Loss of polycystin-2 (PC2) in mice (Pkd2Ϫ/Ϫ ) results in total body edema, focal hemorrhage, structural cardiac defects, abnormal left-right axis, hepatorenal and pancreatic cysts, and embryonic lethality. The molecular mechanisms by which loss of PC2 leads to these phenotypes remain unknown. We generated a model to allow targeted Pkd2 inactivation using the Cre-loxP system. Global inactivation of Pkd2 produced a phenotype identical to Pkd2 Ϫ/Ϫ mice with undetectable PC2 protein and perinatal lethality.Using various Cre mouse lines, we found that kidney, pancreas, or time-specific deletion of Pkd2 led to cyst formation. In addition, we developed an immortalized renal collecting duct cell line with inactive Pkd2; these cells had aberrant cell-cell contact, ciliogenesis, and tubulomorphogenesis. They also significantly upregulated ␤-catenin, axin2, and cMyc. Our results suggest that loss of PC2 disrupts normal behavior of renal epithelial cells through dysregulation of ␤-catenin-dependent signaling, revealing a potential role for this signaling pathway in PC2-associated ADPKD.

Backgroud: Bladder cancer (BLCA) is one of the most fatal types of cancer worldwide. However, there are limited methods for us to provide a prognostic prediction of BLCA patients. Therefore, we aimed at developing a lncRNA signature to improve the prognosis prediction of BLCA.Results: An eight-lncRNA signature was significantly associated with recurrence free survival in BLCA patients from both discovery and validation groups. Furthermore, genes involved in the signature were enriched in extracellular matrix organization pathway. Finally, functional experiments demonstrated that six out of the eight lncRNAs significantly regulated the invasion of BLCA cells.Method: A total of 343 BLCA patients from The Cancer Genome Atlas (TCGA) were employed and randomly divided into training (n=172) and validating (n=171) groups. The lncRNA expression profiles of BLCA patients were screened and a risk-score formula were created and validated according to the Cox regression analysis. Next, WGCNA method was employed to cluster genes that highly correlated with the risk scores based on the profiling data of TCGA dataset and transwell assay was also performed to further investigate the role of these lncRNAs.Conclusions: Our results suggested that the eight-lncRNA signature was a candidate prognostic biomarker for predicting tumor recurrence of patients with BLCA.

BackgroundAcademic burnout refers to students who have low interest, lack of motivation, and tiredness in studying. Studies concerning how to prevent academic burnout are rare.ObjectiveThe present study aimed to investigate the impact of core self-evaluations on the academic burnout of university students, and mainly focused on the confirmation of the mediator role of life satisfaction.MethodsA total of 470 university students accomplished the core self-evaluation scale, Satisfaction with Life, and academic burnout scale.ResultsBoth core self-evaluations and life satisfaction were significantly correlated with academic burnout. Structural equation modeling indicated that life satisfaction partially mediated the relationship between core self-evaluations and academic burnout.ConclusionsCore self-evaluations significantly influence academic burnout and are partially mediated by life satisfaction.

Bicaudal-C (Bic-C) gene was originally discovered in Drosophila melanogaster. The gene product Bic-C is thought to serve as an RNA-binding molecule targeting diverse proteins at the posttranscriptional level. Recent research has shown this gene to be conserved in many species, from Caenorhabditis elegans to humans. Disruption of this protein can disturb the normal migration direction of the anterior follicle cell of Drosophila oocytes, while mutation of a mouse Bicc1 (a mouse homologue of Bic-C) results in phenotypes mimicking human hereditary polycystic kidney disease (PKD). However, the cellular function of Bicc1 gene products in mammalian system remains largely unknown. In this study, we established stable IMCD (mouse inner medullary collecting duct) cell lines, in which Bicc1 was silenced by short hairpin RNA inhibition (shRNA). We show that inhibition of Bicc1 disrupted normal tubulomorphogenesis and induced cystogenesis of IMCD cells grown in three dimensional cultures. To determine what factors contributed to the defect, we systematically examined biological changes of Bicc1-silenced IMCD cells. We found that the cells had significant defects in E-cadherin-based cell-cell adhesion, along with abnormalities in actin cytoskeleton organization, cell-extracellular matrix interactions, cell proliferation, and apoptosis. These findings suggest that lack of Bicc1 leads to disruption of normal cell-cell junctions, which in turn impedes establishment of epithelial polarity. These cellular defects may initiate abnormal tubulomorphogenesis and cystogenesis of IMCD cells grown in vitro. The observation of aberrant cellular behaviors in Bicc1-silenced IMCD cells reveal functions for Bicc1 in renal epithelial cells and provides insight into a potential pathogenic mechanism of polycystic kidney disease.

