Objective:　To explore the correlation between cognition disorder and morphologic change of hippocampal neurons after traumatic brain injury (TBI). 　　Methods:　Wistar rat models with severe TBI were made by Marmarous method. The histopathological change of the neurons in the hippocampus area were studied with hematoxylin-eosin (HE) staining and terminal deoxynucleotidyl transferase-mediated X-dUPT nick end labeling (TUNEL), respectively. The cognitive function was evaluated with the Morris water maze test.　　Results:　The comprehensive neuronal degeneration and necrosis could be observed in CA2-3 regions of hippocampus at 3 days after injury. Apoptotic positive neurons in CA2-4 regions of hippocampus and dentate gyrus increased in the injured group at 24 hours following TBI. They peaked at 7 days and then declined. Significant impairment of spatial learning and memory was observed after injury in the rats. 　　Conclusions:　The rats have obvious disorders in spatial learning and memory after severe TBI. Meanwhile, delayed neuronal necrosis and apoptosis can be observed in the neurons in the hippocampus area. It suggests that delayed hippocampal cell death may contribute to the functional deficit.

Objective:　To investigate the spatial and temporal profile of neural cell apoptosis following traumatic brain injury (TBI).　　Methods:　In addition to morphological evidence of apoptosis, TUNEL histochemistry assay was used to identify DNA fragmentation in situ at both light and electron microscopic levels, whereas characteristic internucleosomal DNA fragmentation of apoptosis was demonstrated by DNA gel electrophoresis.　　Results:　Using TUNEL method, we detected massive cells with extensive DNA fragmentation in different regions of the brains of rats subjected to experimental traumatic brain injury. Compared with the sham controls, in the injured cortex, the apoptotic cells were detectable for up to 24 h and reached a peak at 1 week after injury. The number of apoptotic cells in the white matter had a significant increase as early as 12 h after injury and peaked at 1 week. The number of apoptotic cells increased in the hippocampus at 72 h, whereas in the thalamus, the peak of apoptotic cells was at 2 weeks after injury. The number of apoptotic cells in most regions returned to sham values 2 months after injury. Gel electrophoresis of DNA extracted from affected areas of the injured brain revealed only internucleosomal fragmentation at 185-bp intervals, a feature originally described in apoptotic cell death. And no DNA ladder was detectable in the cortex and hippocampus contralateral to the injured hemisphere.　　Conclusions:　These data suggest that in addition to the well described necrotic cell death, a temporal course of apoptotic cell death is initiated after brain trauma in selected brain regions.

Objective:　To investigate the characteristics of bone fractures from road traffic accidents and analyze their injury mechanisms so as to provide reference for the research and medical care of traffic trauma.　　Methods:　Three hundred and six patients with fractures from road traffic accidents were included into this study. A total of 507 fractures were identified and the injury mechanism, location distribution and frequency were analyzed. 　　Results:　The most common location of fractures was the lower extremities, followed by the upper extremities, skull and maxillofacial region, and the rarest was the spine. A total of 56% of the patients suffered from multiple fractures. The fractures of the patella, femur and pelvis and the fractures of the olecranon, humerus and shoulder often happened simultaneously.　　Conclusions:　The injury mechanisms can be classified into four types: impact, incoordinate movement, stretch injury and crush and extrusion. The fractures from traffic accidents have the following characteristics: centrifugal distribution of the injuries, multiple fractures, force transmission and ipsilateral occurrence.

Objective:　To observe the change of nitric oxide (NO) levels in the blood and the morphological change of the muscles in the limbs of rats during the (IR) injury and after being intervened by L-arginine (L-Arg) and L-nitroarginine (L-NNA).　　Methods:　Sixty-six male Sprague-Dawley (SD) rats were used and grouped into the normal controls, the sham injury controls, the IR injury group and the intervention groups (L-Arg group and L-NNA group). After 6 hours of ischemia, followed by reperfusion for 3, 12 or 24 hours, the samples in the IR injury group were obtained. The rats in the intervention groups were given L-Arg (100 mmol/L) and L-NNA (10 mmol/L), respectively, through the abdominal cavity. Then the anterior tibial muscle in the right limb was obtained for histological examination, the anterior tibial muscle in the left limb for ultrastructure observation and the blood for assay of NO in all the rats. NO was assayed by indirect measurement of NO2/NO3 with Griess method. 　　Results:　There was no significant difference of NO between the normal controls and the sham injury controls (P>0.05). But NO significantly decreased in the IR injury group (P<0.01), and further decreased with reperfusion (P<0.01) and reached the lowest point at 12 hours after reperfusion. The level of NO in the L-Arg group was significantly higher than that in the IR injury group (P<0.01), but was not significantly different from that in the controls (P>0.05). In the L-NNA group, NO decreased to the undetectable level (P<0.01). Histological examination and ultrastructure observation showed the muscles were normal in the control groups. After 6 hours of ischemia, the skeletal muscles displayed injuries, and they were most severely injured after 12 hours of reperfusion. In the L-Arg group, the skeletal muscles were less injured, while in the L-NNA group, the injury was similar to that in the IR injury group. 　　Conclusions:　When the limbs of the rats sustain IR, NO in the blood decreases. Meanwhile, the muscles in the limbs are injured. When L-Arg is given, NO in the blood is restored and the muscles are protected. When L-NNA completely inhibits NO, no protection of the muscles is shown.

