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 effects and potential mechanisms of melatonin on cognitive dysfunction induced by long-term anesthesia with isoflurane.Methods:Male C57BL/6J mice aged 2 months were divided into control group, isoflurane group, melatonin group, and isoflurane+ melatonin group by random number table, with 6 mice in each group.Three days after anesthesia, cognitive function of mice was assessed by Y-maze and fear conditioning (FC) tests. ATP content in the hippocampus was measured by an ATP assay kit. Western blot was used to detect the expression of DRP1, pDRP1, MFN2, pAMPK and SIRT1 proteins in the hippocampus. Cultured HT-22 cells derived from mouse hippocampal neurons in vitro were divided into control group, isoflurane group, melatonin group, and isoflurane + melatonin group, and the levels of reactive oxygen species (ROS) in each group were detected by flow cytometry after intervention. Statistical analysis was performed by SPSS 22.0 software, and one-way ANOVA was used for comparisons among multiple groups.Results:(1) There was a statistically significant difference in the percentage of freezing behavior in contextual fear memory among the four groups of mice ( F=39.09, P<0.05). The percentage of freezing behavior in the isoflurane group was lower than that in the control group ((44.23±8.88)% vs (75.87±5.90)%, P<0.05), while the percentage of freezing behavior in the isoflurane+ melatonin group((67.45±14.89)%)was higher than that in the isoflurane group ( P<0.05). There was also a statistically significant difference in the percentage of exploration in the novel arm among the four groups of mice ( F=13.87, P<0.05). The percentage of exploration in the novel arm in the isoflurane group was lower than that in the control group((33.64±6.53)% vs (47.13±3.87)%, P<0.05), while the percentage of exploration in the novel arm in the isoflurane+ melatonin group((43.05±1.64)%)was higher than that in the isoflurane group ( P<0.05). (2) Statistically significant difference in the levels of ATP in the hippocampus was found among the four groups of mice ( F=49.22, P<0.05). The level of ATP in the hippocampus in the isoflurane group was lower than that in the control group((2.29±0.15)nmol/mg vs (3.58±0.12)nmol/mg, P<0.05), while the level of ATP in the hippocampus in the isoflurane+ melatonin group ((3.02±0.27)nmol/mg)was higher than that in the isoflurane group ( P<0.05). There was a statistically significant difference in the levels of ROS in HT-22 cells among the four groups ( F=18.36, P<0.05). The level of ROS in HT-22 cells in the isoflurane group was higher than that in the control group after anesthesia ( P<0.05), while the level of ROS in HT-22 cells in the isoflurane+ melatonin group was lower than that in the isoflurane group after anesthesia ( P<0.05). (3) There were statistically significant difference in the levels of pDRP1, pAMPK and SIRT1 protein in the hippocampus among the four groups of mice ( F=19.87, 21.20, 25.65, all P<0.05). The levels of pDRP1 and SIRT1 protein in the hippocampus in the isoflurane group were both lower than those in the control group (both P<0.05), while the levels of pDRP1 and SIRT1 protein in the hippocampus in the isoflurane+ melatonin group were both higher than those in the isoflurane group (both P<0.05). In the isoflurane group, the expression of pAMPK protein in the hippocampal region was higher than that in the control group ( P<0.05), while the expression of pAMPK protein in the isoflurane+ melatonin group was lower than that in the isoflurane group ( P<0.05). Conclusion:Melatonin improves long-term isoflurane anesthesia-induced cognitive dysfunction by regulating mitochondrial homeostasis through the AMPK/SIRT1 signaling pathway.

