Solving the problem of weapon injuries is of primary importance in military medical research. This article aims at presenting an inquiry into hightech weapon injuries in terms of the following: (1)classify hightech weapons into special, hightech conventional and new concept weapons, and expound their characteristics; (2)demonstrate from different angles the pressing necessity to step up researches on special (nuclear, chemical and biological) weapons; (3)discuss the types and injurious effects (high speed projectiles, war heads with numerous shrapnels and cluster bomb, multiple killing factors and high casualty inflicting power) of the everlastingly emerging hightech conventional weapons, and multiple injuries, and combined injuries produced thereby; (4)probe into new concept weapons, mainly the beamed (laser, microwave and infrasound) and non lethal weapon injuries; (5)bring up the question of confrontation of hightech weapons′ in the space in the future; (6)explore the tactics in four levels to confront hightech weapons, and research on medical protection against hightech weapon injuries in terms of basic sciences, medical logistics, and medical equipments.

The principal role of neutrophils in tissue repair has long been thought to be confined to killing bacteria and clearing necrotic tissue. However, recent studies have shown that neutrophils are also one of the sources of pro inflammatory cytokines and growth factors, such as IL 1, TNF ?, bFGF, VEGF,TGF ? 1 that probably serve as the earliest signals to activate local fibroblasts, epidermal cells and vascular endothelial cells and initiate tissue repair. It was also reported that neutrophils improved the proliferation removal of injured epithelial cells in airway and corneal epithelial cells. It is very important for the successful tissue repair that the function of neutrophils is normal.

Irradiation induced tumorigenesis is a complicated process involving several phases such as initiating, promoting and progressing, just like the tumorigenesis induced by other factors. While irradiation induced tumorigenesis has its particularity on molecular mechanism, though the precise process remain unclear. Generally, irradiation can cause serious damage on DNA, which may bring irreversible consequences. For example, the double strand breaks (DSB) can induce the mismatch repair reaction, resulting in mutation of some specific genes or chromosomes in irradiated cells. The mutagenesis then make for the activation of oncogene, inactivation of tumor suppressor gene, uncontrolled cell proliferation and alterations of signal transduction pathway, all these work together to promote tumorigenesis. In addition, the gene instability, cytoplast mutation and cell group by stand effects induced by irradiation also play crucial roles in the process of tumorigenesis. [

One hundred and five rats were equally divided into three groups and inflicted with radiation (550 rads of (?)Co ? ray), burn (15% full thickness burn) and radiation-burn combined injury respectively. Another ten were used as controls. After injuries, the outstanding changes in adrenal cortex included the following: (a) Transformation between clear cells and compact cells, on the basis of ultrastructural and cytochemical changes. (b)Acidophilic masses appeared in the cytoplasm of cortex cells, as a result of the formation of mitochondria-lipid droplets-lysosomes-hyperplastic SER complex, (c) The cortex cells or their cytoplasm entered the blood sinuses.This phenomenon is considered as an unusual pattern of discharge of endocrine secretion. Similar dynamic changes and distributing characteristics of cortical lesions were observed in all three groups of injured animals, and signifying hyperfunction of this gland. The degree of effect on the adrenal cortex in combined injury group was more marked than any of either single injurious factor. That is considered as an important feature of combined effect on the adrenal cortex.

Objective To measure the collagen content in the granulation tissue of skin wound surface in rats with depression in order to explore the possible mechanism about depression to wound healing.Methods Totally 126 Sprague-Dawley rats were randomly and equally allocated to 3 groups: simple wound group,depression plus wound group,wound plus depression group.Unpredictable stimuli,including fasting,electrocution,water deprivation,swimming in cold water and others,were performed for 18 d to establish depression model of rats.A full-thickness dermal wound(2.2 cm in diameter) was made on the back of rats to build wound model.Rats from depression plus wound group received 18 days' stimuli and then wound cutting.For those of wound plus depression,stimuli were carried out from the next day of wounding.The basal tissue in the center of the wound was taken out from 6 rats of every group in 3,5,7,10,14,18 and 21 d after wounding.Hydroxyproline reagent kit was used to detect the content of hydroxyproline in collected tissue.Wound collagen depositions in every time point were stained by nitroxanthic acid sirius red and then observed by polarization microscopy.Results Hydroxyproline content and collagen deposition in wound granulation tissue of depression plus wound group rats were lower than those in the other 2 groups.From 18 d after wounding,rats of depression plus wound group had a tendency to the same level as wound plus depression group.Conclusion Depression plus wound significantly decreases hydroxyproline synthesis,reduces collagen deposition in wound,and then delays the wound healing.

