The gut microbiota regulates intestinal nutrient absorption, participates in modulating host glucolipid metabolism, and contributes to ameliorating glucolipid metabolism disorder. Dysbiosis of the gut microbiota can compromise the integrity of the intestinal mucosal barrier, induce inflammatory responses, and exacerbate insulin resistance and abnormal lipid metabolism in the host. Dangua Humai Oral Liquid, a hospital-developed formulation for regulating glucolipid metabolism, has been granted a national invention patent and demonstrates significant clinical efficacy. This study aimed to investigate the effects of Dangua Humai Oral Liquid on gut microbiota and the intestinal mucosal barrier in a mouse model with glucolipid metabolism disorder. A glucolipid metabolism disorder model was established by feeding mice a high-glucose and high-fat diet. The mice were divided into a normal group, a model group, and a treatment group, with eight mice in each group. The treatment group received a daily gavage of Dangua Humai Oral Liquid(20 g·kg~(-1)), while the normal group and model group were given an equivalent volume of sterile water. After 15 weeks of intervention, glucolipid metabolism, intestinal mucosal barrier function, and inflammatory responses were evaluated. Metagenomics and untargeted metabolomics were employed to analyze changes in gut microbiota and associated metabolic pathways. Significant differences were observed between the indicators of the normal group and the model group. Compared with the model group, the treatment group exhibited marked improvements in glucolipid metabolism disorder, alleviated pathological damage in the liver and small intestine tissue, elevated expression of recombinant claudin 1(CLDN1), occluding(OCLN), and zonula occludens 1(ZO-1) in the small intestine tissue, and reduced serum levels of inflammatory factors lipopolysaccharides(LPS), lipopolysaccharide-binding protein(LBP), interleukin-6(IL-6), and tumor necrosis factor-α(TNF-α). At the phylum level, the relative abundance of Bacteroidota decreased, while that of Firmicutes increased. Lipid-related metabolic pathways were significantly altered. In conclusion, based on the successful establishment of the mouse model of glucolipid metabolism disorder, this study confirmed that Dangua Humai Oral Liquid effectively modulates gut microbiota and mucosal barrier function, reduces serum inflammatory factor levels, and regulates lipid-related metabolic pathways, thereby ameliorating glucolipid metabolism disorder.
Animals ; Gastrointestinal Microbiome/drug effects* ; Mice ; Intestinal Mucosa/microbiology* ; Male ; Drugs, Chinese Herbal/administration & dosage* ; Mice, Inbred C57BL ; Humans ; Glycolipids/metabolism* ; Lipid Metabolism/drug effects* ; Administration, Oral ; Disease Models, Animal

Objective The leptin receptor,encoded by the LEPR gene,is involved in tumorigenesis.A potential functional variant of LEPR,rs1137101(Gln223Arg),has been extensively investigated for its contribution to the risk of digestive system(DS)cancers,but results remain conflicting rather than conclusive.Here,we performed a case-control study and subsequent meta-analysis to examine the association between rs1137101 and DS cancer risk. Methods A total of 1,727 patients with cancer(gastric/liver/colorectal:460/480/787)and 800 healthy controls were recruited.Genotyping of rs1137101 was conducted using a polymerase chain reaction-restriction fragment length polymorphism(PCR-RFLP)assay and confirmed using Sanger sequencing.Twenty-four eligible studies were included in the meta-analysis. Results After Bonferroni correction,the case-control study revealed that rs1137101 was significantly associated with the risk of liver cancer in the Hubei Chinese population.The meta-analysis suggested that rs1137101 is significantly associated with the risk of overall DS,gastric,and liver cancer in the Chinese population. Conclusion The LEPR rs1137101 variant may be a genetic biomarker for susceptibility to DS cancers(especially liver and gastric cancer)in the Chinese population.

