Rhegmatogenous retinal detachment: a review of current practice in diagnosis and management.

Rhegmatogenous retinal detachment (RRD) is a common condition with an increasing incidence, related to the ageing demographics of many populations and the rising global prevalence of myopia, both well known risk factors. Previously untreatable, RRD now achieves primary surgical success rates of over 80%-90% with complex cases also amenable to treatment. The optimal management for RRD attracts much debate with the main options of pneumatic retinopexy, scleral buckling and vitrectomy all having their proponents based on surgeon experience and preference, case mix and equipment availability. The aim of this review is to provide an overview for the non-retina specialist that will aid and inform their understanding and discussions with patients. We review the incidence and pathogenesis of RRD, present a systematic approach to diagnosis and treatment with special consideration to managing the fellow eye and summarise surgical success and visual recovery following different surgical options

The Role of Intrinsically Unstructured Proteins in Neurodegenerative Diseases

The number and importance of intrinsically disordered proteins (IUP), known to be involved in various human disorders, are growing rapidly. To test for the generalized implications of intrinsic disorders in proteins involved in Neurodegenerative diseases, disorder prediction tools have been applied to three datasets comprising of proteins involved in Huntington Disease (HD), Parkinson's disease (PD), Alzheimer's disease (AD). Results show, in general, proteins in disease datasets possess significantly enhanced intrinsic unstructuredness. Most of these disordered proteins in the disease datasets are found to be involved in neuronal activities, signal transduction, apoptosis, intracellular traffic, cell differentiation etc. Also these proteins are found to have more number of interactors and hence as the proportion of disorderedness (i.e., the length of the unfolded stretch) increased, the size of the interaction network simultaneously increased. All these observations reflect that, “Moonlighting” i.e. the contextual acquisition of different structural conformations (transient), eventually may allow these disordered proteins to act as network “hubs” and thus they may have crucial influences in the pathogenecity of neurodegenerative diseases

Rhegmatogenous retinal detachment: a review of current practice in diagnosis and management (vol 5, e000474, 2020)

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Th17 cells induce a distinct graft rejection response that does not require IL-17A.

IL-17A-producing helper T (Th17) cells have been implicated in the pathogenesis of autoimmune disease, inflammatory bowel disease and graft rejection, however the mechanisms by which they cause tissue damage remain ill-defined. We examined what damage Th17 cell lines could inflict on allogeneic skin grafts in the absence of other adaptive lymphocytes. CD4(+) Th17 cell lines were generated from two TCR transgenic mouse strains, A1(M).RAG1(-/-) and Marilyn, each monospecific for the male antigen Dby. After prolonged in vitro culture in polarizing conditions, Th17 lines produced high levels of IL-17A with inherently variable levels of interferon gamma (IFNγ) and these cells were able to maintain IL-17A expression following adoptive transfer into lymphopenic mice. When transferred into lymphopenic recipients of male skin grafts, Th17 lines elicited a damaging reaction within the graft associated with pathological findings of epidermal hyperplasia and neutrophil infiltration. Th17 cells could be found in the grafted skins and spleens of recipients and maintained their polarized phenotype both in vivo and after ex vivo restimulation. Antibody-mediated neutralization of IL-17A or IFNγ did not interfere with Th17-induced pathology, nor did it prevent neutrophil infiltration. In conclusion, tissue damage by Th17 cells does not require IL-17A