Objective To explore the protective effects of lycium barbarum polysaccharides(LBP) on fibroblast in vitro irradiated by ultraviolet A(UVA). Methods Taking the primary cultured fibroblast as objects, the fibroblast was irradiated by UVA ( irradiation intensity: 2.4 J/cm2). The fibroblast was randomly divided into six groups, control group, UVA radiated group and four protective groups(0.1 mg/ml LBP, 0.2 mg/ml LBP, 0.4 mg/ml LBP and 0.8 mg/ml LBP). The activities of cell proliferation were measured by MTT methods. The contents of MDA, the activities of SOD in the fibroblasts, and the activities of LDH in the supernatants of fibroblasts were determined by biochemical methods. Results The fibroblasts were irradiated by UVA (irradiation intensity: 2.4 J/cm2),the activities of cell proliferation was decreased,the activities of SOD was decreased too, the content of MDA and LDH increased. Compared with UVA irradiated group,in the given concentration,LBP could improve the activities of cell’s proliferation,improve the activities of SOD and decrease the contents of MDA in the cell, and decrease the content of LDH in the supernatants of cells significantly (P

Objective: To investigate the intervention effect of SB431542, which inhibits the TGF-β/Smad3 signaling pathway, on silicotic fibrosis in rats. Methods: A total of 40 specific pathogen-free Sprague-Dawley rats were divided into normal saline control group, model group, SB431542 inhibitor group, and SB431542 inhibitor control group using a random number table, with 10 rats in each group. All rats except those in the normal saline control group were given non-exposed single intratracheal instillation of free silicon dioxide dust suspension 1 mL (50 mg/mL) ; the rats in the SB431542 inhibitor group were given intraperitoneal injection of SB431542 (5 mg/kg) on days 7 and 30 after dust exposure, those in the SB431542 inhibitor control group were given intraperitoneal injection of SB431542 cosolvent (5 mg/kg) on days 7 and 30 after dust exposure, and those in the normal saline control group were given intratracheal instillation of an equal volume of normal saline (5 mg/kg). On day 60 after dust exposure, the paraffin-embedded section of the right upper lobe of lung was collected for HE staining; the left upper lobe of lung was collected to measure the mRNA levels of fibronectin (FN) , collagen type I (COL-I) , and collagen type III (COL-III) by quantitative real-time PCR; the right inferior lobe of lung was collected to measure the protein levels of FN, COL-I, COL-III, phosphorylated Smad3 (p-Smad3) , and Smad3. Results: Compared with the normal saline control group, the model group had nodules with various sizes in lung tissue, with rupture of some alveolar septa, emphysema changes, and pulmonary interstitial fibrosis, as well as significant increases in the mRNA expression of FN, COL-I, and COL-III and the protein expression of FN, COL-I, COL-III, p-Smad3, and Smad3 in lung tissue (P<0.05) . Compared with the SB431542 inhibitor control group, the SB431542 inhibitor group had a relatively complete structure of lung tissue without marked nodules and with a small amount of exudate in alveolar space and the lumen of bronchioles, as well as significant reductions in the mRNA expression of FN, COL-I, and COL-III and the protein expression of FN, COL-I, COL-III, p-Smad3, and Smad3 in lung tissue (P<0.05) . There were no significant differences in the mRNA expression of FN, COL-I, and COL-III and the protein expression of FN, COL-I, COL-III, p-Smad3, and Smad3 between the model group and the SB431542 inhibitor control group (P>0.05) . Conclusion SB431542 exerts an intervention effect on silicotic fibrosis by blocking the TGF-β/Smad3 signaling pathway and reducing the expression of the downstream fibrosis factors FN, COL-I, and COL-III.

OBJECTIVE: To investigate the factors for hydrocephalus secondary to severe traumatic brain injury after surgery, and to explore a new theory and guideline for clinical early prevention and treatment for hydrocephalus.
 METHODS: The clinical data regarding 107 patients with severe traumatic brain injury, who were admitted to our hospital from June 2010 to June 2013, were analyzed. Logistic multi-factor regression was used to analyze the different factors including ages, gender, the Glasgow coma scale (GCS) score before or after surgery, the situation of ventricular system bleeding secondary to surgery, the situation of midbrain aqueduct and ambient cistern before or after surgery, the relationship between early lumbar puncture and the hydrocephalus. The risk and protective factors for postoperative hydrocephalus were discussed.
 RESULTS: The results showed that patients with low GCS score in pre/postoperative (OR=0.099, 95%CI: 0.028-0.350)/(OR=0.088, 95%CI: 0.012-0.649), ventricular system bleeding in postoperative (OR=0.168, 95%CI: 0.029-0.979) and dim CT image for midbrain aqueduct and ambient cistern (OR=0.134, 95%CI: 0.038-0.473)/(OR=0.221, 95%CI: 0.055-0.882) are risk factors. Whereas lumbar puncture (OR=75.885, 95%CI: 9.612-599.122) is a protective factor for postoperative hydrocephalus in STBI patients. The secondary hydrocephalus was mainly occurred in 2 weeks and 2 weeks to 3 months after operation. The incidence of the control group that occurred secondary hydrocephalus is higher than that of the lumbar puncture group (P<0.05). The secondary hydrocephalus were mainly occurred in 2 weeks and 2 weeks to 3 months after operation, with no statistical significance between the 2 groups after 3 months of operation (P>0.05).
 CONCLUSION For patients with stable vital signs, early lumbar puncture could significantly reduce the incidence of secondary hydrocephalus in acute and subacute stage after severe traumatic brain injury.
Brain Injuries ; complications ; Cerebral Ventricles ; physiopathology ; Glasgow Coma Scale ; Humans ; Hydrocephalus ; etiology ; prevention & control ; Incidence ; Logistic Models ; Risk Factors ; Spinal Puncture ; Treatment Outcome

