Temporomandibular joint (TMJ) diseases are common clinical conditions. The number of patients with TMJ diseases is large, and the etiology, epidemiology, disease spectrum, and treatment of the disease remain controversial and unknown. To understand and master the current situation of the occurrence, development and prevention of TMJ diseases, as well as to identify the patterns in etiology, incidence, drug sensitivity, and prognosis is crucial for alleviating patients′suffering.This will facilitate in-depth medical research, effective disease prevention measures, and the formulation of corresponding health policies. Cohort construction and research has an irreplaceable role in precise disease prevention and significant improvement in diagnosis and treatment levels. Large-scale cohort studies are needed to explore the relationship between potential risk factors and outcomes of TMJ diseases, and to observe disease prognoses through long-term follw-ups. The consensus aims to establish a standard conceptual frame work for a cohort study on patients with TMJ disease while providing ideas for cohort data standards to this condition. TMJ disease cohort data consists of both common data standards applicable to all specific disease cohorts as well as disease-specific data standards. Common data were available for each specific disease cohort. By integrating different cohort research resources, standard problems or study variables can be unified. Long-term follow-up can be performed using consistent definitions and criteria across different projects for better core data collection. It is hoped that this consensus will be facilitate the development cohort studies of TMJ diseases.

Background::Acute-on-chronic liver failure (ACLF) is a severe liver disease with complex pathogenesis. Clinical hypoglycemia is common in patients with ACLF and often predicts a worse prognosis. Accumulating evidence suggests that glucose metabolic disturbance, especially gluconeogenesis dysfunction, plays a critical role in the disease progression of ACLF. Lon protease-1 (LONP1) is a novel mediator of energy and glucose metabolism. However, whether gluconeogenesis is a potential mechanism through which LONP1 modulates ACLF remains unknown.Methods::In this study, we collected liver tissues from ACLF patients, established an ACLF mouse model with carbon tetrachloride (CCl 4), lipopolysaccharide (LPS), and D-galactose (D-gal), and constructed an in vitro hypoxia and hyperammonemia-triggered hepatocyte injury model. LONP1 overexpression and knockdown adenovirus were used to assess the protective effect of LONP1 on liver injury and gluconeogenesis regulation. Liver histopathology, biochemical index, mitochondrial morphology, cell viability and apoptosis, and the expression and activity of key gluconeogenic enzymes were detected to explore the underlying protective mechanisms of LONP1 in ACLF. Results::We found that LONP1 and the expressions of gluconeogenic enzymes were downregulated in clinical ACLF liver tissues. Furthermore, LONP1 overexpression remarkably attenuated liver injury, which was characterized by improved liver histopathological lesions and decreased serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in ACLF mice. Moreover, mitochondrial morphology was improved upon overexpression of LONP1. Meanwhile, the expression and activity of the key gluconeogenic enzymes were restored by LONP1 overexpression. Similarly, the hepatoprotective effect was also observed in the hepatocyte injury model, as evidenced by improved cell viability, reduced cell apoptosis, and improved gluconeogenesis level and activity, while LONP1 knockdown worsened liver injury and gluconeogenesis disorders.Conclusion::We demonstrated that gluconeogenesis dysfunction exists in ACLF, and LONP1 could ameliorate liver injury and improve gluconeogenic dysfunction, which would provide a promising therapeutic target for patients with ACLF.

The concept of the glial-vascular unit (GVU) was raised recently to emphasize the close associations between brain cells and cerebral vessels, and their coordinated reactions to diverse neurological insults from a "glio-centric" view. GVU is a multicellular structure composed of glial cells, perivascular cells, and perivascular space. Each component is closely linked, collectively forming the GVU. The central roles of glial and perivascular cells and their multi-level interconnections in the GVU under normal conditions and in central nervous system (CNS) disorders have not been elucidated in detail. Here, we comprehensively review the intensive interactions between glial cells and perivascular cells in the niche of perivascular space, which take part in the modulation of cerebral blood flow and angiogenesis, formation of the blood-brain barrier, and clearance of neurotoxic wastes. Next, we discuss dysfunctions of the GVU in various neurological diseases, including ischemic stroke, spinal cord injury, Alzheimer's disease, and major depression disorder. In addition, we highlight the possible therapies targeting the GVU, which may have potential clinical applications.
Humans ; Neuroglia ; Nervous System Diseases ; Blood-Brain Barrier ; Alzheimer Disease ; Glymphatic System

