LITERARY REVIEW OF KAPHAJA YONI VYAPAD (NON SPECIFIC VULVO VAGINITIS)

A healthy woman is a promise of a healthy family. In different phases of a womans life, from puberty to menopause, the concept of healthy yoni has been mentioned in Ayurveda as well as in modern. Now a days, infection related to yoni is a burning problem irrespective of their age or socioeconomic status. Due to infection, there may be sign and symptoms like vaginal discharge, itching, coldness. in Ayurveda, these types of sign and symptoms are found in Kaphaja yoni vyapad and some of symptoms are similar with Non Specific Vulvovaginitis.Gynaecological disorders have found its immense importance in the field of medicine due to fact that women have a unique function of giving birth. In Ayurveda, women health care is related in separate section, where the term Yoni vyapad includes majority of gynaecological disorders. Before knowing the management, literature of the disease should be known. Therefore, in this study an effort has been put forth to make a conceptual study covering almost all the aspects of Kaphaja yoni vyapad as per Ayurveda as well as per modern

HIV risk behaviours among injecting drug users in Northeast India following scale-up of a targeted HIV prevention programme

BACKGROUND: In the Northeast Indian states of Manipur and Nagaland there has been an ongoing HIV epidemic among injecting drug users (IDUs) since the mid-1990s. Project ORCHID is an Avahan-funded HIV prevention project that has been working in selected districts of Manipur and Nagaland since 2004. It supports local partner non-government organisations (NGOs) to deliver a range of harm reduction interventions, and currently reaches approximately 14,500 IDUs across the two states. To assess changes in HIV risk behaviours two Behavioural Tracking Surveys (BTS) were undertaken among IDUs in 2007 and 2009. METHODS: The BTS used respondent driven sampling (RDS) to recruit adult male IDUs (18 years of age and above) from Ukhrul and Chandel districts in Manipur, and Kiphire and Zunheboto districts in Nagaland. This paper reports on analysis of socio-demographics, drug use and injecting practices, sexual behaviour and condom use, knowledge of HIV, and exposure to interventions. Descriptive data were analysed using RDSAT, and odds ratios were calculated in SPSS. RESULTS: The proportion of IDUs reporting NOT sharing needles / syringes at last injection increased substantially in Ukhrul (59.6% to 91.2%) and Zunheboto (45.5% to 73.8%), remained high in Chandel (97.0% to 98.9%), and remained largely unchanged in Kiphire (63.3% to 68.8%). The use of condoms with regular partners was low in all districts at both time points. In Ukhrul, Kiphire and Zunheboto the proportion of IDUs using condoms during sexual intercourse with a casual partner increased substantially to approximately 70-85%, whilst in Chandel the increase was only marginal (57.4% to 63.6%). Exposure to NGO HIV prevention interventions was significantly associated (p<0.05) with lower odds of sharing needles during the previous month (Nagaland, OR=0.63; Manipur, OR 0.35). CONCLUSION: Despite district-level differences, the results from this BTS study indicate that exposure to HIV prevention services, predominately delivered in this region by NGOs, is associated with a reduced likelihood of engaging in HIV risk behaviours. IDUs using HIV prevention services are more likely to engage in safe injecting and sexual practices, and effort is required to sustain / increase opportunities for IDUs to access these services. These outcomes are a noteworthy achievement in a very challenging context

MATERNAL HEALTH CARE PRACTICES OF LOTHA NAGA TRIBAL WOMEN IN INDIA

Tribal Women in India are more privileged in various ways as in comparison with the women of caste hierarchy. However, due to geographic isolation, they are deprived of access to basic amenities like livelihood opportunities, education, health, and sanitation. The twin factors of distance and cost of intensive maternal health care expenses hinders the tribal women in accessing to the health care services. For this reason, the traditional health care practitioners are profoundly preferred and they have been the largest maternal health care providers to the tribal women. The Maternal Mortality Rate (MMR) in India was 174 in 2015 (WHO, 2018) and the MMR in the State of Nagaland accounts of 160 (GOI-UNDP Report Nagaland, 2016). The Nagaland State also indicates as the lowest and poorest in maternal health care among the Northeastern States in India with an institutional delivery of only 33 percent. The institutional delivery in Wokha District of Nagaland accounts of 34 percent (NFHS-4, 2016). Thus, the study has been undertaken with an objective to portray the maternal health care status of the Lotha tribal women; to describe the maternal health care practices among Lotha tribal women; and to determine the health care infrastructure in the study areas. The Sequential Explorative Research Design has been adopted, and the study ponders on the maternal health care practices of Lotha Tribal women residing in Yanpha and Old Ralan Villages of Wokha District in the State of Nagaland, India. The study therefore, intends to contribute in achieving Sustainable Development Goals (SDGs) at the national and global level.&nbsp

