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.

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.

The biological clock(also known as the circadian rhythm)is the fundamental reliance for all organisms on Earth to adapt and survive in the Earth's rotation environment.Circadian rhythm is the most basic regulatory mechanism of life activities,and plays a key role in maintaining normal physiological and biochemical homeostasis,disease occurrence and treatment.Recent studies have shown that the biologi-cal clock plays an important role in the development of oral tissues and in the occurrence and treatment of oral diseases.Since there is cur-rently no guiding literature on the research methods of biological clock in stomatology,researchers mainly conduct research based on pub-lished references,which has led to controversy about the research methods of biological clock in stomatology,and there are many confusions about how to rationally apply the research methods of circadia rhythms.In view of this,this expert consensus summarizes the characteristics of the biological clock and analyzes the shortcomings of the current biological clock research in stomatology,and organizes relevant experts to summarize and recommend 10 principles as a reference for the rational implementation of the biological clock in stomatology research.

Objective : To investigate the drug resistance and pathogenicity of six clinical isolates of Klebsiella pneu- moniae (Kp) ，and to provide a basis for prevention and treatment of Kp infection． Methods : The six strains from different hospitals were isolated ，cultured ，and identified by species-specific gene khe． Their whole genome se- quences (WGS) were obtained using next-generation sequencing technology (NGS) ．Based on the WGS，the cap- sular serotypes，sequence types (ST) and drug-resistance genes of six strains were identified．The capsular sero- type genes and virulence genes were validated or identified using PCR. Broth microdilution tests were conducted to validate their drug susceptibility，and mice were challenged with Kp aerosols by MicroSprayer aerosolizer to evaluate their pathogenicity. Results : The six strains were all serotype K2 but belonged to four ST types ( ST14 ，ST65， ST700，and ST86) ，and collectively carried six virulence genes and 23 drug-resistance genes．All the six strains were resistant to ampicillin，but only one strain was multidrug-resistant．Four strains exhibited high mucoid charac- teristics．Five strains could cause mortality in mice，which were preliminary identified as high virulence strains. Conclusion For the six Kp clinical isolates from different sources，only one strain named NY 13294 is both multi- drug-resistant and highly virulent，and other four highly virulent strains are resistant to one or two types of antibiot- ics.

Objective To compare the influence of whole sevoflurane inhaling and target-controlled infusion of propofol for the myocardial protective effect on patients with heart valve replacement surgery. Methods 30 adult patients who went through heart valve replacement surgery with cardiopulmonary by pass were selected, including ASA staging II-III and cardiac function classification (NYHA) II-III. All patients were randomly divided equally into sevoflurane group (Group S) and propofol group (Group P) . Patients were monitored before anesthetic induction. Group S got 1%sevoflurane (fresh gas flow 6 L/min) with concentration of the vaporizer increased from 1%to 3%with 1 minute interval during anesthetic induction. Group P got target-controlled infusion of propofol during anesthetic induction,the initial target plasma concentration was set at 0.8μg/mL,and the concentration increased 0.5 μg/mL every minute until intubation. All the patients got fentanyl 5 μg/kg and rocuronium 0.6 mg/kg, and intubation was conducted when BIS decreased lower than 60 and mean arterial pressure (MAP) <20%basic MAP. During anesthesia maintaince,patients got 0.5-2 MAC sevoflurane inhaling or target-controlled infusion of propofol 2-4μg/mL with discontinuous intravenous fentanyl and rocuronium, and maintained BIS 40-60, MAP<±20%basic MAP, central venous pressure 5-15 cm H2O. Outcome variables included demographic characteristics of patients. The following parameters were also recorded, including cardiac troponin I (cTnI), creatine kinase (CK), creatine kinase isoenzyme (CK-MB) and lactate (LAC) in before anesthetic induction (T0), aortic inbation (T1),30 minutes after aorta opening (T2), 6 hours after aorta opening (T3) and 24 hours after aorta opening (T4) . Results There was no statistical significance in demographic characteristics during peri-operation between the two groups ( > 0.05) . The pre-opertaive cTnI, CK, CK-MB and LAC were within the normal range, but increased siginicantly on T2, T3 and T4, and was more significant on T3 ( < 0.01) between two groups, and the intra-group comparison showed no difference on other time points. Conclusion When myocardial injury markers used as myocardial protection outcome variables, whole sevoflurane inhaling could not reduce the release of cTnI compared to propofol TIVA in heart valve replacement surgery.

AIM : To investigate the effects of angiotensin II (AngII) in different concentrations and different action times on the rate of apoptosis and expression of apoptosis genes in vascular smooth muscle cells and the influences of fosinopril on it. METHODS : Flow cytometer was used to measure the apoptosis rate and the expression of apoptosis genes (Fas and Bcl 2) induced by AngII in different concentrations and different action times and the influence caused by fosinopril. RESULTS BZ : The rate of apoptosis and the expression of apoptosis genes were induced and increased by AngII with the increase of concentrations and action times compared with that in the control group. The expression of Fas was increased and Bcl 2 was decreased with the increase of the concentrations and action times of AngII in fosinopril group compared with that in the AngII group. CONCLUSION : The apoptosis rate and the expression of apoptosis genes are induced and increased by angiotensin II with the increase of the concentrations and the action times. Fosinopril has the regulation effect on the apoptosis rate and the expression of apoptosis genes in vascular smooth muscle cells.