Biomedical subjects

S Sen

Publications and source records attributed to S Sen.

At least 559 records · Page 31Linked to original sources

PubMedDate not supplied

Distribution, severity and risk factors for aortic atherosclerosis in cerebral ischemia.

Significant thoracic aortic plaques (>4 mm) are an independent risk factor for ischemic stroke. Within 1 week of stroke/transient ischemic attack (TIA) onset, 105 consecutive patients underwent transesophageal echocardiography assessment of aortic plaque thickness using the criteria of Amarenco et al. (N Engl J Med 1994;331:1474-1479). A proximo-distal gradient was found in the distribution of aortic atheroma >4 mm (p = 0.04). Symptomatic coronary artery disease was associated with plaque in the proximal aorta (p = 0.03); extracranial carotid stenosis >70% was associated with plaque in the arch and descending aorta (p < 0.01). The severity of aortic plaque was associated with age on multivariable analysis (p = 0.0003 to p < 0.01). Only smoking showed predictive regional specificity (p = 0.03);no other risk factors were associated with aortic atheroma in any segment. In stroke/TIA patients, carotid stenosis >70% predicts aortic arch atheroma plaques >4 mm which may predispose to reinfarction after endarterectomy. Atheroma of the ascending aorta is associated with ischemic heart disease, and cardiac screening should be considered in asymptomatic patients.

Adult↗

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Separation of dog brain renin-like activity from acid protease activity.

A renin-like enzyme and acid protease (cathepsin) from whole and saline-pefused dog brains were separated by CM-cellulose chromatography with a linear NaCl gradient. Plasma renin and cathepsin were also separated using the same system. During the separation steps (in all the above cases) the specific activity of the brain renin-like enzyme was increased, while the specific activity of the brain cathepsin was decreased. Approximately a 70-fold increase in the specific activity of brain renin-like enzyme and a sixfold decrease in brain cathepsin specific activity was obtained from saline-perfused brain. The separation made it possible to study the pH optimum of the brain renin-like enzyme and acid protease. The brain renin-like enzyme showed optimal activity in the range of pH 6-7. Immunologically, the renin-like enzyme was distinctly different from dog kidney renin.

Animals↗

PubMedDate not supplied

Role of renin-angiotensin system in chronic renal hypertensive rats.

The role of renin-angiotensin system has been examined in the maintenance of hypertension in acute and chronic two-kidney (36 weeks) and chronic one-kidney (12 weeks) Goldblatt hypertensive rats using three inhibitors of this system. The inhibitors used were URI-73A, a synthetic analog of lysophosphatidylethanolamine, which inhibits renin both in vivo and in vitro, SQ14,225, a potent converting enzyme inhibitor, and [Sar1, Thr8] angiotensin II, an angiotensin II antagonist. When the inhibitors were administered in acute (high renin) hypertensive rats, they all lowered blood pressure significantly. However, in the chronic (low renin) hypertensive phase, both renin and converting enzyme inhibitors lowered blood pressure, whereas, Sar1, Thr8 failed to lower blood pressure. The renin inhibitor lowered plasma renin activity (PRA), and SQ14,225 and [Sar1, Thr8] Ang II increased PRA. Further studies on water and electrolyte balance with one-kidney model hypertensive and uninephrectomized control rats showed no change in plasma volume. However, there was increased 24-hour urinary output and increased sodium excretion. This study indicates that in chronic renal hypertensive rats, blood pressure reduction is possible by either renin on converting enzyme inhibitor, but not by angiotensin antagonists. Since volume did not change either during the development or reversal of hypertension, volume did not appear to play a major role in the maintenance of hypertension.

Angiotensin II↗

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Effect of converting enzyme inhibitor (SQ14,225) on myocardial hypertrophy in spontaneously hypertensive rats.

