Publications by authors named "B A O'Hara"

Three alkali metal salt forms of the diuretic chlorothiazide (systematic name: 6-chloro-1,1-dioxo-2H-1,2,4-benzothiazine-7-sulfonamide, HCTZ) are described. When crystallized from aqueous solution, the Na and K salts, namely, poly[[μ-aqua-aqua(μ-6-chloro-1,1-dioxo-7-sulfamoyl-2H-1,2,4-benzothiadiazin-2-ido)sodium] hemihydrate], {[Na(CHClNOS)(HO)]·0.5HO}, and poly[[diaqua(μ-6-chloro-1,1-dioxo-7-sulfamoyl-2H-1,2,4-benzothiadiazin-2-ido)potassium] hemihydrate], {[K(CHClNOS)(HO)]·0.

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The neuronal ceroid lipofuscinoses (NCLs) are a group of recessively inherited neurodegenerative diseases characterizsed by lysosomal storage of fluorescent materials. CLN3 disease, or juvenile Batten disease, is the most common NCL that is caused by mutations in the Ceroid Lipofuscinosis, Neuronal 3 (CLN3) gene. Sleep disturbances are among the most common symptoms associated with CLN3 disease that deteriorate the patients' life quality, yet this is understudied and has not been delineated in animal models of the disease.

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Condensed droplets of protein regulate many cellular functions, yet the physiological conditions regulating their formation remain largely unexplored. Increasing our understanding of these mechanisms is paramount, as failure to control condensate formation and dynamics can lead to many diseases. Here, we provide evidence that matrix stiffening promotes biomolecular condensation in vivo.

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The human polyomavirus JCPyV is an opportunistic pathogen that infects greater than 60% of the world's population. The virus establishes a persistent and asymptomatic infection in the urogenital system but can cause a fatal demyelinating disease in immunosuppressed or immunomodulated patients following invasion of the CNS. The mechanisms responsible for JCPyV invasion into CNS tissues are not known but direct invasion from the blood to the cerebral spinal fluid via the choroid plexus has been hypothesized.

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Unlabelled: The human polyomavirus, JCPyV, establishes a lifelong persistent infection in the peripheral organs of a majority of the human population worldwide. Patients who are immunocompromised due to underlying infections, cancer, or to immunomodulatory treatments for autoimmune disease are at risk for developing progressive multifocal leukoencephalopathy (PML) when the virus invades the CNS and infects macroglial cells in the brain parenchyma. It is not yet known how the virus enters the CNS to cause disease.

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