Acute small-bowel obstruction following mesenteric perforation by CAPD catheter.
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Biomedical subjects
Publications and source records attributed to S Gupta.
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UNLABELLED: We investigated the cerebral hemodynamic effects of 0.5 and 1.5 minimum alveolar anesthetic concentration (MAC) sevoflurane during propofol anesthesia in 10 patients undergoing supratentorial tumor resection. All patients received a standardized anesthetic, and their lungs were ventilated with a mixture of air and oxygen to produce mild hypocapnia. Anesthesia was then maintained with a propofol infusion. Muscle relaxation was obtained by infusion of atracurium. A transcranial Doppler probe was used to measure red cell flow velocity in the right middle cerebral artery (Vmca). A right-sided jugular bulb catheter was inserted for sampling of jugular bulb blood. After a 30-min period of stabilization and before the start of surgery, baseline arterial and jugular bulb blood samples were drawn to define the arterial-venous oxygen content difference (AVDO2). Mean arterial pressure and Vmca were recorded. Sevoflurane (0.5 and 1.5 MAC) in oxygen/air was then administered, and all measurements were repeated. Administration of sevoflurane at 0.5 MAC did not change Vmca or AVDO2. Sevoflurane (1.5 MAC) did not change Vmca. There was an approximately 25% reduction in AVDO2 (P < 0.05). This suggests that during propofol anesthesia, although 1.5 MAC sevoflurane does not increase red blood cell velocity, there is a relative increase in flow with respect to metabolism. Administration of large-dose sevoflurane may be associated with a degree of luxury perfusion. IMPLICATIONS: We investigated the cerebral hemodynamic effects of sevoflurane in patients undergoing neurosurgery. Small-dose sevoflurane (1%) did not change brain blood flow or oxygen consumption. Large-dose sevoflurane (3%) did not change flow velocity but reduced brain oxygen consumption by 25%. Sevoflurane may provide a degree of luxury perfusion.
The role of type-1 fimbriae in the pathogenesis of chronic pyelonephritis was studied for two Escherichia coli strains. Although both strains produced a similar total oxidative burst of chemiluminescence in macrophages from uninfected mice, the extracellular oxidative burst was greater with the non-fimbriate mutant E. coli BH-5 than its type-1 fimbriate parent E. coli 31-B. Moreover, macrophages from mice infected with the non-fimbriate mutant gave a much greater oxidative burst when stimulated with latex particles than that given by macrophages from mice infected with the type-1 fimbriate parent. These results correlated with the degree of renal inflammation and scarring as measured by malondialdehyde formation. Hence, the role of type-1 fimbriae in the pathogenesis of chronic UTI although documented does not appear to be significant.
2-Methoxyestradiol (2-ME) is an endogenous metabolite of estradiol-17beta and the oral contraceptive agent 17-ethylestradiol. 2-ME was recently reported to inhibit endothelial cell proliferation. The current study was undertaken to explore the mechanism of 2-ME effects on endothelial cells, especially whether 2-ME induces apoptosis, a prime mechanism in tissue remodeling and angiogenesis. Cultured bovine pulmonary artery endothelial cells (BPAEC) exposed to 2-ME showed morphological (including ultrastructural) features characteristic of apoptosis: cell shrinkage, cytoplasmic and nuclear condensation, and cell blebbing. 2-ME-induced apoptosis in BPAEC was a time- and concentration-dependent process (EC50 = 0.45 +/- 0.09 microM, n = 8). Nucleosomal DNA fragmentation in BPAEC treated with 2-ME was identified by agarose gel electrophoresis (DNA ladder) as well as in situ nick end labeling. Under the same experimental conditions, estradiol-17beta and two of its other metabolites, estriol and 2-methoxyestriol (< or =10 microM), did not have an apoptotic effect on BPAEC. 2-ME activated stress-activated protein kinase (SAPK)/c-Jun amino-terminal protein kinase in BPAEC in a concentration-dependent manner. The activity of SAPK was increased by 170 +/- 27% and 314 +/- 22% over the basal level in the presence of 0.4 and 2 microM 2-ME (n = 3-6), respectively. The activation of SAPK was detected at 10 min, peaked at 20 min, and returned to basal levels at 60 min after exposure to 2-ME. Inhibition of SAPK/c-Jun amino-terminal protein kinase activation by basic fibroblast growth factor, insulin-like growth factor, or forskolin reduced 2-ME-induced apoptosis. Immunohistochemical analysis of BPAEC indicated that 2-ME up-regulated expression of both Fas and Bcl-2. In addition, 2-ME inhibited BPAEC migration (IC50 = 0.71 +/- 0.11 microM, n = 4) and basic fibroblast growth factor-induced angiogenesis in the chick chorioallantoic membrane model. Taken together, these results suggest that promotion of endothelial cell apoptosis, thereby inhibiting endothelial cell proliferation and migration, may be a major mechanism by which 2-ME inhibits angiogenesis.
