In the present and future, nuclear terror raid may be tremendously hazardous to human health and social security. The governments of many countries have already established specific organizations to strike and smash nuclear terror raid. The government of our country also pays high attention to it. In order to help people understand and prevent the nuclear terror raid, the article summarizes the effects of each injurious factor, kinds and ranges of injurious effects, medical prevention and treatment at the scene of nuclear terror raid.

Bone growth factors play an important role in the process of bone metabolism and perform a variety of physio -logical functions such as regulating bone growth , differentiation and remodeling .Meanwhile , these cytokines are associated with orthopedic disorder and therapy .The curative effect of the overturned sartorius iliac flap in repair of acetabular defect in developmental dysplasia of the hip proves to be good , but mechanism between the overturned flap and the surrounding bone tissue is unclear .This review briefly summarizes the functions and applications of several major cytokines in bone for -mation and remodeling , which may provide new ideas and methods for illuminating the mechanism of these cytokines during the repair of the acetabular defect .

Altogether 80 Wistar rats were used for an animal model of cerebral concussion, which were sacrificed on days 1,3,7,14 and 30 after injury and the brain tissue was collected. The pathologic changes of cerebral concussion and apoptosis of nervous cells were studied by means of light microscopy, electron microscopy and in situ terminal end labeling method. The results showed that the clinical situation for cerebral concussion occurred in rats struck by 100g standard weight from 1 meter high. The basic pathologic changes were the cerebral vascular dilatation, congestion, hemorrhage, and edema of cerebral tissue. Nervous cells underaent degeneration, apoptosis and necrosis, and the Nissl bodies obviously decreased, even disappeared. On days 1～3 after injury, dot or piece necrosis was seen in brain tissue, around which the tissue rarefied. Monocytes and foam cells increased, and lots of neurons underwent degeneration, apoptosis and necrosis. The edema of cerebral tissue reached its peak on day 7. Hippocampal pyramidal cells decreased in number and showed the changes of obvious ischemia. On days 14～30, blood vessels also showed dilatation, congestion and hemorrhage, whereas edema alleviated. The neurons in cerebral cortex and hippocampus also showed the changes of chronic ischemia. By in situ terminal end labeling the number of apoptotic neurons increased on day 1, reached its peak on day 3 and still existed on day 30. The results suggested that the main pathologic changes of cerebral concussion were blood circulatory disorder and nervous cell degeneration, apoptosis and necrosis. Apoptosis of nervous cells was one of the main changes in cerebral concussion.

Objective To study comparatively the changes in epi th elial growth factor (EGF) and its receptor (EGFR) in injured intestine induced b y neutron and ?-ray irradiation in mice and their significance. Method s 350 male BALB/C mice were irradiated with neutron and ?-rays, and t hey were sacrificed at 6 and 12 hours and 1, 2, 3, 4, 5, 7, 10, 14, 21 and 28 da ys, respectively, after irradiation. Immunohistochemical method was employed to assess EGF and EGFR in the intestinal tissue of the mice. Results After the neutron radiation with 2.5Gy dosage, the expressions of EGF and E GFR in the cytoplasm of mucosa epithelial cells and crypt cells were obviously u p-regulated within 1 day, decreased after 1~2 days, increased again on 3~7 days , reached the peak value at the 5th day, and returned to normal values in 14 day s. Whereas EGF and EGFR were increased at 6 hours and progressively decreased fr om 12 hours up to 4 days after 4.0 and 5.5Gy neutron and 12Gy g-ray radiation . They were increased progressively within 3 days, reaching peak value on the 3r d day, and returned to normal values 5 days after 5.5Gy g-ray irradiation. Conclusions The expressions of endogenous EGF and EGFR showed diffe rent regularities after neutron and g-ray radiation, and they were involved in the pathologic courses of radiation damage and recovery of the intestine.

