Status of glaciers and climate change of East Karakoram in early twenty-first century.

This study aims to assess the glaciers change status in Shyok basin, East Karakoram in terms of area and mass balance, and to ascertain if glaciers in this part of Karakoram also display similar anomaly like central or western counterparts. The spatio-temporal monitoring of glaciers during the time frame of 24 years (1990/2000/2014) suggests major percentage of stable glaciers and insignificant retreat in the total glaciated area. The percentage of retreating glaciers has increased after year 2000. Area change analysis of glaciers having size >1 km2 (569 glaciers) suggests the number of fluctuated glaciers have substantially increased i.e. overall 56% glaciers remained stable, 35% retreated and 9% advanced during 1990-2014. The geodetic based findings using SRTM-C (2000) and Cartosat-1 (2010/2011/2014) stereo-imageries for 201 glaciers suggest the mass loss at the rate of -0.10 ± 0.07 m w.e. a-1. To better apprehend the status of glaciers changes in the region, climatic studies using in-situ observations as well as reanalysis dataset (ERA-I) were also undertaken of past 30 years. Therefore, this study is also a maiden attempt to ascertain if along with Karakoram anomaly, a climatic anomaly exists in the Eastern parts of Karakoram or not. A long term field collected snow-meteorological data of East Karakoram region suggests overall warming trend in annual temperature and no trend for snowfall during 1985-2015. The statistically significant increased rates of warming and decreased snowfall after year 2000 support the spatial variations in glaciers of East Karakoram and marginal mass loss. The observations of the marginal mass loss along with warming temperatures indicate that no Karakoram or climatic anomaly is existent over the East Karakoram region. Our study further refutes the prevalence of the elevation-dependent warming (EDW) over East Karakoram region vis-à-vis North-West Himalayan ranges. The impact of hiatus in global warming was also not observed over studied region.

Bacterial isolates and its antibiotic susceptibility pattern in NICU.

BACKGROUND: Neonatal sepsis is one of the major causes of morbidity and mortality among the newborns in the developing world. OBJECTIVES: To determine the common bacterial isolates causing sepsis in neonatal intensive care unit and its antibiotic susceptibility pattern. METHODS: A one year discriptive prospective study was conducted in neonatal intensive care unit to analyse the results of blood culture and to look into the sensitivity of the commonly used antibiotics. RESULTS: The blood culture yield by conventional method was 44.13% with nosocomial sepsis accounting for 10.79%. 84.08% were culture proven early onset sepsis and 15.95% were late onset sepsis. Klebsiella infection was the commonest organism isolated in early, late and nosocomial sepsis but statistically not significant. Gram positive organisms were 39.36% in which Staphylococcus aureus was the leading microorganism followed by coagulase negative staphylococcus areus. Gram negative organisms were 60.64% amongst them Klebsiella was the most often encountered followed by Pseudomonas. The most common organism Klebsiella was 87.5% and 78.3% resistance to ampicillin and gentamycin respectively. Among gram negative isolates 87.5% and 77.2% were resistance to ampicillin and gentamycin respectively. Among gram positive isolates 58.5% and 31.5% resistance were noted to ampicillin and gentamycin respectively. Resistance to cefotaxim to gram negative and gram positive isolates were 87.34% and 59.35% respectively. CONCLUSION: Klebsiella is most common organism which is almost resistance to first line antibiotics. Resistance to both gram negative and gram positive isolates among firstline antibiotics and even with cefotaxim is emerging and is a major concern in neonatal intensive care unit.

Propagation of Turing patterns in a plankton model.

The paper is devoted to a reaction-diffusion system of equations describing phytoplankton and zooplankton distributions. Linear stability analysis of the model is carried out. Turing and Hopf stability boundaries are found. Emergence of two-dimensional spatial structures is illustrated by numerical simulations. Travelling waves between various stationary solutions are investigated. Transitions between homogeneous in space stationary solutions and Turing structures are studied.

Scenario of extrapulmonary tuberculosis in a tertiary care center.