The effect of bile on the expression of cholera toxin (CT) and the major subunit of the toxin-coregulated pilus (TcpA) and on motility was examined in the Vibrio cholerae O1 classical-biotype strains 0395 and 569B. Although the motility of the cells increased significantly in the presence of bile, transcription of the ctxAB genes, encoding CT, and of the tcpA gene was drastically reduced. In toxR mutant strains, motility is higher than in the wild-type strain and was further increased, by about 150%, in the presence of bile. Bile represses CT production in strain 569B-55, a toxR mutant of strain 569B, which normally produces more than 80% of the amount of CT synthesized in the wild-type cells. These results suggest that bile may target some factor other than ToxR that is involved in the regulation of CT production and motility. Bile has no effect on the relative amounts of the two outer membrane porins, OmpU and OmpT, which are under ToxR control.
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Previous evidence suggests an increased cardiovascular morbidity in patients with panic disorder. In this study, we compared 24-hour ECG in patients with panic disorder (n = 22; age: 36.1 +/- 7.6 years) and healthy controls (n = 21; age: 34.6 +/- 10.0 years). The QTc intervals during the day or night were not significantly different between patients and controls. Ventricular ectopic beats were also not significantly different between the two groups. These results do not suggest any overt cardiac arrhythmias in this age group of patients with panic disorder.
BACKGROUND AND PURPOSE: The poor outcome observed in stroke patients with visual neglect may be due to greater stroke severity or nonspecialist management. METHODS: The effects of visual neglect were studied prospectively in 150 consecutive stroke patients with comparable stroke pathology and motor severity managed on a stroke unit. A randomized study was subsequently undertaken in 50 stroke patients with visual neglect to evaluate the effectiveness of spatial cueing during motor activity on functional outcome and resource use in these patients. RESULTS: Visual neglect was present in 47 (32%) of a selected group of 146 patients (mean age, 77.0 +/- 8.2 years; 42% men) with moderate stroke severity. There were no differences in demography, prestroke function, or motor power in the arm (2.6 +/- 1.7 versus 2.3 +/- 2.1) or the leg (3.2 +/- 1.4 versus 3.0 +/- 1.6) on the affected side compared with 99 patients with no visual neglect. Although patients with visual neglect had lower median initial (4 versus 5, P < .01) and discharge (14 versus 16, P < .01) Barthel Index scores, equal proportions of patients were discharged home (60% versus 65%) or to institutions (34% versus 33%) in both groups. The durations of hospitalization (64 versus 36 days, P < .001) and therapy input (47.7 versus 27.8 hours; P < .01), however, were significantly greater in patients with visual neglect. The randomized controlled study showed a trend toward higher Barthel scores at 12 weeks (14 versus 12.5, P = NS) and significant reduction in median length of hospital stay (42 versus 66 days) in patients receiving spatiomotor cueing and early emphasis on functional rehabilitation. CONCLUSIONS: Patients with visual neglect managed on a stroke unit have similar destination of discharge despite lower Barthel Index scores compared with patients of equal stroke severity who do not have this deficit. Spatiomotor cueing and early emphasis on function can improve outcome and reduce resource use in these patients.
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Atheroembolic renal failure (AERF) is often seen after vascular procedures in elderly atherosclerotic patients. To estimate the incidence of AERF after coronary angiography, all patients undergoing coronary angiography at the V.A. Medical Center, Dayton, were prospectively evaluated for AERF. Since, unlike contrast nephropathy, AERF develops about a week after the vascular procedure and persists or progresses over weeks and months, serum creatinine was measured just prior to and 3 weeks after coronary angiography. Peripheral signs of cholesterol emboli were also looked for at follow-up visits. Two hundred sixty-seven patients underwent coronary angiography over a fifteen-month period. Most of the patients were sixty years old or older. Mean serum creatinine in these patients prior to coronary angiography was 1.2 mg/dL. Mean serum creatinine after coronary angiography was unchanged (1.2 mg/dL). Only 7 patients had serum creatinine > 2 mg/dL prior to coronary angiography. Two patients died within a week of coronary angiography and 2 did not return for follow-up. Of the remaining 263 patients, 5 had a serum creatinine increase by 0.5 mg/dL or more at three weeks after coronary angiography. Three of 5 had a serum creatinine increase by 1.0 mg/dL or more. Two of these 3 patients eventually died of renal failure. None of these 5 patients had peripheral signs of cholesterol emboli. In selected patients, the incidence of AERF after coronary angiography appears to be very low (< 2%).
