Objective To investigate the changes of endothelial function during myocardial ischemia and reperfusion (I/R) injury of rabbits, and the protection of ShenFu injection (SFI) for the injury, as well as the related mechanism. Methods Twenty one Japanese white rabbits were randomly divided into 3 groups (7 each): sham operated group (A), I/R group (B) and SFI-treated I/R group (C). The activity of serum endothelial nitric oxide synthase(eNOS), the concentrations of serum nitric oxide products (NOP) and plasma endothelin (ET) before ligation of coronary artery, 40min after ischemia and 40min after reperfusion were determined. The concentration of total superoxide dismutase (T-SOD) and malonyl-dialdehyde (MDA) in myocardial tissue were determined. Ultrastructure of myocardial cell was observed by electro microscope. Results 1) Serum eNOS and NOP decreased and plasma ET increased ingroup B than that ingroup A after 40min of ischemia (P<0.01), even more significant after 40min of reperfusion. NOP was correlated positively with ETafter 40min of ischemia (P<0. 05) and after 40min of reperfusion ( P<0. 01). In 40min after reperfusion, T-SOD was decreased and MDA was increased ingroup B than that in group A, significantly (P<0. 01). NOP were correlated positively with T-SOD, while were correlated negatively with MDA (P<0.05). ET was correlated positively with MDA, while was correlated negatively with T-SOD (P<0.05). Ultrastructure of myocardial cell changed abnormally. 2) SFI can increase eNOS and NOP after 40min ischemia and 40min reperfusion, and decrease ET after 40min reperfusion, significantly (P<0. 01). SFI can increase T-SOD and decrease MDA significantly (P<0. 01), the abnormality of myocardial cells can be relieved obviously. Conclusion SFI can improve the endothelial function in which free radicals are involved, and prevent myocardial tissue from I/R injury.

Objective To evaluate the iron metabolism in host-pathogen interplay.MethodsA total of 13 expression profiles of iron metabolism related genes of RAW264.7 murine macrophages uninfected or infected with Salmonella typhimurium were stuldied by real-time PCR.Results The live wild-type Salmonella typhimurium induced the expression of the transferrin receptor(Tfr1)in host cell macrophages,which resulted in a sustained increase of the labile iron pool inside the host oell 1h or 24h after infection.Gene expression analysis showed that wild-type Salmonella typhimurium drove an active iron acquisition program with induction of ferrireductase(Steap3),iron membrane transporter Dmtl,and iron regulatory proteins(Irpl and Irp2),and a little of iron efflux change through ferriportin(Fpnl).On the other hand,the Salmonella mutant strain spiC-used in present studies did not cause an increase mRNA level for Tfrl at 1h or 24h,but led to an increase mRNA level for Epnl at 24h as compared with 1h. The assessment was that the labile iron pool decreased after infection with spiC-Salmonella for 24h.Conclusion Wild-type Salmonella typhimurium appears to drive an active transferrin-mediated iron uptake program after infection 1h or 24h.The spiC-Salmonella mutant strain used in our studies shows an increased iron efflux from infected cells at 24h as comparde with 1h.

Objective To investigate the differently expressed genes in human ovarian carcinoma, and to reveal the molecular mechanism of the cancerous development. Methods The specimens of human ovarian serous adenocarcinoma tissues in stage III, and of normal human ovarian tissues as control were excised during surgery for present study. Clinical stages were determined by the Federation International of Gynecology and Obstetrids (FIGO). Total RNA was isolated from human ovarian tissues, and cDNA probe was labeled and purified. The amount of radioactivity incorporated into the cDNA probes was checked by a scintillation counter. The profiles of gene expression were compared between carcinomas and normal ovarian tissues by cDNA microarray which contained 588 genes totally. Results Forty-four differentially expressed genes were identified from the 588 genes which were from ovarian carcinoma and normal ovarian tissues and compared with cDNA expression array and analyzed by AtlasImage 1.01 software. 11 of the 44 genes were up-regulated in ovarian carcinoma tissues (including c-erbB2, neu, c-fos, c-myc proto-oncogenes, HER2 receptor, and so on), and the other 33 genes were down-regulated (including RAR, MMP18, MMP19, p21, DNA-PK, and so on). Conclusion The gene expressions in human ovarian carcinoma have been detected in present study. It is the differently expressed genes that help us to disclose the potential molecular mechanisms of the developmental process of human ovarian carcinogenesis. The differently expressed genes may provide a useful hallmark for the early diagnosis of human ovarian carcinoma.

