Patients with severe trauma require an extremely timely treatment and transfusion plays an irreplaceable role in the emergency treatment of such patients. An increasing number of evidence-based medicinal evidences and clinical practices suggest that patients with severe traumatic bleeding benefit from early transfusion of low-titer group O whole blood or hemostatic resuscitation with red blood cells, plasma and platelet of a balanced ratio. However, the current domestic mode of blood supply cannot fully meet the requirements of timely and effective blood transfusion for emergency treatment of patients with severe trauma in clinical practice. In order to solve the key problems in blood supply and blood transfusion strategies for emergency treatment of severe trauma, Branch of Clinical Transfusion Medicine of Chinese Medical Association, Group for Trauma Emergency Care and Multiple Injuries of Trauma Branch of Chinese Medical Association, Young Scholar Group of Disaster Medicine Branch of Chinese Medical Association organized domestic experts of blood transfusion medicine and trauma treatment to jointly formulate Chinese expert consensus on blood support mode and blood transfusion strategies for emergency treatment of severe trauma patients ( version 2024). Based on the evidence-based medical evidence and Delphi method of expert consultation and voting, 10 recommendations were put forward from two aspects of blood support mode and transfusion strategies, aiming to provide a reference for transfusion resuscitation in the emergency treatment of severe trauma and further improve the success rate of treatment of patients with severe trauma.

Pulmonary blast injury has become the main type of trauma in modern warfare, characterized by externally mild injuries but internally severe injuries, rapid disease progression, and a high rate of early death. The injury is complicated in clinical practice, often with multiple and compound injuries. Currently, there is a lack of effective protective materials, accurate injury detection instrument and portable monitoring and transportation equipment, standardized clinical treatment guidelines in various medical centers, and evidence-based guidelines at home and abroad, resulting in a high mortality in clinlcal practice. Therefore, the Trauma Branch of Chinese Medical Association and the Editorial Committee of Chinese Journal of Trauma organized military and civilian experts in related fields such as thoracic surgery and traumatic surgery to jointly develop the Clinical treatment guideline for pulmonary blast injury ( version 2023) by combining evidence for effectiveness and clinical first-line treatment experience. This guideline provided 16 recommended opinions surrounding definition, characteristics, pre-hospital diagnosis and treatment, and in-hospital treatment of pulmonary blast injury, hoping to provide a basis for the clinical treatment in hospitals at different levels.

Objective:To evaluate the effects of intranasal administration of glial cell line-derived neurotrophic factor (GDNF) on postoperative cognitive dysfunction in aged rats.Methods:Forty healthy Sprague-Dawley rats of both sexes, aged 21-23 months, weighing 480-600 g, were divided into 4 groups ( n=10 each) using a random number table method: sham operation group (group S), operation group (group O), intranasal administration of low-dose GDNF group (group G1) and intranasal administration of high-dose GDNF group (group G2). Rats underwent exploratory laparotomy under anesthesia with chloral hydrate in O, G1 and G2 groups, while the rats in group S only received sham operation.The rats in group G1 and group G2 were intranasally treated with GDNF 25 and 50 μg (in 25 μl of PBS), respectively, and PBS 25 μl was nasally administered in group S and group O every day for 3 consecutive days after operation or sham operation.Morris water maze test was performed on days 3-7 after surgery, and then the rats were sacrificed, and hippocampal tissues were removed for determination of the expression of GDNF, high mobility group box 1 (HMGB1), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), activated caspase-3 and Bax (by Western blot). Results:Compared with group S, the escape latency was significantly prolonged on days 5-7 after operation, the number of crossing the platform was reduced, time spent in the target quadrant was shortened, expression of GDNF was down-regulated, and expression of IL-1β, TNF-α, HMGB1, activated caspase-3 and Bax in hippocampi was up-regulated in group O, and the number of crossing the platform was reduced, time spent in the target quadrant was shortened, and expression of IL-1β and TNF-α was up-regulated in G1 and G2 groups ( P<0.05). Compared with group O, the escape latency was significantly shortened on days 5-7 after operation, the number of crossing the platform was increased, time spent in the target quadrant was prolonged, expression of GDNF was up-regulated, expression of TNF-α, HMGB1, activated caspase-3 and Bax in hippocampi was down-regulated in G1 and G2 groups, and IL-1β in hippocampi was down-regulated in group G1 ( P<0.05). Compared with group G1, the expression of TNF-α in hippocampi was down-regulated ( P<0.05), and no significant change was found in the other parameters mentioned above in group G2 ( P>0.05). Conclusions:Intranasal administration of GDNF can improve postoperative cognitive dysfunction, and the mechanism may be related to inhibiting neuroinflammatory responses and neuroapoptosis in aged rats.

