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Biomedical subjects

L Cherian

Publications and source records attributed to L Cherian.

At least 19 recordsLinked to original sources
PubMed2001

Circadian coupling between pancreatic secretion and intestinal motility in humans.

Human interdigestive intestinal motility follows a circadian rhythm with reduced nocturnal activity, but circadian pancreatic exocrine secretion is unknown. To determine whether circadian changes in interdigestive pancreatic secretion occur and are associated with motor events, pancreatic enzyme outputs, proximal jejunal motility, and plasma pancreatic polypeptide concentrations were measured during consecutive daytime and nighttime periods (12 h each) in seven healthy volunteers using orojejunal multilumen intubation. Studies were randomly started in the morning or evening. Nocturnally, motility decreased (motor quiescence: 67 +/- 22 vs. 146 +/- 37 min; motility index: 3.59 +/- 0.33 vs. 2.78 +/- 0.40 mmHg/min; both P < 0.05) but amylase output increased (273 +/- 78 vs. 384 +/- 100 U/min; P < 0.05) and protease output remained unchanged (P > 0.05); consequently, enzyme/motility ratio increased. Amylase outputs were always lowest during phase I. Motor but not pancreatic circadian activities were associated with sleep. Pancreatic polypeptide plasma concentrations were unchanged. Consequently, intestinal motor and pancreatic exocrine functions may have different circadian rhythms, i.e., decreased motor and stable secretory activity during the night. However, the association between individual phases of interdigestive motor and secretory activity is preserved. The nocturnal increase in enzyme/motility ratio is probably not caused by increased cholinergic tone.

Amylases↗
PubMed2000

Brain nitric oxide changes after controlled cortical impact injury in rats.

Nitric oxide (NO) and the NO end products, nitrate and nitrite, were measured at the impact site after a 5-m/s, 3-mm deformation controlled cortical impact injury in rats. Immediately after the impact injury and the NO and microdialysis probes could be replaced, there was an increase from baseline in NO concentration of 83 +/- 16 (SE) nM, compared with 0.5 +/- 4 nM in the sham injured animals (P < 0.001). This marked increase in NO occurred at the time of the initial rise in blood pressure (BP) and intracranial pressure (ICP) in response to the injury. After the initial increase in BP and ICP, the BP decreased and stabilized at a value which was approximately 20 mmHg below the preinjury values, and ICP plateaued at an average value of 20 mmHg, compared with 8 mmHg in the sham-injured animals. This provided an average cerebral perfusion pressure of 40-50 mmHg, compared with 65-75 mmHg for the sham-injured animals. These values were relatively constant for the remainder of the 3-h monitoring period. The NO values also stabilized during this time period. By 1 h after the impact injury the NO concentration measured directly using the NO electrode had decreased from baseline values by an average value of 25 +/- 6 nM. NO concentration remained significantly lower than baseline values throughout the remainder of the 3-h monitoring period. The concentration of nitrate/nitrite in the dialysate fluid also decreased by an average value of 341 +/- 283 nM 20-40 min after the injury. Dialysate nitrite/nitrate concentrations remained less than the preinjury baseline values throughout the remainder of the 3-h monitoring period. Preinjury treatment with L-nitro-arginine methyl ester (L-NAME) blunted the injury-induced increase in NO and resulted in more severe immediate intracranial hypertension and more severe systemic hypotension at one hour after injury. Mortality was also 67% with L-NAME pretreatment, compared with 1% in untreated animals.

Animals↗
PubMed1999

Cerebral hemodynamic effects of phenylephrine and L-arginine after cortical impact injury.

