Evaluation of C Library Function rand() and the Associated Compilers Available Off the Shelf for Windows 10 and Kubuntu 19.04

This paper documents the observations made with respect to library function rand() on Windows 10 and Kubuntu 19.04 platform with various compilers such as TDM-GCC 4.9.2 64 bit for Windows 10, clang for Windows 10,Microsoft Visual Studio VC++ compiler for Windows 10 and gcc for Kubuntu 19.04 for a very simple C program. The observations were with respect to uniqueness of the generated random numbers and execution speed of the whole program

Clustering of Lyman alpha emitters at z ~ 4.5

We present the clustering properties of 151 Lyman alpha emitting galaxies at z ~ 4.5 selected from the Large Area Lyman Alpha (LALA) survey. Our catalog covers an area of 36' x 36' observed with five narrowband filters. We assume that the angular correlation function w(theta) is well represented by a power law A_w = Theta^(-beta) with slope beta = 0.8, and we find A_w = 6.73 +/- 1.80. We then calculate the correlation length r_0 of the real-space two-point correlation function xi(r) = (r/r_0)^(-1.8) from A_w through the Limber transformation, assuming a flat, Lambda-dominated universe. Neglecting contamination, we find r_0 = 3.20 +/- 0.42 Mpc/h. Taking into account a possible 28% contamination by randomly distributed sources, we find r_0 = 4.61 +/- 0.6 Mpc/h. We compare these results with the expectations for the clustering of dark matter halos at this redshift in a Cold Dark Matter model, and find that the measured clustering strength can be reproduced if these objects reside in halos with a minimum mass of 1-2 times 10^11 Solar masses/h. Our estimated correlation length implies a bias of b ~ 3.7, similar to that of Lyman-break galaxies (LBG) at z ~ 3.8-4.9. However, Lyman alpha emitters are a factor of ~ 2-16 rarer than LBGs with a similar bias value and implied host halo mass. Therefore, one plausible scenario seems to be that Lyman alpha emitters occupy host halos of roughly the same mass as LBGs, but shine with a relatively low duty cycle of 6-50%.Comment: 23 pages in preprint format, 4 figures, ApJ accepte

Mucoadhesive carbamazepine gel for in situ olfactory delivery

Purpose: To formulate mucoadhesive carbamazepine gel for delivery to the brain via the olfactory mucosa. Methods: Carbamazepine transfersomes were formulated using Lipoid S 100 and sodium cholate. The transfersomes were evaluated for entrapment efficiency, in vitro release transmission electron microscopy, zeta potential, polydispersity index. The transfersomes were then incorporated into gellan gum gel, and the in situ gel formulation was evaluated for drug content, gel strength, in vitro release and mucoadhesive force. Transfersomes were also evaluated for bioanalytical study in rats. Result: TEM analysis showed good regular spheres. The negative zeta potential ensures resistance to aggregation. The gel strength of the formulations was in the range of 0.6 to 7.4 g. In vitro diffusion study of transfersomal gel showed Fickian diffusion mechanism. Formulation F6 was optimized depending for gel strength (6.4 g) , drug content (99.47 ± 0.25 %), and good mucoadhesive force (50.24 ± 0.76 dyne/cm2). Bioanalytical study of F6 showed increased drug concentration in brain. Conclusion: Mucoadhesive carbanmazepine gel can be used effectively to achieve increased concentration of drug in the brain via olfactory mucosal rout

High Mobility Group Box Protein 1 (HMGB1): The Prototypical Endogenous Danger Molecule

High mobility group box protein 1 (HMGB1) is an evolutionary ancient nuclear protein that exerts divergent biological tasks inside and outside of cells. The functions of HMGB1 depend on location, binding partners and redox states of the molecule. In the nucleus, HMGB1 organizes DNA and nucleosomes and regulates gene transcription. Upon cell activation or injury, nuclear HMGB1 can translocate to the cytoplasm, where it is involved in inflammasome activation and pyroptosis, as well as regulation of the autophagy/apoptosis balance. When actively secreted or passively released into the extracellular milieu, HMGB1 has cytokine, chemokine, neuroimmune and metabolic activities. Thus, HMGB1 plays multiple roles in the pathogenesis of inflammatory diseases and mediates immune responses that range from inflammation and bacterial killing to tissue repair. HMGB1 has been associated with divergent clinical conditions such as sepsis, rheumatoid arthritis and atherosclerosis. HMGB1 initiates and perpetuates immune responses during infectious and sterile inflammation, as the archetypical alarmin and damage-associated molecular pattern (DAMP) molecule. We here describe advances in the understanding of HMGB1 biology with focus on recent findings of its mission as a DAMP in danger sensing and as a therapeutic target in inflammatory diseases

Exciton transition and electronic structure of PbMoO4 crystals studied by polarized light

Published in Physica status solidi. B, Basic solid state physics, Vol. 247, No. 2, pp405-410, 2010.Polarized reflectivity spectra of PbMoO4 crystals have been measured using synchrotron radiation up to 20 eV. The optical constants for the crystallographic axes are derived by using a Kramers-Kronig analysis. It is found that the exciton band at 3.6 eV shows a doublet structure with distinct dichroism. X-ray photoemission spectroscopy (XPS) and the calculation of the elec-tronic structure by a discrete variational Xα method are also carried out. The calculation shows that the va-lence band and the conduction band are mainly com-posed of the O 2p and Mo 4d states, respectively, and the Pb state contributes appreciably to the top of the valence band and the bottom of the conduction band. The valence-band XPS spectrum of PbMoO4 is com-pared with that of PbWO4, which reveals a remarkable difference between them. This difference reflects dif-ferent magnitude of hybridization of Mo 4d or W 5d state to the valence band. The exciton transition is ex-plained in terms of the cationic Pb 6s → 6p excitation model taking into account the crystal-field splitting and the spin-orbit interaction of Pb 6p state. From a comparison of the doublet structure of the exciton band of PbMoO4 and PbWO4, it is suggested that the electron-hole exchange interaction plays an important role for the exciton transitions in both materials.ArticlePhysica status solidi. B, Basic solid state physics. 247(2):405-410 (2010)journal articl

The Ayurveda Education in India: How Well Are the Graduates Exposed to Basic Clinical Skills?

