Since the emergence of the new syndrome, termed multiple system organ failure (MSOF), about two decades age, it has aroused an outburst of enthusiasm in clinical and experimental studies among many clinicians and investigators both abroad and at home. Nevertheless, it has also created much confusion in the concept as well as the diagnosis of the syndrome, mainly because the present term does not clearly differentiate this syndrome from some other irrelevant clinical conditions, such as senile dysfunction of multiple organs, agonal state etc. As it has been documented to occur almost as a rule after a septic state and also under the intricate interaction of many humoral and cellular mediators, we suggest that the diagnosis of MSOF should at least include two concurrent conditions, i. e. septic response and organ failure.Inasmuch as the present diagnosis of MSOF designates only the terminal state of a series of pat-hophysiological process, namely systemic inflammatory response---sepsis--septic syndrome--MSOF,it is not conducive to an early diagnosis, which is of utmost importance in the prevention and early treatment of this frequently fatal syndrome. In the light of current investigations, we propose that the name of the syndrome be changed to "sepsis and organ dysfunction" or "mediator injury of organs*. Our humble opinion welcomes further comments and discussion.

Objective To investigate the causer of, and the way to deal with the measurement of protecting from vascular compromise in free flap transplantation. Methods To retrospectively study the clinical data collected from the 89th Hospital of PLA including 305 cases of vascular compromise in free flap transplantation held on June, 1983 to December, 2006. Accoding to the different tissue flaps and different sites to be repaired, 11 factors of vascular compromise of free flap transplantation were to be investigated including operation design, the recipe of free flap, the variation of vascellum, the skill of recipe, the operation opportunity, the match of vascellum, the debride of vascellum, the vascellum angiotasis, the vascular anastomosis, the management of vascular articulo and the infection. Results Among the 305 cases of free flap transplantation, arterial compromise existed in 270 cases, 10 cases developed arterial compromise during operation, 6 cases were due to the injury of nutrient vessel, the flap survived after the revascularization. 4 cases obtained part necrosis of 10 cases, and the rotation flap and skingrafting covered the raw surface. The rest 213 cases survived and 47 cased failed. Another 35 cases of vein compromise were obtained. Among them, 5 cases survived, part necrosis of 10 cases, and 20 cases failed. Conclusion Vascular compromise is the factor of necrosis in free flap transplantation. It is of cardinal importance to timely and correctly treat the vascular compromise in free flap transplantation whether happened intra-or postoperatively. This is the key to access high successful rate. Preventive measures are even more beneficial than proper management after its occurrence. The venous return disorder was the main factor of free flap transplantation failure.

High mobility group A1 belongs to the family of high mobility group. It is widespread in human,and involved in the physiological and pathological situations. It is overexpressed in many human cancers including haematological malignancies as the oncogene.

Objective To investigate the efficacy and toxicity of neoadjuvant regional arterial chemotherapy in the treatment of advanced gastric cancer. Methods The clinical data of 158 patients with advanced gastric cancer and with the same clinical stages who were admitted to Renji Hospital of Shanghai Jiaotong University from February 2002 to May 2005 were retrospectively analysed. Preoperative regional arterial chemotherapy was applied to 76 patients (test group) and the remaining 82 patients only received surgical treatment (control group). The chemotherapy regimen was epirubicin (50 mg/m2) + cisplatin (60 mg/m2) + 5-fluorouracil (1000 mg/m2).This regimen was modified to oxaliplatin (130 mg/m2) + 5-fluorouracil (1000 mg/m2) since 2003, and surgery was performed 6-11 days after the chemotherapy. All patients received postoperative intravenous chemotherapy.The clinical effects, radical resection rate, operative complications and long-term survival of the two treatment methods were evaluated. All data were analysed using the chi-square test and Kaplan-Meier analysis. Results The radical resection rate was significantly higher at 86% (65/76) in the test group compared with 71% (58/82)in the control group ( x2 = 5.01, P ＜ 0. 05 ). The toxicity of the chemotherapy in the test group was mild. The postoperative complication rate was 20% (15/76) in the test group and 16% (13/82) in the control group, with no significant difference between the two groups (x2 = 0.41, P＞0.05). The median survival time was 41 months in the test group and 23 months in the control group. The 5-year overall survival rate was higher in the test group (44.6%) than that in the control group (29.1%) (x2 =3.95, P＜0. 05). Conclusions Neoadjuvant regional arterial chemotherapy is well tolerated by patients with advanced gastric cancer. It is also effective for increasing the radical resection rate and improving the long-term survival.

