Objective:To explore the current status of surgery for portal hypertension to grasp current status and future development of surgery in China.Methods:This study is jointly sponsored by China Hepatobiliary & Pancreatic Specialist Alliance & Portal Hypertension Alliance in China (CHESS).Comprehensive surveying is conducted for basic domestic situations of surgery for portal hypertension, including case load, surgical approaches, management of postoperative complications, primary effects, existing confusion and obstacles, liver transplantation(LT), laparoscopic procedures and transjugular intrahepatic portosystemic shunt(TIPS), etc.Results:A total of 8 512 cases of portal hypertension surgery are performed at 378 hospitals nationwide in 2021.Splenectomy plus devascularization predominated(53.0%)and laparoscopy accounted for 76.1%.Primary goal is preventing rebleeding(67.0%) and 72.8% of hospitals used preventive anticoagulants after conventional surgery.And 80.7% of teams believe that the formation of postoperative portal vein thrombosis is a surgical dilemma and 65.3% of hospitals practiced both laparoscopy and TIPS.The major reasons for patients with portal hypertension not receiving LT are due to a lack of qualifications for LT(69.3%)and economic factors(69.0%).Conclusions:Surgery is an integral part of management of portal hypertension in China.However, it is imperative to further standardize the grasp of surgical indications, the handling of surgical operation and the management of postoperative complications.Moreover, prospective, multi-center randomized controlled clinical studies should be performed.

Deficiencies in the clearance of peripheral amyloid β (Aβ) play a crucial role in the progression of Alzheimer's disease (AD). Previous studies have shown that the ability of blood monocytes to phagocytose Aβ is decreased in AD. However, the exact mechanism of Aβ clearance dysfunction in AD monocytes remains unclear. In the present study, we found that blood monocytes in AD mice exhibited decreases in energy metabolism, which was accompanied by cellular senescence, a senescence-associated secretory phenotype, and dysfunctional phagocytosis of Aβ. Improving energy metabolism rejuvenated monocytes and enhanced their ability to phagocytose Aβ in vivo and in vitro. Moreover, enhancing blood monocyte Aβ phagocytosis by improving energy metabolism alleviated brain Aβ deposition and neuroinflammation and eventually improved cognitive function in AD mice. This study reveals a new mechanism of impaired Aβ phagocytosis in monocytes and provides evidence that restoring their energy metabolism may be a novel therapeutic strategy for AD.
Animals ; Mice ; Alzheimer Disease ; Amyloid beta-Peptides ; Monocytes ; Cognition ; Energy Metabolism ; Phagocytosis

The present study investigated the therapeutic effect and mechanism of Di'ao Xinxuekang(DXXK) on non-alcoholic steatohepatitis(NASH) in mice. Sixty-five C57 BL/6 J mice were randomly divided into a normal group and an experimental group for model induction with the high-fat diet for 16 weeks. Then the mice in the experimental group were randomly divided into a model group, an atorvastatin group(4 mg·kg~(-1)·d~(-1)), and high-(200 mg·kg~(-1)·d~(-1)), medium-(60 mg·kg~(-1)·d~(-1)), and low-dose(20 mg·kg~(-1)·d~(-1)) DXXK groups, with 10 mice in each group. Drugs were administered by gavage for eight weeks. Serum lipid, liver lipid, serum alanine aminotransferase(ALT), aspartate aminotransferase(AST), malondialdehyde(MDA), superoxide dismutase(SOD), and glutathione reductase(GSH-Px) were determined. Interleukin-1β(IL-1β) and tumor necrosis factor-α(TNF-α) were measured by enzyme-linked immunosorbent assay(ELISA). The liver index was calculated. The liver pathological change and lipid accumulation were observed by HE and oil red O staining. The liver ultrastructure was observed by the transmission electron microscope. The mRNA and protein expression of nuclear factor-erythroid 2 related factor 2(Nrf2) and heme oxygenase-1(HO-1) was detected by real-time fluorescence-based quantitative PCR and Western blot, respectively. The results showed that compared with the normal group, the model group displayed serum lipid and liver lipid metabolism disorders, elevated transaminase, lipid deposition, steatosis, and inflammation, suggesting that the NASH model in mice was properly induced. Compared with the model group, the DXXK groups showed decreased serum lipid, liver lipid, ALT, AST, MDA, IL-1β, and TNF-α, increased SOD and GSH-Px, alleviated hepatic steatosis, ballooning, and inflammation, and up-regulated Nrf2 and HO-1 gene and protein expression. In conclusion, DXXK can significantly alleviate NASH in mice, which is related to the inhibition of oxidative stress and inflammatory damage by up-regulating the Nrf2/HO-1 signaling pathway.
Animals ; Drugs, Chinese Herbal ; Inflammation/metabolism* ; Lipids ; Liver ; Mice ; NF-E2-Related Factor 2/metabolism* ; Non-alcoholic Fatty Liver Disease/metabolism* ; Oxidative Stress ; Signal Transduction ; Superoxide Dismutase/metabolism* ; Tumor Necrosis Factor-alpha/metabolism*

