Objective To investigate the sensitivity and specificity of transcranial Doppler (TCD) diagnosis for intracranial posterior circulation artery stenosis or occlusion.Methods Seventy-two cases of patients treated for posterior circulation intracranial artery stenosis or occlusion were chosen,TCD and CT angiography (CTA) tests were carried out and the results were compared and analyzed.Results Compared with CTA,the sensitivity for period of posterior circulation intracranial arteries by TCD was 82.50％,while specificity reached 94.64％.Positive predictive value attained 91.67％,while negative predictive value reached 88.33％ and the accuracy was 89.58％.Conclusions TCD diagnosis for period of posterior circulation intracranial arterial has high specificity,normal sensitivity,and the highest diagnosis accuracy for intracranial segment of vertebral artery.TCD can serve as early inspecting method for intracranial artery.

Objective:To revise the Psychological Security-insecurity Questionnaire(S-I) developed by Maslow and examine its reliability and validity.Methods:Data were collected from 1893 junior middle school students with the original S-I.Results:The revised S-I consisted of 44 items,including 10 first-order factors and 3 second-order factors.It had good test-retest reliability,homogeneity reliability and criterion validity.Conclusion:The revised S-I has satisfying reliabilities and validities,and is suitable to asses the psychological security and insecurity for Chinese junior school students.

Objective To analyze the factors of Protein A/G affinity column,influencing purification effect,and get the best condition to improve application effect of Protein A/G affinity column. Methods We Purified anti-HCV-IgG serum with different disposal modality,different sample input modality and different application number of affinity column before detecting and analyzing the purified samples. Results The Protein A/G affinity column had the best purified effect after using saturated ammonium sulfate to first purification,which increased the affinity column adsorption effect within 30 minutes adsorption. Conclusion Using antibody with first purification and adding the adsorption time could improve utilization rate of affinity column and prolong the service life.

Objective To evaluate the middle-term effect of laparoscopic uterine artery occlusion combined with ascendant myomectomy (LUAO-M) for multiple uterine myomas. Methods The uterine artery was isolated and occluded with Kleppinger bipolar forceps (Sabre 2400,ASPEN LABS USA) or PK forceps (Gyrus Medical Limited Inc UK) under a laparoscope. Then dissection was performed on the surface of pseudo capsule with Kleppinger unipolar needle (Sabre 2400,ASPEN LABS USA) or PK needle (Gyrus Medical Limited Inc UK),and the target myoma was stripped out of the tumor bed with the Separate-Scoop device. Afterwards,repair of the incision was carried out in one layer with interrupted single stitch by Absorbable VICRYL suture (Johnson VICRYL ETHICON USA). Results The mean operation time was (102?36) min and mean blood loss was (88.7?58.4) ml. The mean hospital stay after the operation was (7.9?0.2) d,and febrile morbidity was 5.1% (5/98). Complications included two cases of subcutaneous emphysema and one case of ileus;no other severe complications occurred. Of the patients,98 cases were followed-up for 21 to 52 months (mean,36.3 months),during the period they were visited by a mean of 3.6 times,which showed a correction rate of menstruation abnormality of 95.9% (4/98),rate of uterine volume reduction of 57.7%,and rate of recurrent myoma of 3.1% (3/98). Conclusion LUAO-M shows a good clinical outcome and middle-term effect for multiple uterine myomas.

We reported a simple and fast fluorescence system based on quantum dots ( QDs ) to detect glutamate dehydrogenase ( GLDH) , which inverted glutamate to α-ketogrutarate using NAD+ as a coenzyme. The fluorescence of CdTe QDs was quenched by nicotinamide adenine dimucleotide ( NAD+) through an electron transfer pathway, and the quencher NAD+ could be consumed by adding NAD+-dependent enzymes and corresponding substrates. Based on this principle we introduced GLDH to consume NAD+ in the QDs/NAD+ system, leading to the enhancement of the fluorescence intensity of QDs, which was in proportional to the amounts of GLDH added. Using this fluorescence system, we measured GLDH in a wide concentration range from 10 U/L to 1000 U/L, which was of significance in clinical diagnosis of different kinds of liver diseases.

