Recent studies have shown that the physiological homeostasis of oral mucosal cells is regulated by the circadian clock.Dis-ruption or dysfunction of the circadian clock is closely associated with the development of oral squamous cell carcinoma(OSCC).Research based on the circadian clock offers a novel perspective on the pathogenesis and therapeutic strategies for OSCC.However,there is current-ly limited research on this topic,and people generally have insufficient understanding and recognition of the circadian clock.Given the complexity and challenges of circadian clock which is the fourth dimension of medical research,we organize relevant experts based on summarizing the current research results of circadian clock in the pathogenesis and precision diagnosis and treatment of OSCC,combining the scientific principles of the circadian clock's role and their long-term research experience,then summarizes and recommends the con-sensus opinions for the research of circadian clock in the pathogenesis mechanism and precision diagnosis and treatment of human OSCC,with the hope of providing guidance for the basic research and clinical application of circadian clock or circadian rhythm in the pathogene-sis mechanism and precision diagnosis and treatment of oral and maxillofacial squamous cell carcinoma.

Turning to critical illness is a common stage of various diseases and injuries before death. Patients usually have complex health conditions, while the treatment process involves a wide range of content, along with high requirements for doctor′s professionalism and multi-specialty teamwork, as well as a great demand for time-sensitive treatments. However, this is not matched with critical care professionals and the current state of medical care in China. Telemedicine, which shortens the distance of medical professionals and the gap of disease diagnosis and treatments in various regions through electronic information, can effectively solve the current problem. Therefore, there is an urgent need to develop a standardized, high-quality visualization telemedicine round system .Therefore, experts have been organized to search domestic and foreign literature on telemedicine round for critically ill patients and to form this consensus based on clinical experiences so as to further improve the level of critical care treatments in regions.

OBJECTIVE To investigate the in vitro inhibitory mechanism of allicin against carbapenem-resistant Klebsiella pneumoniae(CRKP).METHODS The standard microbroth dilution method was employed to determine the minimum inhibitory concentration(MIC)of allicin against the experimental CRKP.Growth curve experiments were conducted to verify the relationship between allicin concentration and antibacterial action.RNA sequencing(RNA-seq)was performed on allicin-treated CRKP and a normal control group to explore the molecular mecha-nism of allicin inhibiting CRKP growth.RESULTS The MIC of allicin against CRKP was 140 mg/ml.A total of 1 775 differentially expressed genes were screened from the normal control group and the allicin-treated group,with 845 genes upregulated and 930 genes downregulated.The expression of bacterial phosphotransferase system(PTS)genes showed significant differences between the control group and the treated group(P＜0.05),and the expression levels of EIIA-EIID genes decreased(P＜0.05).CONCLUSION Based on the analysis of RNA-seq re-sults,it is found that allicin may inhibits the growth of CRKP by disrupting its sugar transport system,thereby affecting its biofilm formation.

Turning to critical illness is a common stage of various diseases and injuries before death. Patients usually have complex health conditions, while the treatment process involves a wide range of content, along with high requirements for doctor′s professionalism and multi-specialty teamwork, as well as a great demand for time-sensitive treatments. However, this is not matched with critical care professionals and the current state of medical care in China. Telemedicine, which shortens the distance of medical professionals and the gap of disease diagnosis and treatments in various regions through electronic information, can effectively solve the current problem. Therefore, there is an urgent need to develop a standardized, high-quality visualization telemedicine round system .Therefore, experts have been organized to search domestic and foreign literature on telemedicine round for critically ill patients and to form this consensus based on clinical experiences so as to further improve the level of critical care treatments in regions.

Recent studies have shown that the physiological homeostasis of oral mucosal cells is regulated by the circadian clock.Dis-ruption or dysfunction of the circadian clock is closely associated with the development of oral squamous cell carcinoma(OSCC).Research based on the circadian clock offers a novel perspective on the pathogenesis and therapeutic strategies for OSCC.However,there is current-ly limited research on this topic,and people generally have insufficient understanding and recognition of the circadian clock.Given the complexity and challenges of circadian clock which is the fourth dimension of medical research,we organize relevant experts based on summarizing the current research results of circadian clock in the pathogenesis and precision diagnosis and treatment of OSCC,combining the scientific principles of the circadian clock's role and their long-term research experience,then summarizes and recommends the con-sensus opinions for the research of circadian clock in the pathogenesis mechanism and precision diagnosis and treatment of human OSCC,with the hope of providing guidance for the basic research and clinical application of circadian clock or circadian rhythm in the pathogene-sis mechanism and precision diagnosis and treatment of oral and maxillofacial squamous cell carcinoma.