The potent converting enzyme inhibitor (CEI) SQ14,225, which is known to prevent the formation of angiotensin II (AII) has been used to evaluate the role of AII in the development and reversal of cardiac hypertrophy. The present study describes the effect of CEI on blood pressure (BP) and myocardial hypertrophy (prevention and reversal) in the spontaneously hypertensive rat (SHR). A group of 3-week- and 8-week-old male SHR was treated with CEI (30 mg/kg in drinking water) for 6 weeks. An additional group of SHR was also treated with a combination of CEI and a diuretic (hydrochlorothiazide, 500 mg/liter). Heart weight, BP, deoxyribonucleic acid (DNA), ribonucleic acid (RNA), hydroxyproline, myocardial catecholamines, and plasma renin activity (PRA) were determined. In the prevention study, we found a significant reduction in the ratio of heart weight to body weight along with the prevention of hypertension (200 vs 145 mm Hg, p less than 0.001). Similar reductions in BP and heart weights were obtained with the reversal group. A better BP control was noted in the CEI and hydrochlorothiazide group. The reduction of heart weight was associated with a reduction in RNA and hydroxyproline content. In all groups, we found a significant increase in PRA (p less than 0.001) and a slight increase in tissue catecholamine concentration. No change in kidney weight was found in any group. Data clearly showed that oral administration of CEI prevented and reversed cardiac hypertrophy in SHR. Reversal was associated with a decrease in myocardial collagen content. These data indicate that prevention of AII formation in combination with BP control can prevent and reverse cardiac hypertrophy in SHR. Of course, whether or not CEI acts only through the renin angiotension system is still speculative.

Animals↗

PubMedDate not supplied

Isolation of aldosterone-stimulating factor (ASF) and its effect on rat adrenal glomerulosa cells in vitro.

A protein fraction has been isolated from normal human urine which upon chronic administration produced hypertension in rats. The hypertension is associated with retention of sodium and increased circulating aldosterone. The protein fraction has been purified to homogeneity, and its molecular weight has been determined to be 26,134 daltons by equilibrium ultracentrifugation. The compound has been identified to be clearly different from ACTH, angiotensin II, and beta-lipotropin. It stimulated aldosterone production from rat glomerulosa cells in vitro in a dose-dependent fashion from 10(-9) to 10(-4)M with a maximum stimulation at 10(-7) where a fourfold increase was obtained during 2 hours of incubation. Removal of some carbohydrate moieties by insoluble neuraminidase caused a twofold increase in aldosterone production in vitro. The protein fraction has been named "aldosterone-stimulating factor" or "ASF." Further studies are in progress to define its physiological role.

Adrenal Cortex↗

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Responses of juxtaglomerular cell suspensions to various stimuli.

Cell suspensions were prepared from rat renal cortical tissue by dispersion with 0.1% collagenase. Unit gravity sedimentation in a 1%-4% Ficoll gradient resulted in a single-cell suspension enriched in juxtaglomerular (JG) cells. Both the cellular renin activity and the amount of renin released into the supernatant increased with time when the suspensions were incubated for 1 hour at 37 degrees C in tissue culture medium. These cells responded to epinephrine and norepinephrine by increasing both synthesis and release of renin. The response was blocked by timolol but not by phenoxybenzamine. Cell suspensions prepared in the same manner but using 0.25% trypsin as the dispersing enzyme neither synthesized nor released renin into the tissue culture medium when similarly incubated. Trypsin-dispersed cells did not respond to catecholamine stimulation. Renin synthesis and release in collagenase-dispersed JG cells were unaltered by changes in Na, K, or Ca ion concentrations. Angiotensin II inhibited release, while saline extracts of clipped kidney from renal hypertensive rats stimulated renin release by these cells.

Angiotensin II↗

PubMedDate not supplied

Steroidogenic characteristics of a new aldosterone-stimulating factor (ASF) isolated from normal human urine.