BACKGROUND: Tuberculosis is a worldwide disease and one of the major health problems of Nepal. Extrapulmonary tuberculosis is increasing all over the world. The main aim of this study was to assess the frequency of extrapulmonary tuberculosis in various organ systems of the body and to assess the pattern of disease in different age groups and gender. METHODS: This observational retrospective study was carried out from December 2003 to October 2009 at the Department of Pathology, Kathmandu University Hospital, Kavre, Nepal. A total of 259 extrapulmonary tuberculosis cases diagnosed by fine needle aspiration cytology and biopsy were included. Frequency of extrapulmonary tuberculosis in the lymph nodes in relation to age and sex were studied. RESULTS: Lymph nodes tuberculosis was present in 179 (69.11%) cases. Among all extrapulmonary tuberculosis, 132 (50.56%) cases were in males and 127 (49.04%) were in females. Out of total 179 tuberculosis of lymph nodes, 116 (74.35%) were seen in age group of 25 years and above (p=0.018) and 86 (48.04%) in males and 93 (51.95%) in females (p=0.18). CONCLUSIONS: Extrapulmonary tuberculosis is common in lymph nodes, equally in both sexes and more in age group of 25 and above. Therefore, this age group should be focused upon more for investigation and management of extrapulmonary tuberculosis.

Laser Raman spectroscopy of THF clathrate hydrate in the temperature range 90-300 K.

In situ Raman and Fourier transform infrared (FTIR-NIR) spectroscopic studies on tetrahydrofuran (THF-C(4)H(8)O) clathrate hydrate (CH) were reported. The Raman results in lattice (64 cm(-1)), ring breathing and C-H stretching mode regions are in conformity with earlier reports, while the FTIR (NIR) studies in second order mode region were reported for the first time. Comparison of the results indicate that the band assigned to ring breathing mode around 922 cm(-1) (in Raman) and corresponding second order mode in NIR around 4295 cm(-1) broadens and shifts in enclathrated THF. The ring breathing mode at lower temperatures (T<120 K) is highly asymmetric and splits into two and are due to different host-guest interactions at lower temperatures.

Cerivastatin, a hydroxymethylglutaryl coenzyme a reductase inhibitor, improves endothelial function in elderly diabetic patients within 3 days.

BACKGROUND: The short-term effects of hydroxymethylglutaryl coenzyme A reductase inhibitors (statins) on endothelial function at doses that do not affect plasma lipid levels are not known. METHODS AND RESULTS: We investigated the short-term effects of cerivastatin, a hydroxymethylglutaryl coenzyme A reductase inhibitor, on endothelial function and endothelium-related products in elderly diabetic patients. Twenty-seven elderly diabetic patients (aged 69.3+/-3.4 years), with or without mild hypercholesterolemia, were enrolled in this study, which tested cerivastatin treatment (0.15 mg/d) for 3 days. Endothelium-dependent flow-mediated dilatation, endothelium-independent dilatation by nitroglycerin in the brachial artery, nitric oxide-related products (nitrite/nitrate and cGMP), endothelium-related products (von Willebrand Factor, soluble vascular cell adhesion molecule-1, and soluble intercellular adhesion molecule-1), and a marker of oxidant stress (8-isoprostane) were assessed. Levels of plasma lipids were not changed before and after treatment with cerivastatin. Flow-mediated dilatation was significantly increased by cerivastatin treatment, as were plasma nitrite/nitrate levels (from 16.9+/-3.4 to 22.0+/-3.7 micromol/L, P<0.05) and cGMP values. The percent of nitroglycerin-induced dilatation was not changed. Plasma concentrations of 8-isoprostane decreased, and levels of soluble vascular cell adhesion molecule also tended to decrease with cerivastatin. CONCLUSIONS: Improvement of endothelial function was in line with antiatherosclerotic effects. Cerivastatin improved impaired endothelial function in the short-term without affecting lipid profiles in elderly diabetic patients. This effect may be partly due to upregulation of endothelial nitric oxide synthase.

HMG-CoA reductase inhibitor stabilizes rabbit atheroma by increasing basal NO and decreasing superoxide.

