Objective To determine the effects and mechanisms of somatostatin analogues (sandostatin) on pancreatic repair and regeneration in caerulein induced pancreatitis. Methods Acute pancreatitis was induced by intra abdominal infusion of caerulein in rats, sandostatin was administered intra abdominally at the time of induction of pancreatitis and 24, 48 and 72 hours after. Rats were sacrificed at 6, 24, 48, 72 and 96 hours after the operation. The mRNA expression for Transforming growth factor ? 1 (TGF ? 1) was evaluated by reverse transcription polymerase chain reaction, pancreatic tissue DNA synthesis was measured by 3H thymidine method in vitro and protein content was detected by Lowry's method. Results The serum amylase level was decreased significantly in the sandostatin treated group. Expression of TGF ? 1 mRNA was undetectable in the normal pancreas and the treated group at 6 hours. TGF ? 2 was observed at 24 hours after the induction of pancreatitis, reaching maximum at 72 hours. It could be detected in the sandostatin treated group at 6 hours, reaching maximum at 24 hours, the expression of TGF ? 1 was increased significantly in the sandostatin treated group as compared with the non treated group at 24, 48 hours. Pancreatic tissue DNA synthesis showed a significant decrease during the first 72 hours following the induction of pancreatitis and a marked increase was observed at 96 hours after treatment with sandostatin. Within 48 hours of the induction of pancreatitis, total protein content in pancreatic tissue declined, and there was a significant increase in the sandostatin treated group at 48 hours, reaching maximum at 96 hours. Conclusions Effects of somatostatin analogues (sandostatin) on pancreatic tissue regeneration in acute pancreatitis in rats might be attributed to the enhancement of TGF ? 1 gene expression which subsequently stimulates formation of extracellular matrix components, increases protein content and DNA synthesis, thus accelerates pancreatic repair and regeneration.

Objective To investigate the expressions of aquaporin 4 (AQP4) in the bacterial meningitis in rats and to explore the molecular mechanism for brain edema caused by bacterial meningitis.Methods Totally 40 of 3-week-old-Sprague-Dawley healthy rats,body weight 60-80 g,male or female,were divided into a normal control group(n =10),and infection groups:24 hours after injection(n =10),48 hours after injection(n =10),and 5 days after injection(n =10).The expressions of AQP4 in the brain were detected by immunohistochemistry and Western blot methods respectively after 24 hours,48 hours,5 days of inoculation.Results Mortality rate:no rats in the control group and the infection group after 24 hours were dead.Two rats in the infection group after 48 hours and 4 rats in the infection group after 5 days were dead because of serious sickness,with the mortality rates 20％ and 40％,respectively.AQP4 expression was slightly positive under light microscope,and the positive cells mainly surrounded glial cells and blood vessels,while neurons were not dyed.Immunohistochemical staining showed that AQP4 expression in the model group increased with the severity of edema;compared with the control group,the AQP4 expression in the brain tissues increased in different periods after rats were infected,and the differences between groups were statistically significant (F--91.84,P ＜ 0.01).Western blot analysis showed that after the brain received streptococcus pneumoniae injection,expression of AQP4 began to increase in 24 hours after streptococcal injection,and reached to the peak in 48 hours,but decreased in 5 days,but the expression still remained higher than that of the normal control group.Each group had statistically significant difference(F =14.23,P ＜ 0.01).Conclusions Expression of AQP4 in the models with bacterial meningitis may increase initially and decrease later.It suggests that AQP4 plays a protective role during the development of infectious brain edema.

Abstract: Upon monitoring cytoplasmic aberrant double-stranded DNA, cGAS-STING signaling pathway induces the expression of type I interferons and pro-inflammatory cytokines, which activates the host immune response and enhances anti-tumor immune response and resistance to pathogen infection. However, sustained activation of the cGAS-STING signaling pathway drives diseases such as autoimmune diseases, aging-associated inflammation, and neurodegenerative pathologies. Herein, we describe the mechanism by which cGAS-STING signaling pathway participates in regulating the development of various immune-related diseases, with a particular review of the research and development progress of STING agonists, cGAS inhibitors, and STING inhibitors, aiming to provide some theoretical reference for the future development of cGAS-STING modulators.

"The Expert Group on Tumor Ablation Therapy of Chinese Medical Doctor Association, The Tumor Ablation Committee of Chinese College of Interventionalists, The Society of Tumor Ablation Therapy of Chinese Anti-Cancer Association and The Ablation Expert Committee of the Chinese Society of Clinical Oncology" have organized multidisciplinary experts to formulate the consensus for thermal ablation of pulmonary subsolid nodules or ground-glass nodule (GGN). The expert consensus reviews current literatures and provides clinical practices for thermal ablation of GGN. The main contents include: (1) clinical evaluation of GGN, (2) procedures, indications, contraindications, outcomes evaluation and related complications of thermal ablation for GGN and (3) future development directions.
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