【摘要】 目的 探討顱腦損傷(BI)死亡的法醫病理學特點,以及繼發性腦干損傷、并發癥的發生與死亡之間的因果關系。方法 從性別、年齡、致傷方式、損傷類型、生存時間、死亡原因等方面,對四川大學華西法醫學鑒定中心1998年1月-2008年12月127例BI死亡尸檢案例進行回顧性統計研究分析。結果 127例法醫病理學檢案中,原發性BI死亡51例(402%),繼發性腦干損傷死亡61例(480%),并發癥死亡15例(118%),其中傷后12 h內死亡者直接死因均為嚴重原發性腦損傷,存活12 h～1周者直接死因以繼發性腦干損傷居多,生存時間超過1周者約半數死于并發癥。結論 在BI案例的死亡原因確定時,應在全面系統的病理學檢驗基礎上,結合案情及臨床資料進行綜合分析。【Abstract】 Objective To explore the characteristics of forensic pathology in traumatic brain injury and the relationships between secondary brainstem damage, complications and the causes of death. Methods 127 cases were reviewed from gender, age, manner of injury, survival time and the direct causes of death from January 1998 to December 2008. Results Of the 127 cases, the key direct cause of death was secondary brainstem damage, followed by severe primarily brain injury and complications. For those who died within 12 hours after injury, the direct cause was severe primarily brain injury; for those who survived between 12 hours to one week, secondary brainstem damage was in the majority of the causes and for those who survive more than one week time, complication was an important cause. Conclusion In the cases of traumatic brain injury, we should take comprehensive and systematic examination of forensic pathology, and refer to clinical data at the same time to determine the direct cause of death.
Objective To observe the effect of exogenous basic fibrob last growth factor (bFGF) on apoptosis of cultured human retinal pigment epithelial (RPE) cells exposed to visible light,and determine the role of bFGF, fibroblast growth factor receptor 1 (FGFR1),bcl-2 and caspase-3. Methods 2000±500) lx cold white light was used. Exogenous bFGF was utilized during culture. Annexin annexin V-fluoresce in isothiocyanate/propidium iodium (V-FITC/PI) labeling,flow cytometry, Immunocytochemical staining, enzyme associated absorb examing and reverse transcriptional polymerase chain reaction (RT-PCR) were used to determine the apoptosis, the expression levels of bFGF, FGFR1, bcl-2, as well as the activity of caspase-3. Results No protective effect of bFGF was observed under the concentration 5 ng/ml.A significant inhibition of apoptosis was found in 10 ng/ml and 20 ng/ml groups （P＜0.05）. The upregulation of bcl-2 was observed in bFGF (10 ng/ml, 20 ng/ml) protreated groups（P＜0.01）.Compared to no light exposure group,all light exposure groups (including bFGF pro-treated) had higher endogenous bFGF and FGFR1 levels （P ＜0.05）, and the increase was concentration dependent.The bFGF and FGFR1 levels were higher in exogenous bFGF applied (gt;5 ng/ml) groups than light exposure groups（P＜0.05）. The caspase-3 activity was significantly inhibited in bFGF (10 ng/ml) pro-treated groups. Conclusions Human RPE cells exposed to visible light were rescued by application of exogenous bFGF in vitro.The probable protective mechanism of bFGF partly is directly binding to FGFR1 or potentiating endogenous bFGF autocrine loop,to upregulate bcl-2 and to inhibit caspase-3 activation. (Chin J Ocul Fundus Dis，2003，19：24-28)
Objective To further investigate pathologic mechanism of retinal phototrauma. Methods Twenty Wistar rats were divided into control and experimental groups.Their eyes were extracted in 12，24 and 36 hours after light exposure.HE stained retina samples were examined and TDT-mediated dUTP nick end labelling(TUNEL)method was employed to distinguish apoptotic cells. Results After 12-hour light exposure,slight vesiculation was observed in the rod outer segment of the retinas.After 24-hour light exposure,the outer nuclear layer showed predominant fractured and condensed nuclei and fragmented DNA.After 36-hour light exposure,the rod outer and inner segments were lysed and most of the nuclei in the outer nuclear layer were disappeared. Conclusions Apoptosis of photoreceptor cell is one of the important mechanisms which cause experimental retinal photoinjury of rats. (Chin J Ocul Fundus Dis, 1999, 15: 167-169)