The glymphatic system plays a pivotal role in maintaining cerebral homeostasis. Chronic cerebral hypoperfusion, arising from small vessel disease or carotid stenosis, results in cerebrometabolic disturbances ultimately manifesting in white matter injury and cognitive dysfunction. However, whether the glymphatic system serves as a potential therapeutic target for white matter injury and cognitive decline during hypoperfusion remains unknown. Here, we established a mouse model of chronic cerebral hypoperfusion via bilateral common carotid artery stenosis. We found that the hypoperfusion model was associated with significant white matter injury and initial cognitive impairment in conjunction with impaired glymphatic system function. The glymphatic dysfunction was associated with altered cerebral perfusion and loss of aquaporin 4 polarization. Treatment of digoxin rescued changes in glymphatic transport, white matter structure, and cognitive function. Suppression of glymphatic functions by treatment with the AQP4 inhibitor TGN-020 abolished this protective effect of digoxin from hypoperfusion injury. Our research yields new insight into the relationship between hemodynamics, glymphatic transport, white matter injury, and cognitive changes after chronic cerebral hypoperfusion.
Animals ; Brain Ischemia ; Carotid Stenosis/drug therapy* ; Cognitive Dysfunction/etiology* ; Digoxin ; Disease Models, Animal ; Mice ; Mice, Inbred C57BL ; White Matter

Objective:To assess the validity and reliability of the depression and somatic symptoms scale among patients with coronary heart disease.Methods:Totally 246 patients with coronary heart disease were assessed with depression and somatic symptoms scale (DSSS), Hamilton depression rating scale for depression (HAMD) and patients’ health questionnaire depression scale-9 item (PHQ-9). The structural validity was evaluated with exploratory factor analysis and confirmatory factor analysis. The validity as a screening tool was evaluated with the gold standard diagnosed by psychiatrists who were trained with the mini international neuropsychological interview (MINI) according to ICD-10. Receiver operating characteristic (ROC) curve was used to identify cutoff scores for depression. Cronbach α coefficient was used to evaluate the internal consistency.Results:Exploratory factor analysis yielded two factors: depression factor and somatic factor, and the cumulative variance was 51.8%. The fitting indexes of confirmatory factor analysis were as follows: χ2/ df=3.636, RMR=0.077, RMSEA=0.104, IFI=0.804, TLI=0.781, CFI=0.802. The intraclass correlation coefficient of DSSS and HAMD was 0.54. The area under ROC curve (AUC) was 0.828, and the best boundary value was 17 points (sensitivity and specificity: 81% and 75%, respectively). The total scores and subscale scores for internal consistency of DSSS were higher in the depression group than those in the non-depression group ( P<0.01). Cronbach α coefficient for internal consistency of DSSS was 0.917. Conclusion:The DSSS has good validity and reliability among patients with coronary heart disease for screening depression, and can be used to screen depression among patients with coronary heart disease in general hospital.

Objective:To investigate the nutritional risk and prevalence of malnutrition in patients with terminal stage gastrointestinal malignant tumors in a tertiary hospital in Changsha.Methods:Cluster sampling was used to conduct a cross-sectional survey of inpatients from Departments of Gastroenterology, Gastrointestinal Surgery, Hepatobiliary Surgery and Oncology in Hunan Provincial People's Hospital from January 2019 to July 2020. Nutritional Risk Screening 2002 (NRS 2002) was used to assess the prevalence of nutritional risk with malnutrition defined as concurrent presence of BMI < 18.5 kg/m 2, poor general condition and NRS 2002 nutritional impairment score of 3. Step 2 of Global Leadership Initiative on Malnutrition (GLIM) diagnostic criteria (without whole body muscle mass) was adopted to diagnose malnutrition. Step 3 of GLIM criteria was used to evaluate the prevalence of severe malnutrition. Results:A total of 802 patients registered in the 4 departments were selected for screening via cluster sampling and 514 were enrolled according to the inclusion/exclusion criteria. The prevalence of nutritional risk in patients with terminal stage gastrointestinal cancer was 49.8% (256/514). The prevalence of malnutrition and severe malnutrition per GLIM criteria were 41.6% (214/514) and 18.3% (94/514), respectively.Conclusions:Although nutritional support therapy is not recommended for patients with end-stage cancer. This paper suggests that the prevalence of nutritional risk and malnutrition in patients with end-stage gastrointestinal cancer is not as high as described in some articles.

Objective:To investigate the feasibility and effectiveness of percutaneous transhepatic cholangioscopy(PTCS) in the treatment of bilioenteric anastomotic stricture after choledochojejunostomy.Methods:From April 2016 to April 2020, the clinical data of 9 patients (7 males and 2 females, aged 40-76 years) who underwent percutaneous transhepatic cholangioscopy(PTCS) for stricture expansion and lithotomy at Department of Hepatobiliary and Pancreatic Surgery, Second Affiliated Hospital of Zhejiang University School of Medicine were retrospectively analyzed. The operation was divided into two stages. In the first stage, ultrasound-guided percutaneous intrahepatic bile duct puncture was performed, and the sheath tube was inserted and fixed. In the second stage, percutaneous choledochoscopy was used for anastomotic stricture after sinus formation.The clinical outcome was evaluated by related biochemical indexes.Results:The operation time was (53.3±31.0)minutes(range:15-120 minutes).The postoperative hospital stay was (4.4±2.3)days(range:2-9 days).After systematic treatment, the preoperative symptoms, such as abdominal pain, jaundice, fever and shivering, disappeared in 8 patients. The range of alkaline phosphatase was 122-1 334 U/L before operation and 85-702 U/L after operation. The range of gamma glutamyl transpeptidase was 44-1 219 U/L before operation and 46-529 U/L after operation.Conclusion:PTCS is a safe and effective option for minimally invasive treatment of bilioenteric anastomotic stricture.