Background Long-term exposure to free silica particles will lead to fibrosis of lung tissue, and abnormal expression of microRNA (miRNA) may affect the occurrence and process of fibrosis. Objective To observed possible intervention effect of miR-204-3p overexpression adenovirus on silicosis fibrosis induced by silica dust using a silicosis rat model via non-exposed intratracheal instillation. Methods Forty SD rats were randomly divided into four groups: control group, silicosis model group, miRNA-NC group, and miR-204-3p intervention group. Under ether anesthesia, rats in the silicosis model group, miRNA-NC group, and miR-204-3p intervention group were injected with 1 mL (50 mg·mL⁻¹) of free silica dust suspension into the trachea, while the control group was injected with the same volume of normal saline. After 30 d of dust exposure, the miR-204-3p intervention group was injected with rno-mir-204 adenovirus vector to overexpress miR-204-3p, and the miRNA-NC group was given empty virus vector. After 30 d of normal feeding, the animals were sacrificed by chloral hydrate anesthesia, and the lung tissue was taken for subsequent experiments. The relative expression level of miR-204-3p in lung tissue of rats in each group was detected by real-time fluorescence quantitative PCR (RT-qPCR). HE staining, Masson staining, and Sirius red staining were used for pathological observation. Immunohistochemistry was used to detect the expression of Fibronectin and Collagen I in lung tissue of rats in each group. RT-qPCR was used to detect the relative gene expression levels of fibrosis markers Fibronectin, Vimentin, Collagen I, and Collagen III in lung tissue of rats in each group. Western blot was used to detect the protein expression levels of fibrosis markers Fibronectin, Vimentin, Collagen I, and Collagen III in lung tissue of rats in each group. Results The anatomical features of lung tissue in the control group were pink lung tissue with soft texture and smooth surface, while those in the silicosis model were grayish white tissue with hard texture and scars and grayish white silicon nodules on the surface. Compared with the silicosis model group, the color of lung tissue in the miR-204-3p intervention group became ruddy, the surface was smooth, and the texture became soft. The staining results showed that the alveolar wall of the control group was thin, there were a small number of capillaries in the alveoli, and the alveolar structure was clear and complete. In the silicosis model group, the alveolar wall became thicker, the pulmonary septum was partially broken, the alveolar structure was defective, and a large amount of collagen fibers were deposited. The alveolar structure of the miR-204-3p intervention group was relatively clear and there was a small amount of collagen fiber deposition. RT-qPCR results showed that compared with the control group, the relative expression levels of miR-204-3p in lung tissue of the silicosis model group and the miRNA-NC group were decreased (P<0.05), and the relative expression level of miR-204-3p in lung tissue of the miR-204-3p intervention group was increased (P＜0.05). The results of immunohistochemistry showed that compared with the control group, the expression levels of Fibronectin and Collagen I in lung tissue of the silicosis model group were increased (P＜0.05). Compared with the silicosis model group, the relative expression levels of Fibronectin and Collagen I in lung tissue of the rats in the miR-204-3p intervention group were significantly decreased (P<0.05). The results of RT-qPCR and Western blot showed that compared with the control group, the relative protein and gene expression levels of fibrosis factors Fibronectin, Vimentin, Collagen I, and Collagen III in lung tissue of the silicosis model group increased (P＜0.05). Compared with the silicosis model group, the relative gene and protein expression levels of fibrosis factors Fibronectin, Vimentin, Collagen I, and Collagen III in lung tissue of rats in the miR-204-3p intervention group were decreased (P＜0.05). Conclusion Silica dust can cause lung fibrosis in rats, and overexpression of miR-204-3P in vivo can reduce silicosis fibrosis in rats caused by silica dust.