摘要:目的:探討急診醫療過程中意外死亡的原因,以引起廣大同道的重視。方法:對急診就診過程中24 h內死亡且符合入選標準的68例患者進行死亡原因分析,分析意外死亡常見的病因并探討死亡原因與就診之初臨床特征的關系。結果:68例意外死亡患者占同期死亡人數的4.39％,其中主動脈夾層31例,占同期死亡2％,占意外死亡的45.6％;心臟性猝死(急性心肌梗塞9例,心肌炎4例,)13例占同期死亡病人的0.84％,占意外死亡總數的191％;急性腦血管病(小腦出血5例,小腦梗塞8例)13例,占同期死亡人數的0.84％,占意外死亡總數的19.1％;重癥哮喘3例;不明原因死亡5例。臨床特征多為胸痛、胸背痛、頭痛、上腹痛、眩暈等為首發癥狀。結論:急診就診過程意外死亡發生取決于多種因素,由于這些病例癥狀多不典型,病情復雜多樣,臨床醫師極易忽視,臨床極易漏診、誤診,一旦發生,都將引起較大的醫療糾紛,耗費大量的人力物力。因此對急診就診過程中的不典型特征高度重視及時考慮主動脈夾層、心臟性猝死、急性腦血管病,早期治療,避免意外死亡的發生。Abstract: Objective: To explore the character of accidental death during treatment in emergency department, and get more attention of other emergent doctors to avoid death in emergent treatment.Methods: To analysis death causes of 68 qualified patients, who died within 24 hours after they went to hospital; To analysis familiar accidental death causes and the relationship between them and initial clinical signs. Results:These 68 accidental dead patients occupied 4.39% in all dead patients during the same period, including 31 cases of aortic dissecting hematoma(2% in all dead patients vs 45.6% in accidental dead patients); 13 cases of sudden cardiac death(0.84% in all dead patients vs 19.1% in accidental dead patients), which included 9 cases of acute myocardial infaction, 4 cases of myocarditis; 13 cases of acute cerebravascular diseases(0.84% in all dead patients vs 19.1% in accidental dead patients),which included 5 cases of cerebella hemorrhage and 8 cases of cerebella infarction; 3 severe asthma and other 5 cases without exact reasons. Clinical initial showed frequently the pain of breast, breast and back, head and upper belly, and dizzling. Conclusion: The happening of accidental death during treatment in emergent department was decided by many complicated factors. Because being nontypical and complicated, these factors always were ignored by clinical doctors, resulting wrong diagnosis or leaked diagnosis, which brought many clinical dissensions. Clinical dissensions cost much money and energy. So to know and pay more attention to these nontypical signs is very important to diagnosis aortic dissecting hematoma, sudden cardiac death and acute cerebravascular diseases, and is helpful to treat in time, and consequently the death was avoided.
Objective To determine the effects of lensspecific overexpression of OSM on the eye development. Methods A truncated mouse OSM c DNA (661 bp) was linked to the αA-crystallin promoter. Transgenic mice were characterized by routine histological and immunohistochemical techiniques. TUNEL assays were used to de tect cell death. The mRNA expression of caspase-3 was detected by in situhybridization, Rabbit anti-cleavage caspase-3 antibody was used to detectactive capase-3. Results At embryonic day (E) 14.5 and 17.5, expression of the OSM transgenic protein was detected specifically in lens fiber cells. The onset of retinal degeneration in the mid portion of the transgenic retinae was observed started from E17.5. By the time of birth 50% or more of the retinal cells were missing. The OSM transgenic retinal cells underwent apoptosis indicated by TUNEL assays. Most strikingly, activation of caspase-3 protein were observed throughout the transgenic retinas. Conclusions Lens-specific overexpression of OSM activate caspase-3, leading to abnormal eye development,apoptosis and widespread retinal degeneration. (Chin J Ocul Fundus Dis，2003，19：201-268)
ObjectiveTo understand the molecular mechanism of ferroptosis and its research progress and future prospects in pancreatic cancer. MethodThe relevant literature on the molecular mechanism of ferroptosis and its basic and clinical application in the occurrence and development of pancreatic cancer was retrievaled and reviewed. ResultsFerroptosis was a non-apoptotic form of cell death that depended on iron aggregation, and its molecular biological features included iron ion overload, reactive oxygen species accumulation, lipid peroxidation, and so on. Ferroptosis was closely related to cell metabolism, and the imbalance of ferroptosis caused by abnormal metabolism also existed during the tumorigenesis and progression of pancreatic cancer, which in turn triggered the abnormal proliferation of pancreatic cancer cells and leaded to their progression. By regulating the key molecular signaling pathways of ferroptosis, it was expected to find new drug targets and therapeutic pathways for pancreatic cancer treatment. The results of ferroptosis-related studies so far had shown the potential for future translational research in the field of pancreatic cancer treatment. ConclusionsThe mechanism of ferroptosis is of great value in pancreatic cancer research. At present, there are still many uncharted areas in the study of ferroptosis, and the molecular mechanisms involved are still poorly understood. In the future, as the study of ferroptosis continues, it is expected to provide new ideas for pancreatic cancer treatment and discover new targets for drug development.