Objective:To investigate the safety and therapeutic effect of Shakubatrivalsartan in the treatment of pediatric dilated cardiomyopathy.Methods:Clinical information, treatment and prognosis of 5 cases with dilated cardiomyopathy in the First Affiliated Hospital of Xinxiang Medical University from June 2018 to December 2020 were retrospectively analyzed, and relevant literatures were reviewed.Results:A total of 5 cases of children with dilated cardiomyopathy were analyzed, including 3 males and 2 females with age of 12-17 years.Their median left ventricular ejection fraction (LVEF), left ventricular end diastolic dimension (LVDd), N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels were 37% (20%-41%), 61 mm (59-67 mm), and 13 250 ng/L (12 310-21 823 ng/L), respectively.The median conventional treatment time was 5 months (1-12 months), in which, the condition of heart failure gradually progressed, and the median LVEF, LVDd and NT-proBNP levels were reduced to 33% (19%-37%), 61 mm (60-74 mm), 13 144 ng/L (8 086-15 137 ng/L). After less than 3 months of follow-up following conventional treatment plus Shakubatrivalsartan, NT-proBNP level significantly decreased in 5 cases.Besides, 4 cases had improved cardiac function, and the other one′s improvement was not obvious.The blood pressure of 5 cases decreased at varying degrees after medication of Shakubatrivalsartan, which should be closely monitored during drug titration.No adverse reactions were reported.Conclusions:Shakubatrivalsartan for the treatment of pediatric dilated cardiomyopathy is safe and effective, which can alleviate or reverse the process of myocardial remodeling and improve cardiac ejection fraction, thus improving the prognosis.

Objective:To evaluate the effect of glucagon-like peptide 1 and glucose-dependent insulinotropic polypeptide receptor agonist DA-JC4 on postoperative neuroinflammatory responses in aged rats.Methods:Forty-five Sprague-Dawley rats, aged 21-23 months, weighing 530-630 g, provided by the Animal Experiment Center of Medical School of Zhengzhou University, were assigned into 3 groups ( n=15 each) using a random number table method: sham operation group (group S), operation group (group O) and DA-JC4 group (group G). Rats underwent exploratory laparotomy under anesthesia with chloral hydrate in O and G groups.In group G, DA-JC4 10 nmol/kg (dissolved in 1 ml of sterile normal saline) was intraperitoneally injected immediately after the end of operation and at 24 and 48 h after operation.Western blot was used to determine the expression of hippocampal Bax, Bcl-2, activated caspase-3, Beclin-1, microtubule-associated protein 1 light chain 3Ⅱ (LC3Ⅱ), high-mobility group box 1 protein (HMGB1), interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) on day 3 after surgery.The Morris water maze test was performed on days 14-18 after operation to assess the cognitive function. Results:Compared with group S, the escape latency was significantly prolonged on days 15-18 after operation in group O and on day 18 after operation in group G, and the number of crossing the original platform was reduced, the time spent in the target quadrant was shortened, the expression of activated caspase-3, Bax, LC3Ⅱ, HMGB1, IL-1β and TNF-α in hippocampi was up-regulated, and the expression of Bcl-2, LC3Ⅱ and Beclin-1 was down-regulated in O and G groups ( P<0.05). Compared with group O, the escape latency was significantly shortened, and the number of crossing the original platform was increased, the time spent in the target quadrant was prolonged, the expression of activated caspase-3, Bax, LC3Ⅱ, HMGB1, IL-1β and TNF-α in hippocampi was down-regulated, and the expression of Bcl-2, LC3Ⅱ and Beclin-1 was up-regulated in group G ( P<0.05). Conclusion:The mechanism by which DA-JC4 reduces postoperative cognitive dysfunction may be related to inhibiting neuroinflammatory responses in aged rats.