OBJECTIVE: To determine the effects of a pressor agent (phenylephrine and L-arginine) on the abnormal cerebral hemodynamics and on neurologic outcome after a severe cortical impact injury in rats. DESIGN: Prospective, randomized study. SETTING: University laboratory. SUBJECTS: Male Long-Evans rats, weighing 300 to 400 g, fasted overnight. INTERVENTIONS: The animals were anesthetized with isoflurane, and a severe cortical impact injury (velocity, 5 m/sec; deformation, 3 mm) was produced in the right parietal cortex. Five minutes after impact injury, one of the following three treatments were infused: 1 mL saline intravenously for 10 mins, 300 mg/kg L-arginine in 1 mL saline intravenously for 10 mins, or 0.3 microg/kg/min phenylephrine intravenously for 3 hrs. Mean arterial pressure, intracranial pressure (ICP), cerebral perfusion pressure (CPP), and laser Doppler flow (LDF) at the impact site and in the contralateral parietal cortex were monitored for 3 hrs after the impact injury. Histologic examination of the brain was performed at 2 wks after injury in a separate group of L-arginine- and saline-treated animals. MEASUREMENTS AND MAIN RESULTS: The immediate response to the impact injury was an increase in ICP, and a decrease in mean arterial pressure, CPP, and LDF. In the saline-treated animals, LDF decreased to <25% of the baseline values at the impact site and stayed at that level for the entire 3-hr monitoring period. On the contralateral side, LDF decreased initially and recovered gradually to approximately 50% of the preimpact baseline value. Infusion of both phenylephrine and L-arginine increased LDF back to near-baseline levels. However, phenylephrine increased ICP significantly, whereas ICP with L-arginine did not change. L-arginine treatment reduced the contusion volume from a median value of 5.28 mm3 to 0.63 mm3. CONCLUSIONS: Phenylephrine increased cerebral blood flow (CBF) by increasing CPP. L-arginine, however, increased CBF without changing CPP. The improvement in CBF was accompanied by a decrease in neurologic injury. Although the pressor agents are used currently to increase CBF after traumatic brain injury, other strategies may also increase CBF without the potential adverse effects of induced hypertension.

Animals↗
PubMed1999

Minor psychiatric morbidity in South African secondary school pupils.

This study investigated minor psychiatric morbidity ("neurotic": anxiety and depression symptoms) in rural (Black) South African secondary school pupils. The sample included 622 Grade 11 pupils (254 boys and 368 girls) in the age range of 17 to 24 years with a mean age of 19.3 yr. The inventories used were a questionnaire on the socioeconomic and family background, a Cultural Orientation Scale, a Student Stress Scale, a General Self-efficacy Scale, a Perceived Stress Scale, and the Self-reporting Questionnaire-20. The findings are that 12.6% of the pupils had a possible clinically significant psychological disorder. Contributing factors identified were interpersonal, study, finance, illness, perceived stress, low self-efficacy, and low religious orientation.

Adolescent↗
PubMed1998

Effect of glucose administration on contusion volume after moderate cortical impact injury in rats.

Previous studies had shown that pre- and postinjury glucose administration increased brain injury caused by a mild cortical impact injury only when the traumatic injury was complicated by a secondary ischemic insult. The purpose of this study was to examine the effect of pre- and postinjury glucose administration on a more severe cortical impact injury, where primary ischemia occurs at the site of the impact. Long Evans rats who were fasted overnight and anesthetized with isoflurane were subjected to a 5-m/sec, 2.5-mm impact injury. The animals were randomly assigned one of the following treatments: (1) 2.2 g/kg glucose in 4 ml of saline, 20 min prior to injury; (2) 2.0 g/kg glucose in 4 ml of saline, 20 min after injury; or (3) 4 ml of saline either 20 min before injury or 20 min after the injury. At 2 weeks, the animals were sacrificed and the brains were examined for contusion volume and for neuronal loss in CA1 and CA3 regions of the hippocampus. Contusion volume was increased from a median value of 23 mm3 in the saline-infused animals to 34 mm3 in the preimpact glucose infusion animals (p=0.005). Postimpact glucose infusion had no effect on contusion volume. Neuron density in CA1 and CA3 regions of the hippocampus was similar in all three treatment groups. These studies support the hypothesis that glucose administration adversely affects experimental traumatic brain injury in those circumstances where the trauma is complicated by primary cerebral ischemia, such as around cortical contusions.

Animals↗
PubMed1998

Hyperglycemia increases neurological damage and behavioral deficits from post-traumatic secondary ischemic insults.

The effects of post-traumatic administration of glucose 2.0 g/kg was compared to saline infusion with and without control of brain temperature at 37 degrees C on behavioral and histological measures of brain injury after controlled cortical impact injury complicated by a secondary ischemic insult. The glucose infusion increased blood glucose concentration from 114 +/- 4 to 341 +/- 76 mg/dl prior to the secondary ischemic insult. The resulting outcome measures were significantly worse in the glucose infusion group than in either control group. Mortality rate was significantly increased by the glucose administration, from 0% to 55% (p < 0.001). The median contusion volume was increased from 7.9 to 64.2 by glucose administration (p < 0.001) and the neuronal loss in the CA1 and CA3 areas of the hippocampus were greater in the glucose infusion group. In the animals that survived for the 2 weeks of behavioral studies, the duration of beam balance was shorter; the percent of animals that could balance on the beam for at least 60 s was less, the percent of animals that could perform the beam-walking task was less, and the length of time required to find the platform in the Morris water maze task was longer in the glucose infusion group. These studies demonstrate that the infusion of glucose after the cortical impact injury significantly increases the damage caused by post-traumatic ischemic insults. The adverse effect on neurological outcome could not be explained by the temperature effects of glucose infusion.

