Retrospective analysis was conducted for the results of first-aid competitions so as to understand the present status of how emergency doctors of Hubei Province grasp the skills and consciousnesses of cervical immobilization.From 6 out of 19 teams,38 participating doctors from grade 3A hospitals provided patient cervical immobilization while 2 teams offered no cervical protection.It is necessary to intensify the skills and consciousnesses of cervical immobilization in clinical practice.

Objective To investigate a reproducible model of severe crush injury (CI) in rats.Methods A total of 50 clean grade male SD rats were randomly (random number) divided into 5 groups.Both hindlimbs of anesthetized rats were compressed by blocks weighing 3.5 kg,for 6 hours and followed by 3 hours of reperfusion on a specially notched device (group SP,n =10),ordinary compression (group NM,n =10) and simple control (group SHAM,n =10).Arterial tension,serum lactate,and potassium (K+),serum myoglobin (MB),aspartate transferase (AST) and alanine transferase (ALT),BUN and Cr were measured at 10 minutes after cannulaton,and 3 hours after release from compression.Muscles and kidneys were evaluated morphologically.Group D and E were treated in the same way and were observed for 72 h to get the survival rate of the NM group and the specially notched compression group.The SPSS 17.0 statistical software was used for statistical analysis,repeated-measures ANOVA analysis for the differences between groups,Kaplan Meier-estimator for survival analysis.Results The Specially notched compression produced a greater increase in serum lactate (F =39.626,P ＜ 0.05),AST (F =24.965,P ＜ 0.05),ALT (F =19.096,P＜0.05),BUN (F=7.938,P＜0.05),CR (F=14.787,P＜0.05) and MB (F=16.840,P ＜0.05) by the end of experiment than NM group and simple control group.The direct cellular damage and ischemia-reperfusion injury were found under microscope.In crush injury caused by specially notched compression there was acute tubular necrosis found at 24 hours after injury.Mortality rate in the NM group was 20％,whereas mortality rate reached 90％ in rats with specially notched compression (P ＜0.05).Conclusions It successfully developed a severe crush injury model in experimental rats,suggesting it is worthwhile to popularization.

Objective To evaluate the efficacy of multiple injection of morphine combined with phloroglucinol in the treatment of renal colic. Methods One hundred and twenty patients with severe renal colic were equally divided into three groups by random digits table,with 40 cases each group. The group A was administrated with physiological saline 100 ml and phloroglucinol 80 mg intervenous drop infusion combined with morphine 9 mg intravenous injection fractionated into three times, and the group B was administrated with physiological saline 100 ml and phloroglucinol 80 mg intervenous drop infusion,and the group C was administrated with physiological saline 100 ml intervenous drop infusion and morphine 9 mg intravenous injection fractionated into three times. At 10,20 and 40 min after administration, the antalgic efficacy of three groups were analyzed as well as the side effect. Results At 20 min and 40 min both of the total efficacy rates in group A[82.5%(33/40),95.0%(38/40)] were higher than those in group B [62.5%(25/40),80.0%(32/40)] and group C [60.0%(24/40),77.5%(31/40)] (P＜ 0.05),and the colic-exclusion rate in group A was also higher than that in group B and group C (P ＜ 0.05). The difference of the efficacy rates in group A in these two time-points had no statistical significance (P ＞0.05). No increased pain occurred in group A except 1 case of vomiting. Conclusion Multiple injection of morphine combined with phloroglucinol is quick, effective and safe in the early treatment of renal colic.

Objective To construct nursing quality evaluation criteria for operating theatres, basing on the three-dimensional quality assessment model, so as to provide scientific basis for objectively evaluating the quality of care in operating rooms. Methods From August to November 2016, a total of 30 medical and nursing specialists from the 2nd Affiliated Hospital of Harbin Medical University were investigated with two rounds of questionnaires by Delphi method, in order to construct the nursing room quality evaluation standard. Results The response rates of the two rounds of questionnaires were 93.33% and 100.00%. The authority coefficient (Cr) of the experts was 0.87 and the degree of expert coordination was good (P< 0.001). The final operating room care quality evaluation criteria include 3 one-level indicators, 19 two-level indicators, and 51 three-level indicators. Conclusions The final nursing quality evaluation criteria were reliable and valid, which can provide standard for the nursing quality evaluation and management of operating room.

