Objective To investigate the effects of insulin resistance (IR)on hypoxia/reoxygenation (H/R)inj ury in PC1 2 cells and the protective effects of N-actyl-L-cystine (NAC)against H/R inj ury. Methods PC12 cells were treated with 100 nmol/L insulin to induce IR. The H/R injury model was established by Na2 S2 O4. CCK-8 assay was used to detect the cell viability. Glucose consumption was detected by glucose oxidase method. Activity of superoxide dismutase (SOD)was detected by xanthine oxidase method. The levels of malonaldehyde (MDA)were measured by thiobarbituric acid method. Flow cytometry was used to determine the apoptosis and mitochondrial membrane potential (MMP). Results High-insulin inhibited insulin-induced glucose uptake in PC12 cells without affecting the cell viability (P<0. 05). PC12 cells with IR exhibited lower SOD activity and higher levels of MDA (P<0. 05 ),and enhanced apoptosis and depolarization of MMP induced by H/R(P<0. 05). NAC neutralized these effects induced by IR(P<0. 05). Conclusion IR aggravates H/R injury in PC12 cells by enhancing oxidative stress and NAC reduces the H/R injury in PC12 cells with IR via inhibiting oxidative stress and stabilizing MMP.

Intracortical distribution of arteries were studied on thick sections prepared from brains of 11 newborns after injection and fixation. The results are as follows.1. Branches from the cerebral arteries form a pial arterial network on the cortical surface. The larger pial arteries are supplied with vasa-vasorum and perivascular vessels. They send out cortical and medullary arteries penetrating the cortex vertically from the surface.2. The distribution of arteries in the entire cortical area can be represented by the pattern observed in a single gyrus, which serves as a general rule. The cortical arteries arising from the pial arteries penetrate into the cortex vertically and are arranged regularly which appear as a brush border that curves with the cerebral surface in sections. The diameter of the long cortical arteries is 16～31 ?m, while that of the short ones is 7.5～15.4 ?m. All these arteries send out branches at right angles which anastomose with one another to form a dense polygonal or irregular vascular network.The medullary arteries pass directly through the cortex into medulla. The diameter of the long medullary arteries is 48～61 ?m and that of the short ones, 35～47 ?m. Those entering from the top of each gyrus pass directly to the deep medulla, whereas those from the sulcus to the junction between the cortex and medulla exhibit various degrees of curvature. The medullary arteries send out branches at right angle, which, in turn, form T-shaped bifurcations, interconnecting each other in an oblong lattice framework.3. The central arteries penetrate the base of the brain, fan out and arch upward to reach the corpus striatum. Arteries may penetrate into the thalamus from posteriolateral, inferio-medial or superior surface. They branch with acute angles and form dense network with polygonal, triangular, circular and irregular interspaces. The arteries of the internal capsule also branch at right angles, show "T" bifurcations after a short distance and form an oblong vascular network.

