Objective To monitor the protective qualities of personal protective appliances and to ensure the health and safety of radiological working personnel.Methods The lead-equivalent thickness of personal protective appliances and materials was measured by means of standard lead slices.The lead equivalent thickness represents in terms of mm Pb.Results 77 pieces of products and samples were measured altogether.The results indicate that the specific lead equivalents of lead-rubber plates were between 0.20-0.39 mm Pb/mm for 37 pieces of lead-rubber plates and the values of 6 pieces of samples were less than 0.25 mm Pb/mm,which did not accord with the requirement of the relational standard.27 pieces of personal protection appliances were measured altogether.They were 12 pieces of protective clothes,4 pieces of protective headgears,5 pieces of protective neckpieces,4 pieces of protective gloves and 2 pieces of protective masks.13 pairs of lead-glass spectacles among them were measured altogether.The measured results for personal protective appliances and lead-glass spectacles showed that actually measured lead-equivalent were higher than the nominal lead-equivalent.Conclusions The protective qualities are reliable for personal protection materials and appliances to be made in home and imported abroad.But the protective qualities of interventional protection gloves should be improved and made them better.

BackgroundEndostatin (ES) is currently the strongest endogenous angiognesis inhibitor,and it can inhibit the occurrence of neovascularization.Various studies demonstrated that the poly RGD sequence can enhance the function of the ES gene.ObjectiveThis study was to evaluate the use of gene therapy of modified ES for alkaline burn-induced corneal neovascularization (CNV).MethodsOne hundred and two clean SD rats were randomly divided into the normal control group,the pCI empty vector group,the pCI-ES group,and the pCI-RGDRGDES group.Corneal neovascularization models were established by placing a piece of 3 mm filter paper with 1 mol/L NaOH at the central cornea for 40 seconds.3 μg of the pCI blank vector,ES-tranfected pCI blank vector,or RGDRGD-ES-transfected pCI vector was injected into the superior bulbar conjunctiva after the alkali burn twice at 1-week intervals.Area of CNV and edema of the cornea in the various groups of rats were examined daily under the slit lamp biomicroscope.1,4,7 and 14 days after operation,the rats were sacrificed by the excessive anesthesia method and corneal tissues were obtained to evaluate pathological changes.The expression of CD34 in vascular endothelial cells was detected by immunochemistry to calculate the corneal neovascular density.The expressions of VEGF mRNA and Flk-1 protein in the corneas were detected by reverse transcription polymerase chain reaction (RT-PCR) and Western blot analysis.The use and maintenance of animals followed the Statement of ARVO.Results Seven to fourteen days after corneal alkali-burning,the corneal neovascular area was smaller in the pCI-ES group and pCI-RGDRGD-ES group compared with the normal control group and pCI blank vector group (P＜0.05,P＜0.01 ),and nevascular area in the pCI-RGDRGD-ES group was smaller than that in the pCI-ES group (P＜0.05).The expression level of CD34 was significantly lower in the pCI-ES group and pCI-RGDRGD-ES group than that in the normal control group and pCI blank vector group (P＜0.05,P＜0.01 ),and the expression level of CD34 was further declined in the pCI-RGDRGD-ES group compared with the pCI-ES group (P＜0.05 ).Compared with the normal control group and pCI vector group,the expressions of the Flk-1 protein and VEGF mRNA were decreased in the pCI-ES group and pCI-RGDRGD-ES group on the fourth day after corneal alkali-burning (P＜0.01,P＜0.05 ),and those in the pCI-RGDRGD-ES group were less than the pCI-ES group (P＜ 0.05,P＜ 0.05 ).Conclusions Subconjunctival injection of both ES and modified RGDRGD-ES genes result in significant suppression of CNV in vivo,and modified RGDRGD-ES appears to be more effective than native ES.The main mechanism of ES in inhibiting neovascularization is to downregulate the expression of VEGF and Flk-1.