Purpose: This study aimed to investigate the effect of the N6-methyladenosine (m6A) dependent ferroptosis on cisplatininduced Sertoli cell injury. Materials and Methods: A cisplatin exposure mouse model was established by intraperitoneal injection of cisplatin in our study. TM4 cell lines was used for in vitro study. Ferroptosis was detected according to metabolomic analysis and a series of assays, including malondialdehyde, glutathione, and glutathione disulfide concentration detection, 2′,7′-dichlorodihydrofluorescein diacetate and BODIPY 581/591 C11 probe detection, and transmission electron microscope imaging. Key ferroptosis-related genes were identified via transcriptomic analysis, western blot and immunohistochemistry. The m6A modification was demonstrated via m6A RNA immunoprecipitation and luciferase reporter assays. Immune cell infiltration was detected by mass cytometry, and verified by flow cytometry and immunofluorescence. Results: Ferroptosis, but not other types of programmed cell death, is a significant phenomenon in cisplatin-induced testis damage and Sertoli cell loss. Ferroptosis induced by cisplatin in Sertoli cell/TM4 cell is GPX4 independent but is regulated by SLC7A11 and ALOX12. Both SLC7A11 and ALOX12 are regulated via m6A dependent manner by METTL3. Furthermore, overexpressed ALOX12-12HETE pathway may result in macrophage polarization and inflammatory response in cisplatin exposure testis. Conclusions Cisplatin-induced Sertoli cell injury via ferroptosis and promoted ferroptosis in an m6A dependent manner. m6A modification of both SLC7A11 and ALOX12 mRNA could result in ferroptosis in our in vitro model. Further, overexpressed ALOX12 can cause more production of 12-HETE, which may be responsible for testis inflammation caused by cisplatin.

Purpose: This study aimed to investigate the effect of the N6-methyladenosine (m6A) dependent ferroptosis on cisplatininduced Sertoli cell injury. Materials and Methods: A cisplatin exposure mouse model was established by intraperitoneal injection of cisplatin in our study. TM4 cell lines was used for in vitro study. Ferroptosis was detected according to metabolomic analysis and a series of assays, including malondialdehyde, glutathione, and glutathione disulfide concentration detection, 2′,7′-dichlorodihydrofluorescein diacetate and BODIPY 581/591 C11 probe detection, and transmission electron microscope imaging. Key ferroptosis-related genes were identified via transcriptomic analysis, western blot and immunohistochemistry. The m6A modification was demonstrated via m6A RNA immunoprecipitation and luciferase reporter assays. Immune cell infiltration was detected by mass cytometry, and verified by flow cytometry and immunofluorescence. Results: Ferroptosis, but not other types of programmed cell death, is a significant phenomenon in cisplatin-induced testis damage and Sertoli cell loss. Ferroptosis induced by cisplatin in Sertoli cell/TM4 cell is GPX4 independent but is regulated by SLC7A11 and ALOX12. Both SLC7A11 and ALOX12 are regulated via m6A dependent manner by METTL3. Furthermore, overexpressed ALOX12-12HETE pathway may result in macrophage polarization and inflammatory response in cisplatin exposure testis. Conclusions Cisplatin-induced Sertoli cell injury via ferroptosis and promoted ferroptosis in an m6A dependent manner. m6A modification of both SLC7A11 and ALOX12 mRNA could result in ferroptosis in our in vitro model. Further, overexpressed ALOX12 can cause more production of 12-HETE, which may be responsible for testis inflammation caused by cisplatin.

Purpose: This study aimed to investigate the effect of the N6-methyladenosine (m6A) dependent ferroptosis on cisplatininduced Sertoli cell injury. Materials and Methods: A cisplatin exposure mouse model was established by intraperitoneal injection of cisplatin in our study. TM4 cell lines was used for in vitro study. Ferroptosis was detected according to metabolomic analysis and a series of assays, including malondialdehyde, glutathione, and glutathione disulfide concentration detection, 2′,7′-dichlorodihydrofluorescein diacetate and BODIPY 581/591 C11 probe detection, and transmission electron microscope imaging. Key ferroptosis-related genes were identified via transcriptomic analysis, western blot and immunohistochemistry. The m6A modification was demonstrated via m6A RNA immunoprecipitation and luciferase reporter assays. Immune cell infiltration was detected by mass cytometry, and verified by flow cytometry and immunofluorescence. Results: Ferroptosis, but not other types of programmed cell death, is a significant phenomenon in cisplatin-induced testis damage and Sertoli cell loss. Ferroptosis induced by cisplatin in Sertoli cell/TM4 cell is GPX4 independent but is regulated by SLC7A11 and ALOX12. Both SLC7A11 and ALOX12 are regulated via m6A dependent manner by METTL3. Furthermore, overexpressed ALOX12-12HETE pathway may result in macrophage polarization and inflammatory response in cisplatin exposure testis. Conclusions Cisplatin-induced Sertoli cell injury via ferroptosis and promoted ferroptosis in an m6A dependent manner. m6A modification of both SLC7A11 and ALOX12 mRNA could result in ferroptosis in our in vitro model. Further, overexpressed ALOX12 can cause more production of 12-HETE, which may be responsible for testis inflammation caused by cisplatin.