Acute Kidney Injury/therapy* ; Anticoagulants/therapeutic use* ; Blood Coagulation ; Child ; Citrates ; Citric Acid/therapeutic use* ; Continuous Renal Replacement Therapy ; Humans ; Renal Replacement Therapy

Objective : To screen differentially expressed miRNAs and explore its effect and mechanism on cell mi- gration in lung adenocarcinoma (LUAD) ． Methods : Differentially expressed miRNAs in LUAD tissues and normal lung tissues were screened by miRNA microarrays，and then bioinformatics analysis was used to predict their poten- tial biological functions and signaling pathways．The cancer genome atlas (TCGA) analysis and quantitative real- time PCR (qRT-PCR) verified the expression level of hsa-let-7e-5p in LUAD tissues and cell lines．The effect of hsa-let-7e-5p cell migration in LUAD was examined by would healing experiment．After screening the underlying target genes by bioinformatics analysis ，the targeting relationship between hsa-let-7e-5p and DTX2，NME6， C8orf58，GATM and DHX57 were verified by qRT-PCR. Results : The miRNA microarray results showed that 347 miRNAs were down-regulated while 229 miRNAs were up-regulated in lung adenocarcinoma tissues．Compared with normal lung tissue and cells，the expression level of hsa-let-7e-5p was significantly down-regulated．Besides，over- expression of hsa-let-7e-5p inhibitedLUAD cell migration． Conclusion Non-coding RNA hsa-let-7e-5p is down- regulated in LUAD and inhibits the migration of lung adenocarcinoma cells．DTX2，NME6，C8orf58，GATM and DHX57 are the potential target genes of hsa-let-7e-5p.

OBJECTIVE To investigate whether Renqing Changjue has a protective effect on acute respiratory dis?tress syndrome (ARDS) induced by endotoxin lipopolysaccharide (LPS) in rabbits. METHODS Thirty-six healthy male New Zealand white rabbits were randomly divided into six groups: normal control group, model group, dexamethasone group, Renqing Changjue high, middle and low dose group, with six rabbits in each group. LPS was used to replicate the ARDS model after five consecutive days of gavage. Arterial pressure, respiratory rate and anal temperature blood were recorded for arterial blood gas analysis at 0, 0.5, 1, 2 and 4 h, respectively. At the end of the four-hour experiment, rab?bits were killed by bloodletting, and the lung tissue was quickly removed to determine the cytokines, SOD, MDA and pathological examination of rabbit lung. RESULTS Renqing Changjue can significantly reduce the pathological changes of lung in ARDS model group. The expression of AQP1 and MPO in rabbit lung was significantly decreased by immuno?histochemistry (P<0.05) ,reduce the lung wet/dry weight ratio, increase the ratio of PaO2/FiO2, inhibit the release of inflammatory factors and scavenge free radicals and antioxidant effects. CONCLUSION Renqing Changjue can effec?tively protect rabbits with acute respiratory distress syndrome induced by LPS, and may protect the lung by inhibiting the release of cytokines and anti-oxidation.