Objective:To investigate the feasibility and effectiveness of percutaneous transhepatic cholangioscopy(PTCS) in the treatment of bilioenteric anastomotic stricture after choledochojejunostomy.Methods:From April 2016 to April 2020, the clinical data of 9 patients (7 males and 2 females, aged 40-76 years) who underwent percutaneous transhepatic cholangioscopy(PTCS) for stricture expansion and lithotomy at Department of Hepatobiliary and Pancreatic Surgery, Second Affiliated Hospital of Zhejiang University School of Medicine were retrospectively analyzed. The operation was divided into two stages. In the first stage, ultrasound-guided percutaneous intrahepatic bile duct puncture was performed, and the sheath tube was inserted and fixed. In the second stage, percutaneous choledochoscopy was used for anastomotic stricture after sinus formation.The clinical outcome was evaluated by related biochemical indexes.Results:The operation time was (53.3±31.0)minutes(range:15-120 minutes).The postoperative hospital stay was (4.4±2.3)days(range:2-9 days).After systematic treatment, the preoperative symptoms, such as abdominal pain, jaundice, fever and shivering, disappeared in 8 patients. The range of alkaline phosphatase was 122-1 334 U/L before operation and 85-702 U/L after operation. The range of gamma glutamyl transpeptidase was 44-1 219 U/L before operation and 46-529 U/L after operation.Conclusion:PTCS is a safe and effective option for minimally invasive treatment of bilioenteric anastomotic stricture.

Objective: To investigate the roles of N-acetyl-L-cysteine (NAC) against binge drinking-induced fatty liver in mice. Methods: SPF male C57BL/6 mice were randomly divided into 3 groups, i.e. control group, model group, and NAC/ethanol group (n=10). Mice in model and NAC/ethanol groups were exposed to 3 doses of ethanol (6 g/kg bw) to induced fatty liver, while mice in control group received equal volume and equal energy of maltodextrin solution. NAC was administered to mice at 1 h before ethanol exposure (100 mg/kg bw, i.p.). The mice were sacrificed at 6 h after the last ethanol exposure. The liver and epididymal adipose tissues were collected. Histopathological examination and biochemical assay kit were used to evaluate the fat accumulation, while Western-blot was performed to detect the protein levels of some key factors involved in fat metabolism in liver and adipose tissues. Results: Compored with control group mice, the liver index and liver weight were significantly increased compared with model group, the liver index and TG level in NAC/ethanol group mice were all significantly decreased (P<0.05). Histological examination showed NAC effectively suppressed binge drinking-induced fat accumulation in mice liver. In addition, NAC had no significant effects on the protein levels of peroxisome proliferator-activated receptor-α (PPAR-α), Acy-CoA oxidase (ACOX), sterol regulatory element binding protein 1 c (SREBP-1c) and fatty acid synthase (FAS). Furthermore, the protein levels of hormone sensitive lipase (HSL) did not significantly differ among 3 groups, whereas NAC prevented binge drinking-induced increase of HSL phosphorylation at ser563 and ser660. Conclusion NAC could effectively attenuate binge drinking-induced fatty liver, which might be associated with the inhibition of lipid mobilization by suppressing the phosphorylation of HSL.

Objective To explore the effect of 14,15-epoxyeicosatrienoic acids (14,15-EET) on the inflammatory response of BV2 cells under oxygen and glucose depriviation/reoxygenation (OGD/R) conditions.Methods BV2 cells were randomly divided into three groups,blank control group,vehicle control group,and 14,15-EET group.Under treatment of 14,15-EET,the concentration of inflammatory factor in BV2 cell culture media was detected by ELISA at different time points (reoxygenation for 0,3,6,12,24 h) after OGD1h.The viability of BV2 cells was detected by MTT assay at different time points.At the same conditions,using Transwell migration experiment,migration ability of BV2 cells was observed.Results The 14,15-EET group had the lower levels of inflammatory factor secretion,lower viability and weaker ability of migration than the vehicle control group.The above results were most statistically significant at OGD1h/R12h.Conclusion 14,15-EET can inhibit the inflammation of BV2 cells induced by the injury of OGD reperfusion.