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We present photometry and spectroscopy of the peculiar Type II supernova SN 2010jp, also named PTF10aaxi. The light curve exhibits a linear decline with a relatively low peak absolute magnitude of only −15.9 (unfiltered), and a low radioactive decay luminosity at late times that suggests a low synthesized nickel mass of about 0.003 M⊙ or less. Spectra of SN 2010jp display an unprecedented triple-peaked Hα line profile, showing: (1) a narrow central component that suggests shock interaction with a dense circumstellar medium (CSM); (2) high-velocity blue and red emission features centered at −12,600 and +15,400 km s−1; and (3) very broad wings extending from −22,000 to +25,000 km s−1. We propose that this line profile indicates a bipolar jet-driven explosion, with the central component produced by normal SN ejecta and CSM interaction at mid and low latitudes, while the high-velocity bumps and broad line wings arise in a nonrelativistic bipolar jet. Jet-driven SNe II are predicted for collapsars resulting from a wide range of initial masses above 25 M⊙, especially at the sub-solar metallicity consistent with the SN host environment. It also seems consistent with the apparently low 56Ni mass that may accompany black hole formation. We speculate that the jet survives to produce observable signatures because the star's H envelope was very low mass, having been mostly stripped away by the previous eruptive mass loss.
A novel, water-soluble AB-block copolymer of diethylaminoethyl methacrylate (DEAEM) and poly(ethylene glycol) (PEG) was synthesized by anionic polymerization. Poly(ethylene glycol) methyl ether (PEGME) was converted into the corresponding potassium salt by reacting with potassium metal. The PEG salt was used as a macroinitiator for the polymerization of DEAEM to yield a PEG-b-PDEAEM block copolymer. Carbon dioxide was used to terminate DEAEM polymerization with a carboxylic acid group. This polymer, loaded with dye, was tested for pH sensitivity by release studies into solutions of various pH.
Single phase orthorhombic YBa2(Cuy1−xZnx)3O7 samples were formed for 0<x<0.16. The high T superconductivityXfor x=6 (T =90 K) is rapidly depressed with increasing x, and is quenched for x>0.08. Low field (<100 G) cooled magnetization studies show that the superconducting component decreases as x approaches the critical value for suppression of superconductivity, and this is supported by high resolution specific heat measurements in the vicinity of T. Temperature dependent electrical resistivity studies for x<0.08 show metallic behavior; for x>0.10 semiconducting behavior. The electrical resistance was studied at high quasihydrostatic pressures also, and for x=0.08 showed that T is depressed with increasing pressure: T → 0 K for P >10 GPa. This is in°contrast to YBa2(Cuy1−xZnx)3O7 where dT /dP>0. The data support evidence for the high sensitivity to chemical and ice perturbations of the physical properties of samples near the superconducting-normal transition region.
Zn substitution for Cu in YBa2Cu3O7 rapidly reduces the superconducting transition temperature, Tc. Superconductivity is quenched between x=0.08 (T =30 K) and x=0.10. The normal state paramagnetism grows with Zn substu-tition, presumably due to increased localization on the Cu sublattice. Susceptibility studies of oxygen depleted (nonsuperconducting) Zn-substituted samples support this. Strong non-linear isothermal magnetization suggesting an internal magnetic field is found at T=4.2 K in samples with Zn concentration near to the critical value for suppression of superconductivity. The results are discussed in terms of increased localization of d-electrons on the Cu sites with increasing Zn concentration, which is consistent with recent EPR data.
In this paper, we report a novel low thermal budget process (<800°C) for engineered ultra thin oxynitride dielectrics with high nitrogen concentration (>5% a.c.) using vertical high pressure (VHP) process. VHP grown oxynitride films show >1 OX lower leakage current, higher drive current and superior hot-carrier reliability compared to control SiO2 of identical thickness (Tox,eq) grown by RTP in O2.
Pancreatic polypeptide (PP) is a gut hormone released from the pancreas in response to food ingestion and remains elevated for up to 6 h postprandially. Plasma levels are elevated in patients with pancreatic tumours. An intravenous infusion of PP has been reported to reduce food intake in man, suggesting that PP is a satiety hormone. We investigated whether a lower infusion rate of PP would induce significant alterations in energy intake. The study was randomised and double-blinded. Fourteen lean fasted volunteers (five men and nine women) received 90 min infusions of PP (5 pmol/kg per min) and saline on two separate days. The dose chosen was half that used in a previous human study which reported a decrease in appetite but at supra-physiological levels of PP. One hour after the end of the infusion, a buffet lunch was served and energy intake measured. PP infusion was associated with a significant 11 % reduction in energy intake compared with saline (2440 (se 200) v. 2730 (se 180) kJ; P < 0·05). Preprandial hunger as assessed by a visual analogue score was decreased in the PP-treated group compared to saline. These effects were achieved with plasma levels of PP within the pathophysiological range of pancreatic tumours.
To evaluate the risk of transmission of SARS coronavirus outside of the health-care setting, close household and community contacts of laboratory-confirmed SARS cases were identified and followed up for clinical and laboratory evidence of SARS infection. Individual- and household-level risk factors for transmission were investigated. Nine persons with serological evidence of SARS infection were identified amongst 212 close contacts of 45 laboratory- confirmed SARS cases (secondary attack rate 4·2%, 95% CI 1·5–7). In this cohort, the average number of secondary infections caused by a single infectious case was 0·2. Two community contacts with laboratory evidence of SARS coronavirus infection had mild or sub-clinical infection, representing 3% (2/65) of Vietnamese SARS cases. There was no evidence of transmission of infection before symptom onset. Physically caring for a symptomatic laboratory-confirmed SARS case was the only independent risk factor for SARS transmission (OR 5·78, 95% CI 1·23–24·24).