The steroidogenic properties of a glycoprotein fraction (urinary ASF), isolated from normal human urine, were studied in collagenase-dispersed rabbit adrenal capsular cells in 1) define the requirements for its steroidogenic activity, and 2) assess its site and mode of action. When incubated with adrenal cell suspension at 37 degrees C for 2 hours, urinary ASF induced dose-related increases in both aldosterone and corticosterone production. However, urinary ASF was less potent (ED50 = 10(-9) M) than either angiotensin II (ED50 = 8 x 10(-11) M) or ACTH (ED50 = 4 x 10(-11) M). Increases in cyclic AMP accompanized the steroidogenic response to ACTH but not to either urinary ASF or AII. Deprivation of potassium in incubation media or the addition of ouabain (1 mM) during incubation completely inhibited the steroidogenic response to either urinary ASF, ACTH, or AII. Like ACTH and AII, urinary ASF increased conversion of corticosterone to aldosterone. Specific competitive antagonist of AII (Sar1, Thr8, AII) and ACTH ([I1e9]ACTH1-24) did not prevent the ASF-induced increase in aldosterone production. These results suggest that urinary ASF is readily distinguishable from ACTH. Although it shares similar steroidogenic properties with AII, the inability of AII antagonist to block its effects suggests that it acts at a separate receptor site.

Adenosine Triphosphatases↗

PubMedDate not supplied

Localization, purification, and biological activity of a new aldosterone-stimulating factor.

An aldosterone-stimulating factor (ASF) has been isolated from normal human urine and found to be a glycoprotein with a molecular weight of 26,000 daltons. ASF stimulated aldosterone production both in vivo and in vitro. ASF was found to be different from other known aldosterone secretogogues by the use of high performance liquid chromatography (HPLC). The retention time of ASF was different (17.0 minutes) from ACTH (retention time, 28.4 minutes), beta-lipotropin (retention time, 20.5 minutes), and angiotensin II. Proteolytic enzyme digestion and purification of ASF by HPLC yielded a smaller molecule (retention time, 22.0 minutes) with a molecular weight of 4000 daltons. This smaller molecule also stimulated aldosterone production in vitro. This showed that the structural requirement for steroidogenesis may be residing in a smaller molecule. ASF failed to produce hypertension in adrenalectomized rats. By immunofluorescence (using fluorescein conjugated antibodies), ASF was found to be localized in the anterior lobe of the pituitary gland. Data suggest that ASF, a new aldosterone-stimulating hormone that has not been described before, is secreted by the pituitary gland, and the adrenal gland appears to be the target organ for the biological activities.

Adrenalectomy↗

PubMedDate not supplied

Development and preliminary application of a new assay for aldosterone stimulating factor.

A new assay method has been developed to measure aldosterone stimulating factor (ASF) quantitatively. This method utilizes a combination of affinity chromatography and high pressure liquid chromatography (HPLC). Antibodies raised against ASF, coupled to Affi-Gel 10, were used as the affinity column, and adsorbed ASF was eluted with 4 M urea. Quantitation was based on the external standard method of analysis using the area of the standards as controls, which were previously tested by HPLC for purity. The amount of ASF in the unknown samples was calculated on the basis of the area of the peak emerging at the retention time of ASF. A parallel bioassay using adrenal glomerulosa cells was also done to assess the biological activity. In eight normal volunteers, the urinary ASF was 146 +/- 4.6 ng/24 hr urine, whereas in plasma it was 70.5 +/- 6.5 ng/100 ml. The method is reproducible, specific for ASF, and showed less than 3% inter- or intraassay variability. In a preliminary study, when ASF was quantified from the 24-hour urine of two patients with adrenal hyperplasia, a significantly higher level of ASF was found (750 and 1020 ng/24 hr urine). These data suggest that ASF may be of pathological significance in certain hypertensive patients, especially in the hypertension associated with hyperaldosteronism.

Adrenal Glands↗

PubMedDate not supplied

Primary hyperaldosteronism in childhood due to unilateral macronodular hyperplasia. Case report.

We present the first report of primary hyperaldosteronism in childhood due to unilateral macronodular hyperplasia. A 10-year-old white boy with severe hypertension (150/100 mm Hg), hypokalemia (1.4 mEq/liter), and suppressed plasma renin activity (PRA) (less than 0.1 ng/ml/hr) demonstrated fixed PRA and aldosterone (aldo) levels that did not change with alteration of dietary sodium. The paradoxical decrease in serum aldo on assumption of upright posture suggested a tumor. Prolonged ACTH administration produced a continuous rise in blood pressure, but a transient rise in aldo. A minimal decrease in urinary aldo during dexamethasone administration was noted, excluding dexamethasone-suppressible hyperaldosteronism. Blood pressure normalized with spironolactone. Computerized transaxial tomography, iodocholesterol scanning, and adrenal venography were not diagnostic of a discrete adrenal lesion. Although hyperplasia is more common than an adenoma as a cause of hyperaldosteronism in childhood, a tumor was predicted, since adrenal vein hormone sampling with ACTH stimulation lateralized aldosterone secretion unequivocally to the left adrenal gland. However, left adrenalectomy revealed macronodular hyperplasia. Postoperatively, there was reversal of hypertension, hypokalemia, and hyperaldosteronism. Thus, in childhood, unilateral hypersecretion of aldosterone may result from nodular hyperplasia, rather than a discrete adenoma.

