Gastric mucosal endogenous prostacyclin levels are different in Brattleboro rats compared with Wistar strain

Homozygous Brattleboro rats were investigated and compared to normal (physiological) Wistar strain rats regarding their gastric mucosal endogenous prostacyclin (PG-I(2)) level. It seems that the Brattleboro animals have a significantly lower level of this important protective material. Wistar rats having an artificial pituitary stalk lesion (which is the artificial equivalent of homozygous Brattleboro animals) showed no differences in endogenous mucosal prostacyclin level compared to normal Wistar rats. Therefore, we concluded that this hitherto unknown property of the homozygous Brattleboro rats is genetically determined.     

Gastric mucosal integrity: gastric mucosal blood flow and microcirculation. An overview

The stomach is in a state of continuous exposure to potentially hazardous agents. Hydrochloric acid together with pepsin constitutes a major and serious threat to the gastric mucosa. Reflux of alkaline duodenal contents containing bile and pancreatic enzymes are additional important injurious factors of endogenous origin. Alcohol, cigarette smoking, drugs and particularly aspirin and aspirin-like drugs, and steroids are among exogenous mucosal irritants that can inflict mucosal injury. The ability of the stomach to defend itself against these noxious agents has been ascribed to a number of factors constituting the gastric mucosal defense. These include mucus and bicarbonate secreted by surface epithelial cells, prostaglandins, sulfhydryl compounds and gastric mucosal blood flow. The latter is considered by several researchers to be of paramount importance in maintaining gastric mucosal integrity. The aim of this paper is to review the experimental and clinical data dealing with the role of mucosal blood flow and in particular the microcirculation in both damage and protection of the gastric mucosa.     

53BP1 Enforces Distinct Pre- and Post-resection Blocks on Homologous Recombination

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Respiratory mucosal delivery of next-generation COVID-19 vaccine provides robust protection against both ancestral and variant strains of SARS-CoV-2

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肠内营养支持联合益生菌促进重症急性胰腺炎患者恢复的临床机制研究

目的阐述益生菌联合肠内营养支持对改善重症急性胰腺炎患者肠道微生态以及粘膜屏障功能的临床应用价值。方法选取我院收治的100例重症急性胰腺炎患者作为研究对象,随机分为观察组和对照组,各50例。观察组患者接受益生菌制剂联合肠内营养,对照组患者仅接受肠内营养,持续2周。比较两组患者的血浆生化指标、胃肠道功能、肠粘膜屏障功能、并发症发生率、病死率及住院时间。收集两组患者的粪便,检测菌群变化。结果在治疗第7 d,观察组患者的白细胞数和血浆生化指标明显低于对照组。治疗第14 d,观察组生化检测指标均明显低于对照组。胃肠道功能评分方面,治疗第7、14 d,观察组评分均较对照组明显降低；治疗第7 d、14 d,两组患者血浆MDA、ET、CRP水平和尿L/M均出现明显下降,观察组较对照组下降更明显；观察组的总体并发症发生率及住院时间与对照组比较,具有统计学差异。实时荧光定量PCR结果显示,经过14 d治疗后观察组患者大肠埃希菌、肺炎克雷伯菌的数量明显低于对照组。对照组病人双歧杆菌和乳酸菌数量明显高于对照组。结论肠内营养治疗联合益生菌有利于促进重症急性胰腺炎肠道功能的恢复,值得在临床上应用推广。     

Protection from SARS-CoV-2 Delta one year after mRNA-1273 vaccination in rhesus macaques coincides with anamnestic antibody response in the lung

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血流阻断的缺血预处理技术在肝癌切除术中的临床应用价值

目的:探讨血流阻断的缺血预处理技术在肝癌切除术中的临床应用价值。方法:选取2010年4月至2013年7月我院收治的96名原发性肝癌并采用肝脏部分切除术进行治疗的患者,将患者随机分为观察组和对照组,每组各48例,观察组在肝脏部分切除术阻断肝门血流前先分别给予1个5 min缺血和再灌注的处理。对照组不采取任何干预措施。术前、术后1天、3天、7天时分别进行生化检查,并于术前及术后1h对Fas-mRNA表达、Caspasc-3活性及AI进行测定,观察记录患者术后的并发症情况、手术时间、术中出血量以及住院时间。结果:术后1天、3天、7天时两组间的AST、ALT、TBIL等生化指标的含量情况相比,观察组均显著优于对照组(P0.05);术后l d,两组患者ALB均有不同程度的降低,对照组低于观察组(P0.05);术后住院时间观察组为13.28±3.85天,对照组为19.48±4.92天,观察组明显低于对照组(P0.05);术后1h,两组患者的Fas-mRNA表达、Caspasc-3活性相比于阻断前均显著提高,但观察组提高幅度明显低于对照组,差异有统计学意义(P0.05);两组阻断前均未见肝细胞凋亡,术后l h时,两组组均可见肝细胞凋亡,且对照组明显高于观察组组(P0.05)。结论:血流阻断的缺血预处理技术具有操作简便、副作用小的重要特点,应用于肝癌切除术中在保护肝功能方面具有显著的优势。     

Regulation of autophagy protects against liver injury in liver surgery-induced ischaemia/reperfusion

Transient ischaemia and reperfusion in liver tissue induce hepatic ischaemia/reperfusion (I/R) tissue injury and a profound inflammatory response in vivo. Hepatic I/R can be classified into warm I/R and cold I/R and is characterized by three main types of cell death, apoptosis, necrosis and autophagy, in rodents or patients following I/R. Warm I/R is observed in patients or animal models undergoing liver resection, haemorrhagic shock, trauma, cardiac arrest or hepatic sinusoidal obstruction syndrome when vascular occlusion inhibits normal blood perfusion in liver tissue. Cold I/R is a condition that affects only patients who have undergone liver transplantation (LT) and is caused by donated liver graft preservation in a hypothermic environment prior to entering a warm reperfusion phase. Under stress conditions, autophagy plays a critical role in promoting cell survival and maintaining liver homeostasis by generating new adenosine triphosphate (ATP) and organelle components after the degradation of macromolecules and organelles in liver tissue. This role of autophagy may contribute to the protection of hepatic I/R-induced liver injury; however, a considerable amount of evidence has shown that autophagy inhibition also protects against hepatic I/R injury by inhibiting autophagic cell death under specific circumstances. In this review, we comprehensively discuss current strategies and underlying mechanisms of autophagy regulation that alleviates I/R injury after liver resection and LT. Directed autophagy regulation can maintain liver homeostasis and improve liver function in individuals undergoing warm or cold I/R. In this way, autophagy regulation can contribute to improving the prognosis of patients undergoing liver resection or LT.