Objective To evaluate the effect of exercise training on heat shock protein 70 (HSP70) expression during endotoxin-induced acute lung injury (ALI) in rats.Methods Thirty-two SPF healthy male Sprague-Dawley rats,aged 8 weeks,weighing 175-220 g,were divided into 4 groups (n=8 each) using a random number table method:control group (group C),group ALI,low-intensity exercise training group (group ET1) and high-intensity exercise training group (group ET2).The rats in ET1 and ET2 groups received 2-and 4-week treadmill exercise training before establishing the ALI model,while the rats in C and ALI groups received no training.ALI was induced by intravenously injecting 5 mg/kg lipopolysaccharide via the tail vein in ALI,ET1 and ET2 groups,and the equal volume of normal saline was given instead in group C.The animals were sacrificed,and the lungs were harvested for microscopic examination of the pathological changes of lung tissues which were also scored and for determination of wet to dry weight ratio (W/D ratio),concentrations of total protein,interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) in bronchoalveolar lavage fluid (BALF),and expression of HSP70 and nuclear factor kappa B (NF-κB) in lung tissues by Western blot.Results Compared with group C,the W/D ratio and pathological changes of lung tissues were significantly increased,the concentrations of total protein,IL-1 β and TNF-α in BALF were increased,the expression of NF-κB was up-regulated (P＜0.05),and no significant change was found in HSP70 expression in group ALI(P＞0.05).Compared with group ALI,the W/D ratio and pathological changes of lung tissues were significantly decreased,the concentrations of total protein,IL-1β and TNF-α in BALF were decreased,the expression of HSP70 was up-regulated,and the expression of NF-κB was down-regulated in ET1 and ET2 groups (P＜0.05).Conclusion Exercise training can attenuate the endotoxin-induced ALI through relieving the inflammatory responses,which may be related to up-regulating HSP70 expression in the lung of rats.

Objective To establish the Nifedipine-induced liver cell damage model,and to investigate the cellular or molecular mechanism for children's liver cell damage.Methods The HepG2 cells were utilized to establish liver cell damage models.The optimal concentration and the optimal pretreatment time of Nifedipine-induced liver cell injury were confirmed.Western blot and real-time PCR(RT-PCR)were used to check the alteration in proteins and mRNAs level of the liver function-associated classic markers,which contained alkaline phosphatase(ALP),aspartate amino transferase(AST),glutamyl transpeptidase(γ-GT)and alanine aminotransferase(ALT).Additionally,flow cytometry(FCM),colony formation assay(CFA)and cell wound healing assay(CWHA)were utilized to check the effect of Nifedipine on the cell cycle progression and proliferation of HepG2.Results (1)The optimal concentration of Nifedipine was 20 mg/L and the optimal treatment period was 21 days for liver damage.(2)Western blot:intracellular ALT protein content after Nifedipine group was less than that of control group,while the protein levels of AST,γ-GT and ALP in the culture medium after Nifedipine addition(3.55 ± 0.05,4.91 ± 0.055,3.51 ± 0.05,3.08 ± 0.08) were higher than those of control group(0.96 ± 0.02,1.03 ± 0.02,1.00 ± 0.05,0.90 ± 0.13),and the differences were all significant(t = -85.695,-117.582,-47.371,-33.260,all P<0.05).(3)The findings of RT-PCR showed that the mRNA levels of intracellular ALT,γ-GT and ALP in Nifedipine group(0.26 ± 0.02,0.05 ± 0.04, 0.05 ± 0.02)were lower than those of control group(1.13 ± 0.21,0.94 ± 0.10,1.03 ± 0.06),and the differences were all significant(t=7.233,127.436,25.687,all P<0.05).However,the mRNAs levels in purified culture me-dium in Nifedipine group(5.95 ± 0.05,3.13 ± 0.10,3.32 ± 0.08)were higher than those in control group(1.01 ± 0.08,1.00 ± 0.05,1.00 ± 0.05),and the differences were all significant(t= -92.339,-31.250,-43.007,all P<0.05).(4)The portion of G0/G1 phase in Nifedipine group[(84.09 ± 0.43)%]was more than that of control group[(30.93 ± 0.32)%],which had statistical significance(t=173.084,P=0.000).(5)In contrast with control group,the colony formation of cells in Nifedipine group declined from(97.10 ± 1.17)% to(38.56 ± 1.51)%(t=92.088,P=0.000)and the migration rate of cells wound healing was(56.37 ± 2.06)%,(25.00 ± 1.71)% sepa-rately(t=20.285,P=0.000).Conclusion Nifedipine may promote children's liver injury through regulating cell cycle related proteins.