Objective Valsartan, the angiotensin Ⅱ type 1 receptor blocker, is recently proved to reduce urinary albumin at the microalbuminuria stage in human diabetic nephropathy without altering glucose metabolism. But the pathway is still uncertain. In present study, we examined the changes of adrenomedullin receptor (ADMR) mRNA and protein expressions in the renal cortex of diabetic rats to investigate the protective effects of valsartan on an experimental model of diabetic renal injury. Method The SD rats were randomly divided into following groups: normal rats, STZ-induced diabetic rats, and diabetic rats treated with valsartan. STZ-induced diabetic rats were treated with valsartan (10mg/kg body weight) or vehicle for 8 weeks. The expressions of ADMR mRNA in renal cortex were analyzed by RT-PCR, as well as ADMR protein expressions were detected through western blot. Results We found (1) Valsartan treatments reduced urinary albumin excretion in 24h, compared with the untreated. But no notable difference was seen in HbA1c and blood sugar of diabetic rats between the two groups. (2) Valsartan treatments increased the expressions of ADMR mRNA and protein in diabetic rats renal cortex. Conclusion These results indicate that valsartan treatment can upgrade the expressions of ADMR in the renal cortex of diabetic rats. It may be one of renal protective pathways of Ang Ⅱ type 1 receptor blocker.

In the 15 years since the end of the Cold War, the extended task spectrum of the Bundeswehr has included missions abroad. These entail special psychological stress for soldiers. Some develop unspecific stress symptoms, while others develop post-traumatic stress disorders as a result of their exposure to stress. The Bundeswehr has created a medical and psychological stress concept to organize the prevention of stress and trauma. In its military hospitals (particularly in Hamburg), the Bundeswehr has established special facilities for trauma therapy, which will be presented and described in the following article.

Objective To show the capability of NF-κB expression in cochlea. Methods Kanamycin (KA) was subcutaneously injected twice daily for 3 and 7 days with an eight hours interval between two injections, and lipopolysaccharide (LPS) was injected into the tympanic cavity of mice. Equal amount of saline was injected for 7 days as control. Frozen sections of all mice cochleae were examined immmunohistochemichally with rabbit polyclonal NF-κB p50. Expression of NF-κB p50 immunoreactivity of mouse cochleae is identified as showed as brown reaction products characteristic of DAB immunohistochemistry. Results Immnoreactivity NF-κB p50 in mouse cochlea was localized in the organ of Corti, spiral limbus, tectorial membrane, the vascular stria, spiral ligament, spiral ganglion and nerve fibers. The immunoreaction could be observed in all spirals throughout the cochlea. Stronger staining was visible in spiral ligament, tectorial membrane, spiral prominence, spiral ganglion and nerve fibers, and the organ of Corti. The immunoreaction in the vascular stria was weaker than that in the structures mentioned above. The immunoreaction in the organ of Corti was observed in inner hair cells (IHC) and outer hair cells (OHC), inner and outer pillar cells, Deiter's cells, and Boettcher's cells. The immunoreaction was weaker in inner sulcus cells, Hensen's cells and Claudius'cells. The stronger immunoreaction was observed in nucleus of spiral ganglion cells. The nucleus of IHC and OHC remained unstained. Conclusion The injection of LPS/KA can promote NF-κB p50 expression to induce an acute reaction in mouse cochlea.

Objective To investigate the effects of morphine dependence and withdrawal on neurosteroids and amino acid transmitters of rat amygdala. Methods Morphine dependence was induced by pretreatment with increasing doses of morphine for 7 days. Withdrawal was precipitated by naloxone (2mg/kg). Withdrawal syndromes were observed and scored. After decapitation, amygdala was dissected out. Nomadic and conjugated neurosteroids were extracted using liquid-liquid extraction and solid phase extraction. Concentrations of neurosteroids including dehydroepiandrosterone (DHEA), pregnenolone (PREG), allopregnanolone (AP), dehydroepiandrosterone sulfate (DHEAS) and pregnenolone sulfate (PREGS) were detected with HPLC-MS. Concentrations of glycine (GLY), glutamate (GLU) and gamma-aminobutyric acid (GABA) were quantitated by HPLC-ECD with pre-column OPA derivatization. Results Compared with saline control, the DHEA level in rat amygdala of morphine dependent group decreased by 33% (P＜0.01). Compared with naloxone control, the PREG and AP levels in rat amygdala of morphine withdrawal group increased by 45% (P＜0.05) and 42% (P＜0.05) respectively; the GABA level decreased by 18% (P＜0.01). Compared with morphine dependent group, the PREG and PREGS levels in rat amygdala of morphine withdrawal group increased by 60% and 40% respectively (P＜0.05); the glycine level decreased by 14% (P＜0.05). Conclusion The DHEA in rat amygdala may play a role in the development of morphine dependence but not involved in the manifestation of withdrawal symptoms. Other neurosteroids (including PREG, AP and PREGS) in rat amygdala seem to be involved in withdrawal but not in dependence. The synthesis and release of inhibitory amino acids in amygdala were depressed when withdrawal was precipitated by naloxone. The results suggest that different changes of neurosteroids and amino acids exist in stages of morphine dependence and withdrawal.