Male rabbits fed a 0.5% cholesterol diet for 8 wk were divided into three groups. Group 1 was hypercholesterolemic; group 2 was fed a regular diet for an additional 12 wk; and group 3 was fed a regular diet with simvastatin (5 mg x kg(-1) x day(-1)). Simvastatin treatment reduced the atherosclerotic area and total and esterified cholesterol concentrations in the thoracic aorta. Tone-related basal nitric oxide (NO) release was highest in group 3. Acetylcholine-induced, NO-dependent relaxation was improved in group 3 compared with group 2. Amount of endothelial nitric oxide synthase (eNOS) mRNA in vessels increased in group 1, compared with normal aorta, and decreased in group 2; however, it did not decrease in group 3. The amount of O released from vessels increased in group 1 and group 2 compared with normal rabbits; however, it decreased in group 3, especially in the endothelial cells. Peroxynitrite determined by nitrotyrosine staining decreased in group 3. Additionally, the arteries of rabbits fed a regular diet with or without simvastatin were investigated. The aorta from simvastatin-treated group showed increase of tone-related basal NO release and eNOS mRNA and decrease of O release. Taken together, upregulation of eNOS and decrease of O treatment were observed in vivo in the process of the sufficient stabilization of atheroma following simvastatin.

A HMG-CoA reductase inhibitor possesses a potent anti-atherosclerotic effect other than serum lipid lowering effects--the relevance of endothelial nitric oxide synthase and superoxide anion scavenging action.

We have determined whether the anti-atherosclerotic effect of a 3-hydroxy-3-methyl-glutaryl-CoA (HMG-CoA) reductase inhibitor (fluvastatin) is mediated through nitric oxide (NO) as well as affecting plasma lipids. NO related vascular responses, endothelial nitric oxide synthase (eNOS) mRNA and superoxide anion (O(2)(-)) release were examined in vascular walls of oophorectomized female rabbits fed 0.5% cholesterol chow for 12 weeks with or without fluvastatin (2 mg/kg per day). Serum lipid profile was not different between two groups. NO dependent responses stimulated by acetylcholine and calcium ionophore A23187 and tone related basal NO response induced by N(G)-monomethyl-L-arginine acetate (L-NMA); nitric oxide synthase inhibitor were all improved by fluvastatin treatment. Endothelium independent vasorelaxation induced by nitroglycerin was not different between the two groups of rabbits' arteries. Fluvastatin treatment increased cyclic GMP concentration in aorta of rabbits. eNOS mRNA expression and O(2)(-) release were measured in aorta using competitive reverse transcription-polymerase chain reaction (RT-PCR) and with lucigenin analogue, 2-methyl-3,7-dihydroimidazol [1,2-a]pyrazine-3-one (MCLA) chemiluminescence methods. eNOS mRNA in the endothelial cells of aorta was significantly up-regulated and O(2)(-) production was significantly reduced in fluvastatin treated rabbit aorta. Anti-macrophage staining area, but not anti-smooth muscle cell derived actin stained area in the aorta was also reduced by fluvastatin treatment. Conclusion, fluvastatin, a HMG-CoA reductase inhibitor, retards the initiation of atherosclerosis formation through the improvement of NO bioavailability by both up-regulation of eNOS mRNA and decrease of O(2)(-) production in vascular endothelial cells, and this means that part of the anti-atherosclerotic effect of fluvastatin may be due to nonlipid factors.

Up-regulation of endothelial nitric oxide synthase through beta(2)-adrenergic receptor--the role of a beta-blocker with NO-releasing action.

We determined the existence and role of beta(2)-adrenergic receptor in cultured BAECs through the effect of a beta-blocker having NO releasing action; 3,4-dihydro-8(2-hydroxy-3-isopropylamino)-propoxy-3-nitroxy-2H-1-benzopyran; nipradilol on eNOS and eNOS regulatory protein caveolin-1. beta(2) receptor exists in BAECs. eNOS mRNA and protein were up-regulated by its treatment whereas those of caveolin were not altered considerably. This eNOS up-regulatory action was abolished by beta(2) receptor antagonist, ICI-118551. Increase of NO metabolites, protein and mRNA of eNOS was also partially inhibited by co-treatment of NOS inhibitor, L-NA with nipradilol. This is the first investigation of the action of non-selective beta blocker on eNOS through beta(2) receptor. The drug increases NO on incubation with BAECs about 50% as a NO donor and about 50% as results of eNOS up-regulation.