Objective:To investigate the effects and potential mechanisms of melatonin on cognitive dysfunction induced by long-term anesthesia with isoflurane.Methods:Male C57BL/6J mice aged 2 months were divided into control group, isoflurane group, melatonin group, and isoflurane+ melatonin group by random number table, with 6 mice in each group.Three days after anesthesia, cognitive function of mice was assessed by Y-maze and fear conditioning (FC) tests. ATP content in the hippocampus was measured by an ATP assay kit. Western blot was used to detect the expression of DRP1, pDRP1, MFN2, pAMPK and SIRT1 proteins in the hippocampus. Cultured HT-22 cells derived from mouse hippocampal neurons in vitro were divided into control group, isoflurane group, melatonin group, and isoflurane + melatonin group, and the levels of reactive oxygen species (ROS) in each group were detected by flow cytometry after intervention. Statistical analysis was performed by SPSS 22.0 software, and one-way ANOVA was used for comparisons among multiple groups.Results:(1) There was a statistically significant difference in the percentage of freezing behavior in contextual fear memory among the four groups of mice ( F=39.09, P<0.05). The percentage of freezing behavior in the isoflurane group was lower than that in the control group ((44.23±8.88)% vs (75.87±5.90)%, P<0.05), while the percentage of freezing behavior in the isoflurane+ melatonin group((67.45±14.89)%)was higher than that in the isoflurane group ( P<0.05). There was also a statistically significant difference in the percentage of exploration in the novel arm among the four groups of mice ( F=13.87, P<0.05). The percentage of exploration in the novel arm in the isoflurane group was lower than that in the control group((33.64±6.53)% vs (47.13±3.87)%, P<0.05), while the percentage of exploration in the novel arm in the isoflurane+ melatonin group((43.05±1.64)%)was higher than that in the isoflurane group ( P<0.05). (2) Statistically significant difference in the levels of ATP in the hippocampus was found among the four groups of mice ( F=49.22, P<0.05). The level of ATP in the hippocampus in the isoflurane group was lower than that in the control group((2.29±0.15)nmol/mg vs (3.58±0.12)nmol/mg, P<0.05), while the level of ATP in the hippocampus in the isoflurane+ melatonin group ((3.02±0.27)nmol/mg)was higher than that in the isoflurane group ( P<0.05). There was a statistically significant difference in the levels of ROS in HT-22 cells among the four groups ( F=18.36, P<0.05). The level of ROS in HT-22 cells in the isoflurane group was higher than that in the control group after anesthesia ( P<0.05), while the level of ROS in HT-22 cells in the isoflurane+ melatonin group was lower than that in the isoflurane group after anesthesia ( P<0.05). (3) There were statistically significant difference in the levels of pDRP1, pAMPK and SIRT1 protein in the hippocampus among the four groups of mice ( F=19.87, 21.20, 25.65, all P<0.05). The levels of pDRP1 and SIRT1 protein in the hippocampus in the isoflurane group were both lower than those in the control group (both P<0.05), while the levels of pDRP1 and SIRT1 protein in the hippocampus in the isoflurane+ melatonin group were both higher than those in the isoflurane group (both P<0.05). In the isoflurane group, the expression of pAMPK protein in the hippocampal region was higher than that in the control group ( P<0.05), while the expression of pAMPK protein in the isoflurane+ melatonin group was lower than that in the isoflurane group ( P<0.05). Conclusion:Melatonin improves long-term isoflurane anesthesia-induced cognitive dysfunction by regulating mitochondrial homeostasis through the AMPK/SIRT1 signaling pathway.

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.

