This paper introduces the international experiments of risk management in clinical trails, responsibility of sponsor, responsibility of investigator and responsibility of other participators and to help to improve our management level of clinical trails.

Objective To examine neuroinflammation,oxidative damage and neuron loss in the contralateral parie-tal lobecortex of TBI model mice, and to investigate effects of berberine chloride on such secondary damage.Methods TBI model was established by a weight-drop hitting device and mice in berberine group were administered intragastrically with berberine chloride (50mg/kg.day) for 21 days.Immunofluorescence staining was used to assess activity of microglia and astrocyte.Immunohistochemistry was used to assess DNA oxidative damage, neuron loss and expression of COX-2 and iN-OS.Results Activation of microglia and astrocyte, expressions of COX-2 and iNOS and DNA oxidative damage were ob-viously increased by TBI,(19.82 ±1.88)and(16.96 ±1.69)、(13.79 ±4.32)and(8.67 ±0.96)、(27.86 ±5.38) and (16.00 ±7.59)、(31.92 ±6.57)and(24.79 ±2.78)respectively (P<0.01 or P<0.05).Activation of microglia and ex-pressions of COX-2 and iNOS were significantly suppressed by berberine ,(15.49 ±1.88)and(19.82 ±1.88)、(16.83 ± 7.89)and(27.86 ±5.38)、(26.25 ±2.41)and(31.92 ±6.57) respectively(P<0.01 or P<0.05).There was no differ-ence in neuron loss among three groups, (49.05 ±4.38),(48.56 ±3.56)and (47.75 ±4.14) respectively (P>0.05). Conclusions TBI can cause neuroinflammation and oxidative damage but not neuron loss in the contralateral parietal lobe cortex.Berberine chloride can significantly suppress neuroinflammtion in the contralateral parietal lobe cortex after TBI.

In recent years,radiomics has been developed rapidly in the field of clinical medicine,and the artificial intelligence(AI)technology has been utilized to assist diagnosis.This paper introduced the background of radiomics,analyzed the basic research process of radiomics,and looked forward to its application in the identification of bone and joint injuries in the field of forensic medicine.Reviewing the three aspects is expected to provide a theoretical foundation of radiomics,which will be helpful to develop its application in forensic medicine.

Objective:To explore the effect of rapamycin on 1-methyl-4-phenylpyridinium iodide (MPP+ )-induced activation of Nod-like receptor protein 3 (NLRP3) inflammasome in microglia.Methods:The BV2 microglia cells were divided into control group, model group and rapamycin group.The model group and rapamycin group were treated by MPP+ to activate NLRP3 inflammasome, and rapamycin group was pretreated with rapamycin.Quantitative real-time PCR (RT-qPCR) was used to detect the mRNA levels of NLRP3, apoptosis-associated speck-like protein (ASC) and caspase-1.Immunofluorescence was used to detect the protein expression of NLRP3 and interleukin-1β (IL-1β). Western blot was carried out to assess the protein expression of NLRP3, ASC, caspase-1, beclin1 and microtubule-associated protein 1 light chain 3 (LC3).Results:The mRNA levels of NLRP3, ASC and caspase-1 in model group were higher than those in control group ( t=4.825, 3.015, 5.853, all P<0.05). The mRNA levels of NLRP3 and caspase-1 in rapamycin group were lower than those in model group ( t=2.75, 2.89, both P<0.05). In model group, the protein expressions of NLRP3 (1.54±0.22), ASC (1.02±0.13) and caspase-1 (1.42±0.30) were higher than NLRP3 (0.66±0.15), ASC (0.41±0.14) and caspase-1 (0.70±0.10) in control group ( t=5.653, 5.602, 3.964, all P<0.01), while the protein expression of beclin1 (0.28±0.09) and LC3II/LC3I ratio(0.69±0.14) were lower than beclin1 (0.60±0.11) and LC3II/LC3I (1.29±0.23) in control group ( t=4.010, 3.982, both P<0.01). The protein expressions of NLRP3 (0.80±0.18) and ASC (0.68±0.14) in rapamycin group were lower than those in model group ( t=4.413, 3.077, both P<0.05), while the protein expression of beclin1 (0.65±0.20) and LC3II/LC3I ratio(1.42±0.36) were higher than those in model group ( t=2.965, 3.278, both P<0.05). Conclusion:MPP+ activates NLRP3 inflammasome and impairs autophagic function in microglia.Rapamycin inhibits MPP+ -induced activation of NLRP3 inflammasome by restoring autophagic impairment in microglia.

Objective To investigate the effect of berberine chloride on autophagy and β-secretase (BACE) level in mice with traumatic brain injury (TBI).Methods Eighteen female healthy C57BL/6 mice were randomly divided into three groups:control group,model group and berberine group (n=6).TBI models in the later two groups were established by a weight-drop hitting device and mice in berberine group were administered intragastricly with berberine chloride (50 mg/kg) once daily for 21 d.Immunofluorescent staining were used to assess LC3 and BACE expressions in ipsilateral cortex or thalamus,and then,their mean fluorescence intensities were calculated and compared among these three groups.Results LC3 expression in the ipsilateral cortex and thalamus and BACE expression in the ipsilateral cortex (0.02±0.01,0.06±0.02 and 0.04±0.01 in the control group,model group and berberine group) showed significant difference among the three groups (P＜0.05):LC3 expression in ipsilateral cortex and thalamus and BACE expression in the ipsilateral cortex of the model group were significantly increased as compared with those of the control group (P＜0.05);the LC3 expression in the ipsilateral cortex and thalamus and BACE expression in the ipsilateral cortex of the model group were significantly decreased as compared with those of the berberine group (P＜0.05).Conclusion Autophagy is over-activated in the ipsolateral cortex and thalamus and BACE is over-activated in the ipsolateral cortex after TBI,and these changes are significantly suppressed by berberine chloride.

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.