Objective To investigate the expression and significance of ?-endorphin in hippocampus after high power microwave (HPM) radiation. Methods 50 male Wistar rats were sacrificed at 6h, 1d, 3d, 7d, 14d, 28 days after exposure to 12mW/cm~2 HPM imitational source radiation. The hippocampus was harvested, the characteristics of injury to the hippocampus and expression of ?-endorphin were evaluated by means of light microscope, EM, immunohistochemistry and image analysis. Results In the neutrons of hippocampus, mitochondrial swelling and myelin sheath confluence and dissociation were observed 6 hours after radiation, and mitochondrial swelling, cavitation, disruption of crista, concentration margining of chromatin, blurring of synaptic cleft, piling or evacuation of vesicles were observed 3 days after HPM radiation. The expression of ?-endorphin in cytoplasm of neurons was up-regulated continuously from 1 to 7 days, peaking at 7 days, restoring to normal level from 14 to 28 days after radiation. Conclusion HPM can produce injury to the hippocampus at histological and ultrastructural levels. The expression of ?-endorphin is up-regulated, and it might play an important role in the pathophysiological process of injury and repair in the hippocampus.

Objective To study the injury of rat cardiomyocytes exposed to nonionizing radiation and its mechanism. Methods Primarily cultured cardiomyocytes were irradiated by 9 GHz 950 mW/cm2 microwave pulse (MWP)and 0～100 MHz 6?104 V/m electromagnetic pulse (EMP)for 72 h respectively ,then a series of apparatus including atom force microscope,laser scanning confocal microscope and flow cytometer were used to detect the changes of cell membrane conformation,structure and function. Results Slower pulsation,abnormal conformation,lower viability ,the significantly increased percentage of apoptosis and necrosis were observed in cardiomyocytes after irradiation by MWP and EMP respectively (P

Objective To explore the prevention and treatment effect and its mechanism of Xuebijing injec-tion combined with dexamethasone on rats' paraqnat-induced acute and chronic pulmonary injury.Method One hundred and twenty of male Wistar rats were randomly divided into six groups:nomud group(A),administrated with saline;model group(B)and treatment groups(group C,D,E,F)were given 20%PQ(100 mg/kg.ip),and 2 hours later the normal and model groups were administrated with the same volume of saline for treatment,rats in group C and group D received 1.25 g/kg and 2.5 g/kg Xuebijing injection respectively.rdts in group E received 25,ng/kg dexamethasone,rats in group F receired 2.5 g/kg Xuebijing injection combined with 2.5 g/kg dexamethasone,one time per day till to be killed,while rats killed at 28 d were treated for 7 days.At 2 d,3 d,4 d after poisoned,five rats in each group were killed,serum SOD,MDA level and arterial gas(at 3 d)were measured.At 28 d,the rest of rats were killed,and serum TGF-β1,lung tissure HYP were measured.The pathology of the lung tissue was ob-served at 3 d and 28 d in guoup A,B,F.Results Compared with group B,poisoning symptoms in the treatment groups were milder and serum.SOD,MDA,TGV-β1,lung tissure HYP level were better,arterial oxygen content were higer.Among treatment groups,the treatment effects in group F were the best,SOD and MDA of 3 d,HYP and TGF-β1 of 28 d in group B and F were respectively(37.47±13.00,91.86±21.35)nmol/mL;(11.34±3.07,5.63±1.58)nmoL/mL;(2.54±0.63,1.32±0.07)mg/g;(484.13±63.79,202.22±49.83)pg/mL.The difference was significant(P＜0.05).The pathology of the lung tissue showed that acute lung hemorrhage,edema or chronic pulmonary fibrosis in group F were milder than that of group B.Conclusions In early stage,Xuebijing injection combined with dexamethasone has a stronger ability to clear out oxidized free radical and inhibit lipid super oxidized reaction.This may ameliorate acute pulmonary blooding and edema.In later stage,they could ameliorate chronic pulmonary fibrosis by inhibiting TGF-β1 secretion and HYP generation.