OBJECTIVE To investigate the in vitro inhibitory mechanism of allicin against carbapenem-resistant Klebsiella pneumoniae(CRKP).METHODS The standard microbroth dilution method was employed to determine the minimum inhibitory concentration(MIC)of allicin against the experimental CRKP.Growth curve experiments were conducted to verify the relationship between allicin concentration and antibacterial action.RNA sequencing(RNA-seq)was performed on allicin-treated CRKP and a normal control group to explore the molecular mecha-nism of allicin inhibiting CRKP growth.RESULTS The MIC of allicin against CRKP was 140 mg/ml.A total of 1 775 differentially expressed genes were screened from the normal control group and the allicin-treated group,with 845 genes upregulated and 930 genes downregulated.The expression of bacterial phosphotransferase system(PTS)genes showed significant differences between the control group and the treated group(P＜0.05),and the expression levels of EIIA-EIID genes decreased(P＜0.05).CONCLUSION Based on the analysis of RNA-seq re-sults,it is found that allicin may inhibits the growth of CRKP by disrupting its sugar transport system,thereby affecting its biofilm formation.

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.

Objective:To investigate the preventive and therapeutic effects of epigallocatechin gallate (EGCG) on tetracycline-induced acute drug-induced liver injury (DILI) in mice.Methods:Thirty-two BALB/C mice were divided into four groups, with eight mice in each group. The normal group was raised under conventional condition. Tetracycline-induced acute DILI models were established by intraperitoneal injection of tetracycline in the model group, the blank control group was intraperitoneally injected with equivalent 0.9% NaCl soluation, and EGCG prevention/treatment group was treated with EGCG on the basis of modeling. Blood samples, feces, liver and intestinal tissues of mice were obtained and analyzed by flow cytometry, biochemical test, pathological examination, and 16S rRNA sequencing. The effects of EGCG on gut microbiota, serum lipopolysaccharides (LPS) and transaminase, CD64 expression in intestinal mucosa, hepatic macrophage typing, and hepatic steatosis were evaluated. One-way analysis of variance was performed for analysis of significant difference among groups, and independent sample t test was used for further pairwise comparison. Results:Intraperitoneal injection of tetracycline-caused disorder of gut microbiota in the model group with hepatocytes showing steatosis grade 3 in 7 mice and grade 4 in 1 mouse. The serum level of LPS in model group was significantly higher than that of normal group ( (5.50±0.20) EU/L vs. (3.96±0.19) EU/L) and by the gut-liver axis which caused M1-type macrophages in liver tissues more than that of normal group ((40.00±2.91)% vs. (36.12±2.53)%), and the differences were statistically significant( t=15.83, 2.46; P<0.001, =0.034), and CD64 expression in intestinal mucosa also increased. EGCG intervention altered the gut microbiota in mice with tetracycline-induced acute DILI. The Shannon index and Simpson index of the model group were lower than those of the normal group (4.98±0.56 vs. 5.62±0.47, 0.91±0.03 vs. 0.95±0.02), while the Shannon index (4.08±0.62) and Simpson index (0.83±0.07) of the EGCG prevention/treatment group were lower than those of the model group. The differences were statistically significant ( t=-2.30, -2.85, -2.85, 2.82; P=0.038, 0.013, 0.013, 0.014). Compared with those of the model group, liver pathological changes of EGCG prevention/treatment group improved significantly (grade 2 in 8 mice), the serum level of LPS((4.22±0.17) EU/L) decreased, and the difference was statistically significant( t=-13.63, P<0.001), but had no significant effects on the CD64 expression in intestinal mucosa. Hepatic macrophage typing was compared between EGCG prevention/treatment group and model group, M2-type macrophages promoting repair were predominant in EGCG prevention/treatment group (M2-type macrophoges ratio: (6.20±0.17)% vs. (4.74±0.48)%, t=2.84, P=0.017; M1/M2-type macrophages ratio: 6.20±1.25 vs. 8.48±0.66, t=-4.95, P=0.001). Conclusion:EGCG alleviates tetracycline-induced acute DILI by altering gut microbiota to modulate liver innate immune system.

