Investigating the NCQ scaling of elliptic flow at LHC with a multiphase transport model

The number of constituent quark (NCQ) scaling behavior of elliptic flow has been systematically studied at the LHC energy within the framework of a multiphase transport model (AMPT) in this work. We find that the parameters used to generate the initial states and the collision centrality are important for the existence of NCQ scaling even when hadronic rescattering contribution is off in Pb-Pb collisions of $\sqrt{s_{NN}}=2.76$ TeV. By turning on the hadron rescattering process, the hadronic evolution impacts are also found to be significant. Extending the analysis to Pb-Pb collsions of $\sqrt{s_{NN}}=5.02$ TeV, one would observe similar qualitative features

Acute retinal injury and the relationship between nerve growth factor, Notch1 transcription and short-lived dedifferentiation transient changes of mammalian Müller cells

AbstractOur aim is to define related molecular events on how dormant Müller glia cells re-enter the cell cycle, proliferate and produce new retinal neurons from initial injury to glial scar formation. Sodium iodate (NaIO3) was used to induce acute retinal injury. Long-Evans rats were administered with NaIO3 or phosphate-buffered saline by intraperitoneal injection. The proliferation, dedifferentiation and neurogenesis of Müller cells were analyzed by double-labeled fluorescence immunohistochemistry with primary antibodies – against Müller cells and specific cell markers. Possible molecules that limit the regenerative potential of Müller cells were also determined by immunofluorescence staining, quantitative RT-PCR, protein array, ELISA and Western blot. In the first 3–7days after NaIO3 administration, Müller cells were activated and underwent a fate switch, including transient proliferation, dedifferentiation and neurogenesis. Nerve growth factor (NGF) signaling concomitantly increased with the downregulation of p27Kip1 in Müller cells, which may promote Müller cells to re-enter the cell cycle. The transient increase of NGF signaling and the transient decrease of Notch signaling inhibited Hes1, which might enhance the neuronal differentiation of dedifferentiated Müller cells and suppress gliosis. Upregulated Notch and decreased NGF expressions limit dedifferentiation and neurogenesis, but induces retinal Müller cell gliosis at a later stage. We conclude that transient NGF upregulation and Notch1 downregulation may activate the transient proliferation, dedifferentiation and neurogenesis of Müller cells during NaIO3-induced acute retinal injury; which could be a therapeutic target for overcoming Müller cell gliosis. Such therapy could be potentially used for treating retinal-related diseases

Disitamab Vedotin plus anti-PD-1 antibody show good efficacy in refractory primary urethral cancer with low HER2 expression: a case report

Primary urethral carcinoma (PUC) has a low incidence, but with high aggressiveness. Most of the patients are found in late stage, with poor prognosis. At present, chemotherapy is still the main treatment for metastatic PUC, but it has limited effect. Here, we report a case of metastatic PUC with low HER2 expression that developed disease progression after multiline therapy including chemotherapy, programmed death-1 (PD-1) inhibitors and multi-targeted receptor tyrosine kinase (RTK) inhibitor. After receiving Disitamab Vedotin(a novel antibody drug conjugate, ADC) and toripalimab (a PD-1 inhibitor), the patient achieved persistent PR, and the PFS exceeded 12 months up to now. Our report indicates that, despite the patient of metastatic PUC has low expression of HER2, it is still possible to benefit from Disitamab Vedotin combined with PD-1 inhibitor, which may reverse the drug resistance of PD-1 inhibitor and chemotherapy to a certain extent. But larger sample studies are needed to determine the efficacy of this treatment strategy and its impact on survival

Cobrotoxin from Naja naja atra

Chronic kidney disease (CKD) becomes a global health problem with high morbidity and mortality. Adriamycin- (ADR-) induced rodent chronic nephropathy is a classic experimental model of human minimal lesion nephrotic syndrome. The present study investigated the effect of cobrotoxin (CTX) on ADR-induced nephropathy. Rats were given 6 mg/kg ADR once through the tail vein to replicate ADR nephropathy model. CTX was administered to rats daily by placing a fast dissolving CTX membrane strip under the tongue starting from 5 days prior to ADR administration until the end of experiment. The results showed that CTX ameliorated the symptoms of ADR nephropathy syndrome with reduced body weight loss, proteinuria, hypoalbuminemia, dyslipidemia, serum electrolyte imbalance, oxidative stress, renal function abnormities, and kidney pathological lesions. Anti-inflammatory cytokine IL-10 expression was elevated after CTX administration in ADR nephropathy model. CTX inhibited the phosphorylation of IκB-α and NF-κB p65 nuclear translocation. Meanwhile, CTX upregulated the protein level of podocyte-specific nephrin and downregulated the level of fibrosis-related TGF-β. These findings suggest that CTX may be a potential drug for chronic kidney diseases

Ghrelin Stimulates Hepatocyte Proliferation via Regulating Cell Cycle Through GSK3β/Β-Catenin Signaling Pathway

