PubMed Health⌕ Search

Biomedical subjects

R Jindal

Publications and source records attributed to R Jindal.

16 recordsLinked to original sources
PubMed2001

Comparison of the clinical profile and outcome for squamous cell carcinoma and adenocarcinoma of the distal esophagus and cardia in India.

This retrospective review aimed to assess the clinical profile and outcome of squamous cell carcinoma as compared with adenocarcinoma of the lower third of esophagus and cardia following a transhiatal esophagectomy. A total of 169 patients were analyzed retrospectively in this series from 1989 to 1994. There were 100 patients with squamous cell carcinoma (SCC) and 69 patients with adenocarcinoma (ADC). All tumors were assessed by an esophagogram, upper gastrointestinal endoscopy, and abdominal ultrasonography. The surgical procedure performed in all cases was a transhiatal esophagectomy (THE). The mean age of the patients with SCC and ADC was comparable (48 +/- 14 vs 54 +/- 12 years). Male/female ratio was 1.0:1.4 in the SCC group while in the ADC group it was 8.8:1.0. The main symptom in both the groups was grade II dysphagia (62% in SCC and 60% in ADC). The mean length of the tumor was 6.6 +/- 4.5 cm in the SCC group and 4.2 +/- 3.3 cm in the ADC group. The resectability rate of the SCC group was significantly higher (76%) than in the ADC group (55%). The 6-month and 1-year survival for the SCC patients was not significantly different from the ADC patients (83.7% and 49.3% vs 85.0% and 54.0%). The 5-year survival achieved in SCC was higher than in the ADC group (11.6% vs 7.2%) but the difference was not statistically significant. Adenocarcinoma arising from the distal esophagus and cardia was more common in males, and also occurred in a higher age group and had a lower resectability rate than squamous cell carcinoma. No case of Barrett's esophagus was encountered. The short- and long-term survival in both tumors were similar.

Adenocarcinoma↗
PubMed2000

Preliminary randomized double-blind placebo-controlled trial of tryptophan combined with fluoxetine to treat major depressive disorder: antidepressant and hypnotic effects.

OBJECTIVE: Because the initial phase of treatment of depression with a selective serotonin reuptake inhibitor is often complicated by a delayed onset of action of the antidepressant or severe insomnia or both, we investigated whether tryptophan, an amino acid with both antidepressant-augmenting and hypnotic effects, would benefit patients with depression at the beginning of treatment with fluoxetine. DESIGN: Randomized, double-blind, placebo-controlled trial. PATIENTS: Thirty individuals with major depressive disorder. INTERVENTIONS: Treatment over 8 weeks with 20 mg of fluoxetine per day and either tryptophan (2 to 4 g per day) or placebo. OUTCOME MEASURES: Mood was assessed using the 29-item Hamilton Depression Rating Scale (HDRS-29) and the Beck Depression Inventory (BDI). Laboratory sleep studies were done at baseline and after 4 and 8 weeks of treatment using standard procedures. RESULTS: During the first week of treatment, there was a significantly greater decrease in HDRS-29 depression scores, and a similar trend in BDI scores, in the tryptophan/fluoxetine group than in the placebo/fluoxetine group. No significant differences were noted at later time points. With respect to sleep measures, there was a significant group-by-time interaction for slow-wave sleep at week 4. Further analysis revealed a significant decrease in slow-wave sleep after 4 weeks of treatment in the placebo/fluoxetine group, but not in the tryptophan/fluoxetine group. No cases of serotonin syndrome occurred, and the combination was well tolerated, although the 4 g per day dosage of tryptophan produced daytime drowsiness. CONCLUSIONS: Combining 20 mg of fluoxetine with 2 g of tryptophan daily at the outset of treatment for major depressive disorder appears to be a safe protocol that may have both a rapid antidepressant effect and a protective effect on slow-wave sleep. Further large-scale studies are needed to confirm these initial findings.

Adolescent↗
PubMed1999

Mechanisms of Hydrogen Peroxide-Induced Increase in Intracellular Calcium in Cardiomyocytes.

