OBJECTIVE: To analyze the forensic pathological characteristics of sudden death caused by pulmonary thromboembolism and the chronological transformation of thrombus and explore the assessment method of the causal relationship between previous trauma and the following fatal PTE episode. METHODS: All the 23 cases reviewed here were collected from our institute files from the year of 1998 to 2008. RESULTS: Trauma, surgery and braking etc. were all risky factors of PTE. Of these cases, 12 cases were caused by trauma, 21 cases were caused by surgery and 22 cases died in hospitals which were often happened one or two weeks after injury or one week's postoperative time. Of all the cases, 6 cases had single attack of thrombus and the rest 17 cases had the recurrence of thrombus. The number of the leg deep vein to be the embolic source was 16 cases which were often seen in the left leg. CONCLUSION It is important to confirm the embolic source, trauma, surgery and chronological events in determing the sudden death with PTE.
Adolescent ; Adult ; Aged ; Autopsy ; Cause of Death ; Child ; Death, Sudden/etiology* ; Expert Testimony ; Female ; Forensic Pathology ; Humans ; Leg/blood supply* ; Male ; Middle Aged ; Pulmonary Artery/pathology* ; Pulmonary Embolism/pathology* ; Retrospective Studies ; Risk Factors ; Venous Thrombosis/pathology* ; Wounds and Injuries/complications* ; Young Adult

OBJECTIVE: To analyze the pathological characteristics and the death reasons due to postpartum hemorrhage, and to help to deal with the obstetrical medical tangles. METHODS: Thirty-two cases of death caused by postpartum hemorrhage encountered in our department since 1995 had been collected and retrospectively analyzed. RESULTS: Death caused by postpartum hemorrhage could be divided into single factor and multi-factor, with 81.25% due to single factor, 12.50% multi-factor, and 6.25% unknown reason. The single factors included uterine atony, retained placenta, placenta increta, laceration of the lower genital tract, and coagulation defects. The multi-factor included a combination of two or more factors mentioned above. CONCLUSION The causes of death due to postpartum hemorrhage should be analyzed according to the clinical characteristics of the postpartum hemorrhage and the autopsy examination.
Autopsy ; Blood Coagulation Disorders/complications* ; Cause of Death ; Female ; Forensic Pathology ; Humans ; Placenta, Retained ; Postpartum Hemorrhage/etiology* ; Pregnancy ; Retrospective Studies ; Uterine Inertia

Objective To investigate the epidemiological and forensic characteristics of multiple organ dysfunction syndrome （MODS） after severe trauma and explore the reference indexes for determining traumatic MODS. Methods In terms of the number of organs or systems involved in MODS, the number of failures of each organ or system, the first failing organ and the survival time after organ failure, 72 cases of MODS death caused by traffic accidents were retrospectively analyzed. The cases were divided into two groups according to the mean injury severity score （ISS）. The t test was used to analyze the differences in the number of organs or systems involved in MODS in the two groups. Chi-square test was used to analyze the differences in the types of first failing organs and the differences between the two groups in the number of cases of organ or system failure involved in MODS. Wilcoxon signed-rank test was used to analyze the differences between the two groups in survival time of MODS after trauma. Kaplan-Meier survival curve was drawn and Log-Rank test was performed. Results The number of MODS involved organs or systems after trauma in ISS≤35 group was 3-5, and 2-4 in the ISS>35 group （P<0.05）. The cases of MODS organ or system failure after trauma occurred more in brain and lung in the two groups. The first failing organ after trauma was mainly the lung or kidney. The median time of first organ failure after trauma was 2.00 d, the median survival time of MODS after trauma in ISS≤35 group was 6.00 d, and 2.33 d in ISS>35 group （P<0.05）. The survival curve of ISS≤35 group was relatively high and declined gradually, while the survival curve of ISS>35 group was relatively low and the decline was steep （P<0.05）. Conclusion The epidemiological and forensic characteristics of MODS caused by traffic accidents have certain specificity. The ISS and the forensic characteristics of MODS at ISS>35 can be used as reliable reference indexes for evaluation of the causal relationship among trauma, MODS and death.
Accidents, Traffic ; Humans ; Injury Severity Score ; Multiple Organ Failure/etiology* ; Retrospective Studies ; Sensitivity and Specificity ; Wounds and Injuries/complications*

BACKGROUNDThe multidrug resistance (MDR) associated with the expression of the mdr1 gene and its product P-glycoprotein is a major factor in the prognosis of hepatocellular carcinoma cell (HCC) patients treated with chemotherapy. Our study was to establish a stable HCC MDR cell line where a de novo acquisition of multidrug resistance specifically related to overexpression of a transgenic mdr1.

