Erythropoietin-induced hepatocyte receptor A2 regulates effect of pyroptosis on gastrointestinal colorectal cancer occurrence and metastasis resistance

Erythropoietin-induced hepatocyte receptor A2(EphA2)is a receptor tyrosine kinase that plays a key role in the development and progression of a variety of tumors.This article reviews the expression of EphA2 in gastrointestinal(GI)colorectal cancer(CRC)and its regulation of pyroptosis.Pyroptosis is a form of programmed cell death that plays an important role in tumor suppression.Studies have shown that EphA2 regulates pyrodeath through various signaling pathways,affecting the occurrence,development and metastasis of GI CRC.The overexpression of EphA2 is closely related to the aggressiveness and metastasis of GI CRC,and the inhibition of EphA2 can induce pyrodeath and improve the sensitivity of cancer cells to treatment.In addition,EphA2 regulates intercellular communication and the microenvironment through interactions with other cytokines and receptors,further influencing cancer progression.The role of EphA2 in GI CRC and its underlying mechanisms provide us with new perspectives and potential therapeutic targets,which have important implications for future cancer treatment.

The role of donor hepatocytes and/or splenocytes pre-injection in reducing islet xenotransplantation rejection

OBJECTIVE: To observe the effect of tail vein injection with donor hepatocyte and/or splenocyte on islets xenotransplantation rejection. METHODS: New-born male pigs and BALB/C mice were selected as donors and recipients respectively. Islets xenotransplantation was performed in recipients just after the third time of tail vein injection with donor hepatocytes and/or splenocytes. Macrophage phagocytosis, NK killing activity, T lymphocyte transforming function of spleen cells, antibody forming function of B lymphocytes, and T lymphocyte subsets were taken to monitor transplantation rejection. The effects of this kind of transplantation were indicated as variation of blood glucose and survival days of recipients. RESULTS: Streptozotocin (STZ) succeeded in inducing diabetes mellitus models of mice. Pre-injection of donor hepatocytes, and splenocytes or their mixture via tail vein was effective in preventing donor islets transplantation from rejection, which was demonstrated by the mentioned immunological marks. And each group of transplantation could decrease the blood glucose of recipients and prolong the survival days. Pre-injection of mixture of donor hepatocytes and splenocytes was more effective in preventing rejection than pre-injection of donor hepatocytes or splenocytes separately. CONCLUSION: We propose that pre-injection of donor hepatocytes, splenocytes separately or their mixture before donor islets transplantation is a good way to prevent rejection.

Whole-genome resequencing reveals molecular imprints of anthropogenic and natural selection in wild and domesticated sheep

The abundance of domesticated sheep varieties and phenotypes is largely the result of long-term natural and artificial selection. However, there is limited information regarding the genetic mechanisms underlying phenotypic variation induced by the domestication and improvement of sheep. In this study, to explore genomic diversity and selective regions at the genome level, we sequenced the genomes of 100 sheep across 10 breeds and combined these results with publicly available genomic data from 225 individuals, including improved breeds, Chinese indigenous breeds,African indigenous breeds, and their Asian mouflon ancestor. Based on population structure, the domesticated sheep formed a monophyletic group,while the Chinese indigenous sheep showed a clear geographical distribution trend. Comparative genomic analysis of domestication identified several selective signatures, including IFI44 and IFI44L genes and PANK2 and RNF24 genes, associated with immune response and visual function.Population genomic analysis of improvement demonstrated that candidate genes of selected regions were mainly associated with pigmentation,energy metabolism, and growth development.Furthermore, the IFI44 and IFI44L genes showed a common selection signature in the genomes of 30domesticated sheep breeds. The IFI44 c. 54413058C>G mutation was selected for genotyping and population genetic validation. Results showed that the IFI44 polymorphism was significantly associated with partial immune traits. Our findings identified the population genetic basis of domesticated sheep at the whole-genome level, providing theoretical insights into the molecular mechanism underlying breed characteristics and phenotypic changes during sheep domestication and improvement.