Astragalus membranaceus has the effect of tonifying Qi and solid surface， diuretic support poison， discharging pus and astringent sores to produce muscle. It is not only used for syndromes such as deficiency of lung and temper， deficiency of spleen and diarrhea， but also for stroke， chest obstruction and other diseases. Due to the complex chemical composition and diverse pharmacological effect of Astragalus membranaceus， and the main role in invigorating qi and activating blood circulation has not been clarified. Astragaloside Ⅳ is one of its main active ingredients. In recent years， more and more studies on Astragaloside Ⅳ have been conducted at home and abroad. It has been reported that it has the medicinal value of enhancing immune function， strengthening heart and lowerin blood glucose， diuresis， anti-aging and anti-fatigue， et al， and has extensive pharmacological activity. Among them， the role of cardiovascular and cerebrovascular diseases in particular has attracted increasing attention. Cardiovascular and cerebrovascular diseases are ischemic or hemorrhagic diseases occurring in the heart， brain and systemic tissues due to blood viscosity， atherosclerosis， hypertension， hyperlipidemia， etc.， including cardiovascular and cerebrovascular diseases. Such diseases are a serious threat to mankind and are the leading cause of death worldwide. At present， western medicine is the main treatment， with many adverse reactions and poor long-term prognosis. TCM believes that the imbalance of qi and blood is the basic pathogenesis of this kind of disease. Qi deficiency and blood stasis are more common.At present， Astragaloside Ⅳ in the treatment of cardiovascular and cerebrovascular diseases in a number of studies， and achieved some results， but this review in recent years， Astragaloside Ⅳ in the treatment of cardiovascular and cerebrovascular diseases play the pharmacological activity， in order to explore whether Astragaloside Ⅳ is the main role of astragalus qi to find a theoretical basis for material basis， but also for the innovation of traditional Chinese medicine drug research and development of theoretical basis and practical guidance.

Objective:To analyze the negative effect of prolonged postoperative ileus on postoperative recovery in patients underwent open alimentary tract surgery.Methods:This study was a retrospective cohort study. The subjects of the study were patients who underwent open gastrointestinal surgery at the General Surgery Department of Beijing Friendship Hospital, Capital Medical University from October 2016 to November 2018. According to the PPOI diagnostic criteria proposed by the University of Auckland, the included patients were classified as PPOI Group ( n=14) and non-PPOI group ( n=112). The postoperative complications, postoperative hospital stay and medical expenses during hospitalization were selected as the study endpoint indicators. T-test or Fisher′s exact test were performed to compare the differences between the two groups, and linear regression analysis was used to explore the independent effects of PPOI on hospital stay and medical expenses. Results:The incidence of PPOI in this study cohort was 11.1%. The total postoperative complications occurred more frequent in PPOI group (64.29% vs 38.39%, P=0.08). The average postoperative hospital stay of patients in the PPOI group was longer than that in non-PPOI group [(21.21±14.83) d vs (13.98±14.21) d, P=0.070]. Adjusting for various possible confounding factors, the PPOI regression coefficient beta (95% CI) that affects the length of hospital stay was [-0.43 (-7.16, 6.3), P=0.90]. The average medical cost of patients in the PPOI group was more than that in non-PPOI group [(104 389.64±52 427.66)元比(79 111.41±50 832.29)元, P=0.070]. Adjusting for various possible confounding factors, the PPOI regression coefficient beta (95% CI) that affects medical expenditure was [-134.12 (-21656.85, 21388.62), P=0.99]. Conclusions:Prolonged postoperative ileus leads to delayed postoperative recovery, which is related to increased postoperative complications, hospital stay duration and medical cost. But it needs further confirmation from large sample data.

To evaluate whether the polygenic profile modifies the development of sporadic Alzheimer's disease (sAD) and pathological biomarkers in cerebrospinal fluid (CSF), 462 sAD patients and 463 age-matched cognitively normal (CN) controls were genotyped for 35 single-nucleotide polymorphisms (SNPs) that are significantly associated with sAD. Then, the alleles found to be associated with sAD were used to build polygenic risk score (PRS) models to represent the genetic risk. Receiver operating characteristic (ROC) analyses and the Cox proportional hazards model were used to evaluate the predictive value of PRS for the sAD risk and age at onset. We measured the CSF levels of Aβ42, Aβ42/Aβ40, total tau (T-tau), and phosphorylated tau (P-tau) in a subgroup (60 sAD and 200 CN participants), and analyzed their relationships with the PRSs. We found that 14 SNPs, including SNPs in the APOE, BIN1, CD33, EPHA1, SORL1, and TOMM40 genes, were associated with sAD risk in our cohort. The PRS models built with these SNPs showed potential for discriminating sAD patients from CN controls, and were able to predict the incidence rate of sAD and age at onset. Furthermore, the PRSs were correlated with the CSF levels of Aβ42, Aβ42/Aβ40, T-tau, and P-tau. Our study suggests that PRS models hold promise for assessing the genetic risk and development of AD. As genetic risk profiles vary among populations, large-scale genome-wide sequencing studies are urgently needed to identify the genetic risk loci of sAD in Chinese populations to build accurate PRS models for clinical practice.