Objective To observe the morphologic characteristics of the post-traumatic cerebral infarction and discriminate it from brain contusion. Methods From 81 severe brain injury samples 15 were selected which met the criteria of the secondary necrosis and hemorrhage of brain. Another 15 simple brain contusion samples were selected as control. They were cut according to various requirements either coronary or saggittally or horizontally and observed grossly and histologically. Results The post-traumatic cerebral infarctions were found mainly in 5 localities: basal ganglia (3 cases), cingulate gyrus (2 cases), both cuneus of the occipital lobes (2 cases), lateral occipito-temporal gyrus (6 cases, 5 of them complicated with hemorrhage in the midbrain and pons), and occipital gyrus (2 cases). All of the infarctions were located not at the point of coup or contrecoup. They were localized and had clear boundaries. All of the lesions could be traced back to be related to brain hernia. Microscopically, there were extravasation of blood, and necrosis in the infarction, and usually severe congestion and edema with white blood cells infiltration and glia cell reaction. If the lesion was in the cerebrum, it was usually located at the junction of cortex and medulla, in severe cases extended to whole thickness of the cortex and the subarachnoid space, but the pia mater was not ruptured. There were marked ischemic and hypoxia changes in the neurons. The lesions of brain contusion, on the contrary, were always ruptured. The contused brain tissue may be necrotic. Conclusion The Post-traumatic cerebral infarction is synonymous with secondary necrosis and hemorrhage of the brain. The mechanism of the infarction is compression of intra-cerebral blood vessels due to cerebral hernia. It could be differentiated from cerebral contusion by the relation with cerebral hernia, the location of the lesion, the in-tactness of the pia mater, as well as other related histological changes.

[Summary] Considerable efforts have been made to understand the cellular and molecular mechanisms of metformin ,a potent antihyperglycemic agent now recommended as the first‐line treatment of patients with T2DM. The main effect of this drug is to reducethe hepatic glucose output ,primarily through inhibition of the mitochondrial respiratory chain complex Ⅰ and then activating AM P‐activated protein kinase (AMPK) ,which provide a generally acceptable mechanism for the action of metformin on hepatic gluconeogenesis. Beyond its effect on glucose metabolism ,metformin has been reported to improve ovarian function of patients with polycystic ovary syndrome (PCOS) and to reduce the risk of microvascular and macrovascular complications in patients with T2DM. In addition ,metfomin has also recently been suggested as an adjuvant treatment of cancer. Here we reviewed the progress of mechanism research and clinical application of metformin.

For the purpose of diagnosis of sudden manhood death syndrome, immu- nohistochemical study of ANP was performed in right atria of 10 cases of sudden manhood death syndrome (SMDS) and 10 cases of noncardiac death controls with LSAB-method. It was found that the ANP granulus in right atria of SMDS were obviously depleted, compared with that in the control groups. The results showed that depletion of ANP granules in atria plays an important role in the causes of death of SMDS. This experiment also provides a new approach for studying the causes of SMDS.

To explore the demarcation between the normal variation and the developemental anomaly of the cardiac conduction system (CCS). Using the method of sampling CCS designed by this research group, CCS of 737 cases died of non cardiac causes of death and 149 cases died of sudden cardiac deaths were sampled, serial sections were made, stained with HE method or Masson trichrome method,and observed under the light microscope.Results:(1)There were morphological variations in size, position and structure of normal human CCS; (2) In 4 cases died of sudden cardiac deaths, developemental anomalies were found in both AVN and HB. The morphological variations observed in our cases include: displacement of the bifurcation of HB into the pars membrancea of the interventricular septum,of the HB toward the left or the left lower sides of the interventricular septum or of less than 1/2 AVN into the central fibrous body , as well as of ordinary cardiomyfibers into the HB or BB. The developmental anomalies observed in our cases include: preservation of fetal type AVN in adults, displacement of whole AVN into the central fibrous body, complete division of HB into more than 3 bundles, and the displacement of the bifurcating portion of HB into the root of tricupid valves.

Objective To study the pathological changes related to cardiac sudden death. Methods The CCS from 179 cases with cardiac sudden death were examined histopathologically. Result There were 8 cases with hemorrhage, inflammation, or tumor infiltration in the cardiac nervous tissue or cardiac ganglion. Pathological changes such as edema, degeneration or necrosis could be found in the nervous tissue. However, no lethal pathological changes were observed out of cardiac nervous tissue. Conclusion Either primary or sencondary pathological changes in the cardiac nervous tissue might cause sudden death.

Objective To study the ultrastructural changes of gunshot wounds at the brain stem and the cause of the death. Method A case died of the head injury and two cases died of gunshot wounds of the brain stem were studied. Brain stem tissues were taken 25 min after death. Tissue blocks from the tegmentum of the midbrain and the pons as well as the gray matter of the medulla oblongata in the deep portion of the base of the fourth ventricle were taken and were examined with ultramicroscopy and scanning electron microscopy. Results (1) The gunshot wound injuries inside the brain including burn and injuries caused by punch and pressure; (2) Although the primary gunshot wounds were located at the midbrain, the pathological changes extended to the whole brain stem; (3)The injuries of the axons and the nerve cells were more severe and extensive than those of the glia fibers. (4)The changes of the burn included condensation and degeneration of the myelin sheath and axonal cytoplasm, especially the mitochondria as well as edema of the myelin sheath and the axonal cytoplasm. The punch and pressure injuries included the torsion, deformation, fusion, compression, breach, torn and displacement of the axons with loss of cytoplasm as well as the deviation of mitochondria, micro ?neuro - fibrils and micro - tubules in the axons. Conclusion The severe and extensive injuries of the axons of nerve fibers in the brain stem might play an important role in the cause of death of gunshot.