Objective To investigate the clinical efficacy of percutaneous closure of foramen ovale guided by transthoracic echocardio-graphy with simply delivery sheath.Methods The clinical data of patients with patent foramen ovale underwent interventional closure and percutaneous closure guided by transthoracic echocardiography with simply delivery sheath in our hospital from January 2020 to December 2022 were analyzed retrospectively,the patients were divided into interventional closure group(40 cases)and simply delivery sheath group(39 cases).The operation time,incidence of surgical complications,and surgical success rates of patients in the two groups were compared.The closure effect were evaluated by ultrasound immediately after surgery.All the patients were followed up for 6 months after surgery to evaluate remission of the symptoms.Results The surgical success rate of simply delivery sheath group(100%)was higher than that of interventional closure group(90.0%),with statistically significant difference(P<0.05).The operation time of simply delivery sheath group was longer than that of interventional closure group,with statistically significant difference(P<0.05).One patient in the interventional closure group had small amount of pericardial effusion during the operation.Two patients had decreased blood pressure and slowed heart rate in simply delivery sheath group,and symptoms disappeared after treatment.There was no significant difference in the incidence of complications between the two groups(P>0.05).After 6-month follow-up,all occluders were in good position and no residual leakage was found.The symptoms of headache or dizziness disappeared in 28 patients in interventional closure group,significantly relieved in 8 patients;the symptoms of headache or dizziness disappeared in 30 patients in simply delivery sheath group,and significantly relieved in 9 patients.Conclusion Percutaneous closure for patent foramen ovale under the guidence of transthoracic echocardiography with simply delivery sheath is safe and feasible with satisfactory efficacy and higher successful rate without radiation hazard.It is worthy of clinical promotion.

Endo-beta-N-acetylglucosaminidase (ENGase) is widely distributed in various organisms. The first reported ENGase activity was detected in Diplococcus pneumoniae in 1971. The protein (Endo D) was purified and its peptide sequence was determined in 1974. Three ENGases (Endo F1-F3) were discovered in Flavobacterium meningosepticum from 1982 to 1993. After that, the activity was detected from different species of bacteria, yeast, fungal, plant, mice, human, etc. Multiple ENGases were detected in some species, such as Arabidopsis thaliana and Trichoderma atroviride. The first preliminary crystallographic analysis of ENGase was conducted in 1994. But to date, only a few ENGases structures have been obtained, and the structure of human ENGase is still missing. The currently identified ENGases were distributed in the GH18 or GH85 families in Carbohydrate-Active enZyme (CAZy) database. GH18 ENGase only has hydrolytic activity, but GH85 ENGase has both hydrolytic and transglycosylation activity. Although ENGases of the two families have similar (β/α)8-TIM barrel structures, the active sites are slightly different. ENGase is an effective tool for glycan detection andglycan editing. Biochemically, ENGase can specifically hydrolyze β‑1,4 glycosidic bond between the twoN-acetylglucosamines (GlcNAc) on core pentasaccharide presented on glycopeptides and/or glycoproteins. Different ENGases may have different substrate specificity. The hydrolysis products are oligosaccharide chains and a GlcNAc or glycopeptides or glycoproteins with a GlcNAc. Conditionally, it can use the two products to produce a new glycopeptides or glycoprotein. Although ENGase is a common presentation in cell, its biological function remains unclear. Accumulated evidences demonstrated that ENGase is a none essential gene for living and a key regulator for differentiation. No ENGase gene was detected in the genomes of Saccharomyces cerevisiae and three other yeast species. Its expression was extremely low in lung. As glycoproteins are not produced by prokaryotic cells, a role for nutrition and/or microbial-host interaction was predicted for bacterium produced enzymes. In the embryonic lethality phenotype of the Ngly1-deficient mice can be partially rescued by Engase knockout, suggesting down regulation of Engase might be a solution for stress induced adaptation. Potential impacts of ENGase regulation on health and disease were presented. Rabeprazole, a drug used for stomach pain as a proton inhibitor, was identified as an inhibitor for ENGase. ENGases have been applied in vitro to produce antibodies with a designated glycan. The two step reactions were achieved by a pair of ENGase dominated for hydrolysis of substrate glycoprotein and synthesis of new glycoprotein with a free glycan of designed structure, respectively. In addition, ENGase was also been used in cell surface glycan editing. New application scenarios and new detection methods for glycobiological engineering are quickly opened up by the two functions of ENGase, especially in antibody remodeling and antibody drug conjugates. The discovery, distribution, structure property, enzymatic characteristics and recent researches in topical model organisms of ENGase were reviewed in this paper. Possible biological functions and mechanisms of ENGase, including differentiation, digestion of glycoproteins for nutrition and stress responding were hypothesised. In addition, the role of ENGase in glycan editing and synthetic biology was discussed. We hope this paper may provide insights for ENGase research and lay a solid foundation for applied and translational glycomics.