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We demonstrated previously that TSH activates phospholipase D (PLD) via stimulation of protein kinase C (PKC) in Fischer rat thyroid line (FRTL)-5 thyroid cells. To examine the role of the cAMP pathway in the regulation of PLD, we studied the effects of forskolin (0-100 microM; 30 min) and dibutyryl cAMP (dbcAMP; 0-1 mM; 30 min) on PLD activation. FRTL-5 thyroid cells were labeled mainly in phosphatidylcholine with [3H]myristate followed by incubation with 200 mM ethanol before the addition of agonist. PLD was assessed by the measurement of [3H]phosphatidylethanol. Forskolin (100 nM to 100 microM) and dbcAMP (100 pM to 100 microM) increased PLD activity significantly. Maximal responses to forskolin and dbcAMP exceed the PLD responses produced by 100 microU/ml of TSH. To determine whether the effects of forskolin and dbcAMP on PLD occurred as a consequence of PKC activation, FRTL-5 thyroid cells were preincubated for 10 min with the PKC inhibitors, chelerythrine (1 microM) or calphostin C (1 microM), or they were pretreated for 24 h with phorbol myristate acetate (100 nM) to down-regulate PKC. Unlike TSH-mediated PLD activation, these treatments had no effect on PLD activation by cAMP agonists. Forskolin (10 microM; 30 min) had no effect on the subcellular distribution of PKC alpha-, epsilon-, or zeta-isoforms, confirming the lack of involvement of PKC. The protein kinase A (PKA) inhibitors, H-89 (10 microM; 30 min) and dideoxyadenosine (5 nM; 10 min) significantly decreased the forskolin- and dbcAMP-mediated PLD activation without any effect on the phorbol ester-mediated PLD response. Following pretreatment with H-89 or dideoxyadenosine, the TSH-mediated PLD response was also significantly reduced. These studies indicate that forskolin and dbcAMP stimulate PLD in FRTL-5 thyroid cells directly via PKA without involvement of PKC. Studies of cells in the presence and absence of ethanol revealed approximately 60% of the phosphatidate plus diacylglycerol produced via TSH occurs via PLD activation. Although TSH-mediated inositol phosphate generation occurred with similar concentrations of TSH that led to PLD activation, 10-fold higher TSH concentrations were required to increase intracellular Ca2+. These results and the lack of a rapid Ca2+ transient following physiological TSH concentrations suggest that alternatives to conventional hydrolysis of phosphatidylinositol 4,5-bisphosphate may initiate PKC activation. Thus, the two major signal transduction systems in the FRTL-5 thyroid cell (PKA and PKC) appear to converge on PLD activation. Stimulation of both of these pathways by TSH may be required for optimal physiological activation of PLD.
Diabetic women present an interesting challenge to the reproductive health-care physician and gynecologist. Good preconceptual counselling reduces the risk of adverse consequences of the pregnancy to the mother and the fetus and should be encouraged. Poor metabolic control has been linked with an increased risk of congenital malformations. The low-dose combined pill (COC) does not appear to increase the risk of diabetes in women with a history of gestational diabetes. Young healthy diabetic women under 25 years old may be prescribed the low-dose COC with careful metabolic monitoring. The copper intrauterine contraceptive device is a useful choice in diabetic women with vascular disease, proliferative retinopathy and nephropathy. The progestogen-only pill and barrier methods may sometimes have unacceptable failure rates in diabetic women who may require to avoid a pregnancy at any cost. When a couple's family is complete, sterilization and vasectomy should be encouraged.
Although panic disorder has been associated with impaired quality of life (QOL) and financial dependence, no prior study has examined whether a clinical intervention will improve these outcomes. This study examines the effects of clinically titrated doses of clonazepam versus placebo on QOL and work productivity (WP) in patients with panic disorder. QOL and WP were measured in conjunction with a randomized, double-blind, placebo-controlled trial. The Medical Outcomes Study 36-Item Short Form Health Survey (SF-36) and Work Productivity and Impairment questionnaire were used to assess QOL and WP, respectively. Baseline assessments were obtained before randomizing patients to receive clinically titrated doses of clonazepam or placebo. Follow-up assessments were obtained after 6 weeks of therapy with the test drug or at premature termination from the study. Improvement on the SF-36 Mental Health Component Summary scale was more than twice as great with clonazepam than with placebo (P = 0.03). Clonazepam patients improved (P < 0.05) on all five measures of mental health-related QOL, and both measures of physical health-related QOL, and both measures of WP. Placebo patients improved on three of five measures of mental health-related QOL, but on no other measures. Patients with marked improvements on clinical measures of panic disorder severity, especially avoidance and fear of the main phobia, showed the greatest gains on the SF-36 Mental Health Component Summary scale. Clinically titrated doses of clonazepam significantly improved mental health-related QOL and WP in panic disorder patients. Lesser improvements were obtained with placebo.
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