BACKGROUND:Cel membrane microparticles CD31 and CD54 lead to microvascular injury in the femoral head by mediating vascular inflammatory response, promoting blood clotting, affecting vasomotion and promoting vascular endothelial injury. Studies have verified that membrane particles play an important role in steroid-induced necrosis of the femoral head, but there is no studies concerning relationship between microparticles and alcohol-induced avascular necrosis of femoral head. METHODS/DESIGN:This is a randomized control ed animal study. Healthy male Wistar rats wil be randomly assigned to two groups. In the model group, rats wil be intragastrical y administered hard liquor for 6 consecutive months to prepare models of alcohol-induced avascular necrosis of the femoral head. Blank controls wil be intragastrical y given an equal volume of physiological saline. In 1-6 months of intervention, six rats wil be randomly selected from each group every month. Blood wil be col ected separately. Flow cytometry wil be used to detect serum cel membrane particles CD31, CD54 levels. Bilateral femoral head wil be fixed, decalcified, embedded in wax, and then sections. After hematoxylin-eosin staining, empty bone lacuna wil be quantified under a light microscope to identify femoral head necrosis. Verhoff’s staining and MSB microthrombosis staining wil be used to observe microvascular injury and microvascular thrombosis in the femoral head, and to analyze the correlation of CD31 and CD54 levels with femoral head necrosis, vascular endothelial injury and microvascular thrombosis. DISCUSSION:This study wil investigate the effects of CD31 and CD54 on alcohol-induced avascular necrosis of the femoral head, explore the pathogenesis of alcohol-induced avascular necrosis of the femoral head, provide a new theoretical basis for early diagnosis and early treatment, and may provide a new target for its treatment. ETHICS APPROVAL:The protocol has been approved by the Animal Experimental Ethics Committee of Inner Mongolia Medical University (approval number YKD2016154). Experimental procedures and materials of rats wil be in accordance with the Guide for the Care and Use of Laboratory Animals, which is consistent with the guide of National Institutes of Health. Subject headings:Femur Head Necrosis;Membrane Proteins;Tissue Engineering

BACKGROUND:The relationship between long-term heavy drinking and alcohol-induced necrosis of the femoral head has long been clear, but thepathogenesis of alcohol-induced necrosis of the femoral head is currently not fuly understood.
OBJECTIVE:To establish a rat model of alcohol-induced avascular necrosis of femoral head and to study its pathogenesis.
METHODS: Eighty Wistar rats were randomly divided into experimental and control groups (40 rats per group). Rats in the experimental group were intragastricaly administered strong wine 10 mL/kg, once a day, for 6 consecutive days. Rats in the control group were given physiological saline 10mL/kg, once a day, for 6 consecutive days. Bilateral femoral heads were randomly colected from six rats every month for histomorphological observation.
RESULTS AND CONCLUSION:(1) Osteonecrosis: in the experimental group, at 3 months, trabecular bone became thin, arranged disorderly, and the number of empty lacuna began to increase. At 6 months, typical osteonecrosis appeared, and vacant lacunaes increased significantly. In the control group, trabecular bone was complete and neatly arranged. Osteocytes were visible in bone lacuna, and normal morphology of cels was seen. (2) Injury of blood vessels: in the experimental group, at 3 months, micro-intimal hyperplasia was observed. Elastic fibers of partial vascular endothelium were reduced. Elastic fiber andmiddle-layer smooth muscle breakage and proliferation were found. At 6 months, above manifestations were more remarkable. In the control group, arteriole film was not thickened, and vessel wal was normal. (3) Formation of microthrombus, in the experimental group, the number of microthrombus was increased at 3 months, and became significant at 6 months. In the control group, the number of microthrombus was not altered. (4) Results indicated that chronic alcohol intake can lead to microvascular endothelial injury in the rat femoral head. Abnormal blood microcirculation was detected in local region, and resulted in avascular necrosis of the femoral head. The degree of necrosis was associated with alcohol intake.