The histological and ultrastructural changes in cerebellum of mice exposed whole-body irradiation with high doses of 60Coy-ray were studied in this paper. The animals suffered from acute radiation sickness of CNS form, intermediate form and intestinal form after 16000, 8000 and 4000 rads irradiation respectively. The nuclear shrinkage of the cerebellar granular cells was the most prominent change after irradiation. The cellular necrosis was found only in individural cells. The shrinkage of nucleus, different from necrosis, with characteristic ultrastructural features, tended to recover as manifested by the appearance of nucleolus, increase of free polysomes and well development of Golgi apparatus. It was considered that the cerebellar granular cells were rather resistent to, the radiation. Some pathological changes of small blood vessels in cerebellum were also observed, but was not responsible for the degeneration of the neurons.

Objective To construct a bait vector containing human glucocorticoid receptor(GR) ligand binding domain (LBD) in yeast two hybrid system in order to screen its cDNA library Methods PCR was used to amplify GR LBD fragment from the fetal liver cDNA library with the primers designed in accordance with the sequence in GenBank GR LBD The product was inserted into pGEM(r) T Vector Systems After verified with restriction endonuclease digestion of SmaⅠ/SalⅡ, the vector was inserted into the "bait plasmid" pGBKT7 (named as pGBKT7 GR LBD) After confirmation with restricted endonuclease digestion and sequence analysis, the plasmid was transformed into the yeast cell AH109, and the transformants were selected on SD/ Trp plates The interaction between GR and SRC 1 was tested by ? gal activity with yeast two hybrid system Results The amplified product of 893 bp was inserted into pGEM(r) T Vector and proven to be successful with double restriction enzyme digestion Sequence analysis revealed that the sequence was correctly inserted into pGBKT7 with a right reading frame AH109 [pGBKT7 GR LBD] grew on SD/ Trp plates, but not on the other selective media GR could interact with SRC 1 Conclusion The bait plasmid pGBKT7 GR LBD constructed expresses GR LBD correctly, and can't activate the transcription of reporter gene alone in yeast two hybrid system

Objective　To study the effect of glucagon-like peptide 2 (GLP-2) on mitogen-activated protein kinase (MAPK) activity in small intestinal epithelia in mice after radiation injury and its relation with the change of small intestinal epithelial proliferation. Methods　Mice were given a single dose of 8 Gy of total body 60Co gamma irradiation and then divided into GLP-2 and control groups. The activity of MAPK and proliferation rate in small intestinal epithelia were measured. Results　The activity of MAPK in small intestinal epithelia was higher in GLP-2-treated mice than in irradiated mice, and the proliferation rate in small intestinal epithelia significantly increased in GLP-2-treated mice. These two indices were of significantly positive correlated. Conclusion　GLP-2 can promote small intestinal epithelial proliferation in irradiated mice, and this may be related to activation of MAPK in small intestinal epithelia.

Objective　To investigate the effects of glucagon-like peptide 2 (GLP-2) on recovery of small intestinal epithelia from radiation injury in mice. Methods　Mice received a single 8 Gy dose of total body irradiation from 60Co gamma ray followed by treatment with GLP-2 or vehicle. DNA and protein content in small intestinal mucosa were measured, and small intestine was processed for histological examination with light microscope and scanning electron microscope. Results　Small intestinal mucosal DNA and protein content, villus height, and villus number significantly decreased in irradiated mice, partial villus tips were ulcerated. GLP-2 administration caused increase in DNA and protein content, villus height, and villus number as compared with irradiated control group. Meanwhile, the villus tips were lack of ulceration. Conclusion　GLP-2 can promote recovery of small intestinal epithelia from radiation injury in mice.

Objective　To study the effects of systemic irradiation and conglutinant drug W11-a12 on the number and some functions of wound nentrophils (Neu). Methods　Wound Neu was collected from sponges which were implanted in rat's dorsum incision. The number of Neu, as well as the phagocytic function and motility of wound Neu were measured. Results　After 4,6,8 Gy systemic irradiation, the number of white blood cells and Neu in wound, as well as the phagocytic function and chemotactic motility of wound Neu, were significantly decreased at 24 h, 48 h after wounding. W11-a12 markedly increased the number of wound Neu, improved the phagocytic function and chemotactic motility of wound Neu at 24 h, 48 h after wounding despite the rats were radiated or not. Conclusion　The results indicated that the decreased number and function of wound Neu in the early stage of wound healing contributed to the impairment of repair after systemic irradiation. W11-a12 accelerated normal and irradiation-impaired wound healing partly by increasing the number of wound Neu and improving the Neu function.