For the study of venae cerebri profundae of the Chinese, 50 previously fixed adult cerebral hemispheres and 11 brains of the newborn were investigated. The adult cerebral hemispheres were dissected under the stereoscopic microscope. All the 11 brains of the newborn were treated within 24 hours after death. Six percent gelatin solution containing 6% vermilion was injected into arteria carotis interna while a mixture of Indian ink with 3% gelatin was injected into vena jugularis interna. The specimens were fixed, sectioned into slices of 1～3 mm thick, cleared and observed under stereoscopic microscope. The findings were summarized as follows:1. vena cerebri interna was mostly formed by the continuation of v. thalamostriata superior after it curved inward and backward. In 38.00%?6.86 of the cases it united with v. choroidea superior and v. septi pellucidi at the site of the curvature. In 32.00%?6.6 it didn't receive any veins. In 12.00%?4.60 it united with v. septi pellucidi and 80.00%?3.84 with v. choroidea superior, while other occurrences were rare.In 80.00%?5.66 of the cases, Vena cerebri interna took its course at the posterior margin of the interventricular foramen. The rest started at the anterior one third (12.00%?4.60)and middle one third (8.00%?3.84) of the thalamus respectively.The source, position and course of v. thalamostriata superior, v. choroidea superior, v. septi pellucidi and v. ventriculi lateralis medialis were observed and described.2. v. basalis was formed by the union of the v. cerebri anterior, v. cerebri media profunda and v. ventricularis lateralis inferior. 70% of v. cerebri anterior emptied into v. basalis whereas the other 30% into the adjacent venous sinuses. v. cerebri media profundae, most of which received vv. thalamostriata inferior, emptied into v. basalis in 68.00%?6.60 cases and the adjacent venous sinuses in 32.00%?6.60 v. ventricularis lateralis inferior emptied into v. basalis in 96.00%?2.77 cases and into v. cerebri magna in 2.00%?1.98, while in 2.00%?1.98 it was absent.3. The longitudinal anastomotic vein. was formed by the "T" shaped bifurcations of the small branches of v. thalamostriata superior, v. septi pellucidi and v. ventricularis lateralis medialis in the white matter within an area of 2 mm by the lateral angle of the lateral ventricle. It received numerous radially arranged small veins in the medulla of the cerebral hemisphere. The longer ones of these veins might extend to the cortex and anastomoses between them and superficial cortical veins were demonstrated.

AIM: To investigate the effect of suberoylanilide hydroxamic acid (SAHA) on the apoptosis of hu-man small-cell lung cancer H446 cells and its possible mechanism.METHODS: H446 cells were incubated in the medi-um containing SAHA.CCK-8 assay was used to detect the anti-tumor effect of SAHA on the H446 cells, and IC50 values of SAHA were calculated.Flow cytometry was used to analyze the apoptosis.After Notch3 gene was silenced, the pro-apopto-tic effect of SAHA on the H446 cells was inhibited ( P <0.05).Eukaryotic expression plasmid containing N3ICD was transfected into the H446 cells, so that N3ICD was expressed in the H446 cells.The mRNA expression of Notch3 was measured by RT-PCR.The protein levels of Notch3, N3ICD, Puma and cleaved caspase-3 were determined by Western blot.RESULTS: SAHA remarkably reduced the cell viability in a dose-dependent manner (P <0.05), and the IC50 value of SAHA was 1.91 μmol/L.SAHA induced apoptosis in a dose-dependent manner (P <0.05).The expression of Notch3 gene was negative in the H446 cells, SAHA reactivated Notch3 gene and Notch3 pathway in a dose-dependent manner (P <0.05).Notch3 knockdown inhibited apoptosis induced by SAHA (P <0.05).Over-expression of N3ICD up-regula-ted the protein levels of Puma and cleaved caspase-3.CONCLUSION: SAHA induces apoptosis in human small-cell lung cancer H446 cells by activating Notch3 pathway and up-regulating the protein level of Puma.

Ginseng root saponins ( GRS ) was extracted from native ginseng.The dosage used was calculated according to the content of saponins.Immunosuppression in mice was induced in 15 days after implar- ting Ehrlich ascites carcinoma (EAC) subcutaneously in armpit, and in 5-11 days after implanting EAC into peritoneal cavity. GRS administered orally 50mg/kg- for 8 days did not prevent the atrophy of the thymus in tumor-bearing mice but rather aggravated it. GRS administered orally 50mg/kg for 14 days partially restored the suppressed phagocytosis of peritoneal macrophages in tumor-bearing mice. GRS administered orally 50mg/kg for 6 days somewhat restored the suppression of hemolysin formation in tumor-bearing mice 5 days after implanting EAC, But GRS given in the same route and dosage for 9 days, showed no effect on the suppression of hemolysin formation. GRS administered orally 50mg/kg for 10 days partially restored the suppression of delayed hypersensitive reaction in tumor-bearing mice.

