197 research outputs found

    Update on the Risk of Hepatocellular Carcinoma in Chronic Hepatitis B Virus Infection

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    Chronic hepatitis B virus infection is an important cause of liver-related morbidity and mortality, with hepatocellular carcinoma being the most life-threatening complication. Because of the highly variable clinical course of the disease, enormous research efforts have been made with the aim of revealing the factors in the natural history that are relevant to hepatocarcinogenesis. These include epidemiological studies of predisposing risk groups, viral studies of mutations within the hepatitis B viral genome, and clinical correlation of these risk factors in predicting the likelihood of development of hepatocellular cancer in susceptible hosts. This update addresses these risks, with emphasis on the latest research relevant to hepatocarcinogenesis

    Structural basis for delta cell paracrine regulation in pancreatic islets

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    International audienceLittle is known about the role of islet delta cells in regulating blood glucose homeostasis in vivo. Delta cells are important paracrine regulators of beta cell and alpha cell secretory activity, however the structural basis underlying this regulation has yet to be determined. Most delta cells are elongated and have a well-defined cell soma and a filopodia-like structure. Using in vivo optogenetics and high-speed Ca2+ imaging, we show that these filopodia are dynamic structures that contain a secretory machinery, enabling the delta cell to reach a large number of beta cells within the islet. This provides for efficient regulation of beta cell activity and is modulated by endogenous IGF-1/VEGF-A signaling. In pre-diabetes, delta cells undergo morphological changes that may be a compensation to maintain paracrine regulation of the beta cell. Our data provides an integrated picture of how delta cells can modulate beta cell activity under physiological conditions

    A Severe Lack of Evidence Limits Effective Conservation of the World's Primates

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    Threats to biodiversity are well documented. However, to effectively conserve species and their habitats, we need to know which conservation interventions do (or do not) work. Evidence-based conservation evaluates interventions within a scientific framework. The Conservation Evidence project has summarized thousands of studies testing conservation interventions and compiled these as synopses for various habitats and taxa. In the present article, we analyzed the interventions assessed in the primate synopsis and compared these with other taxa. We found that despite intensive efforts to study primates and the extensive threats they face, less than 1% of primate studies evaluated conservation effectiveness. The studies often lacked quantitative data, failed to undertake postimplementation monitoring of populations or individuals, or implemented several interventions at once. Furthermore, the studies were biased toward specific taxa, geographic regions, and interventions. We describe barriers for testing primate conservation interventions and propose actions to improve the conservation evidence base to protect this endangered and globally important taxon

    Cooperation, coalition and alliances

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    Congenital Hydrocephalus and Abnormal Subcommissural Organ Development in Sox3 Transgenic Mice

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    Congenital hydrocephalus (CH) is a life-threatening medical condition in which excessive accumulation of CSF leads to ventricular expansion and increased intracranial pressure. Stenosis (blockage) of the Sylvian aqueduct (Aq; the narrow passageway that connects the third and fourth ventricles) is a common form of CH in humans, although the genetic basis of this condition is unknown. Mouse models of CH indicate that Aq stenosis is associated with abnormal development of the subcommmissural organ (SCO) a small secretory organ located at the dorsal midline of the caudal diencephalon. Glycoproteins secreted by the SCO generate Reissner's fibre (RF), a thread-like structure that descends into the Aq and is thought to maintain its patency. However, despite the importance of SCO function in CSF homeostasis, the genetic program that controls SCO development is poorly understood. Here, we show that the X-linked transcription factor SOX3 is expressed in the murine SCO throughout its development and in the mature organ. Importantly, overexpression of Sox3 in the dorsal diencephalic midline of transgenic mice induces CH via a dose-dependent mechanism. Histological, gene expression and cellular proliferation studies indicate that Sox3 overexpression disrupts the development of the SCO primordium through inhibition of diencephalic roof plate identity without inducing programmed cell death. This study provides further evidence that SCO function is essential for the prevention of hydrocephalus and indicates that overexpression of Sox3 in the dorsal midline alters progenitor cell differentiation in a dose-dependent manner

    Search for an Invisibly Decaying Z\u27 Boson at Belle II in e⁺e⁻ → μ⁺μ⁻(e±^{\pm}μ^{\mp}) Plus Missing Energy Final States

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    Measurements of the branching fractions for BKγB \to K^{*}\gamma decays at Belle II

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    This paper reports a study of BKγB \to K^{*}\gamma decays using 62.8±0.662.8\pm 0.6 fb1^{-1} of data collected during 2019--2020 by the Belle II experiment at the SuperKEKB e+ee^{+}e^{-} asymmetric-energy collider, corresponding to (68.2±0.8)×106(68.2 \pm 0.8) \times 10^6 BBB\overline{B} events. We find 454±28454 \pm 28, 50±1050 \pm 10, 169±18169 \pm 18, and 160±17160 \pm 17 signal events in the decay modes B0K0[K+π]γB^{0} \to K^{*0}[K^{+}\pi^{-}]\gamma, B0K0[KS0π0]γB^{0} \to K^{*0}[K^0_{\rm S}\pi^{0}]\gamma, B+K+[K+π0]γB^{+} \to K^{*+}[K^{+}\pi^{0}]\gamma, and B+K+[K+π0]γB^{+} \to K^{*+}[K^{+}\pi^{0}]\gamma, respectively. The uncertainties quoted for the signal yield are statistical only. We report the branching fractions of these decays: B[B0K0[K+π]γ]=(4.5±0.3±0.2)×105,\mathcal{B} [B^{0} \to K^{*0}[K^{+}\pi^{-}]\gamma] = (4.5 \pm 0.3 \pm 0.2) \times 10^{-5}, B[B0K0[KS0π0]γ]=(4.4±0.9±0.6)×105,\mathcal{B} [B^{0} \to K^{*0}[K^0_{\rm S}\pi^{0}]\gamma] = (4.4 \pm 0.9 \pm 0.6) \times 10^{-5}, B[B+K+[K+π0]γ]=(5.0±0.5±0.4)×105, and\mathcal{B} [B^{+} \to K^{*+}[K^{+}\pi^{0}]\gamma] = (5.0 \pm 0.5 \pm 0.4)\times 10^{-5},\text{ and} B[B+K+[KS0π+]γ]=(5.4±0.6±0.4)×105,\mathcal{B} [B^{+} \to K^{*+}[K^0_{\rm S}\pi^{+}]\gamma] = (5.4 \pm 0.6 \pm 0.4) \times 10^{-5}, where the first uncertainty is statistical, and the second is systematic. The results are consistent with world-average values

    Erratum: The Belle II Physics Book (Progress of Theoretical and Experimental Physics (2019) 2019 (123C01) DOI: 10.1093/ptep/ptz106)

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