Small-scale continuum robots hold promise for interventional diagnosis and treatment, yet existing models struggle to achieve small size, precise steering, and visualized functional treatment simultaneously, termed an "impossible trinity". This study introduces an optical fiber-based continuum robot integrated imaging, high-precision motion, and multifunctional operation abilities at submillimeter-scale. With a slim profile of 0.
View Article and Find Full Text PDFHuman ANP32A/B (huANP32A/B) poorly support the polymerase activity of avian influenza viruses (AIVs), thereby limiting interspecies transmission of AIVs from birds to humans. The SUMO-interacting motif (SIM) within NS2 promotes the adaptation of AIV polymerase to huANP32A/B via a yet undisclosed mechanism. Here we show that huANP32A/B are SUMOylated by the E3 SUMO ligase PIAS2α, and deSUMOylated by SENP1.
View Article and Find Full Text PDFParaneoplastic cerebellar degeneration (PCD) with anti-Yo antibodies represents a rare immune-mediated paraneoplastic neurological syndrome. Its diagnosis and management remain clinically challenging. Here, we present a case of PCD with confirmed anti-Yo antibodies, validated through anti-cerebellar degeneration protein 2 (CDR2) and anti-CDR2-like antibodies detection, which demonstrated a favorable response to ofatumumab therapy.
View Article and Find Full Text PDFVirus-encoding RNA-dependent RNA polymerase (RdRp) is essential for genome replication and gene transcription of human coronaviruses (HCoVs), including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). We previously identified the interaction between the catalytic subunit NSP12 of SARS-CoV-2 RdRp and the host protein CREB-regulated transcription coactivator 3 (CRTC3), a member of the CRTC family that regulates cyclic AMP response element-binding protein (CREB)-mediated transcriptional activation. Currently, the implication of CRTC3 in the pathogenesis of HCoVs is poorly understood.
View Article and Find Full Text PDFNon-alcoholic fatty liver disease (NAFLD) is expected to become the leading risk factor for liver cancer, surpassing viral hepatitis. Unlike viral hepatitis-related hepatocellular carcinoma (HCC), the role of excessive nutrient supply in steatotic HCC is not well understood, hindering effective prevention and treatment strategies. Therefore, it is crucial to identify key molecules in the pathogenesis of steatotic HCC, investigate changes in metabolic reprogramming due to excessive fatty acid (FA) supply, understand its molecular mechanisms, and find potential therapeutic targets.
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