ObjectiveAfter establishing the rabbit brain death model, TUNEL, western blotting, and immuno-histochemical methods were used to detect hepatocyte apoptosis to study hepatocyte apoptosis level from rabbit donors after brain death. MethodsSixty healthy male New Zealand rabbits were divided into brain death group (n=30) and sham group (n=30). The rabbits of brain death group were established by increasing intracranial pressure in a modified, slow, and intermittent way, collecting liver tissues after corresponding treatment respectively, using TUNEL to detect apoptosis rate, western blotting and immunohistochemical methods to detect the expression of Cleaved-caspase 3. ResultsThe hepatocyte apoptosis rate at each time point of brain death group were higher than those of the corresponding time point of sham group (P<0.05), and the rate of hepatocyte apoptosis increased gradually with the extension of brain death time (P<0.05). The results of Western blot assay and immunohistochemistry assay showed that the relative expression amount of Cleaved-caspase 3 protein increased gradually with the extension of brain death time (P<0.05), and relative expression amount of Cleaved-caspase 3 protein at each time point of brain death group were higher than those of the corresponding time point of sham group (P<0.05). ConclusionsThe relationship between brain death donor liver and cell apoptosis is closely related. Along with the extension of the brain death time in rabbits, the level of apoptosis of liver cells gradually increased, which affects the quality of liver donors after brain death.
Objctive To explore the relationship between the expression of Fas/FasL and the apoptosis occurs in retinal ischemia/reperfusion injury of rats , as well as the therapeutic effects of bFGF on the ischemic retina.Methods Th emodels of retinal ischemia/reperfusion injury was made by transient elevating introcular pressure. A total of 28 rats were divided into normal and operation group.The latter were subdivided into 1 hour, 6, 12, 24, 48 and 72 hours after reperfusion group, in which the left eyes of the rats were in the ischemia/reper fusion groups and the right ones were in the treatment groups (bFGF intracameral injection). Apoptosis was assessed by the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labelling (TUNEL) method, and the expression of Fas and Fas ligand was studied by strept avidin-biotin complex （SABC）immunohistochemistry. Results No positive cells were observed in the normal rats′retinae, but there was a significant number of TUNEL positive cells in 6-24 hours after transient ischemia followed by a decrease at the 48th hour. The number of TUNEL positive cells reached a maximum at the 24th hour after ischemia. The expression of Fas gradually increased as early as when it was at the 6th hour, reached a peak at the 24th hour, and then decreased at the 48th hour. Similarly, the expression of Fas ligand was at peak in 24-48 hours in GCL and INL of retina. Conclusions Retinal ischemia-reperfusion after transient elevated IOP induced apoptosis of cells in the retina. Fas/FasL may play an important role in the early events of the apoptotic pathways. bFGF can rescue RGCs from retinal ischemia/reperfusion injury through downregulation of the expression of Fas/FasL and may represent an important mechanism for therapeutic neuroprotection. (Chin J Ocul Fundus Dis，2003，19：160-163)
Cancer is a heterogeneous disease characterized by maladjustment of cell death. The types of cell death were mainly divided into two forms including accidental cell death and regulated cell death (RCD). In recent years, researchers have discovered dozens of RCD modes, among which apoptosis, pyroptosis, necroptosis, and ferroptosis are the most widely studied. Cuproptosis is a new cell death mechanism that first proposed on 17 March 2022. It is recognized as a unique and both copper and mitochondria dependent RCD. The research and development of targeted drugs for regulating different cell death pathways will be hots and difficulties in the treatment of refractory cancer in the future.
Objective To investigate the risk factors of early allograft dysfunction (EAD) following C-Ⅱ donation after cardiac death (DCD) liver transplantation. Methods The data of 46 donors and recipients of C-ⅡDCD liver transplantation between March 2012 and August 2015 were retrospectively analyzed. The baseline data such as democracy, death cause, donor warm ischemic time (DWIT) and cold ischemic time (CIT) in EAD group and the non-EAD group (control group) was compared, and whether these factors were risk factors of EAD was investigated by univariate and multivariate analyses. Statistical cut-off values for significant factors of the unfavorable analysis were defined by receiver operating characteristics (ROC) analysis. The 6-month and 1-year graft survival rate were compared. Results The EAD group had a longer DWIT compared with the group [(17.6±4.7) and (12.7±6.2) minutes, P=0.009]; meanwhile, the EAD group had a longer CIT compared with the control group [(13.7±4.7) and (11.0±3.5) hours, P=0.020]. The other factors in both groups showed no statistical significance (P>0.05). The ROC curve revealed the cut-off values of DWIT and CIT were 17.50 minutes [area under the curve (AUC)=0.713, P=0.020] and 9.85 hours (AUC=0.723, P=0.015), respectively. The multivariate logistic regression analysis showed the DWIT [odds ratios (OR)=1.340, 95% confidence interval (CI)(1.042, 1.654), P=0.008] and CIT [OR=1.396, 95% CI (1.075, 1.698), P=0.015] were all independent risk factors of EAD. The 6-month and 1-year graft survival rate of the EAD group and the control group was 85.7% vs. 92.3% (P=0.607) and 71.4% vs. 84.6% (P=0.587), respectively. Conclusions EAD may occured in C-Ⅱ donors with DWIT≥17.50 minutes or CIT≥9.85 hours in DCD liver transplantation. The livers can be used as a resource for clinical use and also have a good outcome.