Animals↗
PubMed1998

Endothelial-mediated dilations following severe controlled cortical impact injury in the rat middle cerebral artery.

The mechanisms associated with dysfunction of the cerebral vasculature following head trauma have not yet been fully elucidated. In an attempt to shed more light on the matter, we investigated the endothelial-mediated dilations in the rat middle cerebral artery (MCA) following severe traumatic brain injury (TBI). Rats were subjected to severe controlled cortical impact injury (CCI; 5 m/s, 130 ms duration, 3 mm deformation) over the right parietal cortex. At 24 h postinjury, ipsilateral segments of MCA and corresponding contralateral segments were isolated, mounted in a vessel chamber, and pressurized. The responses to 2 methylthio-ATP (2MeSATP), a selective agonist for the P2Y1 purinoceptors, N(omega)-nitro-L-arginine (L-NAME), an NO synthase inhibitor, and S-nitroso-N-acetylpenicillamine (SNAP), an exogenous NO donor, were determined. 2MeSATP elicited concentration dependent dilations in all MCAs studied. Ipsilateral MCAs harvested following TBI or sham-TBI, showed similar maximum dilations to 2MeSATP [70 +/- 4% (n = 17) and 72 +/- 6% (n = 13), respectively]. However, TBI reduced the concentration of 2MeSATP necessary to elicit one-half of the maximum dilation (EC50) from 15 to 9 nM (p < 0.05). Inhibition of NO synthase with 10(-5) M L-NAME abolished the dilation to 2MeSATP in both TBI and sham-TBI MCAs. The constriction to L-NAME was significantly reduced in TBI MCAs compared to sham vessels. Dilations to SNAP, an NO donor, were not altered by TBI indicating that the mechanisms of dilation involving NO in the vascular smooth muscle were not affected. Unlike other pathological conditions which often diminish endothelial-mediated responses, severe TBI enhanced the sensitivity to 2MeSATP without altering the maximum response.

Adenosine Triphosphate↗
PubMed1998

University students' adjustment problems.

Considerable information is available on the adjustment problems of first-year university students in developed countries, but comparatively little is known about such problems in Asia and Africa. This study of a representative sample of 1257 first-year students conducted at the University of the North showed that 33 to 85% of the first-year students experienced various adjustment problems.

Adaptation, Psychological↗
PubMed1998

AIDS awareness of secondary school pupils in the northern province of South Africa.

This study investigated AIDS awareness in secondary school pupils (mainly Northern Sotho and Xitsonga) in the Northern Province of South Africa. The randomly chosen sample included 622 Standard 9 pupils (254 boys and 368 girls) in the age range of 17 to 24 years (M of 19.3), who were administered a questionnaire on awareness of AIDS and socioeconomic status. Over 72% of the questions about AIDS were correctly answered, which suggests a fair amount of accurate information about AIDS; however, 18% were of the opinion that "AIDS does not exist" and 19% that "there is a cure for AIDS." Analysis of variance indicated no relationships for sex, age, ethnicity, or socioeconomic status with correct answers.

Acquired Immunodeficiency Syndrome↗
PubMed1998

Brain fag symptoms in rural South African secondary school pupils.

The study investigated brain fag symptoms in rural South African Secondary School pupils. The sample included 622 Grade 11, Secondary School pupils in the age range of 17 to 24 years (M age 19.3 yr., SD = 2.6) chosen at random from schools throughout the Northern Province of South Africa. A Cultural Orientation Scale, a Student Stress Scale, a General Self-efficacy Scale and Self-reporting Questionnaire were administered to collect data on socioeconomic status, cultural orientation, stress events, self-efficacy, perceived stress, "neurotic" disorder, and brain fag symptoms. Analysis indicated that 25% of the pupils suffered from the brain fag symptoms. There were positive significant relations for collectivism, socioeconomic status, female birth order, depression score on the Self-reporting Questionnaire, total score but not the anxiety score of the questionnaire with brain fag symptoms. This suggests the brain fag syndrome is basically a depressive disorder and to some extent an anxiety and depressive disorder. The findings are discussed in relation to the nature of brain fag symptoms, precipitating factors, and socioeconomic status.

