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Background: Kidney transplantation (kTx) is by far the most effective method of treating end-stage renal disease, with immunosuppressive therapy being obligatory for all, except identical twins. Despite kTx being the most effective treatment for end-stage renal disease, the patients face significant morbidity. They are often burdened with diabetes, anaemia, lipid disorders, all of which pose heightened risks for cardiovascular disease.

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Ossification of the posterior longitudinal ligament of the vertebral column (OPLL) is a disease characterised by ectopic bone formation in the spinal ligament that causes progressive neurological impairment. However, there are no suitable treatments for OPLL. Here, we compared the general characteristics and haemostasis of patients with OPLL and those with cervical spondylotic myelopathy.

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Cryo-EM structure determination of protein-free RNAs has remained difficult with most attempts yielding low to moderate resolution and lacking nucleotide-level detail. These difficulties are compounded for small RNAs as cryo-EM is inherently more difficult for lower molecular weight macromolecules. Here we present a strategy for fusing small RNAs to a group II intron that yields high resolution structures of the appended RNA.

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The vertebrate visual cycle hinges on enzymatically converting all--retinol (at-ROL) into 11--retinal (11c-RAL), the chromophore that binds to opsins in photoreceptors, forming light-responsive pigments. When struck by a photon, these pigments activate the phototransduction pathway and initiate the process of vision. The enzymatic isomerization of at-ROL, crucial for restoring the visual pigments and preparing them to receive new light stimuli, relies on various enzymes found in both the photoreceptors and retinal pigment epithelium cells.

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Chronic exposure to manganese (Mn) induces manganism and has been widely implicated as a contributing environmental factor to Parkinson's disease (PD), featuring notable overlaps between the two in motor symptoms and clinical hallmarks. Here, we developed an adult model of Mn toxicity that recapitulated key parkinsonian features, spanning behavioral deficits, neuronal loss, and dysfunctions in lysosomes and mitochondria. Metabolomics analysis of the brain and body tissues of these flies at an early stage of toxicity identified systemic changes in the metabolism of biotin (also known as vitamin B) in Mn-treated groups.

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