METHODSThe 4.5-kb mdr1 cDNA obtained from the plasmid pHaMDR1-1 was cloned into the PCI-neo mammalian expression vector, later was transferred by liposome to human hepatocarcinoma cell line HepG2. Then the transfected HepG2 cells resisting G418 were clustered and cultured and the specific fragment of mdr1 cDNA, mRNA and the P-glycoprotein (Pgp) in these HepG2 cells were detected by PCR, RT-PCR and flow cytometry, respectively. The accumulation of the daunorubicin was determinated by flow cytometry simultaneously. The nude mice model of grafting tumour was established by injecting subcutaneously HepG2/mdr1 cells in the right axilla. When the tumour diameter reached 5 mm, adriamycin was injected into peritoneal cavity. The size and growth inhibition of tumour were evaluated.

RESULTSThe mdr1 expression vector was constructed successfully and the MDR HCC line HepG2/mdr1 developed. The PCR analysis showed that the specific fragment of mdr1 cDNA in HepG2/mdr1 cells, but not in the control group HepG2 cells. Furthermore, the content of the specific fragment of mdr1 mRNA and Pgp expression in HepG2/mdr1 cells were (59.7 +/- 7.9)% and (12.28 +/- 2.09)%, respectively, compared with (16.9 +/- 3.2)% and (3.07 +/- 1.06)% in HepG2 cells. In the nude mice HCC model, the tumour genes of both groups were identified. After ADM therapy, the mean size of HepG2 cell tumours was significantly smaller than HepG2/mdr1 cell tumours.

CONCLUSIONThe approach using the transfer of mdr1 cDNA may be applicable to the development of MDR hepatocarcinoma cell line, whose MDR mechanism is known. This would provide the experimental basis of MDR research.

ATP-Binding Cassette, Sub-Family B, Member 1 ; genetics ; metabolism ; Animals ; Carcinoma, Hepatocellular ; drug therapy ; genetics ; pathology ; Cell Line, Tumor ; Doxorubicin ; pharmacology ; therapeutic use ; Drug Resistance, Multiple ; genetics ; Drug Resistance, Neoplasm ; genetics ; Female ; Flow Cytometry ; Genetic Vectors ; genetics ; Humans ; Liver Neoplasms, Experimental ; drug therapy ; genetics ; pathology ; Mice ; Mice, Nude ; Mitomycin ; pharmacology ; therapeutic use ; Reverse Transcriptase Polymerase Chain Reaction ; Xenograft Model Antitumor Assays ; methods

