Management of Degenerative Lower back Spinal Stenosis inside the Aged

From Selfless
Jump to navigation Jump to search

Intimate partner violence (IPV) and reproductive coercion (RC)-largely in the form of pressuring pregnancy-appear to contribute to low use of contraceptives in India; however, little is known about the extent to which these experiences differentially affect use of specific contraceptive methods. The current study assessed the association of IPV and RC with specific contraceptive methods (Intrauterine Devices [IUDs], pills, condoms) among a large population-based sample of currently married women (15-49 years, n = 1424) living in Uttar Pradesh. Outcomes variables included past year modern contraceptive use and type of contraceptive used. Primary independent variables included lifetime experience of RC by current husband or in-laws, and lifetime experiences of physical IPV and sexual IPV by current husband. Multivariate logistic regression models were developed to determine the effect of each form of abuse on women's contraceptive use. Approximately 1 in 7 women (15.1%) reported experiencing RC from their current husband or in-laws ever in their lifetime, 37.4% reported experience of physical IPV and 8.3% reported experience of sexual IPV by their current husband ever in their lifetime. Women experiencing RC were less likely to use any modern contraceptive (AOR 0.18; 95% CI 0.9-0.36). Such women also less likely to report pill and condom use but were more likely to report IUD use. Neither form of IPV were associated with either overall or method specific contraceptive use. Study findings highlight that RC may influence contraceptive use differently based on type of contraceptive, with less detectable, female-controlled contraceptives such as IUD preferred in the context of women facing RC. Unfortunately, IUD uptake remains low in India. Increased access and support for use, particularly for women contending with RC, may be important for improving women's control over contraceptive use and reducing unintended pregnancy.Ciliary microtubules are subject to post-translational modifications that act as a "Tubulin Code" to regulate motor traffic, binding proteins and stability. In humans, loss of CCP1, a cytosolic carboxypeptidase and tubulin deglutamylating enzyme, causes infantile-onset neurodegeneration. In C. elegans, mutations in ccpp-1, the homolog of CCP1, result in progressive degeneration of neuronal cilia and loss of neuronal function. To identify genes that regulate microtubule glutamylation and ciliary integrity, we performed a forward genetic screen for suppressors of ciliary degeneration in ccpp-1 mutants. We isolated the ttll-5(my38) suppressor, a mutation in a tubulin tyrosine ligase-like glutamylase gene. We show that mutation in the ttll-4, ttll-5, or ttll-11 gene suppressed the hyperglutamylation-induced loss of ciliary dye filling and kinesin-2 mislocalization in ccpp-1 cilia. We also identified the nekl-4(my31) suppressor, an allele affecting the NIMA (Never in Mitosis A)-related kinase NEKL-4/NEK10. In humans, NEK10 mutation causes bronchiectasis, an airway and mucociliary transport disorder caused by defective motile cilia. C. elegans NEKL-4 localizes to the ciliary base but does not localize to cilia, suggesting an indirect role in ciliary processes. This work defines a pathway in which glutamylation, a component of the Tubulin Code, is written by TTLL-4, TTLL-5, and TTLL-11; is erased by CCPP-1; is read by ciliary kinesins; and its downstream effects are modulated by NEKL-4 activity. Identification of regulators of microtubule glutamylation in diverse cellular contexts is important to the development of effective therapies for disorders characterized by changes in microtubule glutamylation. By identifying C. elegans genes important for neuronal and ciliary stability, our work may inform research into the roles of the tubulin code in human ciliopathies and neurodegenerative diseases.The major glycerophospholipid phosphatidylethanolamine (PE) in the nervous system is essential for neural development and function. There are two major PE synthesis pathways, the CDP-ethanolamine pathway in the endoplasmic reticulum (ER) and the phosphatidylserine decarboxylase (PSD) pathway in mitochondria. However, the role played by mitochondrial PE synthesis in maintaining cellular PE homeostasis is unknown. Here, we show that Drosophila pect (phosphoethanolamine cytidylyltransferase) mutants lacking the CDP-ethanolamine pathway, exhibited alterations in phospholipid composition, defective phototransduction, and retinal degeneration. Induction of the PSD pathway fully restored levels and composition of cellular PE, thus rescued the retinal degeneration and defective visual responses in pect mutants. Disrupting lipid exchange between mitochondria and ER blocked the ability of PSD to rescue pect mutant phenotypes. These findings provide direct evidence that the synthesis of PE in mitochondria contributes to cellular PE homeostasis, and suggest the induction of mitochondrial PE synthesis as a promising therapeutic approach for disorders associated with PE deficiency.The autonomous parvovirus Minute Virus of Mice (MVM) localizes to cellular DNA damage sites to establish and sustain viral replication centers, which can be visualized by focal deposition of the essential MVM non-structural phosphoprotein NS1. How such foci are established remains unknown. Here, we show that NS1 localized to cellular sites of DNA damage independently of its ability to covalently bind the 5' end of the viral genome, or its consensus DNA binding sequence. Many of these sites were identical to those occupied by virus during infection. However, localization of the MVM genome to DNA damage sites occurred only when wild-type NS1, but not its DNA-binding mutant was expressed. Additionally, wild-type NS1, but not its DNA binding mutant, could localize a heterologous DNA molecule containing the NS1 binding sequence to DNA damage sites. These findings suggest that NS1 may function as a bridging molecule, helping the MVM genome localize to cellular DNA damage sites to facilitate ongoing virus replication.At present nearly half of the world's population is under some form of government restriction to curb the spread of COVID-19, an extremely contagious disease. Nanchangmycin In Bangladesh, in the wake of five deaths and 48 infections from COVID-19, between March 24 and May 30, 2020, the government imposed a nationwide lockdown. While this lockdown restricted the spread of COVID-19, in the absence of effective support, it can generate severe food and nutrition insecurity for daily wage-based workers. Of the 61 million employed labor force in Bangladesh, nearly 35% of them are paid on a daily basis. This study examines the food security and welfare impacts of the COVID-19 induced lockdown on daily wage workers both in the farm and nonfarm sectors in Bangladesh. Using information from more than 50,000 respondents complied with the 2016-17 Household Income and Expenditure Survey (HIES) in Bangladesh, this study estimates daily wage rates as Bangladesh Taka (BDT) 272.2 in the farm sector and BDT 361.5 in the nonfarm sector. Using the estimated daily wage earnings, this study estimates that a one-day complete lockdown generates a US$64.