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The present study was an endeavor to explore whether and how hypothyroidism plays a role in the etiology of polycystic ovarian syndrome (PCOS). A composite picture of the hormone profile was assessed in different groups of subjects (control women and hypothyroid women with or without PCOS). Comparative analysis of the results suggests that hypothyroidism is invariably followed by a lowering of sex hormone binding globulin and an increment in the free testosterone level, but further metabolism of testosterone (T) may or may not be directed towards an overproduction of estriol (E₃). The factors that dictate the route of T metabolism, and the way by which E₃ acts to rescue the ovaries from the development of PCOS under the hypothyroid state are discussed.

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Aggregation of alpha synuclein has strong implications in Parkinson’s disease. The heterogeneity of folding/aggregation landscape and transient nature of the early intermediates result in difficulty in developing a successful therapeutic intervention. Here we used fluorescence measurements at ensemble and single molecule resolution to study how the late and early events of alpha synuclein aggregation modulate each other. In-vitro aggregation data was complemented using measurements inside live neuroblastoma cells by employing a small molecule labeling technique. An inhibitor molecule (arginine), which delayed the late event of amyloidosis, was found to bind to the protein, shifting the early conformational fluctuations towards a compact state. In contrast, a facilitator of late aggregation (glutamate), was found to be excluded from the protein surface. The presence of glutamate was found to speed up the oligomer formation at the early stage. We found that the effects of the inhibitor and facilitator were additive and as a result they maintained a ratio at which they cancelled each other’s influence on different stages of alpha synuclein aggregation.