in other plasma membrane markers or in total protein, although plasma membrane protein decreased by 15% in STZ-treated rats. When total recoveries of transporters were calculated (i.e. picomoles of transporters recovered per g tissue), the number of transporters in the plasma membrane fraction from STZ-treated rats was decreased by 68% relative to that in control animals. In the intracellular membranes and in total crude membranes from diabetic rats the transporters were decreased by 45%. This suggests that in STZ-treated rats there is an overall decrease in the number of glucose transporters, and that the plasma membrane is further specifically depleted of transporters. The decrease in glucose transporter number in the plasma membrane could at least in part be the cause of the diminished glucose uptake in diabetic muscle and for overall drop in total body glucose utilization of this condition.

Animals↗
PubMed1986

Biomechanical aspects of femoral fractures in automobile accidents.

A medical and engineering study was made of 1074 car accidents involving 2520 vehicle occupants. The injuries they sustained were correlated with details of the crash and with contact points inside the cars. Where possible the forces which were generated in the crash were estimated and related to the injuries. In all, 39 car occupants suffered femoral shaft fracture, with an incidence of 1.7% and 0.8% for front and rear seat occupants respectively. Of these, 31 had associated injuries to other regions of the body; these were the cause of 13 of the 14 deaths in this group. Associated injuries were more severe in car occupants who were not wearing seat belts but the incidence of femoral fracture was not significantly different. The mean velocity change (delta-V) causing femoral fracture was 26 mph (42 km/h) and there was a higher incidence of femoral shaft fracture when delta-V was over 30 mph. Estimates of forces needed to cause fracture were higher than those found in cadaver studies. The time to union of femoral fractures did not correlate with the severity of the crash but was longer (mean 19 weeks) than the average for other femoral fractures.

Accidents, Traffic↗
PubMed1985

Effect of seat belts on injuries to front and rear seat passengers.

Data on 2520 occupants of cars involved in accidents were analysed in relation to injury and the severity of the crash to investigate the effect of rear seat passengers on injury to restrained and unrestrained front seat occupants and vice versa. Unrestrained front seat occupants showed a higher incidence of serious injury when there were rear seat passengers. The presence of a rear seat passenger did not affect significantly the overall incidence of injury among restrained front seat occupants within the range of crash severity considered. Unrestrained rear seat passengers behind unrestrained front seat occupants showed a higher incidence of moderate injury and a lower incidence of no injury than those behind restrained front seat occupants. It is concluded that legislation on seat belts has not greatly increased the risk of person to person injury.

Accidents, Traffic↗
PubMed1985

Hyperkalemic renal tubular acidosis: effect of furosemide in humans and in rats.

Furosemide increases urinary acidification in control subjects and in certain patients with normokalemic or hypokalemic distal renal tubular acidosis (RTA). We studied the effect of furosemide in 14 patients with hyperkalemic distal RTA. In a group of patients with pure selective aldosterone deficiency, furosemide increased net acid and K excretion in a fashion indistinguishable from controls. This effect of furosemide was observed both in the presence and in the absence of acute mineralocorticoid administration. In another group of patients with hyperkalemic distal RTA, furosemide failed to decrease urine pH and to increase net acid excretion despite acute mineralocorticoid administration. Plasma aldosterone was variable in this group in that some patients had appropriate levels of aldosterone for the degree of hyperkalemia, whereas in the other patients the levels were low. The failure of these patients to respond to furosemide, despite pharmacologic doses of mineralocorticoid, suggests that these patients had a defect in H+ secretion other than that attributable to aldosterone deficiency alone. To gain insight into the mechanism whereby furosemide increases urinary acidification, we studied control and amiloride-treated rats pretreated with mineralocorticoid. In response to furosemide, control rats had a significantly lower urine pH and higher net acid and K excretion than that observed in amiloride-treated rats. These data suggest that furosemide increases H+ and K excretion, at least in part, by creating a favorable electric gradient for secretion of these ions since these effects were blunted in presence of inhibition of distal Na transport by amiloride.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Renal Tubular↗
PubMed1984

Rupture of the thoracic aorta and its relationship to road traffic accident characteristics.

A 3-year prospective study of road traffic accidents was carried out in Oxfordshire by a combined team of surgeons and engineers. This liaison permitted the comparison of injuries with details of the collisions. Twelve cases of rupture of the thoracic aorta were recorded and in 10 cases the lesion was just distal to the origin of the left subclavian artery. The mean velocity change during the impacts was 38.3 mph, and it is suggested that oblique and transverse forces to the chest as well as rapid deceleration are aetiological factors in this condition.

Accidents, Traffic↗
PubMed1983

A clinical study of post polio infantile paralysis.

This study reports on 3,000 cases of poliomyelitis seen at the Rehabilitation and Artificial Limb Centre at Lucknow between January 1976 and December 1980. Factors such as age and sex incidence, extremity involvement, incidence of deformities at hip, knee and ankle, lower limb discrepancy, treatment and orthoses prescribed are discussed.

Age Factors↗
PubMed1983

Metabolic acidosis.

Explore the source record for details and available documents.

Acid-Base Equilibrium↗
PubMed1982

Morphological distance between Rastogis and certain other caste groups of Uttar Pradesh, India.

150 male Rastogis from Lucknow (Uttar Pradesh) have been investigated anthropometrically. The results are compared with those obtained in some other population samples from Uttar Pradesh. The T2 test showed that Rastogis are nearest to Pasis and at the largest distance from Brahmin and Chattri. This is in conformity with the results of blood group analysis. The possible reasons for these morphological distance differences are discussed.

Anthropometry↗
PubMed1980

A clinical study of amputations of the lower limb.

A retrospective study of 525 cases of lower limb amputation attending the Outpatient Department of the Rehabilitation and Artificial Limb Centre and various rural clinics from January 1976 to March 1978 was carried out. Males outnumbered females and the majority of cases were in the 3rd decade. Trauma was the most common cause of amputation followed by peripheral vascular disease and neoplastic lesions. The stump was considered to be satisfactory in more than half of the cases studied. Proper postoperative care was lacking in most of those amputated at other centres.

Adolescent↗