ObjectiveTo investigate the effect of mucin 1 (MUC1) on the proliferation and apoptosis of nasopharyngeal carcinoma (NPC) and its regulatory mechanism. MethodsThe 60 NPC and paired para-cancer normal tissues were collected from October 2020 to July 2021 in Quanzhou First Hospital. The expression of MUC1 was measured by real-time quantitative PCR (qPCR) in the patients with PNC. The 5-8F and HNE1 cells were transfected with siRNA control (si-control) or siRNA targeting MUC1 (si-MUC1). Cell proliferation was analyzed by cell counting kit-8 and colony formation assay, and apoptosis was analyzed by flow cytometry analysis in the 5-8F and HNE1 cells. The qPCR and ELISA were executed to analyze the levels of TNF-α and IL-6. Western blot was performed to measure the expression of MUC1, NF-кB and apoptosis-related proteins (Bax and Bcl-2). ResultsThe expression of MUC1 was up-regulated in the NPC tissues, and NPC patients with the high MUC1 expression were inclined to EBV infection, growth and metastasis of NPC. Loss of MUC1 restrained malignant features, including the proliferation and apoptosis, downregulated the expression of p-IкB、p-P65 and Bcl-2 and upregulated the expression of Bax in the NPC cells. ConclusionDownregulation of MUC1 restrained biological characteristics of malignancy, including cell proliferation and apoptosis, by inactivating NF-κB signaling pathway in NPC.

Peroxisome proliferator-activated receptor gamma(PPAR-γ)is a member of the ligand-activated nuclear tran-scription factor superfamily.Activated PPAR-γ is involved in the regulation of many central nervous system(CNS)events,and is involved in cholesterol metabolism by inducing or inhibi-ting a series of gene pathways,thereby inhibiting the deposition of β-amyloid protein(Aβ).It plays an important neuroprotec-tive role in Alzheimer's disease(AD),improves memory and cognition in AD,and is a potential target for AD.Drug develop-ment aimed at restoring cholesterol homeostasis may be a poten-tial strategy to counteract AD.By analyzing the distribution and structure of PPAR-γ,focusing on the biological correlation be-tween PPAR-γ-mediated cholesterol metabolism and AD,this paper describes the mechanism regulation of PPAR-γ on key proteins,genes and their corresponding molecules,providing a new reference for the treatment of AD.

Objective:To investigate the current status of the use and management of medical devices in various primary medical and health institutions under hierarchical medical diagnosis and treatment.Methods:A stratified random cluster sampling method was used to select 450 medical personnel from 50 township and urban primary medical and health institutions of Shijiazhuang from May to August 2023 and a questionnaire network survey on the use and management of medical devices was conducted,which covered 16 items across three dimensions including the use of commonly used medical devices in primary medical institutions,maintenance and quality control management.Results:A total of 450 questionnaires were distributed and 450 valid questionnaires were collected,including 239 from township primary level medical institutions and 211 from urban primary level ones.According to the results of 211 urban primary level questionnaires,the proportions of the training and examination carried out by the medical staff of urban grass-roots medical and health institutions prior to the use of medical devices,understanding parameters of medical devices and timely detection of malfunction of medical devices were 62.6%(132/211),77.7%(164/211)and 70.1%(148/211),respectively,which were higher than those at the township primary level,the difference was statistically significant(x2=17.750,29.649,22.384,P<0.05).The proportions of urban primary medical and health institutions with maintenance system,inspection and maintenance standards,regular calibration provisions,and equipment calibration standards were 64.0%(135/211),53.6%(112/211),55.9%(118/211)and 55.0%(116/211),respectively,which were higher than those of the township primary level,the difference was statistically significant(x2=5.834,34.728,6.004,25.540,P<0.05).The difference was not statistically significant between urban primary level and township primary level in each item of quality control management(P>0.05).Conclusion:Primary medical and health institutions were required to strengthen training and assessment before medical and health personnel use medical devices;improve related system and standards for medical device maintenance;formulate quality control management system for commonly used medical devices;strengthen analysis and discussion processes after quality control,and promote continuous improvement of medical device quality management.

