Board informal hierarchy, strategic aggressiveness, and corporate ESG performance.

Based on the stakeholder theory, relationship contract theory, and other theories, this study examined how the board informal hierarchy influences corporate ESG (Environmental, Social, and Governance) performance, using Chinese A-share listed enterprises from 2010 to 2022 as the research samples. The results indicated that the clearer the board informal hierarchy, the better the corporate ESG performance. Furthermore, the board informal hierarchy can enhance the ESG performance by promoting more aggressive strategic initiatives.

HSF1 promotes CD69 Treg differentiation to inhibit colitis progression.

Regulatory T cells (Tregs) are critical for generating and maintaining peripheral tolerance. Treg-based immunotherapy is valuable for the clinical management of diseases resulting from dysregulation of immune tolerance. However, the lack of potency is a potential limitation of Treg therapy.

McKeown esophagectomy: robot-assisted versus conventional minimally invasive technique-systematic review and meta-analysis.

Background And Purpose: This meta-analysis assesses the surgical outcomes between robot-assisted minimally-invasive McKeown esophagectomy and conventional one.

Method: This meta-analysis searched the Web of Science, PUBMED, and EMBASE from the database's inception to January 2022. Altogether, 1073 records were identified in the literature search.

Chronic stress induced depressive-like behaviors in a classical murine model of Parkinson's disease.

Depression occurs in around 40 % of patients with Parkinson's disease (PD) and contributes to severe disability and a poor quality of life. The underlying mechanisms and pathophysiology of depression in PD (PDD) remain obscure, due to a lack of stable animal models of PDD. In this study, we established a PDD model by inducing exposure to chronic mild (CMS) and strong stress (CSS) using 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in PD mice.

Metabolic enzyme PDK3 forms a positive feedback loop with transcription factor HSF1 to drive chemoresistance.

: Dysregulation of metabolism plays an important role in the development and progression of cancers, while the underlying mechanisms remain largely unknown. This study aims to explore the regulation and relevance of glycolysis in chemoresistance of gastric cancer. Biochemical differences between chemoresistant and chemosensitive cancer cells were determined by metabolism profiling, microarray gene expression, PCR or western blotting.

SIRT1 deacetylated and stabilized XRCC1 to promote chemoresistance in lung cancer.

Chemoresistance is one of the most important challenges in the clinical management of lung cancer. SIRT1 is a NAD dependent protein deacetylase and implicated in diverse cellular processes such as DNA damage repair, and cancer progression. SIRT1 is upregulated in chemoresistant lung cancer cells, genetic knockdown or chemical inhibition of SIRT1 reversed chemoresistance by enhancing DNA damage and apoptosis activation, accompanied with XRCC1 degradation.

KDM5B demethylates H3K4 to recruit XRCC1 and promote chemoresistance.

Chemotherapy is the main treatment for human cancers including gastric cancer. However, in response to chemotherapeutic drugs, tumor cells can develop drug resistance by reprogramming intracellular metabolic and epigenetic networks to maintain their intrinsic homeostasis. Previously, we have established cisplatin-resistant gastric cancer cells as a drug resistant model, and elucidated the XRCC1 as the core DNA repair mechanism of drug resistance.

Rab5a suppresses autophagy to promote drug resistance in cancer cells.

Cancers are huge problems that need to be investigated thoroughly. Rab5a plays an important part in the regulation of intracellular membrane trafficking. However, its role in cancer and autophagy has not been fully determined.

Enolase 1 stimulates glycolysis to promote chemoresistance in gastric cancer.

Chemotherapy is the major choice for the cancer treatment of early and advanced stages. However, intrinsic or acquired drug resistance significantly restricts the clinical efficacy of chemotherapy. It is critical to develop novel approaches to detect and overcome drug resistance.

Loss of PIG3 increases HIF-1α level by promoting protein synthesis via mTOR pathway in renal cell carcinoma cells.

PIG3 is a target of the tumor suppressor p53 and is thought to be involved in p53-mediated cell apoptosis. Although PIG3 is similar to oxidoreductases involved in generating ROS, whether PIG3 would regulate HIF-1α was never characterized directly. Here we demonstrated that knockdown of PIG3 by transfecting with specific siRNA could increase the expression of HIF-1α in several human cancer cell lines, including CAKI, FTC-133 and A549.

Expression of HIF-1α and HIF-2α correlates to biological and clinical significance in papillary thyroid carcinoma.

Background: The aim of this study was to detect the expression of hypoxia-inducible factor (HIF)-1α and HIF-2α in papillary thyroid carcinoma (PTC) compared with normal thyroid tissues.

Methods: The mRNA levels and protein levels of HIF-1α and HIF-2α were detected by real-time PCR and Western blot separately in 30 pairs of PTCs and normal thyroid cases. The protein levels were also detected by immunohistochemistry (IHC) using 92 samples of PTC group and 46 normal samples as control group for analyzing the biological and clinical significance of the expression of HIF-1α/HIF-2α.

PIG3 plays an oncogenic role in papillary thyroid cancer by activating the PI3K/AKT/PTEN pathway.

The p53-inducible gene 3 (PIG3 or TP53I3) is a downstream gene of p53, which can be involved in the process of apoptosis induced by p53 via the production of reactive oxygen species (ROS). However, the functional significance of PIG3 in cancer remains to be determined. This aim of this study was to examine the mRNA and protein expression of PIG3 in papillary thyroid carcinoma (PTC) and normal thyroid tissues, assess the relationship between PIG3 expression and clinicopathological parameters in PTC and examine its role in the proliferation of PTC cell lines.

Nanofibrous collagen nerve conduits for spinal cord repair.

Nerve regeneration in an injured spinal cord is often restricted, contributing to the devastating outcome of neurologic impairment below the site of injury. Although implantation of tissue-engineered scaffolds has evolved as a potential treatment method, the outcomes remain sub-optimal. One possible reason may be the lack of topographical signals from these constructs to provide contact guidance to invading cells or regrowing axons.

Sustained release of neurotrophin-3 and chondroitinase ABC from electrospun collagen nanofiber scaffold for spinal cord injury repair.

Nerve regeneration after spinal cord injuries (SCI) remains suboptimal despite recent advances in the field. One major hurdle is the rapid clearance of drugs from the injury site, which greatly limits therapeutic outcomes. Nanofiber scaffolds represent a potential class of materials for enhancing nerve regeneration because of its biomimicking architecture.