Inhibition of inducible nitric oxide synthase gene expression by indomethacin or ibuprofen in beta-amyloid protein-stimulated J774 cells.

Recent studies show that a mononuclear phagocyte lineage, including microglia, plays a possible role in the pathogenesis of Alzheimer's disease through nitric oxide (NO)-mediated neurotoxicity. Epidemiological studies show that nonsteroidal anti-inflammatory drugs (NSAIDs) have a protective effect against Alzheimer's disease. Based on these observations, it has been hypothesized that an anti-Alzheimer's disease effect of NSAIDs could result from the inhibition of NO synthesis. We report here that indomethacin or ibuprofen dose-dependently reduce beta-amyloid protein and interferon-gamma-induced NO production, accompanied by an inhibition of inducible nitric oxide synthase mRNA expression in J774 cells, a murine macrophage cell line. Aspirin, however, does not produce such an effect, suggesting that the cyclooxygenases pathway is not involved in the inhibitory effects of NSAIDs on beta-amyloid protein and interferon-gamma-induced NO production in J774 cells.

Physiological concentration of 17beta-estradiol retards the progression of severe atherosclerosis induced by a high-cholesterol diet plus balloon catheter injury: role of NO.

The molecular mechanisms of the antiatherosclerotic effects of estrogen are not yet known. We evaluated the effects of 17beta-estradiol (E(2)) on high cholesterol diet- (HCD; standard diet and 1% cholesterol) and balloon injury-induced atherosclerosis in female New Zealand White rabbits. The abdominal aortas of 40 oophorectomized (Groups 1 through 5) and 8 nonoophorectomized (Group 6) rabbits were injured by balloon catheter, and the animals were then divided into the following groups and treated for 10 weeks: Group 1, standard diet; Group 2, standard diet plus a moderate dose of E(2) (100 microg x kg(-1) x d(-1)); Group 3, HCD; Group 4, HCD plus a moderate dose of E(2); Group 5, HCD plus a low dose of E(2) (20 microg x kg(-1) x d(-1)); and Group 6, HCD in nonoophorectomized rabbits. After the treatment phase, plasma E(2) was increased up to 282.2+/-45.5 pg/mL in Group 2, 263.0+/-41.5 pg/mL in Group 4, 87. 9+/-18.8 pg/mL in Group 5, and 45.6+/-7.3 pg/mL in Group 6. HCD-mediated increases in plasma lipid levels were not changed by E(2) treatment, whereas E(2) decreased the aortic intimal thickening in Group 2 animals compared with those in Group 1 and reduced atherosclerosis in the thoracic and abdominal aortas of Group 4, 5, and 6 rabbits compared with those in Group 3. E(2) restored the impaired abdominal aortic endothelium-dependent relaxation of balloon-injured and HCD-supplemented rabbits, and E(2) increased basal nitric oxide (NO) release. The basal NO-releasing effect showed a significant, inverse relation with the severity of atherosclerosis. Plasma E(2) concentration also showed a significant, inverse relation with atherosclerotic area. In conclusion, physiological concentrations of E(2) can retard the progression of severe atherosclerosis and stabilize atheromas induced by HCD and balloon injury. The retardation may be partially mediated by endothelial NO function in vessels treated with E(2).

Dehydroepiandrosterone retards atherosclerosis formation through its conversion to estrogen: the possible role of nitric oxide.