ObjectiveTo investigate the efficacy and safety of N-acetylcysteine （NAC） in the treatment of severe alcoholic hepatitis （SAH）， and to provide a basis for clinical medication for SAH. MethodsA prospective randomized controlled trial was conducted among 172 SAH patients with a Maddrey discriminant function score of >32 points who were recruited by The Fifth Medical Center of Chinese PLA General Hospital from June 2015 to June 2018， and these patients were divided into NAC group with 84 patients and control group with 86 patients. NAC （8 g/day， 28 days） was assessed in terms of its safety in SAH patients， its impact on 28-day biochemical parameters， and its role in improving 28- and 180-day survival rates. A further analysis was performed to investigate the effect of NAC on the 28- and 180-day survival rates of SAH patients with acute-on-chronic liver failure （ACLF-SAH patients） and those without acute-on-chronic liver failure （non-ACLF-SAH patients）. The independent-samples t test was used for comparison of normally distributed continuous data between two groups， and the Mann-Whitney U test was used for comparison of non-normally distributed continuous data between two groups. The Kaplan-Meier method was used to plot survival curves， and the Log-rank test was used for comparison of survival curves. Univariate and multivariate Cox proportional-hazards regression model analyses were used to investigate independent influencing factors. ResultsNo serious adverse events were observed during NAC treatment， suggesting that NAC had a good safety profile. Compared with the control group， NAC did not significantly improve the 28-day biochemical parameters （all P>0.05） and survival rate of SAH patients （P=0.081）， but it could improve the 180-day survival rate of SAH patients （67.4% vs 81.0%， χ²=4.280， P=0.039）. NAC did not improve the 28- and 180-day survival rates of ACLF-SAH patients （both P>0.05）； NAC did not improve the 28-day survival rate of non-ACLF-SAH patients （P>0.05）， but it could improve the 180-day survival rate of these patients （68.4% vs 88.9%， χ²=4.883， P=0.027）. The multivariate Cox regression survival analysis showed that NAC treatment （hazard ratio ［HR］=2.530， 95% confidence interval ［CI］： 1.334‍ ‍— 4.796， P=0.004，）， Maddrey discriminant function score （HR=3.852， 95%CI： 2.032 — 7.304， P<0.001）， and serum sodium level （HR=1.948， 95%CI： 1.079‍ ‍—‍ ‍3.517， P=0.027） were independent influencing factors for 180-day survival rate in SAH patients. ConclusionNAC has a good safety profile in the treatment of SAH and can improve the 180-day survival rate of SAH patients， and in particular， non-ACLF-SAH patients can benefit from NAC treatment in terms of middle- and long-term survival rates.

Renal interstitial fibrosis（RIF） is the main pathological manifestation of chronic kidney disease. Due to the complexity of the mechanism， there is no specific treatment for RIF in clinical practice. The abnormal activation of the phosphatidylinositol 3-kinase （PI3K）/protein kinase B（Akt） signaling pathway and the activation of downstream target genes are key drivers of RIF induction and progression. Traditional Chinese medicine has the characteristics of precise efficacy and minimal toxic side effects， and the occurrence and development of RIF can be regulated by multiple targets and mutual coordination. This review focuses on the PI3K/Akt signaling pathway and summarizes the potential targets and regulatory mechanisms of traditional Chinese medicine in the treatment of RIF. It is found that various effective ingredients （such as sinomenine， mangiferin， coumarin derivates from Hydrangea paniculata， etc.） and formulas （such as Fushengong decoction， Qi-Bang-Yi-Shen formula， etc.） of traditional Chinese medicine can inhibit fibroblast proliferation， improve inflammation and oxidative stress， maintain mitochondrial stability， and slow down ferroptosis through this pathway， thereby delaying the occurrence and progression of RIF.

Objective This study aims to investigate the primary target and potential mechanism of mangiferin(MF)in treating oral submucous fibrosis(OSF)through Gene Expression Omnibus(GEO)database chip mining,network pharmacology,and molecular docking techniques.Methods Potential therapeutic targets for OSF were identified using GEO chip data.The potential targets of MF were predicted,and disease-related targets for OSF were col-lected from databases.A Venn diagram was created using the EVenn platform to identify overlapping targets.The protein-protein interaction(PPI)network was constructed using the STRING database.Gene ontology(GO)and Kyoto Encyclope-dia of Genes and Genomes(KEGG)enrichment analyses were performed using the DAVID platform.Cytoscape 3.10.1 software was used to visualize a drug-target-pathway-disease network,while AutoDocktools 1.5.6 software was employed for molecular docking analysis.Results A total of 356 potential targets for MF and 360 disease-related targets for OSF were obtained from multiple databases.The top 15 key target proteins in the PPI network were selected as significant candi-dates.GO function and KEGG pathway enrichment analyses revealed that MF treatment primarily involved advanced gly-cation end products-receptor(AGE-RAGE),epidermal growth factor receptor(EGFR),and other signaling pathways associ-ated with OSF pathogenesis.Molecular docking analysis demonstrated that MF exhibited a strong binding activity toward AKT serine kinase 1(AKT1),tumor necrosis factor(TNF),and other core targets.Conclusion These findings suggest that MF may exert its therapeutic effects on OSF through a multitarget approach involving various signaling pathways.