Adolescent↗
PubMed1998

Attitudes toward suicide among South African secondary school pupils.

This study investigated attitudes towards suicide among 622 Standard 9 (U.S. Grade 11) secondary school pupils chosen at random from schools throughout the Northern Province in South Africa. The pupils were 254 (41%) boys and 368 (59%) girls in the age range of 17 to 24 years, with a mean age of 19.3 yr. A questionnaire was administered to obtain data on attitudes and other measures. There were 31 (17%) parasuicidal boys and 34 (13%) girls. Major intentions or reasons to commit suicide mentioned were "failing to solve problems" and "mental illness." Most frequent possible suicide methods were firearms, pills, or poison. Significant associations were found with having a friend or relative who committed suicide, parasuicide (oneself), depression, stress events, ethnicity, and attitudes towards suicide.

Adolescent↗
PubMed1998

The factor-structure of the Self Reporting Questionnaire (SRQ-20) in South Africa.

This study investigated the factor structure of the Self Reporting Questionnaire (SRQ-20) on a sample of 624 standard nine (Grade 11) school pupils selected at random from the Northern Province of South Africa. Factor analysis technique was used to extract the factors of the SRQ-20. The findings which indicate the extraction of four factors; (i) anxiety-depression; (ii) depression; (iii) anxiety and; (iv) somatic complaints are discussed in relation to previous studies.

Adolescent↗
PubMed1997

Hyperglycemia increases brain injury caused by secondary ischemia after cortical impact injury in rats.

OBJECTIVE: To examine the effects of glucose infusion on the histologic brain damage caused by controlled cortical impact injury alone and by cortical impact injury complicated by secondary ischemia. DESIGN: Prospective, randomized study. SETTING: University laboratory. SUBJECTS: Male Long-Evans rats. INTERVENTIONS: Three experimental conditions were studied: a) 2.5-mm deformation impact (velocity 4 m/sec) injury followed by 40 mins of bilateral carotid occlusion; b) sham impact injury followed by 40 mins of bilateral carotid occlusion; and c) 2.5-mm deformation impact (velocity 4 m/sec) injury followed by sham carotid occlusion. For each experimental condition, animals were randomized to receive either glucose solution or saline solution before the induced injury and the sham impact injury. Contusion volume and neuron density in the CA1 and CA3 regions of the hippocampus were measured 2 wks after the injury. MEASUREMENTS AND MAIN RESULTS: Parenteral administration of 2.2 g/kg glucose solution increased the blood glucose concentration from 6.7 +/- 3.3 to 17.9 +/- 10.6 mmol/L before the impact injury, and to 12.3 +/- 5.6 mmol/L before carotid occlusion. Hyperglycemia had the greatest effect on the consequences of the impact injury complicated by secondary ischemia, increasing contusion volume from 1 to 30.6 mm3 in the animals that received saline or glucose solution, respectively (p = .005), and reducing the density of normal appearing neurons in the CA1 area of the hippocampus from 201 to 144 cells/mm2 in the animals that received saline solution and glucose solution, respectively (p = .038). The impact injury alone and bilateral carotid occlusion alone caused minimal neuronal loss in the hippocampus and minimal contusion or infarction at the impact site. Individually, these mild injuries were not adversely affected by infusion of glucose solution. CONCLUSION: Hyperglycemia increases brain damage when traumatic brain injury is complicated by secondary ischemia.

Animals↗
PubMed1996

Secondary insults increase injury after controlled cortical impact in rats.