Dehydroepiandrosterone (DHEA) is speculated to have an antiatherosclerotic effect, although the mechanism of action remains unclear. The objective of the current study was to determine whether the antiatherosclerotic effect of DHEA is related to its conversion to estrogen and to define the role of nitric oxide (NO) in the antiatherosclerotic effect of DHEA. Forty-eight oophorectomized rabbits were divided into 5 groups and fed the following diets for 10 weeks: group 1, a regular rabbit diet plus 1% cholesterol (a high-cholesterol diet [HCD]); group 2, an HCD plus 0.3% DHEA; group 3, an HCD plus 0.3% DHEA and fadrozole (2.0 mg x kg(-1) x d(-1)), a specific aromatase inhibitor; group 4, an HCD plus 17beta-estradiol (20 microg x kg(-1) x d(-1)); and group 5, a regular diet. Atherosclerotic lesions, lipid deposition in aortic vessels, and basal and stimulated NO release were measured in the aforementioned groups of rabbits. NO release was measured by using an NO-selective electrode as well as by measuring vascular responses and the plasma NO metabolites nitrite and nitrate. The plasma total cholesterol level was increased, but there were no significant differences in lipid profile in the 4 groups of rabbits that were fed the HCD. The area occupied by atherosclerosis in the thoracic aorta was diminished by approximately 60% in the DHEA-treated rabbits (group 2) compared with the HCD group of rabbits (group 1); there was a corresponding 80% decrease in the estradiol group (group 4) but only a 30% decrease in the DHEA plus fadrozole group (group 3). In the aortas of rabbits from groups 1 and 3, the acetylcholine-induced and tone-related basal NO-mediated relaxations were diminished compared with those of the controls (group 5). However, these relaxations were restored in the aortas of group 2 and 4 rabbits, and an increase in NO release was observed in groups 2 and 4 compared with groups 1 and 3, as measured by an NO-selective electrode. Injection of neither solvent (20% ethanol/distilled water) nor fadrozole significantly affected the atherosclerotic area or the NO-related responses described above. We conclude that approximately 50% of the total antiatherosclerotic effect of DHEA was achieved through the conversion of DHEA to estrogen. NO may also play a role in the antiatherosclerotic effect of DHEA and 17beta-estradiol.

A HMG-CoA reductase inhibitor improved regression of atherosclerosis in the rabbit aorta without affecting serum lipid levels: possible relevance of up-regulation of endothelial NO synthase mRNA.

We determined the role of Fluvastatin: HMG-CoA reductase inhibitor on the regression of atherosclerosis following removal of dietary cholesterol. Male rabbits fed a 0.5% cholesterol diet for 12 weeks were divided into three groups: A1, hypercholesterolemic; A2, fed a regular diet for an 12 additional weeks; and A3, fed a regular diet with fluvastatin (2 mg/kg/day). Fluvastatin treatment (A3) did not affect serum lipid levels compared with A2. However, it decreased the atherosclerotic area in the aortic arch and decreased total and esterified cholesterol concentrations in the descending aorta. Tone-related basal NO release in the thoracic aorta was larger in A3 than in A2. eNOS mRNA in vessel was determined by competitive RT-PCR assay. It increased in A1, compared with normal aorta and decreased in A2; however, it did not decrease in A3. This is the first report of a decrease in eNOS mRNA in atherosclerosis after removal of dietary cholesterol and a reversal of it by a HMG-CoA reductase inhibitor, which may contribute to the regression of atherosclerosis.

Oligofurostanosides and oligospirostanosides from roots of Asparagus filicinus.

The ethanolic extract roots of Asparagus filicinus contains a complex mixture of steroidal saponins, from which two oligospirostanosides (Filicinins A and B) and two oligofurostanosides (Filicinosides C and D) were characterized.

Furostanosides from Asparagus filicinus roots.

Two furostanosides have been isolated from an ethanolic extract of the roots of Asparagus filicinus and identified as 3-O-beta-D-glucopyranosyl-26-O-beta-D-glucopyranosyl-22-alpha-methoxy-(2 5S), 5 beta-furostan-3 beta, 26-diol (filicinoside-A) and 3-O-beta-D-glucopyranosyl-26-O-beta-D-glucopyranosyl-25S), 5 beta-furostan-3 beta, 22 alpha, 26-triol (filicinoside-B).

Spawning behaviour of an air-breathing catfish Heteropneustes fossilis (Bloch).

Spawning behavior of H. fossilis was studied by breeding the fish in laboratory through hypophysation using pituitary glands of the Indian major carps (Catla catla and Labeo rohita) at a dose of about 15 mg/100 g body weight of the recipient. The spawning activity started about 6 to 10 hr after the administration of pituitary injection. The activity lasted 2 to 6 hr in various experiments. During this period, intermittent mating acts were observed, the average rate of mating being once every 2 to 3 min in the initial stages and 5 to 10 min or even longer in the later ones.