Objective:To compare results of four glycosylated hemoglobin A1c (HbA1c) detection methods and to evaluate the uncertainty of HbA1C results in clinical laboratory, and to provide method for clinical laboratory on the evaluation of uncertainty.Methods:According to the four uncertainty evaluation methods, which were recommended by "CNAS-TRL-001, the evaluation and expression of measurement uncertainty in medical laboratory", the relative and absolute uncertainty of low, medium and high HbA1c in 33 clinical laboratories measured in 2019 and 35 clinical laboratories measured in 2020 was evaluated by more than 6 months of internal quality control (IQC) data, trueness verification and external quality assessment (EQA) data. The four uncertainty evaluation methods were: IQC data and trueness verification data (method 1), only trueness verification data (method 2), IQC and EQA data (method 3) and only EQA data (method 4). The related statistical methods used in this analysis were Friedman and Wilcoxon signed rank test.Results:For method 1, the median range of relative and absolute uncertainty of low, medium and high HbA1c detection in 2019 and 2020 ranged from 4.21% to 9.24% and from 0.27% to 0.64%, respectively. Compared to method 1, the relative and absolute uncertainties obtained by method 2 were smaller, and the differences were statistically significant ( P<0.016 7, P<0.05). Compared to method 1, the relative uncertainties obtained by method 3 and method 4 were smaller, except for the high concentration of HbA1c level in 2020. Among the 6 pairs of comparisons (low, medium and high HbA1c in 2019 and 2020), there were 3 pairs (high HbA1c in 2019, low and medium HbA1c in 2020) and 2 pairs (low and high HbA1c in 2020) of differences with statistical significance (all P<0.016 7). Conclusion:The uncertainty evaluation of HbA1c detection in clinical laboratory should be evaluated based on IQC and trueness verification data.

Post-stroke cognitive impairment (PSCI) is a series of syndromes caused by stroke, involving impairment of one or more cognitive functions, such as attention, language function, executive function, visuospatial cognition, episodic memory and working memory, etc. The traditional treatment methods of PSCI include drug therapy and cognitive training. The treatment modalities are limited and the maintenance effect is not good. Therefore, an auxiliary treatment method is urgently needed to improve its therapeutic effect. Transcranial direct current stimulation (tDCS) is a safe and mature non-invasive brain stimulation technique, which generates weak direct current (1-2 mA) through electrodes placed on the scalp to change the resting membrane potential of neurons, regulate the excitability of the cerebral cortex, so as to achieve the purpose of treatment. This article reviews the effect of tDCS on PSCI, and hopes to provide reference and guidance for its rehabilitation treatment.