Objective:　To study the changes of partial pressure of oxygen in brain tissue (PbtO2) and brain temperature (BT) in patients in acute phase of severe head injury, and to study the effect of mild hypothermia on PbtO2 and BT. 　　Methods:　The PbtO2 and the BT of 18 patients with severe head injury were monitored, and the patients were treated with mild hypothermia within 20 hours after injury. The rectal temperature (RT) of the patients was kept on 31.5-34.9℃ for 1-7 days (57.7 hours±28.4 hours averagely), simultaneously, the indexes of PbtO2 and BT were monitored for 1-5 days (with an average of 54.8 hours±27.0 hours). According to Glasgow Outcome Scale (GOS), the prognosis of the patients was evaluated at 6 months after injury. 　　Results:　Within 24 hours after severe head injury, the PbtO2 was significantly lower (9.6 mm Hg±6.8 mm Hg, 1 mm Hg=0.133 kPa) than the normal value (16-40 mm Hg). After treatment of mild hypothermia, the mean PbtO2 increased to 28.7 mm Hg±8.8 mm Hg during the first 24 hours, and the PbtO2 was still maintained within the range of normal value at 3 days after injury. The BT was higher than the RT in the patients in acute phase of severe head injury, and the difference between the BT and the RT significantly increased after treatment of mild hypothermia. Hyperventilation (the partial pressure of carbon dioxide in artery (PaCO2)≈25 mm Hg) decreased the high intracranial pressure (ICP) and significantly decreased the PbtO2. 　　Conclusions:　This study demonstrates that PptO2 and BT monitoring is a safe, reliable and sensitive diagnostic method to follow cerebral oxygenation. It might become an important tool in our treatment regime for patients in the acute phase of severe head injury requiring hypothermia and hyperventilation.

Objective:　To investigate the gene expression of two kinds of constitutive nitric oxide synthase (cNOS): neuronal NOS (nNOS) and endothelial NOS (eNOS) in injured spinal cord tissue.　　Methods:　Thirty-six adult Sprague-Dawley rats were divided randomly into six groups: the normal group and the injury groups (2, 6, 12, 24, 48 h after injury, respectively). A compression injury model of the spinal cord was made and gene expression of nNOS and eNOS were examined by reverse transcription polymerase chain reaction (RT-PCR).　　Results:　The gene expression of nNOS and eNOS was detected in the normal group and they were up-regulated quickly after injury, reaching the maximum at 6 h. There was no difference between gene expression of nNOS and eNOS in the normal group, but in each injury group the gene expression of eNOS was much higher than that of nNOS.　　Conclusions:　Expression of constitutive NOS (cNOS) in spinal cord tissue was up-regulated after injury mainly in the early stage. cNOS as a whole offers protection in spinal cord injury, but different cNOS may play different roles.

Objective:　To investigate the diagnosis and treatment of renal trauma. 　　Methods:　Retrospective analysis of 298 patients with renal trauma was carried out. Among them, 272 (91.3%) had blunt renal injuries and 26 (8.7%) had penetrating injuries; 123 (41.3%) had multiple complicated intraabdominal injuries and 56 (18.8%) had concomitant shock. Normal-dose-IVU examination was used in 39 patients and double-dose-IVU in 44 patients, ultrasonography in 109 patients, and CT in 45 patients. Conservative and supportive therapy was done in 193 patients (64.8%) and operation in 105 patients (35.2%). 　　Results:　The positive rate was 48.7% by the normal-dose-IVU examination and 90.9% by double-dose-IVU, 78.8% by ultrasonography, and 95.6% by CT. One hundred and eighty-three patients were cured by conservative therapy and 101 by operation. Fourteen patients died. 　　Conclusions:　B-ultrasound can be conveniently used for primary assessment of renal injuries, while CT shows rapid, accurate and proper condition of a renal trauma patient. The treatment depends on the severity of the injury. The conservative therapy is employed in most cases which present slight or moderate injury and no evident massive bleeding. Severe injury requires surgical exploration. The operative approach is by using a transabdominal incision, which makes it relatively easy to explore intraabdominal organs and control the injured kidney. It is also very important to control shock and prevent other severe complications in the early stage of the treatment.