Objective:To study the protective effect of different doses of single-flavored Coptis， Magnoliae Officinalis Cortex， and their compatibility on ulcerative colitis （UC） model rats and the colonic B lymphoblastoma-2 associated X protein （Bax） and cysteine-containing aspartame-3（Caspase-3） protein， inflammatory cytokines， and other expressions. Method:The 120 healthy adult SD rats were randomly divided into blank group， model group， sulfasalazine group， Coptidis Rhizoma 2.00， 1.00， 0.50 g·kg^-1 group， Magnoliae Officinalis Cortex 2.00， 1.00， 0.50 g·kg^-1 group， Coptidis Rhizoma combine with Magnoliae Officinalis Cortex 4.00， 2.00， 1.00 g·kg^-1 group， 12 groups with 10 rats in each group. The UC model was prepared by 2，4， 6-trinitrobenzene sulfonic acid/ethanol （TNBS/ethanol）. After 24 h of modeling， the rats were gavaged at 10 mL·kg^-1 for one time/d. After modeling， the mental state， activity state， hair luster， stool characteristics， and blood in the stool of each group were observed. After continuous administration for 6 days， colon tissues and spleen were taken after the last administration for 24 h. The ratio of colonic weight to length and spleen index was calculated. The degree of colonic injury was evaluated according to the colonic mucosal injury index （CMDI） score criteria. the histopathological observation was performed using hematoxylin-eosin staining （HE）. The expression levels of tumor necrosis factor （TNF）-α， interleukin-6 （IL-6）， interleukin-10 （IL-10）， and myeloperoxidase （MPO） in the serum of Coptidis Rhizoma 2.00 g·kg^-1 group， Magnoliae Officinalis Cortex 2.00 g·kg^-1 group， Coptidis Rhizoma combine with Magnoliae Officinalis Cortex 4.00 g·kg^-1 were detected by enzyme-linked immunosorbent assay（ELISA） in blank group and model group. Western blot was used to detect the expression of Bax and Caspase-3 proteins in the colon of rats. Result:Compared with blank group， rats in model group were sluggish and less active. The colon weight-length ratio， spleen index， CMDI， and colon tissue pathological damage increased significantly， and the expression of serum TNF-α， IL-6， and MPO increased significantly. Serum IL-10 expression levels were extremely significantly reduced （P<0.01）. Compared with model group， the sulfasalazine group， the Coptidis Rhizoma 2.00， 1.00 g·kg^-1 group， the Magnoliae Officinalis Cortex 2.00 g·kg^-1 group， and the three-dose groups of Coptidis Rhizoma combine with Magnoliae Officinalis Cortex， their colon weight-length ratio and CMDI were significantly reduced （P<0.05，P<0.01）. The colon weight length ratio and CMDI index of the Coptidis Rhizoma 0.50 g·kg^-1 group， Magnoliae Officinalis Cortex 0.50 and 1.00 g·kg^-1 group were not significantly different from the model group but compared with Coptidis Rhizoma and Magnolia 0.50 g·kg^-1 group， the ratio of colon weight to length in the group of Coptidis Rhizoma combine with Magnoliae Officinalis Cortex 1.00 g·kg^-1 group was significantly reduced （P<0.01）. Compared with model group， the spleen index of the sulfasalazine group， the Coptidis Rhizoma 2.00 g·kg^-1， and the Coptidis Rhizoma combine with Magnoliae Officinalis Cortex 4.00 g·kg^-1 group were significantly lower （P<0.05）， compared with model group， the sulfasalazine group， Coptidis Rhizoma 2.00， 1.00 g·kg^-1 and Magnoliae Officinalis Cortex 2.00 g·kg^-1， thre dose groups of Coptidis Rhizoma combine with Magnoliae Officinalis Cortex can significantly improve the depth and scope of histopathological damage and tissue necrosis. Compared with the model group， the preferred Coptidis Rhizoma 2.00 g·kg^-1 group， Magnoliae Officinalis Cortex 2.00 g·kg^-1group， Coptidis Rhizoma combine with Magnoliae Officinalis Cortex 4.00 g·kg^-1 group serum TNF-α， IL-6， MPO expression levels are extremely significantly reduced， the level of IL-10 increased significantly （P<0.01）．Compared with blank group， the expression of 　Bax and Caspase-3 protein in the colon of model group was significantly increased （P<0.01）. Compared with model group， the expression of Bax and Caspase-3 protein in preferred Coptidis Rhizoma 2.00 g·kg^-1 group and Magnoliae Officinalis Cortex 2.00 g·kg^-1 group， Coptidis Rhizoma combine with Magnoliae Officinalis Cortex 4.00 g·kg^-1 group were significantly reduced （P<0.01）． Conclusion:The compatibility of single-flavored Coptidis Rhizoma， Magnoliae Officinalis Cortex， and Coptidis Rhizoma combine with Magnoliae Officinalis Cortex may improve the pathology of UC model rats induced by TNBS/ethanol by down-regulating the expression of Bax and Caspase-3 protein， inhibiting the release of inflammatory cytokines and promoting the release of anti-inflammatory factors injury， it plays a role in protecting colonic mucosa. The compatibility effect of Coptidis Rhizoma and Magnoliae Officinalis Cortex is better than that of single medicine， and Coptidis Rhizoma has a tendency to be better than Magnoliae Officinalis Cortex.