Adrenal Glands↗

PubMedDate not supplied

Primary pulmonary hypertension in cirrhosis of liver.

BACKGROUND: Primary pulmonary hypertension (PPH) is a grave association of portal hypertension, and is potentially fatal in liver transplant candidates. AIM: To investigate the prevalence of PPH among cirrhotics with portal hypertension. METHODS: 43 cirrhotics with portal hypertension (Child B 22, C 14), after screening for cardiopulmonary diseases, were evaluated by hemodynamic study. RESULTS: PPH was detected in 2 cases (4.7%), both in Child B, hepatitis B and C viruses being the etiologies. Neither had portal axis thrombosis. Two other cases also had pulmonary hypertension, but with high pulmonary capillary wedge pressure (PCWP). The 41 cases without and 2 cases with PPH had, respectively, mean pulmonary artery pressure (MPAP) 16.3 (5.9) mmHg, 26 mmHg and 33 mmHg; PCWP 11.5 (6.7) mmHg, 12 mmHg and 11 mmHg; transpulmonary pressure gradient 4.8 (2.6) mmHg (n = 27), 14 mmHg and 22 mmHg; and pulmonary vascular resistance 80.2 (55.8) dyne.sec.cm-5 (n = 27), 155.6 dyne.sec.cm-5 and 366.7 dyne.sec.cm-5. No correlation of MPAP was found with either Child-Pugh scoring (r2 = 0.0347) or with hepatic venous pressure gradient (r2 = 0.0021). CONCLUSION: PPH has a prevalence of 4.7% among cirrhotics with portal hypertension; it bears no relation with severity of liver disease.

Adult↗

PubMedDate not supplied

Massive corneal and conjunctival squamous cell carcinoma.

A patient with massive, protuberant squamous cell carcinoma of conjunctiva invading the whole cornea, so as to hang from the surface, was referred with a visual acuity of hand motion near to face. A microscopically-controlled, frozen section guided excision, followed by double-freeze-thaw cryoapplication to the sclera and the edges of the conjunctival bed and lamello-lamellar sclerokeratoplasty, was performed. Three years later the patient's visual acuity was 20/60 with no evidence of recurrence of the lesion. Frozen section guided excision with adjuvant cryotherapy and lamellar sclerokeratoplasty is a viable therapy for massive squamous cell carcinoma of cornea and conjunctiva.

Carcinoma, Squamous Cell↗

PubMedDate not supplied

Does enalapril prevent peritoneal fibrosis induced by hypertonic (3.86%) peritoneal dialysis solution?

