Single Mothers: Strategies of Family Management and Support Systems in Relation to Health

The status of women in contemporary society is a vital aspect of debates concerning gender inequality, women’s subordination, violence against women, and women’s empowerment. The responses of women to these problems vary across different social and spatial categories. One of the significant responses is the change in the family structure that leads to the emergence of single-parent families, particularly single-mother families. Few studies in the Indian context deal with the causes of rising numbers of single-mother families. Furthermore, there are no significant studies concerning the issues single mothers face. Being single and a mother is a significant challenge for a woman in Indian society. A divorced single mother faces various constraints and challenges while leading a household after the marital disruption. Single mothers face many physical and psychological problems, including taking care of herself and children in matters of health and well-being. The present study investigates the constraints of divorced single mothers concerning their social support systems and family management strategies as they influence mental and physical health. The study is an outcome of twenty-five case studies of divorced single mothers residing in Hyderabad, India. The results are drawn using interpretive phenomenological analysis

Therapeutic potential of mGluR5 targeting in Alzheimer's disease

Decades of research dedicated towards Alzheimer's disease (AD) has culminated in much of the current understanding of the neurodegeneration associated with disease. However, delineating the pathophysiology and finding a possible cure for the disease is still wanting. This is in part due to the lack of knowledge pertaining to the connecting link between neurodegenerative and neuroinflammatory pathways. Consequently, the inefficacy and ill-effects of the drugs currently available for AD encourage the need for alternative and safe therapeutic intervention. In this review we highlight the potential of mGluR5, a metabotropic glutamatergic receptor, in understanding the mechanism underlying the neuronal death and neuroinflammation in AD. We also discuss the role of mGlu5 receptor in mediating the neuron-glia interaction in the disease. Finally, we discuss the potential of mGluR5 as target for treating AD

L'Avenir de Luchon : journal scientifique, littéraire, annonces et réclames : guide général des baigneurs et des touristes aux eaux thermales, bains de mer de la France et de l'étranger

30 août 19311931/08/30 (N514)-1931/08/30.Appartient à l’ensemble documentaire : MidiPyren

Etiogenic factors present in the cerebrospinal fluid from amyotrophic lateral sclerosis patients induce predominantly pro-inflammatory responses in microglia

Abstract Background Microglial cell-associated neuroinflammation is considered as a potential contributor to the pathophysiology of sporadic amyotrophic lateral sclerosis. However, the specific role of microglia in the disease pathogenesis remains to be elucidated. Methods We studied the activation profiles of the microglial cultures exposed to the cerebrospinal fluid from these patients which recapitulates the neurodegeneration seen in sporadic amyotrophic lateral sclerosis. This was done by investigating the morphological and functional changes including the expression levels of prostaglandin E2 (PGE2), cyclooxygenase-2 (COX-2), TNF-α, IL-6, IFN-γ, IL-10, inducible nitric oxide synthase (iNOS), arginase, and trophic factors. We also studied the effect of chitotriosidase, the inflammatory protein found upregulated in the cerebrospinal fluid from amyotrophic lateral sclerosis patients, on these cultures. Results We report that the cerebrospinal fluid from amyotrophic lateral sclerosis patients could induce an early and potent response in the form of microglial activation, skewed primarily towards a pro-inflammatory profile. It was seen in the form of upregulation of the pro-inflammatory cytokines and factors including IL-6, TNF-α, iNOS, COX-2, and PGE2. Concomitantly, a downregulation of beneficial trophic factors and anti-inflammatory markers including VEGF, glial cell line-derived neurotrophic factor, and IFN-γ was seen. In addition, chitotriosidase-1 appeared to act specifically via the microglial cells. Conclusion Our findings demonstrate that the cerebrospinal fluid from amyotrophic lateral sclerosis patients holds enough cues to induce microglial inflammatory processes as an early event, which may contribute to the neurodegeneration seen in the sporadic amyotrophic lateral sclerosis. These findings highlight the dynamic role of microglial cells in the pathogenesis of the disease, thus suggesting the need for a multidimensional and temporally guarded therapeutic approach targeting the inflammatory pathways for its treatment

Additional file 2: Figure S2. of Astroglia acquires a toxic neuroinflammatory role in response to the cerebrospinal fluid from amyotrophic lateral sclerosis patients

Quantification using the inbuilt Leica software (a). The white arrowhead represents the fluorescent area selected for the intensity measurement using poly-line profile for each cell, referred to as the region of interest (ROI). Twenty cells per image were considered for each of the 10 images taken per cover slip. b The report generated by the software. The mean intensity was taken for each ROI and further analyzed. (TIF 7393 KB

Additional file 1: Figure S1. of Astroglia acquires a toxic neuroinflammatory role in response to the cerebrospinal fluid from amyotrophic lateral sclerosis patients

Representative phase contrast (a, c–e) and confocal images of the enriched astroglial cultures (b, f–h). The reactive astrocytes display a process bearing morphology (e, h) as compared to the flat morphology adopted by the non-reactive astrocytes (c, f). The intermediate stages show a semi-reactive morphology with a transformation from flat to process bearing one (d, g). The cultures were found to be free of microglia as seen by the presence of GFAP immunoreactivity (red, j) and absence of Iba1 (green, i). In a similar manner, the cultures were found to be ChAT negative (green, l). The cultures were >99 % pure. Scale bars are indicated. (TIF 14438 kb

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field