Spectral function at high missing energies and momenta

The nuclear spectral function at high missing energies and momenta has been determined from a self-consistent calculation of the Green's function in nuclear matter using realistic nucleon-nucleon interactions. The results are compared with recent experimental data derived from ($e,e'p$) reactions on $^{12}C$. A rather good agreement is obtained if the Green's functions are calculated in a non-perturbative way.Comment: 10 pages, 3 figure

Effects of Ketosis and Hypocalcemia on The Biochemical Parameters and Subsequent Postpartum Reproductive Performance in Buffaloes

Water buffaloes (Bubalus bubalis) are mainly distributed in tropical and subtropical countries that include the Indian sub-continent and some Mediterranean countries such as Egypt. The transition period is the most stressful period for buffaloes, and it is considered as a turning point in the productive cycle from one lactation to the next and includes different metabolic, physiological, and nutritional changes. Metabolic disorders are common causes of lower productivity in buffaloes. Of these metabolic disorders, ketosis and hypocalcemia are most prevalent. This study aimed to study the ketosis- and hypocalcemia-related biochemical changes during the transition period and their impacts on the postpartum reproductive fertility in Buffaloes. Out of 120 total number of examined buffaloes, 40 buffaloes were used in this study; control group (n=10), hypocalcemia-affected (n=15), and ketosis-affected group (n=15). All buffaloes were subjected to thorough clinical and gynecological examination. Both urine and blood samples were collected from all groups. The amounts of ketone bodies were detected in urine. Biochemical parameters were evaluated including concentrations of glucose, triglycerides, cholesterol, non-esterified fatty acids (NEFA), calcium, phosphorus, sodium, potassium, albumin, total protein, urea and progesterone hormone (P4) in blood the following time-points (2-weeks prepartum, 1-week prepartum, partum, 1-week postpartum, and 2-weeks postpartum). Both hypocalcemia- and ketosis affected buffaloes had lower glucose, phosphorus, sodium and albumin and higher NEFA than control group. Hypocalcemia-affected buffaloes showed lower calcium and higher total protein than control group, while, ketosis-affected buffaloes showed lower cholesterol and total protein than control group. Moreover, metabolic disorders negatively affected the reproductive performance. Both ketosis and hypocalcemia significantly prolonged the duration to first estrus, increased both the number of days-open and the number of services per conceptio

Small-Molecule Inhibitors of Dengue-Virus Entry

Flavivirus envelope protein (E) mediates membrane fusion and viral entry from endosomes. A low-pH induced, dimer-to-trimer rearrangement and reconfiguration of the membrane-proximal “stem" of the E ectodomain draw together the viral and cellular membranes. We found stem-derived peptides from dengue virus (DV) bind stem-less E trimer and mimic the stem-reconfiguration step in the fusion pathway. We adapted this experiment as a high-throughput screen for small molecules that block peptide binding and thus may inhibit viral entry. A compound identified in this screen, 1662G07, and a number of its analogs reversibly inhibit DV infectivity. They do so by binding the prefusion, dimeric E on the virion surface, before adsorption to a cell. They also block viral fusion with liposomes. Structure-activity relationship studies have led to analogs with submicromolar IC90s against DV2, and certain analogs are active against DV serotypes 1,2, and 4. The compounds do not inhibit the closely related Kunjin virus. We propose that they bind in a previously identified, E-protein pocket, exposed on the virion surface and although this pocket is closed in the postfusion trimer, its mouth is fully accessible. Examination of the E-trimer coordinates (PDB 1OK8) shows that conformational fluctuations around the hinge could open the pocket without dissociating the trimer or otherwise generating molecular collisions. We propose that compounds such as 1662G07 trap the sE trimer in a “pocket-open" state, which has lost affinity for the stem peptide and cannot support the final “zipping up" of the stem

Ameliorative effects of camel milk and silymarin upon aflatoxin B1 induced hepatic injury in rats

Abstract Aflatoxin B1 (AFB1) poses a major risk to both human and animal health because it contaminates food, feed, and grains. These dangerous effects can be mitigated using natural components. The purpose of this study was to examine the ameliorative effects of camel milk and silymarin supplementation upon aflatoxin B1 induced hepatic injury in rats. This improvement was assessed by measuring leukocytic and deferential counts, serum biochemical parameters, and gene expression of Tumor Necrosis Factor (TNF-α), antioxidant gene (NAD(P)H quinone oxidoreductase 1 (NQO1)), and base excision repair genes (APE1 and OGG1) in the liver tissue, in addition to liver histopathology. Sixty mature males Wister white rats were used to perform the present study; the rats were distributed in six groups (ten rats/group). The control group (without any treatment) received saline by gavage. The camel milk group received 1 ml of camel milk/kg body weight. The silymarin group received 1 ml of silymarin suspension solution at a dose of 20 mg of silymarin/kg of b.wt. The aflatoxin group received an aflatoxin-contaminated diet at a dose of 1.4 mg of aflatoxin /kg of diet and received saline. The camel milk + aflatoxin group received the same previous oral doses of camel milk and an aflatoxin-contaminated diet at the same time. The silymarin + aflatoxin group received the same previous doses of silymarin orally and an aflatoxin-contaminated diet at the same time. The obtained data indicated the deleterious effect of aflatoxin B1 on the leukocytic count, activity of AST and ALT, serum proteins, ferritin, alpha-fetoprotein, carcinoembryonic antigen, liver pathology, and the expression of the studied genes. However, these deleterious effects were mitigated by camel milk and silymarin supplementation. Thus, we could conclude that the ingestion of camel milk and silymarin mitigated the negative effects of AFB1 on the hematology, activity of AST and ALT, serum proteins, ferritin, alpha-fetoprotein, carcinoembryonic antigen, liver pathology, and gene expression in the rat model