Objective To evaluate the clinical application value of transesophageal atrial pacing (TEAP) combined with atropine load experiment in the diagnosis of the lesions of sinoatrial node and atrioventricular node.Methods One hundred and forty-four cases selected from the outpatient and hospitalized patients in the People's Hospital of Changji Hui Autonomous Prefecture from September 2009 to December 2012,who with dizziness, syncope and other clinical symptoms and electrocardiogram showe.TEAP combined with atropine load experiment were given to these patients.Results (1) The authors detected in all patients,83 cases (57.6％) were positive, among which, 48 cases (57.8％) male, 35 cases (42.2％) female.(2) The authors detected 57 cases(39.6％) non-increased vagus nerve tension cases in 83 positive cases,among which 33 cases (57.9％) male, 24 cases (42.1％) female;Among which 29 cases (20.1％) were sinoatrial node hypofunction, and 16 cases(55.2％) male;8 cases(5.6％) were atrioventricular node hypofunction,and 4 cases(50％) male;14 cases(9.7％) were double node hypofunction, and 10 cases (71.4％) male;6 cases (4.2％) were tachycardia-bradycardia syndrome, and 3 cases (50％) male;among which, a long interval of greater than 3 seconds appeared when we stimulate one 84 years old man with S1S1 stimulate way, immediately pressed protective pacemaker until his own sinus rhythm was restored, as a safety precaution, stoped further examination and classified him as sick sinus group.Conclusion Detect the common causes of slow sinus and atrioventricular block,such as the sinoatrial node dysfunction, atrioventricular node dysfunction, double node dysfunction and increased vagus nerve tension through TEAP combined with atropine load experiment.Consider that this methods have the best diagnostic value in decreasing its rate of false positivity,and should be used as a necessary check before implantation of pacemaker in such patients, suitable used in clinical, especially in basic general hospitals.

Objective:To explore the protective effect of vitamin D in acute liver failure through a mouse model.Methods:Acute liver failure was induced by combining D-galactosamine (D-GalN) lipopolysaccharide (LPS) to observe the effect of long-term vitamin D deficiency on liver injury and inflammatory signals in a mouse model. Acute liver failure was induced by thioacetamide (TAA) to observe the effect of vitamin D deficiency on the survival rate, and further high-dose of vitamin D supplementation protective effect was determined in a mouse model. Liver function was evaluated by measuring serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and liver inflammation by hematoxylin-eosin staining. The expressions of tumor necrosis factor (TNF-α), interleukin (IL) -1β, NOD-like receptor family, pyrin domain containing 3 (NLRP-3), chemokines (CCL2, CXCL1 and CXCL2), etc. in liver tissues were detected by RT-qPCR. The quantitation of macrophages in liver tissue was detected by immunohistochemistry. The comparison between groups were performed by t-test. The survival curve was analyzed by log-rank (Mantel-Cox) test.Results:Long-term vitamin D deficiency had increased acute liver failure sensitivity in mice, which was manifested by increased blood cell extravasation, massive necrosis of parenchymal cells, up-regulation of TNF-α, IL-1β, and NLRP-3 mRNA expression ( P < 0.05), and increased macrophages quantitation ( P < 0.05) in liver tissues. At the same time, vitamin D deficiency had increased the mice mortality rate because of liver injury ( P < 0.01). On the contrary, pre-administration of high dose of vitamin D (100 IU/g) had significantly reduced liver injury, inhibited ALT and AST rise ( P < 0.01), alleviated liver necrosis, and down-regulated the mRNA expression of inflammatory factors in liver tissues ( P < 0.05). Conclusion:Mouse model shows that long-term vitamin D deficiency can aggravate drug-induced acute liver failure and reduce survival rates. Furthermore, high-dose of vitamin D has a certain hepatoprotective effect, which can significantly improve liver necrosis condition and inhibit inflammation. Therefore, adequate vitamin D can retain liver physiological balance to resist liver injury.

Objective:To rapidly evaluate the level of healthcare resource demand for laboratory testing and prevention and control of corona virus disease 2019 (COVID-19) in different epidemic situation, and prepare for the capacity planning, stockpile distribution, and funding raising for infectious disease epidemic response.Methods:An susceptible, exposed, infectious, removed infectious disease dynamics model with confirmed asymptomatic infection cases and symptomatic hospitalized patients was introduced to simulate different COVID-19 epidemic situation and predict the numbers of hospitalized or isolated patients, and based on the current COVID-19 prevention and control measures in China, the demands of resources for laboratory testing and prevention and control of COVID-19 were evaluated.Results:When community or local transmission or outbreaks occur and total population nucleic acid testing is implemented, the need for human resources is 3.3-89.1 times higher than the reserved, and the current resources of medical personal protective equipment and instruments can meet the need. The surge in asymptomatic infections can also increase the human resource demand for laboratory testing and pose challenge to the prevention and control of the disease. When vaccine protection coverage reach ≥50%, appropriate adjustment of the prevention and control measures can reduce the need for laboratory and human resources.Conclusions:There is a great need in our country to reserve the human resources for laboratory testing and disease prevention and control for the response of the possible epidemic of COVID-19. Challenges to human resources resulted from total population nucleic acid testing and its necessity need to be considered. Conducting non-pharmaceutical interventions and encouraging more people to be vaccinated can mitigate the shock on healthcare resource demand in COVID-19 prevention and control.