Objective:　To compare the results of femoral head replacement (FHR) and total hip replacement (THR) in treatment of subcapital femoral neck fractures (SFNF). 　　Methods:　Between May 1987 and July 1998, 56 elderly patients (65-90 years; average 73.5 years) with SFNF were treated with prosthetic replacement. Six cases were treated with unipolar FHR, 18 cases with Bateman bipolar FHR, and 32 cases with Bateman bipolar THR. All domestic prostheses were installed with cement. 　　Results:　There was no significant difference between the 2 groups in operating time and blood transfusion. Forty-nine patients were followed-up for an average of 5 years and 10 months. No wound infection or death was related to surgery. Complications in Group FHR were significantly higher than that in Group THR. 　　Conclusions:　Since FHR is difficult to fit the bony acetabulum, it is only indicated for senile cases with poor conditions. However, the bipolar THR installed with cement is indicated for most elderly patients. Since the femoral head and acetabulum can fit each other completely, it is more stable for taking weight-bearing earlier with less complications.

Objective:　To compare the outcome of non-operative treatment with the outcome of surgical intraventricular drainage for patients with posttraumatic hydrocephalus including complications, mortality and favorable outcome.　　Methods:　Thirty-nine patients were assigned to a nonoperative treatment group and 38 patents to a surgical intraventricular drainage group. Each patients outcome was evaluated 3 years after treatment by using Glasgow Outcome Scale. 　　Results:　In the nonoperative treatment group the rate of favorable outcome (good recovery or mild disability) was 89.74% (35 of 39 patients) and the mortality was 2.56% (1 of 39 patients). In the surgical intraventricular drainage group the rate of favorable outcome was 71.05% (27 of 38 patients) and the mortality was 13.16% (5 of 38 patients; P<0.05). Mortality was not significantly different between the two groups. 　　Conclusions:　 Nonoperative treatment may be better than surgical intraventricular drainage for patients with posttraumatic hydrocephalus.

Objective:　To study the mechanism of macrophage injury after trauma-hemorrhagic shock.　　Methods:　Wistar male rats underwent trauma (closed bone fracture) and hemorrhage (mean arterial blood pressure of 35 mm Hg±5 mm Hg for 60 minutes, following fluid resuscitation). Rats without trauma, hemorrhage or fluid resuscitation served as controls. Peritoneal macrophages were harvested at 6 hours and 1, 2, 3, 7 days after traumatic hemorrhagic shock to determine the effects of pertussis toxin (PTX, as a specific inhibitor to Giα) and cholera toxin (CTX, as a stimulant to Gsα) on macrophage-Ia expression and TNF-α production and levels of Giα and Gsα. 　　Results:　The macrophages from the injured rats revealed a significant decrease of Ia positive number and TNF-α release in response to LPS. With pretreatment with PTX 10-100 ng/ml Ia positive cells and LPS-induced TNFα production in both control and impaired macrophages populations were dose-dependently increased. Both macrophages populations were not responding to CTX treatment (10-100 ng/ml). Western blot analyses showed that the levels of Giα protein expression increased as much as 116.5%-148.8% of the control level from 6 hours through 7 days after traumatic hemorrhage. The levels of Gsα protein expression were reduced at 6 hours and decreased to the lowest degree; 36% of the control at day 1, began to return at day 2 and returned to the normal level at day 7, following traumatic hemorrhagic shock.　　Conclusions:　PTX-sensitive G-protein may participate in the modulation of macrophage-Ia expression and TNF-α release following traumatic hemorrhagic shock. Analyses of the alteration of Giα and Gsα protein expressions further supports the concept that G-protein is involved in trauma-induced macrophage signal transduction pathways.