Two patients underwent liver transplantation of blood type incompatibility were collected from Fuzhou General Hospital of Nanjing Military Area Command of Chinese PLA. Case 1: A male who had primary hepatic carcinoma underwent classic orthotopic liver transplantation; the blood of donor was type A, and the blood of recipient was type O. Case 2: A female having history of type B hepatitis underwent classic orthotopic liver transplantation due to pregnancy combining with severe liver disease and coagulation disorder; the blood of donor was type B, and the blood of recipient was type O. Immunohistochemistry staining was used to observe pathological changes and deposition of various immunoglobulin and complement in two cases following liver transplantation of blood type incompatibility under optic microscope and to investigate diagnostic standard of humoral rejection. The results showed that linear or granular depositions of IgG, IgM, IgA, C4c, C4d, and Clq were found in endothelial cells of hepatic sinusoid, suggesting that IgG and other immunoglobulin exhibited a strongly positively diffused deposition on the endothelial cells of hepatic sinusoid, while expression of C4d and other complements was also found. All those mentioned above could be considered as evidences to prove onset of humoral rejection in transplanted liver tissue.

Aim To establish cerebrocardiac syndrome model in rats. Methods Right middle cerebral artery of rat was occluded (MCAO) with nylon thread and Ⅱ lead ECG was monitored continuously within 2 h to record the emerging of arrhythmias. 30 min, 2 h, 24 h after middle cerebral artery occlusion or 6 h reperfusion after 2 h occlusion, left ventricular myocardiums were observed with transmission electron microscope to find the morphological damage and brains were marked with TTC to locate infarction area. Results (14.9?11.4) minutes after MCAO, 71%(60/85)model rats had abnormal ECG changes including 38 %(32/85)premature ventricular contraction, 27 %(23/85)atrial premature beats, 5%(4/85)ventricular tachycardia, 1.2%(1/85)sinus tachycardia. Arrhythmias sustained (29.0?23.2 )minutes. Ventricular myocardial cell injury was obvious: chaotic and broken mitochondria ridges, aggregated chromatin under the nucleus membrane, deposited glycogen granules in the cytoplasma. 30 min, 2h, 24h after MCAO the infarction rates were 8.7%?1.1%,11.4%?2.3% and 13.7%?3.1% respectively. Conclusion A stable cerebrocardiac syndrome model in rat might be induced by means of occluding right middle cerebral artery and the morphological bases of cerebrogenic cardiac arrhythmias are myocardial cell injury caused by cerebral infarction.

Objective To investigate DJ-1 expression and protective effect against H2O2-induced oxidative stress in primary human melanocytes.Methods The expression and location of DJ-1 in primary melanocytes were identified by immunofluorescence.After cultured melanocytes were exposed to H2O2 for 24 hours,modified MTT assay was used to assess the proliferation of cells and to choose the suitable concentration of H2O2 for the following experiment.Western blot was used to detect D J-1 expression in melanocytes after being treated with 0.5 mmol/L H2O2 for 24 hours.Some melanocytes were divided into 3 groups to be reversely transfected with PBS(mock control group),non-targeting siRNA(negative control group)and DJ-1 targeting siRNA(DJ-1 group).Optical microscopy was utilized to observe the morphologic changes of transfected melanocytes.At 48 hours after the transfection,the melanocytes were stimulated with H2O2 for 24 hours.Subsequently,modified MTT assay,2′,7′-dichlorofluorescein diacetate(DCFH-DA)and annexin Ⅴ-fluorescein isothiocyanate/propidium iodide were used to determine cell viability,intracellular reactive oxygen species (ROS)level and apoptosis rate respectively.Results DJ-1 was expressed in both melanocyte nucleus and cytoplasm,and predominantly in the nucleus.H2O2 inhibited the cell viability in a dose dependent manner.After treatment with H2O2 of 0.5 mmol/L for 24 hours,the cell viability began to decrease in melanocytes with the expression level of DJ-1 being 2.23 times that in the untreated melanocytes(both P ＜ 0.05).Compared with the mock control group,the dendrites of melanocytes in DJ-1 group were obviously shortened with cytoplasm vacuolization.After 24-hour treatment with H2O2 of 0.5 mmol/L,the cell viability in the DJ-1 group dropped to 35％ of that in the mock control group(P ＜ 0.05),while the intracellular ROS fluorescence intensity( FI) and apoptosis rate were higher in the DJ-1 group than in the mock control group (902 ± 40 vs.529± 32,58q％ ± 6.1％ vs.30% ± 3.8％,both P ＜ 0.05).Conclusion DJ-1 can protect melanocytes against H2O2induced oxidative stress likely by decreasing intracellular ROS production and inhibiting ceU apoptosis.