Background/Aims: Obesity is associated with a reduction in ghrelin, a 28 aa gastric hormone. Whether reduced ghrelin contributes to the impaired proliferation of hepatocytes associated with obesity-related steatosis remains largely unknown. Here we examined the effects of ghrelin on the proliferation of hepatocytes derived from lean and obese mice. Methods: AML 12 cells or hepatocytes isolated from mice fed normal chow diet (NCD) or high fat diet (HFD) were used. Effects of ghrelin on hepatocyte proliferation were detected with CCK8 assay and EdU staining. Cell cycle was analyzed by flow cytometry. Levels of proliferation markers was examined by Western blot. Results: Growth hormone secretagogue receptor 1a (GHS-R1a) mRNA and protein were present in hepatocytes. Levels of GHS-R1a were increased upon ghrelin treatment. Ghrelin significantly increased hepatocyte proliferation measured by Cell Counting Kit-8(CCK8) assay and EdU staining in a dose- and time-dependent manner. Proportion of cells in S phase was markedly increased upon treatment with ghrelin. Ghrelin significantly increased levels of proliferating cell nuclear antigen (PCNA) and cyclin D1, while reducing p27 in hepatocytes from mice fed NCD or HFD. Deletion of GHS-R1a completely abolished the effects of ghrelin in cultured hepatocytes. Ghrelin stimulated the phosphorylation of glycogen synthase kinase 3 beta (GSK3β), leading to subsequent increase of nuclear β-catenin in hepatocytes derived from lean and obese mice. This effect was dependent on the GHS-R1a. Conclusion: Ghrelin activates GHS-R1a to stimulate hepatocyte proliferation via GSK3/β-catenin signaling pathway

The Role of Eye Movement Driven Attention in Functional Strabismic Amblyopia

Strabismic amblyopia “blunt vision” is a developmental anomaly that affects binocular vision and results in lowered visual acuity. Strabismus is a term for a misalignment of the visual axes and is usually characterized by impaired ability of the strabismic eye to take up fixation. Such impaired fixation is usually a function of the temporally and spatially impaired binocular eye movements that normally underlie binocular shifts in visual attention. In this review, we discuss how abnormal eye movement function in children with misaligned eyes influences the development of normal binocular visual attention and results in deficits in visual function such as depth perception. We also discuss how eye movement function deficits in adult amblyopia patients can also lead to other abnormalities in visual perception. Finally, we examine how the nonamblyopic eye of an amblyope is also affected in strabismic amblyopia

Critical Roles of microRNA-141-3p and CHD8 in Hypoxia/Reoxygenation-Induced Cardiomyocyte Apoptosis

Background: Cardiovascular diseases are currently the leading cause of death in humans. The high mortality of cardiac diseases is associated with myocardial ischemia and reperfusion (I/R). Recent studies have reported that microRNAs (miRNAs) play important roles in cell apoptosis. However, it is not known yet whether miR-141-3p contributes to the regulation of cardiomyocyte apoptosis. It has been well established that in vitro hypoxia/reoxygenation (H/R) model can follow in vivo myocardial I/R injury. This study aimed to investigate the effects of miR-141-3p and CHD8 on cardiomyocyte apoptosis following H/R. Results: We found that H/R remarkably reduces the expression of miR-141-3p but enhances CHD8 expression both in mRNA and protein in H9c2 cardiomyocytes. We also found either overexpression of miR-141-3p by transfection of miR-141-3p mimics or inhibition of CHD8 by transfection of small interfering RNA (siRNA) significantly decrease cardiomyocyte apoptosis induced by H/R. Moreover, miR-141-3p interacts with CHD8. Furthermore, miR-141-3p and CHD8 reduce the expression of p21. Conclusion: MiR-141-3p and CHD8 play critical roles in cardiomyocyte apoptosis induced by H/R. These studies suggest that miR-141-3p and CHD8 mediated cardiomyocyte apoptosis may offer a novel therapeutic strategy against myocardial I/R injury-induced cardiovascular diseases

An Efficient and Privacy-Preserving Multiuser Cloud-Based LBS Query Scheme

Location-based services (LBSs) are increasingly popular in today’s society. People reveal their location information to LBS providers to obtain personalized services such as map directions, restaurant recommendations, and taxi reservations. Usually, LBS providers offer user privacy protection statement to assure users that their private location information would not be given away. However, many LBSs run on third-party cloud infrastructures. It is challenging to guarantee user location privacy against curious cloud operators while still permitting users to query their own location information data. In this paper, we propose an efficient privacy-preserving cloud-based LBS query scheme for the multiuser setting. We encrypt LBS data and LBS queries with a hybrid encryption mechanism, which can efficiently implement privacy-preserving search over encrypted LBS data and is very suitable for the multiuser setting with secure and effective user enrollment and user revocation. This paper contains security analysis and performance experiments to demonstrate the privacy-preserving properties and efficiency of our proposed scheme