ObjectiveTo investigate the mechanism and effect of Qingfei Paidu decoction on transient receptor potential vanilloid-1/Transient receptor potential ankyrin1 （TRPV1/TRPA1） based on heat-sensitive channel and inflammatory response. MethodAccording to body weight， 80 8-week-old C57BL/6 mice were randomly divided into the normal group， model group， dexamethasone group （5 mg·kg^-1）， and low-dose， medium-dose， and high-dose groups of Qingfei Paidu decoction （14.865， 29.73， 59.46 g·kg^-1）， with 12 mice in each group. In addition to the normal group， the other groups were administered 20 μL （1×10^-3 g·kg^-1） to each mouse by airway infusion to establish the acute lung injury （ALI） model. In the administration group， the drug was given 1 h after modeling and again after an interval of 24 h. The lung tissue was taken 36 h after modeling. Double lung wet/dry weight ratio（W/D）， hematoxylin-eosin （HE） staining， enzyme-linked immunosorbent assay （ELISA）， and Western blot were used to observe and detect the pathological changes of lung tissue， expression levels of inflammatory cytokine tumor necrosis factor-α （TNF-α） and interleukin-6 （IL-6）， and expressions of TRPV1 and TRPA1 proteins in heat-sensitive channel， nuclear factor kappa-B （NF-κB）， inhibitor of NF-κB （IκBα） in inflammatory pathway， and phosphorylated proteins. The phosphorylated protein/total protein ratio was calculated. ResultCompared with that in the normal group， the lung tissue of mice in the model group was seriously damaged， and pulmonary capillary permeability increased. Alveolar capillary congestion and dilation destroyed the complete structure of the alveolar， and the alveolar wall thickened. A large number of inflammatory cells and red blood cells were infiltrated， and pulmonary edema was significantly aggravated. The expressions of TNF-α， IL-6， TRPV1， TRPA1， phosphorylated NF-κB p65/NF-κB p65， and phosphorylated IκBα/IκBα were significantly increased （P<0.01）， and the whole lung W/D was significantly increased （P<0.01）. Compared with the model group， the dexamethasone group and low-dose， medium-dose， and high-dose groups of Qingfei Paidu decoction could significantly improve pulmonary edema. TNF-α， IL-6， TRPV1， TRPA1， lung tissue NF-κB p65， and IκBα phosphorylated protein/total protein ratio decreased significantly （P<0.05， P<0.01）. The whole lung W/D also decreased significantly （P<0.05， P<0.01）. ConclusionQingfei Paidu decoction has anti-inflammatory and protective effects on LPS-ALI mice， which can effectively reduce inflammation， induce diuresis， and alleviate edema. Its mechanism may be related to the regulation of the expression of TRPA1 and TRPV1 and the inhibition of the activation of the NF-κB pathway.

Objective To observe the clinical effect of repairing the defect after extended resec-tion of lower lip cancer by modified lip and cheek fan-shaped flap .Methods Six cases of lower lip cancer were treated .The defect of the lower lip was about 1/3-1/2 after 1 cm of enlarged resection outside the margin of the mass .The defect was repaired with modified lip and cheek fan-shaped flaps . The morphology and function were observed 3-36 months after operation .Results All patients healed in one stage ,and the shape and function of lower lip recovered well without complications .Conclusions Lower lip defect about 1/3-1/2 of patients with modified lip and cheek fan-shaped flap is an ideal method of restoration and reconstruction ,with satisfactory results after surgery .

OBJECTIVE: To explore the genetic basis for a child with mental retardation. METHODS: Whole exome sequencing was carried out for the child. Candidate variant was screened based on his clinical features and verified by Sanger sequencing. RESULTS: The child was found to harbor a c.995_1002delAGACAAAA(p.Asp332AlafsTer84) frameshift variant in the SYNGAP1 gene. Bioinformatic analysis suggested it to be pathogenic. The same variant was not detected in either parent. CONCLUSION The c.995_1002delAGACAAAA(p.Asp332AlafsTer84) frameshift variant of the SYNGAP1 gene probably underlay the mental retardation in this child. Above finding has expanded the spectrum of SYNGAP1 gene variants and provided a basis for the diagnosis and treatment for this child.
Child ; Humans ; Intellectual Disability/genetics* ; Frameshift Mutation ; High-Throughput Nucleotide Sequencing ; Computational Biology ; Heterozygote ; Mutation ; ras GTPase-Activating Proteins/genetics*