Mechanism and potential treatments for gastrointestinal dysfunction in patients with COVID-19

The global coronavirus disease 2019(COVID-19)has become one of the biggest threats to the world since 2019.The respiratory and gastrointestinal tracts are the main targets for severe acute respiratory syndrome coronavirus 2 infection for they highly express angiotensin-converting enzyme-2 and transmembrane protease serine 2.In patients suffering from COVID-19,gastrointestinal symptoms have ranged from 12%to 61%.Anorexia,nausea and/or vomiting,diarrhea,and abdominal pain are considered to be the main gastrointestinal symptoms of COVID-19.It has been reported that the direct damage of intestinal mucosal epithelial cells,malnutrition,and intestinal flora disorders are involved in COVID-19.However,the underlying mechanisms remain unclear.Thus,in this study,we reviewed and discussed the correlated mechanisms that cause gastrointestinal symptoms in order to help to develop the treatment strategy and build an appropriate guideline for medical workers.

腐殖酸对富勒烯C_60的悬浮作用(英文)

研究目的:腐殖酸(HA)对富勒烯(C60)粉末的悬浮作用以及pH、离子强度对HA-C60悬浮性能的影响。创新要点:研究水质条件对C60悬浮性能的影响。研究方法:测定C60粉末在HA溶液中的zeta电位,水力学粒径和悬浮浓度;HA存在下,C60悬浮体系的zeta电位与水力学粒径随pH的变化及C60悬浮体系团聚动力学随离子强度的变化。重要结论:HA对C60粉末起到一定的分散作用,但不能使其长时间稳定悬浮于水中。当pH<4时,C60水悬液开始沉淀;而当HA存在时,C60水悬液在pH 3–11范围内都保持稳定,这是由于HA吸附于C60表面,通过静电排斥和空间位阻作用,促进C60分散悬浮。C60水悬液的稳定性随盐离子价位和浓度升高而降低。HA会抑制Na+对C60水悬液的脱稳作用;但高价离子Ca2+和La3+存在时,HA与C60之间会发生桥联从而促进C60水悬液脱稳沉淀。

Upregulated insulin receptor tyrosine kinase substrate promotes the proliferation of colorectal cancer cells via the bFGF/AKT signaling pathway

Background:Some recent studies on insulin receptor tyrosine kinase substrate(IRTKS)have focused more on its functions in diseases.However,there is a lack of research on the role of IRTKS in carcinomas and its mechanism remains ambiguous.In this study,we aimed to clarify the role and mechanism of IRTKS in the carcinogenesis of colorectal cancer(CRC).Methods:We analysed the expression of IRTKS in CRC tissues and normal tissues by researching public databases.Cancer tissues and adjacent tissues of 67 CRC patients who had undergone radical resection were collected from our center.Quantitative real-time polymerase chain reaction and immunohistochemistry were performed in 52 and 15 pairs of samples,respectively.In vitro and in vivo experiments were conducted to observe the effect of IRTKS on CRC cells.Gene Set Enrichment Analysis and Metascape platforms were used for functional annotation and enrichment analysis.We detected the protein kinase B(AKT)phosphorylation and cell viability of SW480 transfected with small interfering RNAs(siRNAs)with or without basic fibroblast growth factor(bFGF)through immunoblotting and proliferation assays.Results:The expression of IRTKS in CRC tissues was higher than that in adjacent tissues and normal tissues(all P<0.05).Disease-free survival of patients with high expression was shorter.Overexpression of IRTKS significantly increased the proliferation rate of CRC cells in vitro and the number of tumor xenografts in vivo.The phosphorylation level of AKT in CRC cells transfected with pLVX-IRTKS was higher than that in the control group.Furthermore,siRNA-IRTKS significantly decreased the proliferation rate of tumor cells and the phosphorylation level of AKT induced by bFGF.Conclusion:IRTKS mediated the bFGF-induced cell proliferation through the phosphorylation of AKT in CRC cells,which may contribute to tumorigenicity in vivo.