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.

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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.

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.

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. [

0.05).But the female offspring in exposure group showed weaker capability of spatial location compared with that of male offspring in exposure group(P

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 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.