Anti-lipid phosphate phosphohydrolase-3 (LPP3) antibody inhibits bFGF- and VEGF-induced capillary morphogenesis of endothelial cells

BACKGROUND: Angiogenesis, or the remodeling of existing vasculature serves as a lifeline to nourish developing embryos and starved tissues, and to accelerate wound healing, diabetic retinopathy, and tumor progression. Recent studies indicate that angiogenesis requires growth factor activity as well as cell adhesion events mediated by α(5)β(1 )and α(v)β(3 )integrins. We previously demonstrated that human lipid phosphate phosphohydrolase-3 (LPP3) acts as a cell-associated ligand for α(5)β(1 )and α(v)β(3 )integrins. Here, we test the hypothesis that an anti-LPP3 antibody can inhibit basic fibroblast growth factor (bFGF)-and vascular endothelial growth factor (VEGF)-induced capillary morphogenesis of endothelial cells (ECs). RESULTS: We report that bFGF and VEGF up-regulate LPP3 protein expression in ECs. Immunoprecipitation analyses show that LPP3 is a cell surface protein and undergoes N-glycosylation. Fluorescent activated cell sorting (FACS) data suggest that anti-LPP3-RGD detects native neoepitope on the surface of activated ECs. Moreover, we demonstrate LPP3 protein expression in tumor endothelium alongside VEGF. The embedding of ECs into three-dimensional type I collagen in the presence of bFGF and VEGF induce capillary formation. Importantly, we show that the addition of an anti-LPP3 antibody specifically and significantly blocks bFGF- and VEGF-induced capillary morphogenesis of ECs. CONCLUSION: These data suggest that activated ECs as well as tumor endothelium express LPP3 protein. In an in vitro assay, the anti-LPP3-RGD specifically blocks bFGF and VEGF induced capillary morphogenesis of ECs. Our results, therefore, suggest a role for LPP3 in angiogenesis

Analysis of VEGF-responsive Genes Involved in the activation of endothelial cells

BACKGROUND: Identification of the genes and pathways associated with the activation of endothelial cells (ECs) could help uncover the role of ECs in wound healing, vascular permeability, blood brain barrier function, angiogenesis, diabetic retinopathy, atherosclerosis, psoriasis, and growth of solid tumors. DESIGN: Herein, we embedded ECs in 3D type I collagen gel, left unstimulated or stimulated with VEGF(165), and subjected to suppression subtractive hybridization followed by differential display (SSHDD). Gene fragments obtained from SSHDD were subjected to DNA sequence analysis. Database search with nucleotide sequence were performed using the BLAST algorithm and expression of candidate genes determined by northern blot analysis. RESULTS: A total of ~32 cDNA fragments, including known regulators of angiogenesis, and a set of genes that were not reported to be associated with activation of ECs and angiogenesis previously were identified. We confirmed the mRNA expression of KDR, α(2 )integrin, Stanniocalcin, including a set of 11 candidate genes. Western immunoblotting results indicated that KDR, α(2 )integrin, MMP-1, MMP-2, and VE-cadherin genes were indeed active genes. CONCLUSION: We have identified a set of 11 VEGF-responsive endothelial cell candidate genes. Their expression in endothelial cell is confirmed by northern blot analyses. This preliminary report forms as a foundation for functional studies to be performed to reveal their roles in EC activation and pathophysiological events associated with the vasculature including tumor growth

Lipid phosphate phosphatase-3 regulates tumor growth via β-catenin and Cyclin-D1 signaling