Objective:To investigate the function of gasdermin D (GSDMD) in intestinal damage of mice with severe acute pancreatitis (SAP).Methods:The healthy C57BL/6 mice were divided into four groups randomly, including normal saline (NS) group, small interfering RNA (siRNA)-NS group, SAP model group and siRNA-SAP group, with 6 mice in each group. The SAP mouse model was reproduced by intraperitoneal injection of caerulein 50 μg/kg combined with lipopolysaccharide (LPS) 10 mg/kg; the NS group was given the same amount of NS; in the siRNA-SAP group and siRNA-NS group, siRNA 50 mg/kg was injected through the tail vein three times before modeling or injection of NS. The blood of mice eyeball in each group was taken 12 hours after modeling, and serum interleukins (IL-1β, IL-18) levels were detected by enzyme linked immunosorbent assay (ELISA). The mice were sacrificed to observe the general changes in abdominal cavity, the pancreas and ileum tissues were taken to observe the pathological changes under a light microscope. The expression of long-chain non-coding RNA uc.173 (lnc uc.173) was detected by reverse transcription-polymerase chain reaction (RT-PCR). Immunohistochemical method was used to detect the expression of tight junction proteins zonula occluden-1 (ZO-1) and Occludin in intestinal mucosal epithelial cells. Western blotting was used to detect the GSDMD protein expression level in the intestinal tissue.Results:The serum levels of IL-1β and IL-18 in the SAP model group were significantly higher than those in the NS group and the siRNA-NS group [IL-1β (ng/L): 146.66±1.40 vs. 44.48±5.76, 81.49±10.75, IL-18 (ng/L): 950.47±177.09 vs. 115.43±16.40, 84.84±21.90, all P < 0.05]; and the levels of IL-1β and IL-18 in the siRNA-SAP group were significantly lower than those in the SAP model group [IL-1β (ng/L): 116.26±15.54 vs. 146.66±1.40, IL-18 (ng/L): 689.96±126.08 vs. 950.47±177.09, both P < 0.05]. General observation showed that there were no obvious abnormalities in the abdominal cavity of the mice in the NS and siRNA-NS groups; the mice in the SAP model group and the siRNA-SAP group had different degrees of edema and congestion in the intestine; compared with the SAP model group, the abnormalities in the siRNA-SAP group was significantly reduced. Under light microscope, there were no obvious changes in the pancreas and intestinal mucosa in the NS group and the siRNA-NS group; the pancreatic tissue of the SAP model group and the siRNA-SAP group had different degrees of edema, inflammatory cell infiltration, and lobular structure damage, and the intestinal mucosa was damaged to a certain degree, and the villi were broken to varying degrees, but the damage in the siRNA-SAP group was lighter. The results of RT-PCR showed that the expression of lnc uc.173 in the intestinal tissues of the model SAP group was significantly lower than that of the NS group and the siRNA-NS group (2 -ΔΔCt: 0.26±0.12 vs. 1.01±0.37, 0.67±0.32, both P < 0.05), while the expression of lnc uc.173 in the siRNA-SAP group was significantly higher than that in the SAP model group (2 -ΔΔCt: 0.60±0.39 vs. 0.26±0.12, P < 0.05). Immunohistochemistry showed that ZO-1 and Occludin proteins in the NS group were distributed along the epithelial cells of the intestinal mucosa, showing a strong expression; ZO-1 and Occludin expressions were significantly reduced in the SAP model group and siRNA-SAP group, but the expressions in the siRNA-SAP group was higher than that in the SAP model group. Western blotting showed that the expression level of GSDMD protein in the intestinal tissues of the SAP model group was significantly higher than that of the NS group and the siRNA-NS group [GSDMD protein (GSDMD-N/β-actin): 1.99±0.46 vs. 1, 1.00±0.78, both P < 0.05]. Compared with the SAP model group, the expression of GSDMD protein in the siRNA-SAP group was significantly decreased [GSDMD protein (GSDMD-N/β-actin): 1.42±0.42 vs. 1.99±0.46, P < 0.05]. Conclusions:The systemic inflammatory response and intestinal mucosal barrier damage of SAP mice may be related to the increase of GSDMD expression in intestinal tissues. GSDMD mediates cell pyrolysis to promote the release of inflammatory factors, cause intestinal injury, and down-regulate the expression of intestinal epithelial cell tight junction proteins such as ZO-1 and Occludin, resulting in intestinal mucosal damage.