To observe the injury process and pathological changes of the facial nerve,a primer was detonated at a distance of 10 cm from the face of each of 36 anesthelized dogs to simulate blast injury of the maxillofacial region. At the same time, a tangential wound of masseter was produced by a steel pellet fired with a musket to simulate a shrapnel injury. At different time points after injury, the action potential of the facial nerves was checke d and the pathological changes in axons and neurons of facial nerves were observed after HE and Nissle′s staining,respectively.One day after the injury,the facial nerve axons were found to be disrupted extensively,although the epineurium was still in continuity. There were degeneration and necrosis of neurons with infiltration of inflammatory cells in the facial nerve.One week later, the inflammation began to become milder, and the necrotic neurons were gradually absorbed. Four weeks later, the survived neurons appeared normal, and axons began to regenerate. Meanwhile, electromyography (EMG) showed that the action potential of facial nerve recovered. All the observations suggested that severe indirect injury to the facial nerve trunks in an explosive injury was the main pathological changes which involved an extensive area with severe damage in neurons.

This article discusses the necessity of the informatization construction and information of traditional Chinese medicine and its position and function in scientific research.Then from six aspects of infrastructure construction,information resource construction,information technology support,information personnel training,information and laws and regulations environment,and information resources product,this paper expounds the major tasks and constructive emphasis in each phase of scientific research informatization construction.Finally,this paper summarizes the prospect of TCM scientific research information construction and its role to the development of Chinese medicine.

Objective To investigate the apoptosis of Kupffer cell (KC) induced by lipsomal clodronate in rat with acute necrotizing pancreatitis (ANP). Methods Lipsomal clodronate was prepared by means of thin film, the model of ANP was established by injection of 5% sodium taurocholate of 4 ml/kg into the pancreatic capsule. The Kupffer cells were obtained from ANP rat. After exposure to different doses of lipsomal clodronate (0, 50, 100, 150 μl) , then the proliferation and apoptosis of KC was measured by MTT, flow cytometry and agarose gel electrophoresis of DNA. Results The prepared lipsomal clodronate had an average size of 100～200 nm, the spherical shape of liposome was uniform and confirmed by transmission electron microscope. When exposed to different concentration of lipsomal clodronate for 24 h, the growth suppression rate was 17. 4% , 24. 2% and 31. 1% , respectively, while the apoptosis rate of the KC was (14. 12 ±0.37)% , (18.74±0.43)% and (27.51 ±0.39)%, respectively; the difference was statistically significantly (P<0. 01) , the DNA of KC began degradation and gradually showed clear and characteristic ladder. Conclusions Lipsomal clodronate could induce apoptosis and suppress the growth of Kupffer cells in ANP rats.

Coloring Agents ; Diagnostic Uses of Chemicals ; Esophageal Neoplasms ; diagnosis ; Esophagoscopy ; Esophagus ; pathology ; Humans ; Iodine

OBJECTIVETo observe the impact of the JNK inhibitor XG-102 in a diet-induced rat model of non-alcoholic steatohepatitis.

METHODSForty-eight Sprague-Dawley male rats were subjected to a percutaneous superior mesenteric vein retention catheter operation and fed with a standard diet for 10 days, after which the rats were randomly divided into the following three groups: normal control (NC) group; high-fat (HF) model group; XG-102 treatment group. The HF group was fed an HF diet and treated with 0.9% sodium chloride for 16 weeks. The XG-102 group was fed an HF diet for 16 weeks and simultaneously treated with XG-102 (1 mg/kg) once per day for 4 weeks. The levels of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), total cholesterol (TC), triglyceride (TG), homeostasis model of assessment insulin resistance (HOMA-IR) and tumor necrosis factor-alpha (TNFa) were measured. Liver histological changes were observed. The protein expressions of phospho-c-Jun and cleaved caspase-3 were detected by western blotting.

RESULTSCompared with the NC group, the HF group showed significantly higher levels of serum ALT, AST, TC, TG, HOMA-IR and TNFa (P<0.05). Compared with the HF group, the XG-102 group showed significantly lower levels of serum ALT, AST, TC, TG, HOMA-IR and TNFa (P<0.05). The HF group also showed significantly higher protein expression of phospho-c-Jun and cleaved caspase-3 than the NC group (P<0.05) and the XG-102 group (P<0.05).

CONCLUSIONThe JNK inhibitor XG-102 may ameliorate lipid metabolism, reduce insulin resistance, decrease liver injury and inhibit hepatocytes apoptosis.

Alanine Transaminase ; Animal Feed ; Animals ; Aspartate Aminotransferases ; Caspase 3 ; Cholesterol ; Insulin Resistance ; Lipid Metabolism ; Male ; Non-alcoholic Fatty Liver Disease ; Peptides ; Protein Kinase Inhibitors ; Rats ; Rats, Sprague-Dawley ; Triglycerides ; Tumor Necrosis Factor-alpha

OBJECTIVETo understand the distribution of esophageal squamous cell cancer and precursor lesions in high-risk areas of China, and to provide evidence for determining the reference ranges of detection rates in high-risk areas.