Purpose: This study aimed to investigate the effect of the N6-methyladenosine (m6A) dependent ferroptosis on cisplatininduced Sertoli cell injury. Materials and Methods: A cisplatin exposure mouse model was established by intraperitoneal injection of cisplatin in our study. TM4 cell lines was used for in vitro study. Ferroptosis was detected according to metabolomic analysis and a series of assays, including malondialdehyde, glutathione, and glutathione disulfide concentration detection, 2′,7′-dichlorodihydrofluorescein diacetate and BODIPY 581/591 C11 probe detection, and transmission electron microscope imaging. Key ferroptosis-related genes were identified via transcriptomic analysis, western blot and immunohistochemistry. The m6A modification was demonstrated via m6A RNA immunoprecipitation and luciferase reporter assays. Immune cell infiltration was detected by mass cytometry, and verified by flow cytometry and immunofluorescence. Results: Ferroptosis, but not other types of programmed cell death, is a significant phenomenon in cisplatin-induced testis damage and Sertoli cell loss. Ferroptosis induced by cisplatin in Sertoli cell/TM4 cell is GPX4 independent but is regulated by SLC7A11 and ALOX12. Both SLC7A11 and ALOX12 are regulated via m6A dependent manner by METTL3. Furthermore, overexpressed ALOX12-12HETE pathway may result in macrophage polarization and inflammatory response in cisplatin exposure testis. Conclusions Cisplatin-induced Sertoli cell injury via ferroptosis and promoted ferroptosis in an m6A dependent manner. m6A modification of both SLC7A11 and ALOX12 mRNA could result in ferroptosis in our in vitro model. Further, overexpressed ALOX12 can cause more production of 12-HETE, which may be responsible for testis inflammation caused by cisplatin.

Purpose: This study aimed to investigate the effect of the N6-methyladenosine (m6A) dependent ferroptosis on cisplatininduced Sertoli cell injury. Materials and Methods: A cisplatin exposure mouse model was established by intraperitoneal injection of cisplatin in our study. TM4 cell lines was used for in vitro study. Ferroptosis was detected according to metabolomic analysis and a series of assays, including malondialdehyde, glutathione, and glutathione disulfide concentration detection, 2′,7′-dichlorodihydrofluorescein diacetate and BODIPY 581/591 C11 probe detection, and transmission electron microscope imaging. Key ferroptosis-related genes were identified via transcriptomic analysis, western blot and immunohistochemistry. The m6A modification was demonstrated via m6A RNA immunoprecipitation and luciferase reporter assays. Immune cell infiltration was detected by mass cytometry, and verified by flow cytometry and immunofluorescence. Results: Ferroptosis, but not other types of programmed cell death, is a significant phenomenon in cisplatin-induced testis damage and Sertoli cell loss. Ferroptosis induced by cisplatin in Sertoli cell/TM4 cell is GPX4 independent but is regulated by SLC7A11 and ALOX12. Both SLC7A11 and ALOX12 are regulated via m6A dependent manner by METTL3. Furthermore, overexpressed ALOX12-12HETE pathway may result in macrophage polarization and inflammatory response in cisplatin exposure testis. Conclusions Cisplatin-induced Sertoli cell injury via ferroptosis and promoted ferroptosis in an m6A dependent manner. m6A modification of both SLC7A11 and ALOX12 mRNA could result in ferroptosis in our in vitro model. Further, overexpressed ALOX12 can cause more production of 12-HETE, which may be responsible for testis inflammation caused by cisplatin.