BACKGROUND: There is no accepted treatment for liver fibrosis recently. Bone marrow meaenchymal stern cells (BMSCs) used in the treatment of liver fibrosis has been reported as an effectively treatment, but the mechanism is unclear.OBJECTIVE: To study the regulation of hepatic stellate cells mediated by human BMSCs in vitro.DESIGN, TIME AND SETTING: The cytological in vitro study was performed at the Center for Stem Cells and Tissue Engineering of Sun Yat-sen University and the Central Laboratory of Third Affiliated Hospital of Sun Yat-sen University from June to December 2008.MATERIALS: Human bone marrow masenchymal stem cells were collected from normal youth volunteers; Human hepatic stellate cells and normal liver call line L-O2 were supplied by the Animal Experimental Center of Sun Yat-sen University.METHODS: The purified human BMSCs and hepatic stellate calls were set up in Transwell co-culture system. The incubation density was 2×104cells/well. L-O2 was set up instead of human BMSCs as negative control. Hepatic stellate cells cultured alone served as blank control group. The culture was performed for 72 hours.MAIN OUTCOME MEASURES: Morphology of hepatic stellate cells and results of immunocytochemical staining. Apoptosis of hepatic stellte calls was determined by flow cytometry. Western blot were used to assay the expression of α-actin.RESULTS: Activated hepatic stellate cells presented fiat and thin shape under an inverted microscope. Fat drop was lack in cytoplasm, a -actin located in hepatic stellate calls, with the presence of high tension fibers. Compared with the L-O2 + hepatic stellate cell and hepatic stellate call groups, the apoptotic rate of hepatic stellate cells was significantly increased in the BMSC + hepatic stellate cell group (P < 0.05). α -actin expression was significantly down-regulated.CONCLUSION: Human BMSCs can inhibit activation of hepatic stellate ceils and promote them apoptosis, which may be the anti-hepatic fibrosis mechanism of BMSCs.

BACKGROUND:It is reported that bone marrow mesenchymal stem cell(BMSC)transplantation might be a promising treatment for liver fibrosis.But the mechanism is still unclear.OBJECTIVE:To observe the hepatic stellate cells apoptosis induced by BMSC transplantation,and to study the mechanism of BMSC in treating hepatic fibrosis in vivo.METHODS:CCl_4 subcutaneous injection was performed to induce rat liver fibrosis.After 8 weeks of CCU injection,20 rats which underwent successful model establishment were randomly divided into experimental group and control group,10 in each group.The experimental group received MSC transplantation via tail vein injection,and the control group were given DMEM instead.The rats were killed and the livers were harvested at three time point,the day of MSC transplantation,3 days after transplantation,and 7 days after transplantation.The hydroxyproline content was detected by HE and Masson staining,and the expression changes of α-smooth muscle actin(α-SMA)proteins were determined using immunohistochemistry.The apoptosis of hepatic stellate cells were determined by α-SMA and TUNEL(terminal dUTP nick-end labeling)dual-staining.RESULTS AND CONCLUSION:After 8 weeks of CCU injection,the hydroxyproline content increased and histology indicated progress of liver fibrosis.At 7 days after MSC transplantation,the hydroxyproline in the liver was decreased,and the liver fibrosis was alleviated in the experimental group but aggravated in the control group.Immunohistochemistry indicated that α-SMA positive cells were increased at 8 weeks after CCU injection.At day 7 after transplantation,α-SMA positive cells in the experimental group were significantly less than control group(P ＜ 0.05).At 3 days after transplantation,the hepatic stellate cells apoptosis in the experimental group was significantly aggravated compared with control group(P ＜ 0.05).This suggested that MSC transplant was an effective treatment for liver fibrosis.MSC inducing hepatic stellate cells apoptosis may be one of the mechanisms.

Objective To explore the therapeutic effect of rhIL-11 and rhG-CSF on mouse bone marrow injury induced by neutron irradiation.Methods 130 male BALB/c mice were irradiated by 3.0 Gy neutron and mice peripheral blood cells,bone marrow pathological changes,bone marrow nucleated cell counts,AgNOR content,apoptosis and necrosis rates and Bax protein content were observed by means of blood cells automatic analyzer,HE staining,AgNOR staining,flow cytometry,immunohistochemistry staining and image analysis.Results In the irradiation group and the rhIL-11 group,the mice peripheral blood white blood cells,bone marrow nucleated cell counts and AgNOR content was decreased progressively.The Bax protein was positively or strongly positively expressed in the cytoplasm of the hematopoietic cells and the Bax protein content was increased progressively at 6 h,1 d,3 d after irradiation.In the irradiation group,the rates of apoptosis and necrosis in the mice hematopoietic cells were greatly increased and that of necrosis was significant at 6 h after irradiation.In the rhIL-11 + rhG-CSF group,the counts of bone marrow nucleated cell and AgNOR were increased and the Bax protein content was decreased at 3 d after irradiation,while in the rhIL-11 group,the indexes mentioned above were not obviously different compared with those of the irradiation group.Conclusions The mice bone marrow hematopoietic function is seriously damaged by 3.0 Gy neutron irradiation,rhIL-11 and rhG-CSF could improve the mice hernatopoietic function after neutron irradiation,and combination of them is more effective to stimulate the hematopoitic function than either of them alone.