Objective To analyze the role of cysteinyl aspartate specific proteinase-1 (caspase-1) in a mouse model of D-galactosamine (D-GalN) and lipopolysaccharide (LPS) induced acute liver failure (ALF) and to study the possible mechanism. Methods C57BL/ 6 mice were randomly divided into four groups including control group, Z-WEHD-FMK (caspase-1 inhibitor) treatment group, ALF model group and Z-WEHD-FMK-treated ALF group. The mouse model of ALF was established by intraperitoneally injec-ting the mice with D-GalN (450 mg/ kg) and LPS (10 μg/ kg). The damages in liver tissues were evaluated based on the histopathological examination and the levels of alanine transaminase (ALT) and aspartate trans-aminase (AST) in serum samples. Western blot assay was performed to analyze the expression of caspase-1 and the phosphorylation of glycogen synthase kinase 3β (GSK-3β). The qRT-PCR was used to measure the expression of inflammatory cytokines at transcriptional level. Results The expression of caspase-1 at both mRNA and protein levels were gradually increased during the development of ALF. Compared with the mice with ALF, those in the Z-WEHD-FMK-treated ALF group showed less severe liver damages on histopatholog-ical examination and decreased levels of ALT and AST in serum samples [ALT: (479. 2±39. 5) U/ L vs (998. 5±60. 4 ) U/ L, P<0. 05; AST: ( 478. 5±28. 6) U/ L vs ( 1 180. 7±91. 4) U/ L, P<0. 05]. The expression of TNF-α, IL-1β, IL-18 and IL-33 at transcriptional level were significantly suppressed in mice with ALF upon the Z-WEHD-FMK intervention. Results of the Western blot assay indicated that Z-WEHD-FMK suppressed the activities of GSK-3β by enhancing its phosphorylation. Conclusion This study demon-strated that caspase-1 could promote the activation of GSK-3β resulting in the development of inflammation responses and liver damages during the development of ALF in mice.

Objective To investigate the effects of peroxisome proliferator-activated receptor α( PPARα) on macrophage-mediated inflammatory responses with the interference of lipopolysaccharide and the possible mechanism.Methods The bone marrow stem cells were isolated from the femora of mice.The granulocyte-macrophage colony stimulating factor ( GM-CSF) was used to stimulate the in vitro differentiation from bone marrow stem cells into primary macrophages.An in vitro model with cultured cells expressing in-flammatory cytokines was established by treating the primary macrophages with lipopolysaccharide ( LPS) .A specific chemical agonist, Wy-14643, was used to activate PPARα. Autophagy inhibitors including 3-methyladenine (3-MA) and small interfering RNA against Atg7 ( Atg7 siRNA) were used to inhibit the autophagy.Western blot assay was performed to detect the expression of autophagy-related proteins ( Atg5, Atg7, Beclin-1 and LC3).The transcriptional levels of TNF-α, IL-1β, IL-6, Atg5, Atg7 and Beclin-1 were analyzed by qRT-PCR.Results Compared with the macrophages treated with LPS alone, those pretreated with various concentrations of Wy-14643 (10 μmol/L, 25 μmol/L and 50 μmol/L) showed inhibited ex-pression of proinflammatory cytokines ( TNF-α,IL-1βand IL-6) and enhanced expression of autophagy-relat-ed proteins (Atg5, Atg7 and Beclin-1) at mRNA level in a dose-dependent manner.The expression of auto-phagy-related proteins (Atg5, Atg7, Beclin-1 and LC3) by macrophages was promoted with the pretreatment of Wy-14643 as indicated by Western blot assay.The transcriptional levels of TNF-α, IL-1βand IL-6 were increased in Wy-14643 pretreated-macrophages after stimulation with 3-MA or Atg7 siRNA .Conclusion PPARαsuppressed the macrophage-mediated inflammatory responses by promoting autophagy, suggesting that the PPARα-autophagy pathway might be one of the signaling pathways regulating LPS induced-inflamma-tory responses.

[ ABSTRACT] AIM:To investigate the effects of sulindac on oxidative stress in autism.METHODS:With an au-tistic model induced by prenatal exposure to valproic acid ( VPA) , we detected the expression of the signaling molecules of canonical Wnt pathway in the prefrontal cortex ( PFC) and hippocampus ( HC) of autistic rats treated with sulindac.The protein expression levels of glycogen synthase kinase 3β(GSK-3β), β-catenin and 4-hydroxynonenal (4-HNE) were ob-served by Western blotting.The mRNA expression of thioredoxin(Trx)1 and Trx2 was assessed by semi-quantitative RT-PCR.RESULTS:The protein level of GSK-3βand mRNA levels of Trx1 and Trx2 were lower, whereas the protein expres-sion levels ofβ-catenin and 4-HNE were higher in VPA group than those in control group.In contrast, the protein levels of GSK-3βwere significantly higher in the animals treated with both VPA and sulindac than those in VPA group, while the lev-els ofβ-catenin and 4-HNE were decreased.CONCLUSION:Sulindac attenuates oxidative stress in the pathogenesis of au-tism, suggesting the up-regulation of the Wnt/β-catenin signaling pathway disrupts oxidative homeostasis and further facili-tates susceptibility to autism.