Objective:To investigate the preventive and therapeutic effects of epigallocatechin gallate (EGCG) on tetracycline-induced acute drug-induced liver injury (DILI) in mice.Methods:Thirty-two BALB/C mice were divided into four groups, with eight mice in each group. The normal group was raised under conventional condition. Tetracycline-induced acute DILI models were established by intraperitoneal injection of tetracycline in the model group, the blank control group was intraperitoneally injected with equivalent 0.9% NaCl soluation, and EGCG prevention/treatment group was treated with EGCG on the basis of modeling. Blood samples, feces, liver and intestinal tissues of mice were obtained and analyzed by flow cytometry, biochemical test, pathological examination, and 16S rRNA sequencing. The effects of EGCG on gut microbiota, serum lipopolysaccharides (LPS) and transaminase, CD64 expression in intestinal mucosa, hepatic macrophage typing, and hepatic steatosis were evaluated. One-way analysis of variance was performed for analysis of significant difference among groups, and independent sample t test was used for further pairwise comparison. Results:Intraperitoneal injection of tetracycline-caused disorder of gut microbiota in the model group with hepatocytes showing steatosis grade 3 in 7 mice and grade 4 in 1 mouse. The serum level of LPS in model group was significantly higher than that of normal group ( (5.50±0.20) EU/L vs. (3.96±0.19) EU/L) and by the gut-liver axis which caused M1-type macrophages in liver tissues more than that of normal group ((40.00±2.91)% vs. (36.12±2.53)%), and the differences were statistically significant( t=15.83, 2.46; P<0.001, =0.034), and CD64 expression in intestinal mucosa also increased. EGCG intervention altered the gut microbiota in mice with tetracycline-induced acute DILI. The Shannon index and Simpson index of the model group were lower than those of the normal group (4.98±0.56 vs. 5.62±0.47, 0.91±0.03 vs. 0.95±0.02), while the Shannon index (4.08±0.62) and Simpson index (0.83±0.07) of the EGCG prevention/treatment group were lower than those of the model group. The differences were statistically significant ( t=-2.30, -2.85, -2.85, 2.82; P=0.038, 0.013, 0.013, 0.014). Compared with those of the model group, liver pathological changes of EGCG prevention/treatment group improved significantly (grade 2 in 8 mice), the serum level of LPS((4.22±0.17) EU/L) decreased, and the difference was statistically significant( t=-13.63, P<0.001), but had no significant effects on the CD64 expression in intestinal mucosa. Hepatic macrophage typing was compared between EGCG prevention/treatment group and model group, M2-type macrophages promoting repair were predominant in EGCG prevention/treatment group (M2-type macrophoges ratio: (6.20±0.17)% vs. (4.74±0.48)%, t=2.84, P=0.017; M1/M2-type macrophages ratio: 6.20±1.25 vs. 8.48±0.66, t=-4.95, P=0.001). Conclusion:EGCG alleviates tetracycline-induced acute DILI by altering gut microbiota to modulate liver innate immune system.

Objective: To explore the effects of protein powder on the bioavailability of perfluoroalkyl substances (PFASs) in blood and kidneys of rats and renal function change. Methods: Twenty-four rats of the SD strain were randomly divided into the negative control group, PFASs group and protein powder group, with 8 rats (half males and half females) in each group. PFASs included 13 perfluorocarboxylic acids (PFCAs) and 8 perfluorosulfonic acids (PFSAs), and the mixture was used as a test subject for intervention. The rats in the negative control group were given deionized water at doses of 20 mL/kg·bw, in the PFASs group were given 5 mL/kg·bw of PFASs mixtures and 15 mL/kg·bw of deionized water, and in the protein powder group were given 5 mL/kg·bw of PFASs mixtures and 15 mL/kg·bw of protein powder (0.258 g/mL). After intervention for 28 successive days, body weight and kidney mass were weighed, and the kidney volume index was calculated. Serum creatinine and blood urea nitrogen were detected by an automatic biochemical analyzer. The PFCAs, PFSAs and PFASs contents were quantified in blood and kidney using ultra-high performance liquid chromatography-electrospray tandem mass spectrometry, and the bioavailability was estimated. Results: There was no significant differences in kidney mass, kidney volume index, serum creatinine and blood urea nitrogen among the negative control group, PFASs group and protein powder group (all P>0.05). The bioavailability of blood PFCAs, PFSAs and PFASs in the protein powder group was not significantly different from the PFASs group (all P>0.05). Compared with the PFASs group, the bioavailability of PFCAs, PFSAs and PFASs were significantly increased in kidneys of male rats in the protein powder group (all P<0.05), while were not significant different in those of female rats (all P>0.05). Conclusion Protein powder at the dose of this study can significantly improve the bioavailability of PFASs in kidneys of male rats, while there no obvious effects on the bioavailability of blood PFASs and renal function.