Objective:To explore the mechanism of miR-205-5p/E2F1 signal axis in regulating the glioma U251, U87 radiotherapy resistance.Methods:X-ray gradual ascending and intermittent induction method was used to irradiate the glioma U251 cells to establish U251/TR, U87/TR radiation-resistant cell lines. Then, the morphology, migration, invasion and proliferation abilities of cells (U251/TR, U87/TR radiation-resistant cells and U251, U87 radiation-sensitive cells) were analyzed. Luciferase gene detection system and point mutation technique were employed to analyze the mechanism of miR-205-5p and E2F1 gene activity on U251 and U87 radiation-resistant cell lines.Results:Compared with the radiation-sensitive U251 cells, the radiation-resistant cells U251/TR, U87/TR showed increased proliferation activity, enhanced migration and invasion abilities and decreased apoptosis under X-ray irradiation. miR-205-5p mimics transfection could down-regulate the expression of E2F1 factor in U251/TR cells, inhibit cell proliferation, invasion and migration and increase the radiosensitivity of U251/TR cells. miR-205-5p mimics transfection combined with with E2F1 down-regulation exerted anti-tumor effect and decreased cell tolerance by suppressing the Wnt/β-catenin signaling pathway activity.Conclusions:The glioma radiation-resistant cell line U251/TR, U87/TR can be established by X-ray gradual ascending and intermittent induction method. The miR-205-5p/E2F1 signal axis exerts tumor-suppressing effect through the classical Wnt/β-catenin signaling pathway, which can be used as an therapeutic target to increase the radiosensitivity of glioma.

Objective:To examine the outcome of off-pump coronary artery bypass (OPCAB) in elderly patients with left ventricular dysfunction.Methods:From June 2008 to July 2016, 252 patients aged over 80 years underwent isolated OPCAB at Department of Cardiovascular Surgery, Beijing Anzhen Hospital, Capital Medical University, these patients′ data were collected. The left ventricular dysfunction group (ejection fraction (EF): 35% to 50%) was comprised of 31 patients aged (82.0±2.1) years (range: 80 to 88 years), including 25 males and 6 females. Through matching one-to-one on propensity scores, 31 patients (EF >50%) were included into the left ventricular normal group. Among them, there were 25 males and 6 females, aged (81.9±1.9) years (range: 80 to 89 years). Postoperative mortality and complications between the matched groups were compared using the t test, Wilcoxon rank-sum test, χ 2 test or Fisher exact test. Results:Between the dysfunction group and normal group, the preoperative serum creatinine was 144.6(66.0) μmol/L vs. 94.9(43.2) μmol/L ( M( Q R), Z=3.177, P=0.033), respectively, while the pre-discharge serum creatinine was 147.0(59.0) μmol/L vs. 92.0(24.0) μmol/L ( Z=-2.685, P=0.007), respectively. In dysfunction group, the perioperative intra-aortic balloon counterpulsation (IABP) utilization rate was higher (25.8%(8/31) vs. 3.2%(1/31), P=0.026), the total hospitalization day was longer (17(15) days vs. 14(8)days, Z=2.054, P=0.012), the preoperative hospitalization day was longer too (7(7) days vs. 5(4) days, Z=-2.457, P=0.014). However, there was no significant difference in the incidence of postoperative mortality (9.7%(3/31) vs. 3.2%(1/31), P=0.612) and other prognostic indicators between the two groups. Conclusions:The elderly patients, with light and moderate left ventricular insufficiency, are characterized by the abnormal increase in renal function and the rise of IABP utilization due to hemodynamic disorder in OPCAB perioperative period. Preoperative treatment for cardiac insufficiency may be the cause of prolonged preoperative and total hospital stay. However, there is no significant difference in the postoperative mortality and other complications compared with the patients of normal left ventricular function.