OBJECTIVE: Peritoneal fibrosis (PF) is one of the most serious causes of failure in continuous ambulatory peritoneal dialysis (PD). Although the underlying mechanism responsible for the genesis of PF is still unknown, transforming growth factor beta (TGFbeta1) has been shown to be associated with PF. Angiotensin converting enzyme inhibitors have been shown to prevent the stimulating effect of growth factors. The aim of the present study was to investigate the effect of enalapril on peritoneal function and morphology in a rat model of experimental PF. METHODS: Twenty-one albino Wistar rats were divided into three groups: (1) the control group (C) received 10 mL isotonic saline intraperitoneally (i.p.), (2) the dextrose (Dx) group 10 mL 3.86% dextrose PD solution i.p., and (3) the enalapril-treated group (ENA) 10 cc 3.86% dextrose PD solution i.p. plus 100 mg/L enalapril in drinking water. After 4 weeks, a 1-hour peritoneal equilibration test was performed with 20 mL 2.27% dextrose PD solution. Dialysate-to-plasma urea ratio (D/P urea), glucose reabsorption (D1/D0 glucose), ultrafiltration (UF) volume, and levels of dialysate protein, TGFbeta1, and cancer antigen 125 (CA125) were determined. The parietal peritoneum was evaluated histologically by light microscopy. RESULTS: Administration of enalapril resulted in preserved UF (-0.2 +/- 0.7 mL vs 1.7 +/- 0.3 mL, p < 0.05), protein loss (2.3 +/- 0.5 g/L vs 1.6 +/- 0.2 g/L, p > 0.05), and peritoneal thickness (77 +/- 7 microns vs 38 +/- 5 microns, p < 0.001). D/P urea increased significantly in the Dx group (p< 0.05). Both higher levels of TGFbeta1 (undetectable vs 298 +/- 43 pg/mL, p < 0.001) and lower levels of CA125 in dialysate effluent (0.94 +/- 0.5 U/L vs 0.11 +/- 0.1 U/L, p > 0.05) were determined in the Dx group. CONCLUSION: These findings show that peritoneal morphology and function tests were dramatically deranged in the Dx group. The same properties were partially preserved in the ENA group. The production of TGFbeta1 was significantly reduced but peritoneal thickness was not completely inhibited. In conclusion, by inhibiting the production of TGFbeta1, enalapril can preserve peritoneal histology, peritoneal function, and remodeling of mesothelial cells.

Angiotensin-Converting Enzyme Inhibitors↗

PubMedDate not supplied

By reducing TGF beta 1, octreotide lessens the peritoneal derangements induced by a high glucose solution.

BACKGROUND: Chronic peritoneal dialysis may eventually result in peritoneal fibrosis, which progressively reduces dialytic efficacy. Although the pathogenesis has not been elucidated, it has been proposed that transforming growth factor beta-1 (TGF beta 1) plays a central role in the onset of peritoneal fibrosis. METHODS: Rats were divided into three groups and given saline, hypertonic peritoneal dialysis solution alone, a hypertonic peritoneal dialysis solution plus octreotide intraperitoneally. After four weeks, a one-hour peritoneal equilibration test was done. Dialysate-to-plasma urea ratio, glucose reabsorption, ultrafiltration volume and levels of dialysate protein, TGF beta 1 and cancer antigen 125 (CA 125) were determined. The peritoneal membrane was examined histologically by light microscopy. RESULTS: Compared to the saline group, peritoneal function tests (ultrafiltration volume 6 (5-7) vs 0.0 ml, dialysate-to-plasma urea ratio 0.51 vs 0.76, glucose reabsorption 0.54 vs 0.40 and morphology (thickness 4.5 vs 75.5 microns) were dramatically deranged in hypertonic peritoneal dialysis solution-treated rats, which also had a higher level of TGF beta 1 and undetectable CA 125. In contrast, in hypertonic peritoneal dialysis solution plus octreotide rats' peritoneal function was protected (ultrafiltration volume 3 mL, dialysate-to-plasma urea 0.60, glucose reabsorption 0.51) but peritoneal thickening (37.7 microns) was not so markedly reduced although the production of TGF beta 1 was significantly inhibited. CONCLUSION: These data show that by inhibiting the production of TGF beta 1, octreotide can preserve peritoneal function and remodeling of the mesothelial cell. Although the production of TGF beta 1 was significantly inhibited, peritoneal thickening cannot be completely prevented.

Animals↗

PubMedDate not supplied

Management of the Budd-Chiari syndrome by balloon cavoplasty.