Objective:To explore the effects of hypoxia on traumatic brain swelling (TBS) in rats with acute subdural hematoma (ASDH).Methods:Forty-five SD rats were divided into 5 groups according to the random number table method, with 9 rats in each group: sham surgery normal oxygen group which underwent sham surgical procedures and were placed in a closed container with ventilation, sham surgery hypoxia group which underwent sham surgical procedures and were placed in a closed container with oxygen volume fraction of 8% for hypoxia induction, ASDH normal oxygen group which made into the ASDH model and placed in a closed container with ventilation, ASDH hypoxia group were made into the ASDH models and placed in a closed container with oxygen volume fraction of 8% for hypoxia induction, and ASDH hypoxia+oxygen inhalation group which inhaled oxygen continuously with oxygen volume fraction of 40% after being made into the ASDH models and induced for hypoxia. Six rats were selected from each group immediately after the modeling and craniotomy was performed to observe the brain swelling during the surgery and evaluate the degree of TBS. Microvascular blood flow was observed by laser speckle imaging system before modeling, before craniotomy, and immediately after craniotomy. The remaining 3 rats in each group were killed directly after modeling and brain tissue specimens were collected. The expression levels of pericellular protein α-smooth muscle actin (α-SMA) and platelet-derived growth factor receptor-β (PDGFR-β) at 0, 30 and 60 minutes after modeling were detected through Western blot analysis. The expression levels of α-SMA, PDGFR-β and microvascular marker platelet-endothelial cell adhesion molecule 31 (CD31) at 0 minute after modeling were tested through immunofluorescent staining.Results:No brain bulge was observed in the sham surgery normal oxygen group. The height of brain bulge in sham surgery hypoxia group was 0.5(0.0, 1.0)mm, with no significant difference from that in the sham surgery normal oxygen group ( P>0.05); it was 2.2(2, 2.5)mm in the ASDH normal oxygen group, significantly higher than that in the sham surgery normal oxygen group and sham surgery hypoxia group ( P<0.01), it was 3.1(2.9, 3.2)mm in the ASDH hypoxia group, significantly higher than that in the sham surgery normal oxygen group, sham surgery hypoxia group and ASDH normal oxygen group ( P<0.01); it was 2.8(2.7, 2.9)mm in the ASDH hypoxia+oxygen inhalation group, not statistically different from that in the ASDH hypoxia group ( P>0.05), but significantly increased compared with that in the sham surgery normal oxygen group, sham surgery hypoxia group and ASDH normal oxygen group ( P<0.01). Before modeling, before craniotomy and after craniotomy, the microvascular blood flow was 224.2±49.7, 224.8±50.3, 225.1±50.3 respectively in the sham surgery normal oxygen group and 224.7±43.7, 220.9±45.9, 221.8±45.5 respectively in the sham surgery hypoxia group, with no significant difference between the two groups ( P>0.05); it was 226.5±52.7, 173.4±40.7, 172.0±40.7 respectively in the ASDH normal oxygen group, significantly decreased compared with that in the sham surgery normal oxygen group and sham surgery hypoxia group ( P<0.05); it was 225.7±46.4, 131.4±23.6 and 131.0±23.5 respectively in the ASDH hypoxia group, significantly decreased compared with that in the sham surgery normal oxygen group, sham surgery hypoxia group and ASDH normal oxygen group ( P<0.05); it was 226.2±56.1, 132.6±21.7 and 131.7±21.9 respectively in ASDH hypoxia+oxygen inhalation group, significantly decreased compared with that in the sham surgery normal oxygen group, sham surgery hypoxia group and ASDH normal oxygen group ( P<0.05), with no significant difference from that in the ASDH hypoxia group ( P>0.05). At 0, 30 and 60 minutes after modeling, the expression levels of α-SMA and PDGFR-β were 0.70±0.02, 0.67±0.01, 0.55±0.05 and 0.65±0.03, 0.56±0.03 and 0.59±0.02 respectively in the sham surgery normal oxygen group and were 0.63±0.04, 0.60±0.01 0.55±0.05 and 0.62±0.01, 0.51±0.01 and 0.60±0.02 respectively in the sham surgery hypoxia group, with no significant difference between the two groups ( P>0.05); they were 0.88±0.06, 0.87±0.05, 0.82±0.03 and 0.85±0.03, 0.85±0.03, 0.88±0.04 respectively in the ASDH normal oxygen group, significantly higher than those in the sham surgery normal oxygen group and sham surgery hypoxia group ( P<0.01); they were 1.19±0.08, 1.10±0.10, 0.97±0.04 and 1.04±0.06, 1.19±0.07, 1.27±0.08 respectively in the ASDH hypoxia group, significantly higher than those in sham surgery normal oxygen group, sham surgery hypoxia group and ASDH normal oxygen group ( P<0.05 or 0.01); they were 1.20±0.07, 1.10±0.04, 0.96±0.04 and 1.04±0.05, 1.15±0.11, 1.20±0.07 respectively in ASDH hypoxia+oxygen inhalation group, significantly higher than those in sham surgery normal oxygen group, sham surgery normal group and ASDH normal oxygen group ( P<0.01), but with no significant difference from those in ASDH hypoxia group ( P>0.05). At 0 minute after modeling, the fluorescence expression of α-SMA and PDGFR-β was weaker in the sham surgery normal oxygen group and the fluorescence expression of CD31 was stronger. There was no significant difference in the fluorescence expressions of α-SMA, PDGFR-β and CD31 between the sham surgery hypoxia group and sham surgery normal oxygen group. The fluorescence expressions of α-SMA and PDGFR-β in the ASDH normal oxygen group were stronger than those in the sham surgery normal oxygen group and sham surgery hypoxia group, while the fluorescence expression of CD31 was weaker. The fluorescence expressions of α-SMA and PDGFR-β in ASDH hypoxia group were stronger than those in the sham surgery normal oxygen group, sham surgery hypoxia group and ASDH normal oxygen group, while the fluorescence expression of CD31 was weaker. The fluorescence expressions of α-SMA and PDGFR-β in the ASDH hypoxia+oxygen inhalation group were stronger than those in the sham surgery normal oxygen group, sham surgery hypoxia group and ASDH normal oxygen group, while the fluorescence expression of CD31 was weaker, with no significant difference from the fluorescence expressions of α-SMA, PDGFR-β and CD31 in ASDH hypoxia group. Conclusions:Hypoxia in ASDH rats will stimulate pericytes contraction, which causes cerebral microcirculatory disturbance, thus leading to TBS. Short-term inhalation of oxygen of medium concentration cannot dilate pericytes or microcirculation vessels, with no obvious effect on improving the conditions of TBS.

