A modified crack closure integral method for calculating stress intensity factors for cracked plates subject to bending loads

A method is developed to calculate strain energy release rates, G, or stress intensity factors, K, using only nodal forces and displacements from a standard finite element analysis code. The method is an extension of the modified crack closure integral (MCCI) approach to the bending of plates with through cracks. An examination of bending of plates with through cracks based on shear deformation theories has shown that the bending K depends strongly on the ratio of plate thickness, h, and half crack length, a. Hence, the need to examine the effect of h/a on the accuracy of G and K obtained by the MCCI approach is examined. The accuracy of the MCCI method is verified by analyzing a square plate with a central crack subjected to a uniform edge moment and comparing the results with those reported in the literature

Nuclear Cusps and Cores in Early-type Galaxies As Relics of Binary Black Hole Mergers

We present an analysis of the central cusp slopes and core parameters of early-type galaxies using a large database of surface brightness profiles obtained from Hubble Space Telescope observations. We examine the relation between the central cusp slopes, core parameters, and black hole masses in early-type galaxies, in light of two models that attempt to explain the formation of cores and density cusps via the dynamical influence of black holes. Contrary to the expectations from adiabatic-growth models, we find that the cusp slopes do not steepen with increasing black hole mass fraction. Moreover, a comparison of kinematic black hole mass measurements with the masses predicted by the adiabatic models shows that they overpredict the masses by a factor of approximately 3. Simulations involving binary black hole mergers predict that both the size of the core and the central mass deficit correlate with the final black hole mass. These relations are qualitatively supported by the present data.Comment: To appear in ApJ. 8 page

Activation of p38 MAPK in the substantia nigra leads to nuclear translocation of NF-κB in MPTP-treated mice: implication in Parkinson's disease

Activation and translocation of the transcription factor nuclear factor kappa B (NF-κB) from cytoplasm to the nucleus has been reported in models of Parkinson's disease (PD). Our focus was to discern the upstream events which ultimately lead to NF-κB nuclear translocation using animal model of PD. We demonstrate that p38 activation results in downstream phosphorylation of NF-κB and accumulation of p65 subunit of NF-κB selectively in ventral midbrain but not in striatum. Treatment with p38 inhibitor, SB239063, prevented downstream phosphorylation of IκBα and p65 translocation to the nucleus in the ventral midbrain. Phosphorylation of anti-apoptotic Bcl2, an NF-κB target gene by p38 to inactive pBcl2ser87 was also attenuated by SB239063. Increased staining of p65 in the nuclei of cells in the substantia nigra but not in the ventral tegmental area of MPTP-treated mice further suggests a role for NF-κB in PD. In agreement with the above, sustained caspase activation is seen in the ventral midbrain but not in striatum. We demonstrate the region specific p38-mediated activation of NF-κB following MPTP treatment demonstrating the role of p38/NF-κB signaling in the pathogenesis and progression of the disease. Selective inhibitors of p38 may therefore, help preserve the surviving neurons in PD and slow down the disease progression

Glutaredoxin is essential for maintenance of brain mitochondrial complex I: studies with MPTP

This article does not have an abstract

Protection and potentiation of MPTP-induced toxicity by cytochrome P-450 inhibitors and inducer: in vitro studies with brain slices

Exposure to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) causes loss of dopaminergic neurons in humans, primates and mice. Exposure of sagittal slices of mouse brain to MPTP (100 pM) caused inhibition of mitochondrial NADH-dehydrogenase activity. Leakage of lactate dehydrogenase from the slice into the medium was observed following incubation of slices with 1 nM MPTP. Neurotoxicity induced by MPTP was prevented by prior exposure of the slices to the dopamine uptake inhibitor GBR 12935. Deprenyl and pargyline (inhibitors of monoamine oxidase), also protected the slices from MPTP-induced toxicity. However, both pargyline and deprenyl also inhibited cytochrome P-450 mediated aminopyrine N-demethylase activity in brain slices. Pargyline, when administered in vivo to mice, decreased brain cytochrome-450 levels significantly. Other cytochrome P-450 inhibitors, namely, piperonyl butoxide and SKF 525A were found to offer protection against MPTP induced neurotoxicity in slices without affecting monoamine oxidase activity. MPTP toxicity was potentiated significantly in brain slices prepared from mice pretreated with phenobarbital, an inducer of cytochrome P-450. The present study suggests the possible involvement of cytochrome P-450 in MPTP-induced neurotoxicity, in vitro, in brain slices

Total free sugars, reducing sugars and glucose

Carbohydrates in the tissues of crustaceans exist as free sugars and as bound with proteins (Saravanan, 1979). The free sugars in haemolymph consist of mono, di and oligosaccharides. All monosaccharides, maltose and its oligosaccharides constitute the total reducing sugars. Trehalose constitutes the non-reducing sugar fraction of the total free sugars. The total free sugars are estimated by Anthrone method and reducing sugar by Nelson-Somogyi method. The difference in the values obtained by these two methods indicates total non-reducing sugar value which is primarily trehalose in crustacean blood. The glucose can be determined by Glucose-oxidase method. The difference between values of glucose and reducing sugars would indicate the concentration of non-glucose reducing sugars

Antibiotic susceptibility pattern of gram-negative bacterial isolates with special mention on colistin resistance from Intensive Care Unit of a tertiary care hospital: a prospective study assessing the impact of microbial resistance on clinical outcomes

Background: The frequent use of broad-spectrum antibiotics in ICU leads to increased rates of antimicrobial resistance and occurrence of multidrug-resistant (MDR) micro-organisms. The aim of this study was to evaluate the antimicrobial resistance pattern and colistin susceptibility among bacterial isolates from ICU patients. Method: It is a prospective study with 70 nonrepetitive isolates from ICU samples. The clinical data was obtained from the department records. The gram-negative bacterial isolates were identified by conventional biochemical tests. The antimicrobial susceptibility was determined by Kirby-Bauer disc diffusion method. ESBL producers were detected by double disc diffusion test using ceftazidime, cefotaxime alone and in combination with clavulanic acid. MBL detection was done by imipenem+ EDTA combined disc diffusion test. Colistin sensitivity was determined by broth microdilution according to CLSI guidelines. Results: Out of 70 culture positive specimens. The most common gram-negative bacteria isolated from the samples was Acinetobacter spp. (41%), followed by Klebsiella spp. (20%). Among these 45% were MBL producers, 38.5% were ESBL producers and 14% were both ESBL and MBL producers. Colistin resistance was present among 5.7% isolates in ICU.          Conclusions: Non-fermenters were the most common agent causing ICU infections. An alarmingly high rate of resistance to antibiotics especially to colistin in ICU-acquired infections, necessitates new therapeutic strategies to prevent the emergence and control of antimicrobial resistance

Solvent Effect on Polarographic Reduction of m-Nitro-acetophenone oxime

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