Objective To investigate the role of transient receptor potential melastatin 7(TRPM7) in sevoflurane preconditioning for inhibiting hippocampal neurons apoptosis and inflammation response induced by oxygen-glucose deprivation(OGD).Methods Fifty SD rats of postnatal 1 d were selected for extracting hippocampal neurons and randomly divided into 5 groups,including the control group(C),sevoflurane preconditioning group (Sev),OGD group,Sev preconditioningt OGD group (Sev + OGD) and Sev preconditioning+ bradykinin+OGD group(combined group).After 1.5 h oxygen-glucose deprivation,reintroduction was performed,and then the normal culture was performed again for preparing the OGD model.Hippocampal neurons in the control group were normally cultured only;which in the Sev group conducted 2 ％ Sev preconditioning for 1 h;which in the OGD group only prepared the OGD model;which in the SEv+OGD conducted 2％ Sev preconditioning for 1 h,and prepared the OGD model after 24 h;which in the combined group was simultaneously added with bradykinin(final concentration 200μmol/L) in Sev preconditioning,other treatment was same to that in the Sev+OGD group.After 24 h normal culture,the mRNA and protein levels of TRPM7,apoptosis rate,survival rate,mRNA and supernatant protein levels of IL-1β and TNF-α of the hippocampal neurons were detected.Results Compared with the control group,hippocampal neurons mRNA and protein levels of TRPM7,apoptosis rate,mRNA and supernatant protein levels of IL-1β and TNF-α in the OGD group were significantly increased(P＜0.05),whereas the survival rate was significantly decreased (P ＜ 0.05).Compared with the OGD group,hippocampal neurons mRNA and protein levels of TRPM7,apoptosis rate,mRNA and supernatant protein levels of IL-1β and TNF-α in the Sev group were significantly decreased(P＜0.05),whereas the survival rate was significantly increased(P＜0.05).Compared with the Sev group,hippocampal neurons mRNA and protein levels of TRPM7,apoptosis rate,the mRNA and supernatant protein levels of IL-1β and TNF-α in the combined group were significantly increased(P＜0.05),whereas the survival rate was significantly decreased(P＜0.05).Conclusion Sev preconditioning can attenuate hippocampal neurons apoptosis and inflammatory response after OGD via alleviating the overexpression of TRPM7.