BACKGROUND: Hydrogen peroxide (H(2)O(2)) in high concentrations has been implicated in heart dysfunction attributable to ischemia-reperfusion. Although H(2)O(2) is also known to increase the intracellular concentration of Ca(2+) ([Ca(2+)](i)) in cardiomyocytes, the mechanisms for such a change are not clear. In this study, the sources and mechanisms of increase in [Ca(2+)](i) caused by high concentrations of H(2)O(2) in cardiomyocytes were explored. METHODS AND RESULTS: Cardiomyocytes were isolated from adult male Sprague-Dawley rats. Cell viability was examined by trypan blue exclusion test. [Ca(2+)](i) was measured by employing cell suspension at room temperature and Fura-2 fluorescence technique. Incubation of cells with 0.25-l mmol/L H(2)O(2) increased [Ca(2+)](i) in a time- and concentration-dependent manner. Catalase attenuated the H(2)O(2)-induced increase in [Ca(2+)](i) significantly, whereas mannitol showed no effect. Neither the presence of verapamil, a sarcolemmal Ca(2+) channel blocker, nor the removal of Ca(2+) from the medium produced any significant reduction in the H(2)O(2)-induced increase in [Ca(2+)](i). Conversely, treatment of cardiomyoctes with staurosporin, a protein kinase C inhibitor, thapsigargin, a sarcoplasmic reticulum Ca(2+)-pump adenosine triphosphatase inhibitor, as well as ryanodine, a sarcoplasmic reticulum Ca(2+)-release channel blocker, markedly prevented the 0.5-mmol/L H(2)O(2)-induced increase in [Ca(2+)](i). The responses of cardiomyoctes to H(2)O(2) and other Ca(2+)-mobilizing agents, such as KCl or adenosine triphosphate, were additive. No changes in cardiomyocyte viability were seen on incubation with 0.5 and 1 mmol/L H(2)O(2). Perfusion of the isolated heart with H(2)O(2) (0.1-0.5 mmol/L) depressed the left ventricular developed pressure, rate of contraction, and rate of relaxation, whereas the left ventricular end-diastolic pressure was increased. CONCLUSIONS: These results indicate that formation of H(2)O(2) under pathophysiological conditions such as ischemic heart disease may induce changes in Ca(2+) homeostasis in cardiomyocytes and may induce contractile dysfunction. Furthermore, the sarcoplasmic reticulum involving a protein kinase C-mediated mechanism appears to be the main site of action of H(2)O(2) in cardiomyocytes.

Journal Article↗
PubMed1998

Modification of cardiac beta-adrenoceptor mechanisms by H2O2.

From the role of oxidative stress in cardiac dysfunction, we investigated the effect of H2O2, an activated species of oxygen, on beta-adrenoceptors, G proteins, and adenylyl cyclase activities. Rat heart membranes were incubated with different concentrations of H2O2 before the biochemical parameters were measured. Both the affinity and density of beta 1-adrenoceptors were decreased, whereas the density of the beta 2-adrenoceptors was decreased and the affinity was increased by 1 mM H2O2. Time- and concentration-dependent biphasic changes in adenylyl cyclase activities in the absence or presence of isoproterenol were observed when membranes were incubated with H2O2; however, activation of the enzyme by isoproterenol was increased or unaltered. The adenylyl cyclase activities in the absence or presence of forskolin, NaF, and Gpp(NH)p were depressed by H2O2. Catalase alone or in combination with mannitol was able to significantly decrease the magnitude of alterations due to H2O2. The cholera toxin-stimulated adenylyl cyclase activity and ADP ribose labeling of Gs proteins were decreased by treatment with 1 mM H2O2, whereas Gi protein activities, as reflected by pertussis toxin-stimulation of adenylyl cyclase and ADP ribosylation, were unaltered. The Gs and Gi protein immunoreactivities, estimated by labeling with respective antibodies, indicate a decrease in binding to the 45-kDa band of Gs protein, whereas no change in the binding of antibodies to the 52-kDa band of Gs protein or the 40-kDa subunit of Gi protein was evident when the membranes were treated with 1 mM H2O2. These results suggest that H2O2 in high concentrations may attenuate the beta-adrenoceptor-linked signal transduction in the heart by changing the functions of Gs proteins and the catalytic subunit of the adenylyl cyclase enzyme.