BACKGROUND: Marrow stromal cells (MSCs) own the characteristic of migration. However, the mechanisms underlying the migration of these cells remain unclear. OBJECTIVE: To explore the roles of stromal cell-derived factor-1 (SDF-1) and its receptor CXCR4 in trafficking of MSCs migration. DESIGN, TIME AND SETTING: The in vivo cytology experiment was performed at Department of Anatomy, National University of Singapore from March 2007 to June 2007. MATERIALS: MSCs were isolated and purified from a Wistar neonatal rat. Forty adult female Wistar rats were randomly divided into sham operation and experimental groups, with 20 animals in each group. METHODS: The chemotaxis assay was performed at a 48 well Boyden chamber, and a total of 25 μL SDF-1 was added to the lower layer of chamber, covered with 8 μm polycarbonate membrane filter; SDF-1 cultured in DMEM conditioned medium was served as a blank control group. Cell concentration was regulated to 1.5×109L-1/L. 50 μL and cell suspension was added into the upper layer of chamber, cultured at CO2 incubator with temperature of 37 ℃ for 10 hours. Rats in the experimental group were prepared for transected spinal cord injury models, and in the sham operation'group, only the vertebral plate was opened. 1.0 mL (1×109L-1/L) MSCs suspension labeled with 5-(and-6)-carboxyfluorescein diacetate succinimidyl ester (CFDA-SE) was injected through internal jugular vein at 1 hour after completely transected spinal cord. MAIN OUTCOME MEASURES: Expression of chemokine receptor CXCR4 in MSCs, as well as the effect of SDF-1 on the migration of MSCs was observed by immunofluorescence, change of SDF-1 in lesion site of spinal cord was detected by real-time PCR analysis, as well as the in vivo migration of intravenously injected MSCs was detected by fluorescence microscopy. RESULTS: The pudfied MSCs were positive to CXCR4. Compared to the blank control group, SDF-1 with concentrations of 5, 50, and 500 μg/L could accelerated the migration of MSCs (P < 0.05), which reached a peak with concentration of 500 μg/L. The expression of SDF-1 RNA was obvious increased in the experimental group than that of the sham operation group (P < 0.05), and returned to a normal level at 14 days. At 2 weeks after cell injection, the number of MSCs migrated to the lesion site of completely transected spinal cord was significant increased than sham operation group (P < 0.05). CONCLUSION: SDF-1 may contribute to MSCs migration in vitro and in vivo. SDF-1 and its receptor CXCR4 are involved in the migration of injected MSCs to the lesion site of completely transected spinal cord.Ding P, Xue LP, Yang ZY, Wang CQ, Wang JH, Feng ZT, Ling EA.Chemokine stromal cell-derived factor-1 and its receptor CXCR4 mediate migration of marrow stromal ceils into the lesion site of completely transected spinal cord.

[Objective] To investigate the anti-proliferative and apoptosis effect induced by Honokiol (HNK) on human myeloid leukemia cell line U937 cells in vitro.[Methods] After treated with different concentration of HNK,Hoechst33342 fluorescent staining was used to detect cell apoptosis;the growth inhibition ration of U937 cells and PBMCs were analyzed by MTT assay;the apoptosis ration was detected by flow cytometry;mitochondrial membrane potential was explored by rhodamine 123 stain;Caspase3/7 protein activity kit was used to test the Caspase3/7 activity;the Caspase-3 and Caspase-7 mRNA levels were detected by real-time fluorescent relative-quantification reverse transcriptional PCR (FQ-PCR).[Results] Honokiol could significantly inhibit the proliferation of U937 cells in terms of the indexes of IC50/U937 11.8 μg/mL and IC50/PBMCs 40.3 μg/mL,and the anti-proliferative effect was in a time and concentration dependent manner;Flow cytometry analysis manifested that Honokiol could induce U937cells apoptosis by Annexin V/PI double Annexin V/PI fluorescein stain;Honokiol significantly inhibited the mitochondrial membrane potential of U937 cells and enhanced the ability of Caspase3/7 and the mRNA expression levels,but not the PBMCs.[Conclusion] HNK can inhibit U937 cells proliferation and induce cells apoptosis via activating Caspase 3/7.

Human cytomegalovirus (HCMV) is the most common cause of congenital infection, resulting in birth defects such as microcephaly. In this study, RT-PCR and Western Blotting were performed to quantify the regulation of endogenic nerve growth factor expression in neuroglia cells by HCMV infection. The results showed that basal, endogenous NGF expression in U251 was unchanged during early HCMV infection. NGF expression is strongly down-regulated during the latent phase of infection. These results suggest that HCMV can depress the NGF expression in U251 cells.