Objective Observe the injuries to the cranial nerves in cases of brain stem injury following head trauma;explore the mechanism of injuries and their relations to the mode and point of impact on the head. Method Brain stem specimens of 465 cases of head trauma were designed to take cross sections at the roots of the 3rd～12th cranial nerves. Among the 465 cases, 171 were proven to have contusion of the brain stem. On these cases, the cranial nerves were observed meticulously. Results Cranial nerve injuries were found in all cases suffering from brain stem contusion. The nerves included were: oculomotor nerve (120 cases, 70.2%), facial and acoustic nerve (92 cases, 53.8%), trigeminal nerve (85 cases, 49.7%), abducent nerve (45 cases, 26.3%), hypoglossal nerve (31 cases, 18.1%), vagus nerve (27 cases, 15.8%), glosso-pharyngeal nerve (24 cases, 14.0%), and trochlear nerve and accessory nerve (10 cases each, 5.8%). The nerve injuries may be unilateral or bilateral, involving single or multiple nerves in a case. The pathological changes included hemorrhage (42 cases, 24.6%), edema (26 cases, 15.2%), structural deformation at the root of the nerves (71 cases, 41.5%), tear of the nerve roots (32 cases, 18.7%). Conclusion Cranial nerve injury is an important part of the cranio-cerebral injury, and also an accompaniment of the brain stem injury. The features of interesting in the injuries were the higher frequencies in the nerves at the upper level and the nerves of larger diameter; of highest frequency were oculomotor nerve, facial nerve and acoustic nerve.

Three young men died of developmental abnormalities of the AVN,HB and BB were reported.The victims collapesed suddenly and died silently after excitation. A variety of abnormalities were observed in the AVCS including fetal the pattern of the AVN, the malformation of the AVN and thepresence of the accessory routes. The histopathological feature, the mechanism and the precipitatingfactors of sudden death were discussed.

Experimental studies on the myocardial ischemia and reperfusion injury in 16 anaethetized SDrats,of which,8 animals were pretreated with morphine(5 mg/kg,i.p.)for preventing of arrhyth-mias,were studied immunocytochemically with anti-muscle actin specific monoclonal antibody (HHF_(35)),8 shan-operated rats were used as control.With HHF_(35) ABC immunocytochemical method,the area of myocardial ischemia and reperfusion injury(without morphine)showed decrease or ab-sence of staining,large areas of staining loss were also seen.In the group with morphine,only smallfoci of staining absence were shown.The myocardium in control animals showed evenly positive stain-ing.No change were seen with HE staining in all groups.The results obtained with HHF_(35) stainingsupport its important value in studying on myocardic reperfusion injury,and indicated that the degreeof myocardic damage may be relative to the arrhythmias in myocardial reperfusion injury.

BACKGROUND:The method of ligating or resecting rat lower limb femoral or iliac artery has been widely used to make rat models of lower limb ischemia, but there have been no stable and efective methods used to establish diabetic models of chronic atherosclerotic occlusive diseases and to evaluate the ischemic status of hindlimbs of models. OBJECTIVE: To establish type 2 diabetes rat models of lower limb ischemia by feeding with high-fat diet and to evaluate them. METHODS:Twenty rats were randomly and evenly divided into diabetes group (n=10) and control group (n=10). Rats in the diabetes group were fed with high-fat diet for 6 months, and were intraperitonealy injected with streptozotocin (50 mg/kg) to induce diabetes. Rats in the control group were fed with normal diet for 6 months. Rats in these two groups were subjected to ligation of femoral artery to establish right lower limb ischemia models. RESULTS AND CONCLUSION:At the first day of modeling, color Doppler flow imaging and CT angiography showed obviously decreased blood flow suggesting the success of establishing ischemia model. At 7 and14 days after modeling, the blood flow of rats in these two groups showed a gradual recovery as detected by color Doppler flow imaging. At 28 days after modeling, blood flow of rats in the diabetes group was significantly slower than that in the control group (P < 0.05). CT angiography showed that at 28 days after modeling, only a smal amount of compensatory increase in blood flow of the blood vessels at the ligation position of proximal right lower limb femoral artery was seen in the diabetes group, while no obvious blow was observed in the distal part. Histopathologic and immunohistochemical staining showed that at 28 days after modeling, destroyed tissue structure and inflammatory cel infiltration were observed in the ischemic region and capilary density on the affected side was lower than that on the healthy side. The protein expression of vascular endothelial growth factor in the ischemic muscle tissue of rats in the diabetes group was significantly increased compared with that in the control group (P < 0.05). These results show that diabetic rat models of lower limb ischemia can be successfuly established by long term high-fat diet feeding and femoral artery ligation and they can be validated by CT angiography.