Sphingosine-1-phosphate [S1P] is a potent bioactive sphingolipid molecule. In response to a stimulus, S1P is produced intracellularly by the action of two sphingosine kinases, and then it is exported to the extracellular environment or acts as an intracellular second messenger. S1P binds to its cognate G-protein coupled receptors, which are known as S1P receptors. There are five S1P receptors that have been identified in vertebrates. By activating S1P receptors, S1P controls a variety of physiological and pathological processes including cell migration, angiogenesis, vascular maturation, inflammation, and invasion, metastasis, and chemoresistance in cancer. S1P has emerged as a critical regulator of leukocyte migration and plays a central role in lymphocyte egress from the thymus and secondary lymphoid organs. In the current review article, we summarize the current understanding of the emigration of lymphocytes and other leukocytes from bone marrow, thymus and secondary lymphoid organs to the circulation, as well as the clinical implications of modulating the activity of the major S1P receptor, S1PR1. Sphingosine-1-phosphate [S1P] is a sphingolipid metabolite and a potent signalling molecule that regulates diverse cellular processes including cell proliferation, survival, differentiation and migration. Intense research by many groups has provided a comprehensive understanding of the role of S1P signalling in diverse physiological processes. These include but are not limited to metazoan and mammalian development, reproduction, angiogenesis, vascular maturation, inflammation,

The miracle of childbirth is often clouded by the adverse effects on the soft tissue of the pelvic floor induced by passage of the fetus through the birth canal, which can ultimately have a significant impact on the quality of life of women.  The aim of this presentation is provide an illustration of the origins and consequences of maternal pelvic floor trauma on the structure and function of the urogenital system and to present a complex realistic approach to surgical management of pelvic floor defects.  An MRI derived 3-D model of the female pelvis with high-resolution images demonstrating key anatomical structures as are visualized during surgery will be utilized. The etiology of pelvic floor trauma during childbirth will be discussed and the biophysical principles underlying the mechanical strain and load on the soft tissues with passage of the fetal head during vaginal delivery will be addressed.  The operative method will be illustrated through a series of photo slides detailing intraoperative technique, identification and utilization of native tissue structures (fascia), suture placement and material as well as a general appreciation for the interconnectedness (tissue mapping) of the pelvic floor muscles, fascia, and paravaginal tissues in the anatomical restoration of the vaginal axis, length, and overall physiological function Lastly, the important role of postoperative physiotherapy and education of women in regaining pelvic floor function should not be underestimated and used concurrently with surgery to insure successful patient outcomes.  

Panax Notoginsenosides (PNS) performs the function of enhancing blood circulation. The aim of this study is to investigate the effect of intrapleural PNS on rabbit pleural inflammation reaction, and determine the levels of transforming growth factor β1 (TGF-β1) and Vascular Endothelial Growth Factor (VEGF). Forty New Zealand white rabbits were divided into four groups. The rabbit pleural inflammation reaction model was established by injection of tetracycline hydrochloride solution into pleural cavity. Then PNS, urokinase (UK) and PBS were injected into the pleural cavity as experiment groups. While tetracycline hydrochloride solution was replaced by phosphate buffer solution (PBS) as control group. The pleural effusion was collected at 24 h, 48 h, 72 h and 96 h in all groups, and then biochemical indicators, TGF-β1 and VEGF were detected. On day 14, all animals were killed and pleural tissues were collected to perform hematoxylin eosin (HE) and Masson trichrome staining. The results indicated that levels of TGF-β1 and VEGF were significantly lower in PNS group than that in UK group and PBS group (Pand inhibit collagen production, which had better effects compared with UK, single gene conferring resistance to P. neglectus, Rlnn1, has been mapped to chromosome 7AL. QTL analysis in several bi-parental mapping populations has identified major QTL for P. thornei resistance on chromosomes 2BS, 6DS and 7BL, which have been verified in sources of resistance from diverse backgrounds. Genotyping-by-sequencing has provided closely linked flanking markers that are now available to Australian breeders through the Australian Wheat and Barley Program to implement marker-assisted selection. Further fine mapping using large segregating populations will allow map-based cloning approaches to identify candidate genes underlying these QTL for RLN reon reaction model was established by injection of tetracycline hydrochloride solution into pleural cavity. Then PNS, urokinase (UK) and PBS were injected into the pleural cavity as experiment groups. While tetracycline hydrochloride solution was replaced by phosphate buffer solution (PBS) as control group. The pleural effusion was collected at 24 h, 48 h, 72 h and 96 h in all groups, and then biochemical indicators, TGF-β1 and VEGF were detected. On day 14, all animals were killed and pleural tissues were collected to perform hematoxylin eosin (HE) and Masson trichrome staining. The results indicated that levels of TGF-β1 and VEGF were significantly lower in PNS group than that in UK group and PBS group (Pand inhibit collagen production, which had better effects compared with UK, single gene conferring resistance to P. neglectus, Rlnn1, has been mapped to chromosome 7AL. QTL analysis in several bi-parental mapping populations has identified major QTL for P. thornei resistance on chromosomes 2BS, 6DS and 7BL, which have been verified in sources of resistance from diverse backgrounds. Genotyping-by-sequencing has provided closely linked flanking markers that are now available to Australian breeders through the Australian Wheat and Barley Program to implement marker-assisted selection. Further fine mapping using large segregating populations will allow map-based cloning approaches to identify candidate genes underlying these QTL for RLN 