Obesity is taking on pandemic proportions. The laws of thermodynamics, however, remain unchanged, as energy will be stored if less energy is expended than consumed; the storage is usually in the form of adipose tissue. Several neural, humeral and psychological factors control the complex process known as appetite. Recently, a close evolutionary relationship between the gut and brain has become apparent. The gut hormones regulate important gastrointestinal functions such as motility, secretion, absorption, provide feedback to the central nervous system on availability of nutrients and may play a part in regulating food intake. Peptide YY (PYY) is a thirty-six amino acid peptide related to neuropeptide Y (NPY) and is co-secreted with glucagon-like peptide 1. Produced by the intestinal L-cells, the highest tissue concentrations of PYY are found in distal segments of the gastrointestinal tract, although it is present throughout the gut. Following food intake PYY is released into the circulation. PYY concentrations are proportional to meal energy content and peak plasma levels appear postprandially after 1 h. PYY3-36 is a major form of PYY in both the gut mucosal endocrine cells and the circulation. Peripheral administration of PYY3-36 inhibits food intake for several hours in both rodents and man. The binding of PYY3-36 to the Y2 receptor leads to an inhibition of the NPY neurones and a possible reciprocal stimulation of the pro-opiomelanocortin neurones. Thus, PYY3-36 appears to control food intake by providing a powerful feedback on the hypothalamic circuits. The effect on food intake has been demonstrated at physiological concentrations and, therefore, PYY3-36 may be important in the everyday regulation of food intake.
Postprandial concentrations of glucose, insulin and triacylglycerols (TG) correlate to risk for CHD. Carbohydrates affect many metabolites that could have a potential effect on cardiovascular risk factors. The objective of the present study was to examine, using a randomised prospective study, the acute (day 1) and ad libitum medium-term (day 24) effects of four diets: a high-fat diet (HIGH-FAT; 50 % fat, >34 % monounsaturated fatty acids); a low-glycaemic index (GI) diet (LOW-GI; high-carbohydrate, low-GI); a high-sucrose diet (SUCROSE; high carbohydrate increase of 90 g sucrose/d); a high-GI diet (HIGH-GI; high-carbohydrate, high-GI). Daytime profiles (8 h) (breakfast, lunch and tea) of lipid and carbohydrate metabolism were completed during day 1 and day 24. Seventeen middle-aged men with one or more cardiac risk factors completed the study. There was no change from day 1 or between diets in fasting glucose, lipids or homeostatic assessment model (HOMA) on day 24. The HIGH-FAT compared with the three high-carbohydrate diets was associated with lower postprandial insulin and glucose but higher postprandial TG and non-esterified fatty acids (NEFA). There was a significant increase in the 6 h (15.00 hours) TG concentration (day 1, 2·6 (SEM 0·3) MMOL/L v. DAY 24, 3·3 (sem 0·3) mmol/l; P<0·01) on the SUCROSE diet. Postprandial HOMA (i.e. incremental area under the curve (IAUC) glucose (mmol/l per min)×IAUC insulin/22·5 (mU/l per min)) median changes from day 1 to day 24 were −61, −43, −20 and +31 % for the HIGH-FAT, LOW-GI, SUCROSE and HIGH-GI diets respectively. The HIGH-GI percentage change was significantly different from the other three diets (P<0·001). Despite being advised to maintain an identical energy intake there was a significant weight change (−0·27 (sem 0·3) kg; P<0·02) on the LOW-GI diet compared with the SUCROSE diet (+0·84 (sem 0·3) kg). In conclusion the HIGH-FAT diet had a beneficial effect on postprandial glucose and insulin over time but it was associated with higher postprandial concentrations of TG and NEFA. Conversely the HIGH-GI diet appeared to increase postprandial insulin resistance over the study period.
The role of nitric oxide (NO) in mediating pancreatic endocrine responses to moderate hypoglycaemia has been investigated in conscious unrestrained calves. The synthesis of endogenous NO was inhibited by the administration of N-nitro-L-arginine methyl ester (L-NAME; 100 mg kg-1 I.A.), while sodium nitroprusside was infused continuously (2-4 μg min-1 kg-1 I.V.) to mimic the tonic production of NO. This effectively abolished the rise in plasma pancreatic polypeptide (PP) concentration during moderate hypoglycaemia (0·7 nmol kg-1 insulin I.V.) and significantly reduced the response to more intense hypoglycaemia (2·0 nmol kg-1 insulin I.V.). In contrast, the glucagon response was not significantly affected in either group, although consistently higher plasma glucagon values were obtained in response to the higher dose of insulin following the administration of L-NAME. It is concluded that, in the absence of L-NAME, production of NO contributes to the PP response, but not the glucagon response to hypoglycaemia in this species under physiological conditions.
Constipation is a frequent effect of treatment with antidepressant and neuroleptic drugs as a result of interference with neuronal control of colonic muscular activity. Motilin, a circulating peptide, is involved in induction of myoelectric complexes in the colon. Significantly elevated circulating basal motilin levels were found in patients receiving tricyclic antidepressant drugs, mean 128±33 pmol/l (control 48±6 pmol/l) or neuroleptic therapy, mean 213±29 pmol/l (control 87±8 pmol/l).
Plasma pancreatic polypeptide concentrations rise by 320±81 per cent following administration of electroconvulsive therapy. This rise is observed in the first ten minutes despite premedication of patients with 0.6 mg atropine. Pancreatic polypeptide release is dependent on cholinergic tone and is very sensitive to atropine. The dramatic rise in pancreative polypeptide observed following electroconvulsive therapy probably results from vagal stimulation and reflects insufficient atropine premedication.