METHODSEndoscopy with Lugol's iodine staining was performed on 15 709 local residents aged 40 to 69 years old in Linzhou of Henan province and Feicheng of Shandong province from 2005-2009. 35 cases without accurate pathology diagnosis and 11 cases with vital disease before screening were excluded. 15 663 subjects were enrolled in this study. Compliance was calculated by the percentage of the people who had endoscopic screening among the target population. Chi-square test and trend chi-square test were used to compare the distribution differences in age, gender and areas of esophageal squamous cell cancer and precancer. 95% CI of the detection rates was then employed to represent the reference ranges of esophageal squamous cell cancer and precursor lesions.

RESULTSThe compliance rate of screening endoscopy of this study was 49.36% (15 709/31 826) of all, and female's compliance (54.05%, 8 447/15 628) was much higher than that of male (44.83%, 7 262/16 198) (χ(2) = 88.14, P < 0.001). The detection rates of basal cell hyperplasia, low grade intraepithelial neoplasia, high grade intraepithelial neoplasia and esophageal squamous cell cancer of males were 4.17% (302/7 246), 17.22% (1 248/7 246), 1.67% (121/7 246), 0.83% (60/7 246), and were higher than that of females (3.45% (290/8 417), 14.82% (1 247/8 417), 1.41% (119/8 417), 0.48% (40/8 417), respectively). Except for high-grade intraepithelial neoplasia, the detection rates of male were higher than that of female (P values were 0.018, < 0.001, 0.960, 0.006). The detection rates of all grades of precursor lesions increased with age rising (all P values < 0.001), among which the detection rates of the mentioned four lesions for 40-44 years old were 2.69% (94/3 500), 8.11% (284/3 500), 0.40% (14/3 500), 0.14% (5/3 500), and that of 65-69 years old were 5.46% (46/843), 23.25% (196/843), 3.68% (31/843), 2.14% (18/843). The proportion of esophageal precursor lesion of Linzhou were higher than that of Feicheng observably except for esophageal squamous cell cancer (P values were < 0.001, < 0.001, < 0.001, 0.437). The detection rates of the four lesions of Linzhou and Feicheng were 4.90% (504/10 287), 17.37% (1 787/10 287), 1.79% (184/1 0287), 0.60% (62/10 287) and 1.64% (88/5 376), 13.17% (708/5 376), 1.04% (56/5 376), 0.71% (38/5 376). The 95% CI of detection rates of various lesions were, 3.78% (3.48%-4.08%) for basal cell hyperplasia, 15.93% (15.37%-16.50%) for low-grade intraepithelial neoplasia, 12.31% (11.79%-12.82%) for mild dysplasia and 3.62% (3.33%-3.91%) for moderate hyperplasia, 1.53% (1.34%-1.72%) for high-grade intraepithelial neoplasia and 0.64% (0.51%-0.76%) for esophageal squamous cell cancer, respectively.

CONCLUSIONUp to 21.88% residents that were asymptomatic were suffered from esophageal squamous cancer or precursor lesions in high-risk areas in China. The distribution of esophageal squamous cell cancer and precursor lesions was closely related to the gender and the age, which suggested that males were supposed to be paid more attention to.

Adult ; Age Distribution ; Aged ; Carcinoma, Squamous Cell ; epidemiology ; China ; epidemiology ; Endoscopy ; Esophageal Neoplasms ; epidemiology ; Female ; Humans ; Iodides ; Male ; Middle Aged ; Precancerous Conditions ; epidemiology ; Sex Distribution

OBJECTIVE: To summarize the research progress on the role of macrophage-mediated osteoimmune in osteonecrosis of the femoral head (ONFH) and its mechanisms. METHODS: Recent studies on the role and mechanism of macrophage-mediated osteoimmune in ONFH at home and abroad were extensively reviewed. The classification and function of macrophages were summarized, the osteoimmune regulation of macrophages on chronic inflammation in ONFH was summarized, and the pathophysiological mechanism of osteonecrosis was expounded from the perspective of osteoimmune, which provided new ideas for the treatment of ONFH. RESULTS: Macrophages are important immune cells involved in inflammatory response, which can differentiate into classically activated type (M1) and alternatively activated type (M2), and play specific functions to participate in and regulate the physiological and pathological processes of the body. Studies have shown that bone immune imbalance mediated by macrophages can cause local chronic inflammation and lead to the occurrence and development of ONFH. Therefore, regulating macrophage polarization is a potential ONFH treatment strategy. In chronic inflammatory microenvironment, inhibiting macrophage polarization to M1 can promote local inflammatory dissipation and effectively delay the progression of ONFH; regulating macrophage polarization to M2 can build a local osteoimmune microenvironment conducive to bone repair, which is helpful to necrotic tissue regeneration and repair to a certain extent. CONCLUSION At present, it has been confirmed that macrophage-mediated chronic inflammatory immune microenvironment is an important mechanism for the occurrence and development of ONFH. It is necessary to study the subtypes of immune cells in ONFH, the interaction between immune cells and macrophages, and the interaction between various immune cells and macrophages, which is beneficial to the development of potential therapeutic methods for ONFH.
Humans ; Femur Head/pathology* ; Osteonecrosis/therapy* ; Macrophages/pathology* ; Inflammation ; Femur Head Necrosis/pathology*