Adenosine Diphosphate Ribose↗
PubMed1997

Progesterone mediates nutritionally induced effects on embryonic survival in gilts.

The role of plasma progesterone as a potential mediator of nutritionally induced effects on embryonic survival in gilts was assessed in two experiments. Gilts were individually fed 2.5 kg/d for one estrous cycle and inseminated 12 and 24 h after onset of next estrus (d 0). In Exp. 1, 52 gilts were randomly allocated to either N (1.5 x maintenance feed/d) or H (twice maintenance/d) groups from d 1. In 21 gilts, blood samples were collected on d -1, 0, 1, and 2, and gilts were slaughtered on d 3 to 5. Interval from LH peak to postovulatory progesterone rise was shorter (P = .02) in N (28.8 +/- 2.3 h) than in H (38.6 +/- 3.2 h) gilts, with no difference in rate of rise. Embryonic survival was 86.5 +/- 2.1 and 74.2 +/- 6.2% in N and H gilts, respectively, with a higher variability in Group H (P < .05). In 31 gilts, blood samples were collected 48 and 72 h after estrus onset, and gilts were slaughtered on d 11 and 12. Plasma progesterone concentrations at 72 h were higher (P = .02) in N than in H gilts (14.7 +/- 1.2 vs 10.8 +/- 1.0 ng/mL). Uterine plasmin/trypsin inhibitor concentrations were higher (P = .03) in H than in N gilts, but IGF-I concentrations did not differ. In Exp. 2, gilts were randomly allocated to either H or HP groups on d 1. The HP gilts were given six injections of progesterone (75 mg every 12 h) starting 24 h after estrus onset. Gilts were slaughtered on d 28 +/- 3. Plasma progesterone concentrations at 36, 48, 60, 84, and 108 h after estrus onset were higher (P < .001) in HP than in H gilts. Embryonic survival was also higher (P = .004) in HP (84.8 +/- 2.6%) than in H gilts (70.0 +/- 4.0%). Thus, periovulatory plasma progesterone can be the mediator of nutritionally induced effects on embryonic survival.

Animal Nutritional Physiological Phenomena↗
PubMed1996

Effect of nutrition on embryonal mortality in gilts: association with progesterone.

The effect of the timing of nutritional changes during the immediate period after mating on early embryonal survival and of progesterone as a potential mediator of such changes was studied. A total of 82 gilts were initially fed 2.5 kg.gilt-1.d-1 for one estrous cycle before they were inseminated at 16 and 24 h after the onset of estrus (d 0) using fresh, pooled semen. After AI, gilts were randomly allocated to one of the three feeding regimens, normal NRC allowance of 1.5 x maintenance per day from d 1 (Group N1) or d 3 (Group N3) or an allowance of 2 x maintenance from d 1 (Group H1). All gilts were fed on an individual basis. Single blood samples were collected 72 h after first detection of standing estrus. From d 15 onward, all gilts were fed 1.8 kg/d until they were slaughtered on d 28 +/- 3. Total and viable empryonal survival were affected by dietary treatment (P = .044 and .027, respectively), and viable embryonal survival in group N1 was greater than in group H1 (84.7 +/- 4.5 vs 64.5 +/- 7.6%; P < .05). Plasma progesterone was greater in group N1 than in groups N3 and H1 (10.5 +/- 1.0 vs 3.7 +/- .8 and 4.5 +/- .7 ng/mL, respectively; P < .05). The timing of the change in feed allowance after mating is therefore crucial for demonstrating effects of nutrition on embryonal survival in gilts, and progesterone may mediate these effects.