Objective To observe the initial mechanism investigation in immune escaping correlated T cell proportion of Lewis lung cancer by Fuzheng-Peiyuan formula. To provide a theoretical basis for the application of the Chinese medicine of strengthening the body resistance in clinics. Methods The healthy C57BL/6J mice were divided into six groups by the random number table: the Chinese medicine group, the Chinese medicine plus chemotherapy group, the chemotherapy group, the model group and the normal control group. There were 6 mice in each group. All the groups expect the normal control group were inoculated subcutaneously with Lewis lung cancer cell suspension 0.2 ml. The medicine given to the Chinese medicine group were orally Fuzheng-Peiyuan formula with 8.17 g/kg. The combination group was given intraperitoneal injection of cyclophosphamide 60 mg/kg and orally Fuzheng-Peiyuan formula 8.17 g/kg. The chemotherapy group received the injection of cyclophosphamide 60 mg/kg and intragastric administration of normal saline. The model group and normal control group were administered with saline. After continuous administration for 13 days, the expressions of CD4, Foxp3, CD8 and CD28 in spleen cells of tumor bearing mice were observed by flow cytometry. Results Compared with the model group, the chemotherapy group and the chemotherapy combined with Chinese traditional medicine group showed that tumor weight (1.76 ± 0.42 g, 1.40 ± 0.43 g vs. 4.37 ± 0.59 g) significantly decreased (P<0.01); and the CD4+ Foxp3+ cells of mouse spleen cells in the Chinese medicine group and Chinese medicine plus chemotherapy group (11.25% ± 1.69%, 9.30% ± 2.68% vs. 14.21% ± 1.50 %) significantly decreased (P<0.05 or P<0.01). Conclusions The result initial proved that the Chinese medicine could strengthen the body resistance, adjust the proportion of Treg and CTL in spleen T cell in tumor-bearing mouse.

Adult ; Arachnoid Cysts ; complications ; Female ; Humans ; Intracranial Aneurysm ; etiology

Ischemic stroke leads to high potentiality of mortality and disability.The current treatment for ischemic stroke is mainly focused on intravenous thrombolytic therapy.However,ischemia/reperfusion induces neuronal damage,which significantly influences the outcome of patients with ischemic stroke,and the exact mechanism implicated in ischemia/reperfusion injury remains unclear,although evidence shows that oxidative stress is likely to be involved.Betulinic acid is mainly known for its anti-tumor and anti-inflammatory activities.Our previous study showed that betulinic acid could decrease the reactive oxygen species (ROS) production by regulating the expression of NADPH oxidase.Thus,we hypothesized that betulinic acid may protect against brain ischemic injury in the animal model of stroke.Focal cerebral ischemia was achieved by using the standard intraluminal occlusion method and reperfusion enabled after 2 h ischemia.Neurological deficits were scored.Infarct size was determined with 2,3,5-triphenyltetrazolium chloride monohydrate (TTC) staining and the mRNA expression of NADPH oxidase 4 (NOX4) was determined by RT-PCR in infarct tissue.ROS generation and apoptosis in ischemic tissue were analyzed by measuring the oxidative conversion of cell permeable 2',7'-dichloro-fluorescein diacetate (DCF-DA) to fluorescent dichlorofluorescein (DCF) in fluorescence microplate reader and TUNEL assay,respectively.In Kunming mice,2 h of middle cerebral artery (MCA) occlusion followed by 24 or 72 h of reperfusion led to an enhanced NOX4 expression in the ischemic hemisphere.This was associated with elevated levels of ROS generation and neuronal apoptosis.Pre-treatment with betulinic acid (50 mg/kg/day for 7 days via gavage) prior to MCA occlusion prevented the ischemia/reperfusion-induced up-regulation of NOX4 and ROS production.In addition,treatment with betulinic acid could markedly blunt the ischemia/reperfusion-induced neuronal apoptosis.Finally,betulinic acid reduced infarct volume and ameliorated the neurological deficit in this stroke mouse model.Our results suggest that betulinic acid protects against cerebral ischemia/reperfusion injury in mice and the down-regulation of NOX4 may represent a mechanism contributing to this effect.

Adult ; Female ; Hemangioma ; surgery ; Humans ; Laparoscopy ; methods ; Male ; Middle Aged ; Spleen ; surgery ; Splenectomy ; methods ; Splenic Neoplasms ; surgery

Objective To evaluate the analgesia effect of lornoxicam versus tramadol patient controlled analgesia in hepatocellular carcinoma patients treated with surgery .Methods A total of 54 hepatocellular car-cinoma patients who were scheduled for operation were included , 28 pa-tients received lornoxicam patients controlled analgesia with lornoxicam 96 mg+0.9% NaCl up to 150 mL.And 26 patients received tramadol patients controlled analgesia with tramadol 96 mg+0.9%NaCl up to 150 mL.The visual analogue scale ( VAS ) and bruggrmann comfort scale (BCS) were recorded in the time point of 4,12,24 and 48 h.The adverse event such as nausea , vomiting and dizziness were compared between the two groups.Results The VAS and BCS had no statistical difference between the two group in each of the time points ( P>0.05 ) . The adverse event incidence were 14.3% and 19.2% in the lornoxicam and tramadol group respectively with no statistical difference ( P>0.05 ) . Conclusion Both lornoxicam versus tramadol were effective in patient con-trolled analgesia for hepatocellular carcinoma patients treated with surgery .

OBJECTIVETo study the clinical features and mutations in methyl-CpG-binding protein 2 (MECP2) gene among children with classical Rett syndrome in China.

