A brief discussion on the inspiration and thinking of the Metaverse concept to promote the innovative development of intelligent medicine in China / 中华外科杂志

Created by digital technology,the Metaverse is a digital platform where the digital virtual world and the actual real world can coexist to some extent. Based on the integration of Metaverse and medical science,this article describes the great development of intelligent medicine in the fields of medical practice,medical education and medical research,especially in the field of surgery. First,the technical source of the Metaverse concept in the field of intelligent medicine can be traced back to technology to generate actual digital data sets from human anatomy. Second,the successful industrial practice of Metaverse in the field of intelligent medicine conforms to the authentic and credible fundamental purpose of "taking people as the first priority and serving people"， that is， "virtual" must be based on "actual" for "actual".

Protective effect of autophagy inhibition on ischemia-reperfusioninduced injury of N2a cells / 华中科技大学学报（医学）（英德文版）

Autophagy is a conserved and programmed catabolic process that degrades damaged proteins and organelles. But the underlying mechanism and functions of autophagy in the ischemiareperfusion (IR)-induced injury are unknown. In this study, we employed simulated IR of N2a cells as an in vitro model of IR injury to the neurons and monitored autophagic processes. It was found that the levels of Beclin-1 (a key molecule of autophay complex, Beclin-1/class III PI3K) and LC-3II (an autophagy marker) were remarkably increased with time during the process of ischemia and the process of reperfusion after 90 min of ischemia, while the protein kinases p70S6K and mTOR which are involved in autophagy regulation showed delayed inactivation after reperfusion. Administration of 3-methyladenine (3MA), an inhibitor of class III PI3K, abolished autophagy during reperfusion, while employment of rapamycin, an inhibitor of mTORC1 (normally inducing autophagy), surprisingly weakened the induction of autophagy during reperfusion. Analyses of mitochondria function by relative cell viability demonstrated that autophagy inhibition by 3-MA attenuated the decline of mitochondria function during reperfusion. Our data demonstrated that there were two distinct dynamic patterns of autophagy during IR-induced N2a injury, Beclin-1/class III PI3K complex-dependent and mTORC1-dependent. Inhibition of over-autophagy improved cell survival. These suggest that targeting autophagy therapy will be a novel strategy to control IR-induced neuronal damage.

Protective effect of autophagy inhibition on ischemia-reperfusion-induced injury of N2a cells / 华中科技大学学报（医学）（英德文版）

Autophagy is a conserved and programmed catabolic process that degrades damaged proteins and organelles. But the underlying mechanism and functions of autophagy in the ischemia-reperfusion (IR)-induced injury are unknown. In this study, we employed simulated IR of N2a cells as an in vitro model of IR injury to the neurons and monitored autophagic processes. It was found that the levels of Beclin-1 (a key molecule of autophay complex, Beclin-1/class III PI3K) and LC-3II (an autophagy marker) were remarkably increased with time during the process of ischemia and the process of reperfusion after 90 min of ischemia, while the protein kinases p70S6K and mTOR which are involved in autophagy regulation showed delayed inactivation after reperfusion. Administration of 3-methyladenine (3MA), an inhibitor of class III PI3K, abolished autophagy during reperfusion, while employment of rapamycin, an inhibitor of mTORC1 (normally inducing autophagy), surprisingly weakened the induction of autophagy during reperfusion. Analyses of mitochondria function by relative cell viability demonstrated that autophagy inhibition by 3-MA attenuated the decline of mitochondria function during reperfusion. Our data demonstrated that there were two distinct dynamic patterns of autophagy during IR-induced N2a injury, Beclin-1/class III PI3K complex-dependent and mTORC1-dependent. Inhibition of over-autophagy improved cell survival. These suggest that targeting autophagy therapy will be a novel strategy to control IR-induced neuronal damage.

Expression of sonic hedgehog signaling pathways in a rat model of chronic pancreatitis.

OBJECTIVE: To establish a rat model of chronic pancreatitis, and to prove the activation of sonic hedgehog (SHH) signaling pathways in chronic pancreatitis. METHODS: This study was conducted between January and July 2008 in the Department of General Surgery, Wuhan General Hospital, Guangzhou Military Command, Wuhan, China. Thirty Wistar rats were randomly divided into 3 groups: control group (A), experimental control group (B), and model group (C) (10 rats in each group). Trinitrobenzene sulfonic acid was infused into the pancreatic duct to induce chronic pancreatitis in the model group rats. In the experimental control group, we opened the abdominal cavity and infused with 0.9% sodium chloride solution. Serum levels of bilirubin and amylase were determined by radioimmunoassay. Histopathological alterations were studied using the optical microscopy. Expression of patched-1 (PTCH-1), smoothened (SMO), and SHH were detected by immunohistochemistry. RESULTS: Compared with the control group (A), the serum bilirubin and amylase in the model group increased significantly after 7 days of treatment, and fibrotic proliferation of pancreatic tissues were found after 35 days; the expression of PTCH-1, SMO, and SHH in the pancreatic tissue increased significantly in the model group. CONCLUSION: Trinitrobeneze sulfonic acid can induce chronic pancreatitis in rat. The SHH signaling pathway is activated in rats with chronic pancreatitis.

Significances of gene differential expression patterns in hepatocirrhosis and non-hepatocirrhosis tissues within different ischemic time / 中华外科杂志

<p><b>OBJECTIVE</b>To investigate the gene differential expression patterns in hepatocirrhosis and non-hepatocirrhosis tissues within different ischemic time.</p><p><b>METHODS</b>The liver tissues were divided into two groups: Group A (non-hepatocirrhosis), Group B (hepatocirrhosis), each of which consisted of 3 groups with different ischemic time: 15, 30 and 45 minutes. The gene differential expression patterns in the two groups within different ischemic time were detected and compared with those in normal liver tissues by using 4000 points gene microarray.</p><p><b>RESULTS</b>In non-hepatocirrhosis tissues, the homeostatic maintenance genes expressed highly during hepatic ischemia for 15 minutes, and no apoptotic gene was expressed; but in hepatocirrhosis tissues, many apoptotic genes expressed highly. As for 30 minutes, in both two groups liver tissue genes expressed to the peak, and the genes related to cell death, oxidative stress and nuclear factors expressed highly. The difference lies in the facts that in Group B pro-apoptosis genes expressed more than those in Group A, and the Ratio values were higher than those in Group A. Many genes of heat shock protein family and antioxidant proteins expressed highly simultaneously in Group A, but comparatively low in Group B. As for 45 minutes, genes of heat shock proteins and antioxidant proteins expressed lowly in Group B.</p><p><b>CONCLUSIONS</b>It suggests that the safe time limit of hepatic ischemia for cell survive is 30 minutes or so. Non-hepatocirrhosis tissues could endure 30 minutes of ischemia and even longer, but it should be restricted within 30 minutes in hepatocirrhosis tissues.</p>