Animal Nutritional Physiological Phenomena↗
PubMed1995

Insulin autoimmune syndrome as a cause of spontaneous hypoglycemia in alcoholic cirrhosis.

Hypoglycemia in fulminant hepatic failure and hyperinsulinemia in cirrhosis are well-described phenomena. A patient with alcoholic cirrhosis who developed fasting hypoglycemia with an extremely high immunoreactive insulin level and a mildly elevated C-peptide level is reported. An insulinoma was excluded by detailed radiological imaging of the pancreas and by endoscopic ultrasonography. Detection of very high levels of insulin autoantibodies with no prior exposure to exogenous insulin confirmed the diagnosis of insulin autoimmune syndrome. During his hospital course, the patient developed another rare syndrome, acquired inhibitors to factor V, which led to the fatal coagulopathy that resulted in his death. Insulin autoimmune syndrome is the third leading cause of spontaneous hypoglycemia in Japan, where it has been associated with a variety of diseases and drugs. Outside of Japan, only approximately 20 cases have been reported and usually have been found in the context of an underlying autoimmune disorder or prior exposure to sulfhydryl drugs. It is believed that this is the first case reported outside Japan occurring in association with alcoholic liver disease, and the first in the world with coexisting acquired inhibitors to factor V.

Autoimmune Diseases↗
PubMed1994

Preservation and storage of pancreatic islets.

UW solution is currently the best available for short-term cold storage of pancreatic islets for up to 3-5 days, culture for up to 10-14 days, and cryopreservation for longer periods. More research needs to be done to find a better solution, specifically for cold storage of islets. It seems that such a solution is likely to be a derivative of the UW solution.

Cryopreservation↗
PubMed1992

Virulence of silver-resistant mutant of Klebsiella pneumoniae in burn wound model.

A silver-resistant mutant of Klebsiella pneumoniae B-5 was produced by passaging in nutrient broth containing graded concentrations of silver nitrate up to 150 ppm. The development of silver resistance in the strain resulted in rough colonies, decrease in cell size, carbohydrate content and change in klebocin pattern. The virulence of the AgR strain as checked by the burn wound model decreased as the mutant could not establish itself in the skin and spleen of the animals and the organism was cleared more efficiently by human lymphocytes than the parent AgS strain.

Animals↗
PubMedDate not supplied

A randomized, double-blind, placebo-controlled crossover study of the effect of exogenous melatonin on delayed sleep phase syndrome.

OBJECTIVE: The effects of exogenous melatonin on sleep, daytime sleepiness, fatigue, and alertness were investigated in 22 patients with delayed sleep phase syndrome whose nocturnal sleep was restricted to the interval from 24:00 to 08:00 hours. This study was a randomized, double-blind, placebo-controlled crossover trial. Subjects received either placebo or melatonin (5 mg) daily for 4 weeks, underwent a 1-week washout period, and then were given the other treatment for an additional 4 weeks. Patients could take the melatonin between 19:00 and 21:00 hours, which allowed them to select the time they felt to be most beneficial for the phase-setting effects of the medication. METHODS: Two consecutive overnight polysomnographic recordings were performed on three occasions: at baseline (before treatment), after 4 weeks of melatonin treatment, and after 4 weeks of placebo treatment. RESULTS: In the 20 patients who completed the study, sleep onset latency was significantly reduced while subjects were taking melatonin as compared with both placebo and baseline. There was no evidence that melatonin altered total sleep time (as compared with baseline total sleep time), but there was a significant decrease in total sleep time while patients were taking placebo. Melatonin did not result in altered scores on subjective measures of sleepiness, fatigue, and alertness, which were administered at different times of the day. After an imposed conventional sleep period (from 24:00 to 08:00), subjects taking melatonin reported being less sleepy and fatigued than they did while taking placebo. CONCLUSIONS: Melatonin ameliorated some symptoms of delayed sleep phase syndrome, as confirmed by both objective and subjective measures. No adverse effects of melatonin were noted during the 4-week treatment period.

Adult↗