Objective:To identify the risk factors affecting the healing of defective bony nonunion.Methods:The studies reporting the risk factors for healing of defective bony nonunion between January 2000 and March 2022 were retrieved by computer from the VIP, Wanfangdata, CNKI, Web of Science, PubMed, and Medline databases. The Newcastle-Ottawa Scale (NOS) was used to evaluate the quality of the included studies. the RevMan 5.3 software was used to perform a meta-analysis of the general factors, injuries and surgical-related factors affecting the healing of defective bony nonunion.Results:Included in this Meta analysis were 17 studies with 1,236 patients. The NOS score of the included studies was from 5 to 8. The meta-analysis showed the following: age ( MD=-4.27, 95% CI: -8.29 to 2.91, P < 0.01), smoking ( OR=3.56, 95% CI: 2.81 to 6.32, P < 0.01), soft tissue defect ( OR=3.54, 95% CI: 2.21 to 5.69, P < 0.01), combined ipsilateral fibular fracture ( OR=4.18, 95% CI: 1.24 to 14.03, P=0.02), venous thrombosis ( OR=4.27, 95% CI: 1.05 to 17.44, P=0.04), and postoperative infection ( OR=2.96, 95% CI: 1.97 to 4.47, P < 0.01) were significant risk factors for the healing of defective bone nonunion. Minor bone defect ( SMD=-0.67, 95% CI: -1.25 to -0.10, P=0.02), proximal to distal bone transport ( OR=-0.42, 95% CI: 0.22 to 0.77, P < 0.01), short-term external fixation ( MD=-3.92, 95% CI: -7.10 to -0.73, P=0.02), and autologous bone grafting ( OR=0.39, 95% CI: 0.16 to 0.95, P=0.04) were protective factors for the healing of defective bony nonunion. Conclusions:High age (senility), smoking, soft tissue defect, ipsilateral fibular fracture, venous thrombosis, and postoperative infection are risk factors affecting the healing of defective bony nonunion. Minor bone defect, proximal to distal bone transport, short-term external fixation, and autologous bone grafting are protective factors affecting the healing of defective bony nonunion. Surgeons can predict early the prognosis of patients with defective bony nonunion based on the above factors.

Odontogenic maxillary sinusitis(OMS)is a subtype of maxillary sinusitis(MS).It is actually inflammation of the maxillary sinus that secondary to adjacent infectious maxillary dental lesion.Due to the lack of unique clinical features,OMS is difficult to distinguish from other types of rhinosinusitis.Besides,the characteristic infectious pathogeny of OMS makes it is resistant to conventional therapies of rhinosinusitis.Its current diagnosis and treatment are thus facing great difficulties.The multi-disciplinary cooperation between otolaryngologists and dentists is absolutely urgent to settle these questions and to acquire standardized diagnostic and treatment regimen for OMS.However,this disease has actually received little attention and has been underrepresented by relatively low publication volume and quality.Based on systematically reviewed literature and practical experiences of expert members,our consensus focuses on characteristics,symptoms,classification and diagnosis of OMS,and further put forward multi-disciplinary treatment decisions for OMS,as well as the common treatment complications and relative managements.This consensus aims to increase attention to OMS,and optimize the clinical diagnosis and decision-making of OMS,which finally provides evidence-based options for OMS clinical management.