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 The aim of this study was to explore the effects of changes in the estrogen receptor alpha 36(ER-α36)expression on the proliferation and membrane-initiated estrogen signaling in glioblastoma U251 cells.Methods The expression and localization of ER-α36 and EGFR glioblastoma U87 cells and U251 cells were determined by immunofluorescence,qRT-PCR and Western blot.The effect of upregulating ER-α 36 on U251 cell proliferation and estrogen signaling pathway activity by low con-centrations of 100 pmol/L icariin isomer(SNG162)was detected by MTT assay and Western blot.Results ER-α36 and EGFR were co-expressed in the cell membrane of glioblastoma.Compared with DMSO(control group),the expression ER-α36(P<0.01)and EG-FR increased in U251 cells treated with SNG162(P<0.05);Further experments also found that low concentrations of SNG162 in-creased the expression of cycle related proteins-cyclin D1,cyclin B,cyclin E and CDK4(P<0.01),and enhanced the proliferative a-bility of U251 cells(P<0.05).Conclusion The low concentration of SNG162 upregulates the expression of ER-α36,activates the estrogen-mediated ERK1/2 MAPK,p38 MAPK,and EGFR/Src signaling pathways,promotes glioblastoma proliferation,and activates the membrane initialized estrogen signaling pathway.

Objective The aim of this study was to explore the effects of changes in the estrogen receptor alpha 36(ER-α36)expression on the proliferation and membrane-initiated estrogen signaling in glioblastoma U251 cells.Methods The expression and localization of ER-α36 and EGFR glioblastoma U87 cells and U251 cells were determined by immunofluorescence,qRT-PCR and Western blot.The effect of upregulating ER-α 36 on U251 cell proliferation and estrogen signaling pathway activity by low con-centrations of 100 pmol/L icariin isomer(SNG162)was detected by MTT assay and Western blot.Results ER-α36 and EGFR were co-expressed in the cell membrane of glioblastoma.Compared with DMSO(control group),the expression ER-α36(P<0.01)and EG-FR increased in U251 cells treated with SNG162(P<0.05);Further experments also found that low concentrations of SNG162 in-creased the expression of cycle related proteins-cyclin D1,cyclin B,cyclin E and CDK4(P<0.01),and enhanced the proliferative a-bility of U251 cells(P<0.05).Conclusion The low concentration of SNG162 upregulates the expression of ER-α36,activates the estrogen-mediated ERK1/2 MAPK,p38 MAPK,and EGFR/Src signaling pathways,promotes glioblastoma proliferation,and activates the membrane initialized estrogen 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.

Since the outbreak of Novel Coronavirus Pneumonia(NCP), hospitals have taken the fight against the virus as its own responsibility, and keep standing in the front line of epidemic prevention and control. The continuous input of anti-epidemic forces in hospitals also brings challenges to the medical supplies support, including the management of protective supplies and the maintenance of medical equipment. In the face of increasing security pressure, the medical materials support team broke the game on multiple fronts. Firstly, the team implements active material procurement strategy, sets material distribution priority according to risk level, releases materials uniformly based on stock and use, and implements traceability management of donated materials to ensure material supply. Secondly, centralized allocation management of equipment, emergency installation, advanced maintenance and emergency maintenance work is effectively completed. Thirdly, disinfection strategies for items and equipment are developed safely and effectively with the aid of disinfection equipment functions. At last, personnel management and training have been strengthened. These measures have provided strong support for the orderly prevention and control of the epidemic.

Aberrant oxidative metabolism in cells is one of the hallmarks of cancer. Overproduction of reactive species promotes carcinogenesis by inducing genetic mutations and activating oncogenic pathways, and thus, antioxidant therapy is considered as an important strategy for cancer prevention and treatment. Caveolin-1 (Cav-1), a constituent protein of caveolae, is involved in not only the formation of the caveolae, vesicular transport, maintaining cholesterol homeostasis directly, but also many cellular physiological and pathological processes including growth, regulation of mitochondrial antioxidant level, apoptosis and carcinomas by interacting with a lot of signaling molecules through caveolin scaffolding domain. Cav-1 has also been shown to mediate tumor genesis and progression through oxidative stress modulation, while Cav-1-targeted treatment could scavenge the reactive species. Intracellular reactive species could modulate the expression, degradation, post-translational modifications and membrane trafficking of Cav-1. More importantly, emerging evidence has indicated that multiple antioxidants could exert antitumor activities in cancer cells by modulating the signaling of Cav-1. This paper reviewed the research progresses on the roles of Cav-1 and oxidative stress in tumorigenesis and development, and would provide new insights on designing strategies for cancer prevention or treatment.
Antioxidants ; Apoptosis ; Carcinogenesis ; Carcinoma ; pathology ; Caveolin 1 ; Humans ; Mitochondria ; Neoplasms ; pathology ; Oxidative Stress ; Signal Transduction