Coronaviruses are a large family of viruses known to cause more serious diseases from the common cold, such as Middle East Respiratory Syndrome (MERS) and Severe Acute Respiratory Syndrome (SARS). Coronaviruses were identified in the mid-1960s. Sars-Corona Virus (SARS-CoV) is a coronavirus that was first seen in China in February 2003 and causes severe acute respiratory failure. As the largest known RNA viruses (because coronaviruses have the largest genome of RNA viruses), CoVs are further divided into four types: alpha coronavirus (α-CoV), beta coronavirus (β-CoV), gamma coronavirus (γ-CoV), and delta coronavirus (δ-CoV); the first two only infect mammals, including bats, pigs, cats and humans. Gamma coronavirus mostly infects birds and Delta coronavirus can infect both birds and mammals. This novel coronavirus is now the seventh member of the Coronaries, which is known to infect humans. All Coronaviruses belong to a genus. All of these geniuses are in the Coronaries family, making up one of the two subfamilies. Coronavirus, Nidovirales, which causes infections mainly in the respiratory and gastrointestinal tract, belongs to the Orthocoronavirinae subfamily, respectively in the Coronaviridae family. Previously, with serological analysis, the differences in the Coronavirus species used were understood and the Coronaviridae family was examined by dividing it into 4 antigenic groups.

But then, by examining the monoclonol antibody analysis and nucleotide sequences in the species and divisio groups, the classification was reduced to 3 antitigenic groups.

The discovery of DNA as the biomolecule of genetic inheritance and disease opened the prospect of therapies in which mutant and damaged genes could be altered for the improvement of the human condition. Genome-editing is a technology that allows specific changes in the genes of interest. This approach is capable of manipulating the genome of living cells or organisms in various ways: insertions or deletions of chosen genes, introduction of point mutations, knockout or correction of specific genes3 Gene therapy provides a unique approach to treat a variety of both inherited and acquired diseases2 by delivering a therapeutic gene material to correct the loss�?�of�?�function caused by mutation or to express the deficient gene product. Despite years of preclinical studies, it was not until the early 1990s that the first gene therapies were studied in humans In fact, the first clinical trial to gain approval for transfer of a foreign gene into humans was conducted at the National Cancer Institute in Bethesda in 1990.6 In spite of numerous setbacks, efficacious gene-based therapies still hold the great promise to revolutionize the clinical management of human diseases. Numerous preclinical and clinical studies of gene therapy strategies for preventing or treating a wide range of neurodegenerative diseases have been carried out in recent decades,8 however, safety concerns remain one of the biggest barriers to successful clinical application on