Purpose: The anterior and medial approaches in open reduction for developmental dysplasia of the hip (DDH) had been widely used. The former could not directly approach the intra-articular interposition, while the latter had been associated with injury to blood vessel and avascular necrosis (AVN) of the femoral head. Meanwhile, the bikini incision had also been mentioned in some studies. The purpose of this study was to introduce a modified anterior approach through a mini-bikini incision and report its short-term outcomes. Methods: Data of DDH patients younger than 2 years at the time of surgery who had received this mini-bikini incision between June 2013 and December 2018 were collected. The surgical technique, operation duration, intraoperative blood loss, and length of incision were recorded in detail. In the latest follow up, the objective measurement of the scar and the subjective feeling towards the scar were collected. X-ray and magnetic resonance imaging (MRI) were performed at the last follow-up, and the incidence of residual dysplasia, redislocation, and femoral head AVN was analyzed. Results: Forty-three cases (49 hips) were included with an averaged follow-up of 43 months. The operation duration was 22 min, and the blood loss was 9.8 ml on average. The length of the scar averaged 2.6 cm. The mean University of North Carolina "4P" scar scale (UNC4P) for the scar was 0.92, and no patients complained numbness. Overall, all the parents were satisfied with the cosmetic appearance. The mean acetabular index (AI) was 27.42°± 6.41°in dislocated hip in the last follow-up. One hip redislocated soon after the operation and was reduced in a closed manner right away. MRI showed improved coverage but still some residual dysplasia that was in accordance with the post-operative recovery nature. Four hips (8%) had signs of AVN in X-ray. Conclusion: Open reduction through the anterior approach with the mini-bikini incision was a safe procedure with comparable outcomes to classical approaches. It would be a complementary approach for DDH patients younger than 2 years old who need an open reduction.

Bicc1 is a mouse homologue of Drosophila Bicaudal-C (dBic-C), which encodes an RNA-binding protein. Orthologs of dBic-C have been identified in many species, from C. elegans to humans. Bicc1-mutant mice exhibit a cystic phenotype in the kidney that is very similar to human polycystic kidney disease. Even though many studies have explored the gene characteristics and its functions in multiple species, the developmental profile of the Bicc1 gene product (Bicc1) in mammal has not yet been completely characterized. To this end, we generated a polyclonal antibody against Bicc1 and examined its spatial and temporal expression patterns during mouse embryogenesis and organogenesis. Our results demonstrated that Bicc1 starts to be expressed in the neural tube as early as embryonic day (E) 8.5 and is widely expressed in epithelial derivatives including the gut and hepatic cells at E10.5, and the pulmonary bronchi at E11.5. In mouse kidney development, Bicc1 appears in the early ureteric bud and mesonephric tubules at E11.5 and is also expressed in the metanephros at the same stage. During postnatal kidney development, Bicc1 expression gradually expands from the cortical to the medullary and papillary regions, and it is highly expressed in the proximal tubules. In addition, we discovered that loss of the Pkd1 gene product, polycystin-1 (PC1), whose mutation causes human autosomal dominant polycystic kidney disease (ADPKD), downregulates Bicc1 expression in vitro and in vivo. Our findings demonstrate that Bicc1 is developmentally regulated and reveal a new molecular link between Bicc1 and Pkd1.

The use of TILs has a better clinical efficiency for malignant pleural effusion and ascites than cisplatin through intrapleural and intraperitoneal infusion without severe adverse effects.

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