BACKGROUND: Obstruction of the suprahepatic inferior vena cava (IVC) by a membrane or stricture is the commonest cause of Budd-Chiari syndrome in the eastern hemisphere. We present our experience with the outcome of balloon cavoplasty in such cases. METHODS: We followed up 40 consecutive cases of Budd-Chiari syndrome over seven years. Doppler study of hepatic venous outflow tract (in all cases), liver biopsy (30 cases) and necropsy (two cases) were performed. Balloon cavoplasty was done in selected cases. RESULTS: Of 40 patients with BCS (mean age 35.2 [SD 8.7] years; 26 men) 5, 5 and 30 had fulminant, acute and chronic presentation, respectively. Inferior vena cavography was performed in 32 cases, and showed membranous obstruction of the IVC in 12, segmental occlusion of the IVC in 11 cases, and block in both the IVC and the main hepatic veins in the rest. Successful balloon cavoplasty was done in 18 cases with obstruction of the IVC (membrane or stricture); 15 of them are well over a mean follow up of 56 (14.6) months. Three patients developed restenosis; two of them, treated with redilatation, are doing well, and one died of septicemia and hepatic failure following a surgical bypass. Pressure gradient between the IVC and right atrium decreased significantly after cavoplasty (15.4 [2.8] vs 6.6 [2.0] mmHg; p< 0.001). CONCLUSION: Balloon cavoplasty gave encouraging results in the management of Budd-Chiari syndrome due to membranous obstruction or stricture of the IVC.

Adolescent↗

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Aureobasidium pullulans scleritis following keratoplasty: a case report.

Fungal scleritis is a rare entity. A 50-year-old patient with culture proven Aureobasidium pullulans corneal ulcer underwent therapeutic keratoplasty. He developed scleritis 5 days following surgery. Although the patient had symptomatic improvement after antifungal therapy, surgical debridement, and cryotherapy, visual improvement was only marginal. Aureobasidium pullulans should be looked for as a cause for keratomycosis and scleromycosis, especially in tropical countries.

Antifungal Agents↗

PubMedDate not supplied

Intussusception in southern Indian children: lack of association with diarrheal disease and oral polio vaccine immunization.

BACKGROUND: Intussusception is the most common cause of intestinal obstruction in young children and has been reported as a complication of a recently withdrawn tetravalent reassortant rotavirus vaccine. METHODS: We studied the history, clinical presentation, management and outcome of intussusception presenting to a tertiary care hospital in southern India over a 10-year period, in order to assess potential association with diarrheal disease and immunization. RESULTS: Data from 137 index cases and 280 control subjects indicated that the risk of diarrheal disease or oral polio vaccine administration in the month prior to presentation was similar in the index cases and controls. Mean time to presentation to hospital after developing symptoms was 1.8 days, and 77.3% of patients required surgery, with 47.4% undergoing intestinal resection. Mortality was 0.006%. CONCLUSIONS: No association could be demonstrated between gastroenteritis or oral poliovirus vaccine immunization and intussusception in southern Indian children. These children presented later and required operative intervention more frequently than has been reported in other studies, but had a good outcome with low mortality.

Case-Control Studies↗

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Survival after percutaneous endoscopic gastrostomy: the role of dementia.

BACKGROUND: Percutaneous Endoscopic Gastrostomy (PEG) is a widely used technique for enteral feeding in nursing home patients. Several factors including malnutrition, hypoalbuminemia, older age, number of co-morbidities and cognitive impairment adversely affect survival. OBJECTIVE: This study evaluated the relative impact of age, serum albumin, number of co-morbid illnesses and dementia on survival in male nursing home patients who had undergone percutaneous endoscopic gastrostomy (PEG). DESIGN: In a retrospective study the hospital records of all North Chicago Veterans Affair (VA) male nursing home residents (n=88) who had PEG placed between 1990 through 2000 were reviewed. Of the 88 charts reviewed, 17 were eliminated from analysis due to incomplete data. Following data was examined: Age, serum albumin, number of co-morbid illnesses, presence of dementia, survival in years following PEG placement. RESULTS: Advancing age was associated with increasing probability of dementia and increased number of co-morbidities. Post PEG survival decreased with increasing age, with lower serum albumin, and increased number of co-morbidities. Age and serum albumin were strong predictors of survival in PEG recipients without the diagnosis of dementia. However, in PEG recipients with a diagnosis of dementia, age and serum albumin no longer predicted survival. Dementia appears to attenuate the effects of age and serum albumin on survival following PEG placement. CONCLUSION: In the presence of dementia, none of the usual predictors of survival in PEG recipients remain significant.

Age Factors↗