“Ayurveda” is an ancient system of healthcare that is native to India. At present, in India, there are more than 240 colleges that offer a graduate-level degree (Bachelor of Ayurvedic Medicine and Surgery—BAMS) in Ayurveda. Even though the Central Council of Indian Medicine, the governing body that monitors the matters related to Ayurveda education, has imposed various educational norms and regulations, the standard of education has been a cause of concern in recent years. The mushrooming of substandard Ayurvedic colleges is the most important factor that is being held responsible for this kind of erosion in the standards. The present study is a mailed survey, which was carried out to evaluate the “Extent of exposure to basic clinical skills during BAMS course” as perceived by the sample groups of students and teachers drawn from 32 Ayurvedic educational institutions spread all over India. A methodically validated questionnaire was used as the tool in the study, to which 1022 participants responded. The study indicates that there are some serious flaws in the existing system of the graduate-level Ayurveda education. Since the Ayurvedic graduates play an important role in the primary healthcare delivery system of the country, governing bodies are required to take necessary steps to ensure the adequate exposure of the students to basic clinical skills. Along with the strict implementation of all the regulatory norms during the process of recognition of the colleges, introducing some changes in the policy model may also be required to tackle the situation

RNase L-Independent Specific 28S rRNA Cleavage in Murine Coronavirus-Infected Cells

We characterized a novel 28S rRNA cleavage in cells infected with the murine coronavirus mouse hepatitis virus (MHV). The 28S rRNA cleavage occurred as early as 4 h postinfection (p.i.) in MHV-infected DBT cells, with the appearance of subsequent cleavage products and a decrease in the amount of intact 28S rRNA with increasing times of infection; almost all of the intact 28S rRNA disappeared by 24 h p.i. In contrast, no specific 18S rRNA cleavage was detected in infected cells. MHV-induced 28S rRNA cleavage was detected in all MHV-susceptible cell lines and all MHV strains tested. MHV replication was required for the 28S rRNA cleavage, and mature cytoplasmic 28S rRNA underwent cleavage. In certain combination of cells and viruses, pretreatment of virus-infected cells with interferon activates a cellular endoribonuclease, RNase L, that causes rRNA degradation. No interferon was detected in the inoculum used for MHV infection. Addition of anti-interferon antibody to MHV-infected cells did not inhibit 28S rRNA cleavage. Furthermore, 28S rRNA cleavage occurred in an MHV-infected mouse embryonic fibroblast cell line derived from RNase L knockout mice. Thus, MHV-induced 28S rRNA cleavage was independent of the activation of RNase L. MHV-induced 28S rRNA cleavage was also different from apoptosis-related rRNA degradation, which usually occurs concomitantly with DNA fragmentation. In MHV-infected 17Cl-1 cells, 28S rRNA cleavage preceded DNA fragmentation by at least 18 h. Blockage of apoptosis in MHV-infected 17Cl-1 cells by treatment with a caspase inhibitor did not block 28S rRNA cleavage. Furthermore, MHV-induced 28S rRNA cleavage occurred in MHV-infected DBT cells that do not show apoptotic signs, including activation of caspase-3 and DNA fragmentation. Thus, MHV-induced 28S rRNA cleavage appeared to differ from any rRNA degradation mechanism described previously

RNase L-Independent Specific 28S rRNA Cleavage in Murine Coronavirus-Infected Cells

We characterized a novel 28S rRNA cleavage in cells infected with the murine coronavirus mouse hepatitis virus (MHV). The 28S rRNA cleavage occurred as early as 4 h postinfection (p.i.) in MHV-infected DBT cells, with the appearance of subsequent cleavage products and a decrease in the amount of intact 28S rRNA with increasing times of infection; almost all of the intact 28S rRNA disappeared by 24 h p.i. In contrast, no specific 18S rRNA cleavage was detected in infected cells. MHV-induced 28S rRNA cleavage was detected in all MHV-susceptible cell lines and all MHV strains tested. MHV replication was required for the 28S rRNA cleavage, and mature cytoplasmic 28S rRNA underwent cleavage. In certain combination of cells and viruses, pretreatment of virus-infected cells with interferon activates a cellular endoribonuclease, RNase L, that causes rRNA degradation. No interferon was detected in the inoculum used for MHV infection. Addition of anti-interferon antibody to MHV-infected cells did not inhibit 28S rRNA cleavage. Furthermore, 28S rRNA cleavage occurred in an MHV-infected mouse embryonic fibroblast cell line derived from RNase L knockout mice. Thus, MHV-induced 28S rRNA cleavage was independent of the activation of RNase L. MHV-induced 28S rRNA cleavage was also different from apoptosis-related rRNA degradation, which usually occurs concomitantly with DNA fragmentation. In MHV-infected 17Cl-1 cells, 28S rRNA cleavage preceded DNA fragmentation by at least 18 h. Blockage of apoptosis in MHV-infected 17Cl-1 cells by treatment with a caspase inhibitor did not block 28S rRNA cleavage. Furthermore, MHV-induced 28S rRNA cleavage occurred in MHV-infected DBT cells that do not show apoptotic signs, including activation of caspase-3 and DNA fragmentation. Thus, MHV-induced 28S rRNA cleavage appeared to differ from any rRNA degradation mechanism described previously