Lumbar adjacent segment degeneration is defined as degenerative changes cranial or caudal to surgical segments.Some patients developed corresponding clinical symptoms in addition to radiological degeneration,which is called adjacent segment disease.Although many new surgical techniques emerged in recent years,the problem of adjacent segment degeneration has not really been resolved.MEDLINE/PubMed,Cochrane Controlled Trials Registry and EMBASE were comprehensively searched.All randomized or nonrandomized clinical studies of lumbar degenerative diseases treated by fusion/fixation,decompression-alone or artificial lumbar disc replacement were included.The number of cases enrolled in these studies was greater than or equal to 20 cases and the minimum age of the patients was 18 years old.Case reports,reviews or meta-analyses,papers with unobtainable text and abstract,and studies of trauma,infection,oncology and inflammatory disease were all excluded.The diagnostic criteria of adjacent segment degeneration,as well as the incidence and risk factors of adjacent segment degeneration and reoperation were reviewed.The concepts of adjacent segment degeneration in different literatures were very confusing,and radiological degeneration was often mixed in use with symptomatic degeneration.It was therefore difficult to make any conclusion due to lack of a standard.In addition,the previous studies did not fully understand the pathogenesis and risk factors of the disease,especially the effect of the index level on adjacent segments.Moreover,most of the current studies were retrospective,therefore,convincing conclusions can hardly be drawn due to lack of high-level evidence.The main reason for reoperation after lumbar fusion is adjacent segment degeneration.Therefore,the most important way to reduce the rate of reoperation is to reduce the incidence of adjacent segment degeneration.In the future,the diagnostic criteria for adjacent segment degeneration should be unified first.And it is extremely important to thoroughly understand the mechanism and risk factors of adjacent segment degeneration by comprehensive studies and clarify them through high-level evidence.

Objective To evaluate the role of nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway in remote ischemic preconditioning-induced reduction of lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice.Methods Sixty-eight healthy male C57BL/6 mice,aged 6-8 weeks,weighing 22-26 g,were divided into 4 groups (n =17 each) using a random number table:control group (group C),ALI group,remote ischemic preconditioning group (group RIPC) and brusatol plus remote ischemic preconditioning group (group B+RIPC).Normal saline 100 μl was intratracheally instilled in group C.ALI was induced by intratracheal instillation of LPS 5 mg/kg in group ALI.Mice in group RIPC were subjected to 6 cycles of 5-min ischemia followed by 5-min reperfusion in the right hindlimbs using a tourniquet,and 1 h later the model of ALI was established.Nrf2 inhibitor brusatol 2 mg/kg (in 100 μl of 1％ dimethyl sulfoxide) was intraperitoneally injected every other day for 10 days prior to establishment of the ALI model in group B.Brusatol 2 mg/kg was intraperitoneally injected every other day for 10 days prior to establishment of the ALI model,and remote ischemic preconditioning was performed at 1 h before establishment of the ALI model in group B+RIPC.Seven mice in each group were selected at 24 h after establishment of the ALI model,and bronchoalveolar lavage fluid (BALF) was collected for determination of protein concentrations and neutrophil count.Mice were then sacrificed and lungs were removed for determination of lung water content,myeloperoxidase (MPO) activity,contents of interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α),and expression of Nrf2,HO-1 and high-mobility group box 1 protein (HMGB1) in lung tissues (by Western blot) and for examination of pathological changes (with a light microscope).Results Compared with group C,the lung water content,MPO activity,contents of IL-1β and TNF-α,and neutrophil count and protein concentrations in BALF were significantly increased,and the expression of Nrf2,HO-1 and HMGB1 was up-regulated in group ALI (P＜ 0.05).Compared with group ALI,the lung water content,MPO activity,contents of IL-1β and TNF-α,and neutrophil count and protein concentrations in BALF were significantly decreased,the expression of Nrf2 and HO-1 was up-regulated,and the expression of HMGB1 was down-regulated (P＜0.05),and the pathological changes were significantly attenuated in group RIPC.Compared with group RIPC,the lung water content,MPO activity,contents of IL-1β and TNF-α,and neutrophil count and protein concentrations in BALF were significantly increased,the expression of Nrf2 and HO-1 was down-regulated,and the expression of HMGB1 was up-regulated (P＜0.05),and the pathological changes were aggravated in group B+RIPC.Conclusion The activation of Nrf2/HO-1 signaling pathway is involved in remote ischemic preconditioning-induced reduction of LPS-induced ALI in mice.