Objective To investigate the effects of electro-acupuncture on gastric emptying and Fos expression in the neuron of vagal-solitary complex (VSC) of rat bulbus after lipopolysaccharide (LPS) intraperitoneal injection (i.p.). Methods 40 male SD rats were randomly assigned to 4 groups: control group, LPS i.p. group, LPS i.p. plus electro-acupuncture at Tsusanli point group and LPS i.p. plus electro-acupuncture at non-meridian-non-acupoint group, 10 rats for each group. Immunohistochemical techniques were used to detect the Fos expression in VSC. The animal's gastric emptying was measured by phenol red method. Results The rats with gastric emptying decreased greatly to (20.7±4.5)% 2.5 hours after LPS injection, and Fos-positive neurons were significantly found in VSC (83.2±6.6) compared with control group. However, in the group of LPS i.p. plus electro-acupuncture at Tsusanli point, the gastric emptying was up-regulated to (44.1±6.2)%, and the expression of Fos -positive neurons were down-regulated to (37.9±3.8) compared with LPS i.p. group. No significant difference was found between the group of LPS i.p. plus electro-acupuncture at non-meridian-non-acupoint and the group of LPS i.p. Conclusion LPS i.p. can retard the gastric motility in rats, electro-acupuncture at Tsusanli point may well regulate the function in LPS model rats. This function may be connected with its protective effects on Fos immunoreactive neurons activity in VSC of rat bulbus.

Objective To study the role the pathogenesis of early acute lung injury (ALI) of rabbits induced by intravascular injection of endotoxin (ET) with the intervening method of Chloroquine. Methods Rabbits were randomly assigned to three groups: control group, ET group, and ET+ chloroquine group. Acute lung injury was induced by intravascular injection of ET (500μg/kg). The arterial gas analyses, leucocyte and platelet counts in peripheral blood, PLA2 activity both in serum and lung tissue, lipid peroxide (LPO) and superoxide dismutase (SOD) in lung tissue were measured. Electron microscope and light microscope were used to observe the pathological injuries in pulmonary tissue. The protective effects of chloroquine in early ALI were evaluated. Results Compared with saline controls, rabbits treated with ET displayed the early lung injuries, such as the decrease of PaO2 (P＜0.05), the decrease of leucocytes and platelets in peripheral blood, the leukocytes sequestration in lung tissue. The PLA2 activity significantly increased in ET group compared with control group and chloroquine group both in serum and pulmonary tissue. In ET group, concentration of LPO increased in lung tissue (P＜0.05), while concentration of SOD decreased (P＜0.05). Severe histopathological injuries were presented in ET group, including pulmonary edema, lung tissue haemorrhage, inflammatory cells infiltration, asphyxial membrand formation, partial pulmonary closure and emphysema.Ultrastructural changes showed both type Ⅰ and type Ⅱ epithelial cells injury in ET group, the edema of endothelial cells, interalveolar septum thickening. In chloroquine group, PaO2 didn't decrease, PLA2 activities in serum and pulmonary tissue were lower than ET group (P＜0.05, P＜0.05), while the concentration of LPO in lung tissue decreased (P＜0.01) and SOD increased significantly (P＜0.01). Pathological examination showed slight pulmonary edema, inflammatory cells infiltration were extenuated, ultrastructural examination proved that the injuries were alleviated by chloroquine compared with ET group. Conclusion Intravascular injection of ET could successfully induce the early ALI models in rabbits. Chloroquine could inhibit the PLA2 activation and reduce the oxidative injury in lung tissue. The experiment result demonstrated PLA2 activation and oxidative stress played important roles in the pathophysiological process of early ET-induced ALI in rabbits.

Objective To study the histopathological features, diagnosis criteria, the relationship of surgery pattern and prognosis of phyllode tumor of breast. Methods To analyze the histopathological features and clinical outcome of different surgery patterns in 203 patients with phyllode tumor of breast by Chi square test, Cluster, Focater, Logistic and Cox multivariate regression according to the request of SPSS 10. 0. Results 203 patients with phyllode tumor of breast were divided into three groups, i.e. benign 133 cases, borderline 42 cases and malignant 28 cases. Local recurrences in three groups were 28, 19 and 18, respectively. The patients died from tumor were 0, 2 and 16, and circulatory metastases were 0, 1 and 10, respectively. Five-year survival were 100 %,92. 0% and 33. 3% in the three groups of 131 patients by a 5 years' follow-up survey. Conclusions Tumor necrosis has important value in the diagnosis of phyllode tumor. Nature of tumor margin, cellular pleomorphism, frequency of mitoses and tumor necrosis were statistically appropriate composition in histological diagnosis of phyllode tumor. Wide local excision is preferred for the benign and borderline phyllode tumor, while simple mastectomy is indicated for recurred borderline and malignant, but tylectomy should be abolished in the treatment of phyllode tumor. Correlation of histotypes of phyllode tumor with local recurrence and tumor death was statistically significant at a level of P＜0. 001; correlation of infiltrative growth of the tumor with local recurrence was statistically significant at a level of P＜0. 001. Tumor necrosis and mitotic activity were independent prognostic factors.