Background Axillary hyperhidrosis characterized by excessive sweating in the axillary regions is a frustrating chronic autonomic disorder leading to social embarrassment, impaired quality of life and usually associated with palmoplantar hyperhidrosis. Identifying the condition and its cause is central to the management. Aim The aim of this article is to discuss treatment options for axillary hyperhidrosis. Methods Comprehensive literature search using PubMed and Google Scholar was performed to review relevant published articles related to diagnosis and treatment of axillary hyperhidrosis. Results Treatment modalities for axillary hyperhydrosis vary from topical and systemic agents to injectables, newer devices and surgical measures. None except for physical measures using devices or surgery, which destroys the sweat glands to remove them, is possibly permanent and most are associated with attendant side effects. Conclusion Several treatments including medical and surgical option are available for the treatment of axillary hyperhydrosis. Patient education is important component of its management. Individualized approach of management is necessary for optimal outcome of treatment.
Alzheimer, a neurodegenerative disease, and a large variety of pathologic conditions are associated with a form of protein aggregation known as amyloid fibrils. Since fibrils and prefibrillar intermediates are cytotoxic, numerous attempts have been made to inhibit fibrillation process as a therapeutic strategy. Peptides, surfactants and aromatic small molecules have been used as fibrillation inhibitors. Here we studied the effects of paclitaxel, a polyphenol with a high tendency for interaction with proteins, on fibrillation of insulin as a model protein. The effects of paclitaxel on insulin fibrillation were determined by Thioflavin T fluorescence, Congo red absorbance, circular dichroism and atomic force microscopy. These studies indicated that paclitaxel considerably hindered nucleation, and therefore, fibrillation of insulin in a dose-dependant manner. The isothermal titration calorimetry studies showed that the interaction between paclitaxel and insulin was spontaneous. In addition, the van der Waal's interactions and hydrogen bonds were prominent forces contributing to this interaction. Computational results using molecular dynamic simulations and docking studies revealed that paclitaxel diminished the polarity of insulin dimer and electrostatic interactions by increasing the hydrophobicity of its dimer state. Furthermore, paclitaxel reduced disrupting effects of insulin fibrils on PC12 cell's neurite outgrowth and complexity, and enhanced their survival.
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