<p>Abstract</p> <p>Background</p> <p>The acquisition of proliferative and invasive phenotypes is considered a hallmark of neoplastic transformation; however, the underlying mechanisms are less well known. Lipid phosphate phosphatase-3 (LPP3) not only catalyzes the dephosphorylation of the bioactive lipid sphingosine-1-phosphate (S1P) to generate sphingosine but also may regulate embryonic development and angiogenesis <it>via </it>the Wnt pathway. The goal of this study was to determine the role of LPP3 in tumor cells.</p> <p>Results</p> <p>We observed increased expression of LPP3 in glioblastoma primary tumors and in U87 and U118 glioblastoma cell lines. We demonstrate that <it>LPP3</it>-knockdown inhibited both U87 and U118 glioblastoma cell proliferation in culture and tumor growth in xenograft assays. Biochemical experiments provided evidence that <it>LPP3</it>-knockdown reduced β-catenin, CYCLIN-D1, and CD133 expression, with a concomitant increase in phosphorylated β-catenin. In a converse experiment, the forced expression of LPP3 in human colon tumor (SW480) cells potentiated tumor growth <it>via </it>increased β-catenin stability and CYCLIN-D1 synthesis. In contrast, elevated expression of LPP3 had no tumorigenic effects on primary cells.</p> <p>Conclusions</p> <p>These results demonstrate for the first time an unexpected role of LPP3 in regulating glioblastoma progression by amplifying β-catenin and CYCLIN-D1 activities.</p

Lipid phosphate phosphatase 3 participates in transport carrier formation and protein trafficking in the early secretory pathway

The inhibition of phosphatidic acid phosphatase (PAP) activity by propanolol indicates that diacylglycerol (DAG) is required for the formation of transport carriers at the Golgi and for retrograde trafficking to the ER. Here we report that the PAP2 family member lipid phosphate phosphatase 3 (LPP3, also known as PAP2b) localizes in compartments of the secretory pathway from ER export sites to the Golgi complex. The depletion of human LPP3: (i) reduces the number of tubules generated from the ER-Golgi intermediate compartment and the Golgi, with those formed from the Golgi being longer in LPP3-silenced cells than in control cells; (ii) impairs the Rab6-dependent retrograde transport of Shiga toxin subunit B from the Golgi to the ER, but not the anterograde transport of VSV-G or ssDsRed; and (iii) induces a high accumulation of Golgi-associated membrane buds. LPP3 depletion also reduces levels of de novo synthesized DAG and the Golgi-associated DAG contents. Remarkably, overexpression of a catalytically inactive form of LPP3 mimics the effects of LPP3 knockdown on Rab6-dependent retrograde transport. We conclude that LPP3 participates in the formation of retrograde transport carriers at the ER-Golgi interface, where it transitorily cycles, and during its route to the plasma membrane

Lipid phosphate phosphatase 3 enables efficient thymic egress

Lipid phosphate phosphatase 3 in endothelial and epithelial cells promotes efficient T cell emigration from the thymus to the periphery

EGFR interacts with the fusion protein of respiratory syncytial virus strain 2-20 and mediates infection and mucin expression.

Respiratory syncytial virus (RSV) is the major cause of viral lower respiratory tract illness in children. In contrast to the RSV prototypic strain A2, clinical isolate RSV 2-20 induces airway mucin expression in mice, a clinically relevant phenotype dependent on the fusion (F) protein of the RSV strain. Epidermal growth factor receptor (EGFR) plays a role in airway mucin expression in other systems; therefore, we hypothesized that the RSV 2-20 F protein stimulates EGFR signaling. Infection of cells with chimeric strains RSV A2-2-20F and A2-2-20GF or over-expression of 2-20 F protein resulted in greater phosphorylation of EGFR than infection with RSV A2 or over-expression of A2 F, respectively. Chemical inhibition of EGFR signaling or knockdown of EGFR resulted in diminished infectivity of RSV A2-2-20F but not RSV A2. Over-expression of EGFR enhanced the fusion activity of 2-20 F protein in trans. EGFR co-immunoprecipitated most efficiently with RSV F proteins derived from "mucogenic" strains. RSV 2-20 F and EGFR co-localized in H292 cells, and A2-2-20GF-induced MUC5AC expression was ablated by EGFR inhibitors in these cells. Treatment of BALB/c mice with the EGFR inhibitor erlotinib significantly reduced the amount of RSV A2-2-20F-induced airway mucin expression. Our results demonstrate that RSV F interacts with EGFR in a strain-specific manner, EGFR is a co-factor for infection, and EGFR plays a role in RSV-induced mucin expression, suggesting EGFR is a potential target for RSV disease