Objective:　To observe dynamic changes of intracellular calcium (［Ca2+］i) after spinal cord injury, and to study the relationship between the changes of ［Ca2+］i and the functional damage of the spinal cord.　　Methods:　The rats were subjected to a spinal cord contusion by using a modified Allens method. The ［Ca2+］i in the injured segment of the spinal cord was measured by the technique of La3+ blockage and atomic absorption spectroscopy at 1, 4, 8, 24, 72, and 168 hours after injury. The motor function on the inclined plane was measured at the same time.　　Results:　The spinal cord ［Ca2+］i increased significantly (P<0.05 or P<0.01) after spinal cord injury. There was a significant correlation (P<0.05) between the changes of ［Ca2+］i and the motor function. 　　Conclusions:　［Ca2+］i overload may play an important role in the pathogenesis of spinal cord injury.

Objective:　To investigate the apoptosis rules of the astrocytes and oligodendrocytes induced by Ca2+ reperfusion. 　　Methods:　The apoptosis of purified cultured astrocytes and oligodendrocytes induced by Ca2+ reperfusion and the relationship between the development of the cell apoptosis and post-reperfusion time was observed. 　　Results:　Both the astrocytes and oligodendrocytes were obviously in a time-dependent fashion, and the apoptosis ratios of the oligodendrocytes (39.73%±4.16%) were higher than the astrocytes (19.64%±4.67%) 24 hours after Ca2+ reperfusion. The TUNEL positive cells were 13.6±1.82 and 21.4±1.95 at every visual field of astrocytes and oligodendrocytes respectively 24 hours after Ca2+ reperfusion.　　Conclusions:　The astrocytes and oligodendrocytes are similar with the development rules on apoptosis and have different susceptiveness to the situation.

Objective:　To explore the effect of homeobox B2 (HOXB2) antisense oligodeoxynucleotides (asodn) on the proliferation and expression of primary human umbilical vein endothelial cells (HUVECs). 　　Methods:　Various concentrations of HOXB2 asodn modified by thiophosphate transfected the induction of liposome into HUVECs. MTT and RT-PCR methods were employed to determine the effect of different concentrations of asodn on the endothelial proliferation and the expression level of HOXB2 mRNA.　　Results:　After the transfection of HOXB2 asodn, the endothelial proliferation was inhibited in a dose-dependent fashion. Simultaneously, the expression of HOXB2 mRNA decreased significantly.　　Conclusions:　HOXB2 plays an important role in the proliferation of endothelia.

Lipopolysaccharide (LPS), or endotoxin, is the major component of the outer surface of gram-negative bacteria. LPS is a potent activator of the cells of the immune and inflammation systems, including macrophages, monocytes and endothelial cells, and contributes to systemic changes seen in septic shock.1,2 It has long been believed that LPS is responsible for several fatal consequences of gram-negative infection. Cell activation by LPS constitutes the first step in the cascade of events believed to lead to the manifestation of gram-negative sepsis, which results in approximately 20 000 annual deaths in the United States3 and 30% mortality rate of known cases in China.Therefore, the action mechanism of LPS is one of the most important problems in the research field of immunity, inflammation and surgery. Researchers have investigated the mechanism of cell activity and injury of LPS for a long time. In 1990, CD14，the glycosyl-phosphatidylinositol (GPI)-linked plasma membrane protein, was identified as a proximal LPS receptor on the cell surface of macrophages, and it was suggested that CD14 and LBP (lipopolysaccharide binding protein) played an important role in the effect mechanism of LPS. CD14 seemed to receive LPS via transfer from the plasma protein LBP. Then, two action patterns were recognized. CD14 positive cells, such as macrophages and leukocytes, were activated after LPS combined with LBP and interacted with CD14. But, CD14 negative cells (for example, endothelial cells), were activated through other receptors that we did not know of in the cell surface after LPS, LBP and soluble CD14 (sCD14) combined with the compounds. However, there are some questions to be answered. Firstly, because CD14 lacks cytoplasmic doman, it is unlikely to act as the transducer. Secondly, the action pattern of LPS through CD14 and LBP may be in dose-dependent mode, but, in conditions of high dosage and long exposure to LPS action, CD14 and LBP do not play an important role in LPS activation effect. Finally, for CD14 negative cells, the receptor combined LPS-LBP-sCD14 compound has not yet been identified. Some details indicated that a “co-receptor” for LPS signal transduction must exist. Although standard biochemical approaches, transfection assay, and immunologic tacties were all employed to search for this co-receptor, it has not yet been found. The find of Toll-like receptor 4 (TLR4) provides a new opportunity to study the mechanism of LPS action.