Secondary ischemic insults are common after severe head injury and contribute to poor neurological outcome. To study the increased vulnerability of the traumatized brain to secondary insults, bilateral carotid occlusion was produced after a controlled cortical impact injury in rats. The injury produced by either the impact injury or the bilateral carotid occlusion was mild to moderate when studied individually. The 1 and 3 m/sec impact injuries alone caused no detectable contusion at the impact side and minimal neuronal loss in the hippocampus. The 5 m/sec impact injury alone resulted in a small contusion with a median volume of 5.4 mm3. The 40-min period of bilateral carotid occlusion alone caused no cortical injury and no neuronal loss in the CA1 region of the hippocampus. When the 40 min of bilateral carotid occlusion was produced 1 h after the impact injury, there was an increase in the damage produced. The contusion volume was significantly larger after the 3 and 5 m/sec impact injuries and the hippocampal neuronal loss was significantly greater after the 1 and 3 m/sec impact injuries. When varying durations of bilateral carotid occlusion were produced 1 h after a 3 m/sec impact injury, contusion volume was significantly larger after bilateral carotid occlusion duration of 40 min, and CA1 neuronal loss was significantly greater after bilateral carotid occlusion durations of 30 and 40 min. When 40 min of bilateral carotid occlusion was produced at different time intervals after a 3 m/sec injury, the increased contusion volume was maximal when bilateral carotid occlusion occurred at 4 h after the impact injury, and the increased neuronal loss in the CA3 region of the hippocampus was maximal when bilateral carotid occlusion occurred at 1 h after the impact injury. By 24 h after the impact injury, 40 min of bilateral carotid occlusion had minimal consequences, similar to the effect in sham-injured animals. These results mimic the clinical situation where secondary insults of a severity that would not cause permanent neurological damage in a normal person are associated with a marked worsening of neurological outcome after head injury and where the injured brain is most susceptible to secondary insults in the first few hours after injury.

Animals↗
PubMed1996

Activation of ornithine decarboxylase and accumulation of putrescine after traumatic brain injury.

Activation of ornithine decarboxylase (ODC), the initial enzyme in polyamine synthesis, and accumulation of putrescine are thought to mediate pathological processes in the ischemic and traumatized brain. Past studies have separately investigated either ODC or polyamines after head injury. The purpose of the present study was to quantify both ODC activity and polyamines in the rat parietal cortex before and after controlled cortical impact injury. Adult, male rats underwent a right craniectomy and were subjected to a 5 m/sec, 2-mm deformation impact injury. Rats were sacrificed 1, 4, 8, and 24 h postimpact and tissues from the injured (right) and contralateral (left) hemisphere were analyzed for ODC and polyamines. ODC activity was determined by measuring the decarboxylation of [14C]ornithine to putrescine. Putrescine, spermidine, and spermine were determined by high performance liquid chromatography. Cortical impact induced a 10- to 20-fold increase in ODC activity and a 4- to 5-fold increase in putrescine in the ipsilateral cortex. Spermidine and spermine did not significantly increase in the ipsilateral (right) cortex compared to controls (right cortex). In contrast, there was a slight increase in spermidine content in the contralateral (left) cortex after injury. The delayed increase in ODC activity and accumulation of putrescine may mediate pathophysiological changes observed after head injury.

Animals↗
PubMed1996

Ileal inhibition and modulation of carbachol-stimulated proximal small intestinal motor functions in humans.

Carbohydrates within the distal small intestine inhibit endogenously stimulated proximal gastrointestinal motor activity and induced an interdigestive-like pattern in humans. In order to further investigate the intermediary mechanisms of the ileal inhibitory effects, we intubated eight healthy volunteers with an oroileal multilumen tube and stimulated small intestinal motility exogenously with a continuous intravenous infusion of the cholinergic agonist carbachol. Additionally, the ileum was perfused for 15-min intervals with either carbohydrates (total load: 18 g) or normal saline as volume control. Ileal carbohydrate perfusion inhibited the carbachol-stimulated motility pattern significantly (p < 0.001) and induced phase-III-like motor activity; ileal saline had no effect. These data suggest that a direct inhibition of cholinergic systems may be involved in the ileal inhibitory effects on proximal small intestinal motility.

Adult↗
PubMed1996

Changes in phospholipids and acetylcholinesterase during early phase of injury to spinal cord--an experimental study in rats.

Injury to spinal cord was produced in rats by the clip compression technique by placing the aneurysm clip extradurally for 30 seconds. The traumatised spinal segment and the adjoining upper segment were used for biochemical estimations. Motor function of the injured rats was evaluated using the inclined plane. Phospholipid phosphorus values were significantly decreased in the injured spinal segment at 24 hrs. AchE activity was also decreased in the traumatised segment one week after injury. Dexamethasone and verapamil reversed the changes in AchE activity at the end of one week. At the one week assessment period, aneurysm clipped rats showed a decrease in the maximum angle in the inclined plane. Dexamethasone and verapamil treated rats showed improvement in the neurologic function, neurologic recovery was better in the dexamethasone treated group.

Acetylcholinesterase↗