Volatile organic compounds (VOCs) in ambient air can participate in photochemical reactions, which lead to the generation of secondary pollutants such as ozone and aerosol. So real-time and accurate monitoring of atmospheric VOCs plays an important role in the study of the causes of air pollution. On the basis of proton transfer reaction mass spectrometry (PTR-MS) research, a novel dipolar proton transfer reaction mass spectrometer (DP-PTR-MS) for real-time and on-line monitoring atmospheric VOCs was developed. Compared with the conventional PTR-MS with one kind of reagent ion H3O+, DP-PTR-MS had three kinds of reagent ions H3O+, OH-, (CH)2COH+, which could be switched according to the actual detection need. So DP-PTR-MS can improve the qualitative ability and expand the detection range effectively. The reagent ion H3O+can be used for detecting VOCs whose proton affinities are greater than that of H2O. The reagent ion OH-can be used to identify VOCs cooperating with the reagent ion H3O+,and can also be used for detecting some inorganic substances such as CO2. The reagent ion (CH3)2COH+can be used for accurately detecting NH3under interference elimination circumstances. The limit of detection (LOD) and sensitivity of DP-PTR-MS were measured by using six kinds of standard gases. The results showed that the LOD for detecting toluene was 7×10-12(V/V) and the sensitivity for detecting ammonia has reached 126 cps/10-9 (V/V). The ambient air in Hefei city was on-line and real-time monitored for continuous 78 hours with DP-PTR-MS. The results showed that the newly developed DP-PTR-MS could be used for long-term and real-time monitoring atmospheric VOCs with the concentration of 10-12(V/V) level. DP-PTR-MS is an important tool for the study of the causes of atmospheric pollution and the monitoring of trace VOCs emissions.

Objective To establish a mouse model of 5-fluorouracil ( 5-FU )-induced intestinal mucositis. Methods Different doses of 5-FU were intraperitonealy injected into mice for once or 5 consecutive days. The body weight and diarrhea score of the mice were recorded every day, and peripheral blood and the morphological changes of small intestine were examined at 24 h or 72 h after the last 5-FU administration. Results Compared with the control group, after administered 5-FU, the dosage groups showed various degrees of body weight loss and diarrhea, and the white blood cell and platelet counts in peripheral blood decreased significantly (P＜0. 05 or P＜0. 01). The small intestine showed evident pathological changes after the single dose 400 mg/kg and the continuous injection of 50 mg/kg, 100 mg/kg. The mortality rate was 100% in the 100 mg/kg group. Conclusions A mouse model of intestinal mucositis can be successfully established by a single injection of 5-FU or for consecutive 5 days, in a dose-dependent manner. The optimal dose for single injection is 400 mg/kg, and that of the continual injection for 5 consecutive days is 50 mg/kg.

Caveolin-1 (Cav-1), as an important structural protein of caveolae, has been proven to be correlated with several signal transduction pathways. Recent studies have shown that Cav-1 may play a critical role in response to DNA damage in irradiated pancreatic cancer cells. However, it is not known whether down-regulation of Cav-1 is required to enhance the damage of other kinds of human cells exposed to X-radiation. In this study, the role of Cav-1 in Chang liver cell line (CHL) exposed to X-radiation was investigated. Cav-1 knockdown cell line (CHL-CAV7) was stably established by the siRNA plasmids transfection, and Cav-1 expression was suppressed by 60%, compared with that of control group (CHL-C) which was transfected with non-targeting plasmids. Cellular survival ability and the expressions of proteins related to DNA damage and repair were examined by colony formation assay and Western blot, respectively. Down-regulation of Cav-1 expression induced a significant decrease of the survival rate in CHL-CAV7 cells exposed to 8 and 10 Gy X-radiation. Compared with CHL-C cells, CHL-CAV7 cells showed increased γH2AX expression, as well as decreased p-ATM, DNA-dependent protein kinase, catalytic subunit (DNA-PKcs) and p53 protein expressions when treated with X-radiation. Meanwhile, the colocalization of Mdm2 and Cav-1 was decreased in CHL-CAV7 cells compared with that in CHL-C cells. These results suggest that the down-regulation of Cav-1 may aggravate DNA damage of CHL cells through reducing the interaction of Cav-1 and Mdm2, which results in the promotion of p53 degradation.

Potassium channels have multitudinous subtypes, which are widely distributed on cell membranes. They affect various cellular physiological functions through participating in processes such as resting potential formation, substance transportation, enzyme activity and cellular communication. Autophagy is a significant mechanism to maintain intracellular metabolic homeostasis. The abnormity of autophagy may lead to the occurrence and development of multiple diseases. Recently, it has been reported that Kchannels and cell autophagy are closely related. Here, we reviewed the recent research progresses on regulation of autophagy signaling, autophagy flux or autophagolysosome formation by Kchannel, and discussed the physiological significance of autophagy regulation by Kchannel.