METHODSPCR and direct sequencing were employed to analyze the three exons of MECP2 gene in 9 children recently diagnosed with Rett syndrome and their parents.

RESULTSHeterozygous mutations were identified in 5 out of 9 patients, with a mutation rate of over 50%; there was one case of insert mutation (c.913insT) and 4 cases of missense mutation (exon 3: c.316C>T (R106W); exon 4: c.502C>T (R168X), c.808C>T (R270X), and c.1126C>T (P376S). A new mutation (c.913insT) was found. No mutations were detected in their parents. Two patients had MECP2 mutations in the transcriptional repression domain (TRD). They had almost lost language functions and were found to have significantly delayed development compared with other patients.

CONCLUSIONSMutations in MECP2 gene were detected in 5 confirmed cases of Rett syndrome, and most of them were on exon 4. Mutations in the TRD of MECP2 protein may affect the language ability and development in children with Rett syndrome.

Child, Preschool ; Female ; Humans ; Infant ; Language Development ; Methyl-CpG-Binding Protein 2 ; genetics ; Mutation ; Rett Syndrome ; genetics ; psychology

OBJECTIVETo investigate the protective effect of exogenous inhibitor of matrix metalloproteinases-9 (MMP-9), batimastat, in the lung injury induced by cardiopulmonary bypass (CPB) in dogs.

METHODSThirty healthy mongrel puppies were randomly divided into 3 groups: control group, low-dose group [batimastat 10 mg/(kg.d) for 3 days before operation] and high-dose group [batimastat 30 mg/(kg.d) for 3 days before operation]. The off-pump puppies' model of acute lung injury was established, and hemodynamic and respiratory parameters were monitored. The preoperative and postoperative alveolar-arterial oxygen difference (A-aDO(2)) and respiratory index (RI) were calculated. From the beginning of surgery, blood samples were taken at the time 0, 60, 120, and 270 min. Plasma concentrations of MMP-9 were measured by ELISA, and blood MMP-9 mRNA expressions were determined by RT-PCR. The myeloperoxidase (MPO) activity of centrifugal bronchoalveolar lavage fluid were measured by Colorimetry. And MMP-9 activity was determined by Gelatin zymography. Light and electronic microscope were used to observe the morphological changes of lung tissue. A small piece of left lung tissue was taken, weighed and baked to calculate the wet weight (W/D) index.

RESULTSAfter cardiopulmonary bypass, the concentrations of MMP-9 and mRNA expressions of the control group were increased significantly, and lung injury was apparent. At 270 min, the MMP-9 plasma concentration of high-dose group (17.36 +/- 1.18) microg/L was significant reducing than control group (30.47 +/- 2.22) microg/L (P < 0.05). After operation, A-aDO(2) and RI of high-dose group were significantly improved than control group (P < 0.05). The W/D index of the high-dose group (2.8 +/- 0.48) was significantly lower than that of control group (4.7 +/- 0.6) (P < 0.05). And the pathological changes of lung tissue were significantly improved in the high-dose group. However, there was no significant difference in the MMP-9 mRNA expression in three groups.

CONCLUSIONSBatimastat plays a role in the protection of the lung injury of CBP by reducing the concentration and activity of MMP-9, the degradation of the cell membrane and pulmonary neutrophil infiltration and reduction of pulmonary edema.

Acute Lung Injury ; etiology ; prevention & control ; Animals ; Cardiopulmonary Bypass ; Disease Models, Animal ; Dogs ; Lung ; pathology ; Matrix Metalloproteinase 9 ; metabolism ; Matrix Metalloproteinase Inhibitors ; Phenylalanine ; analogs & derivatives ; pharmacology ; Postoperative Complications ; prevention & control ; Thiophenes ; pharmacology

OBJECTIVESTo study the in vivo efficacy and the safety of cord blood derived CIK/NK cells stimulated by K562-dendritic cells (DC) fusion vaccines in NOD/SCID mice model for human erythroleukemia.

METHODSDC and CIK /NK cells were both derived from cord blood mononuclear cells. DC were fused with inactivated K562 leukemia cell by PEG to produce K562-DC fusion vaccines. K562-DC fusion vaccines were co-cultured with CIK/NK cells to prepare K562-DC fusion vaccine stimulated CIK/NK cells. NOD/SCID mice were inoculated with 1 x 10(6) K562 cells. 24 hours later, 1 x 10(7) vaccines stimulated CIK/ NK cells and 1 x 10(7) CIK/NK cells were transfused into the NOD/SCID mice. NOD/SCID mice without inoculation of K562 cells were used as control group. CD13 and CD56 positive cells were assayed by flow cytometry.

RESULTSAll the leukemia NOD/SCID mice without therapy died within 39 days, tumor was found in 5 of 8 mice. One of 8 leukemia mice treated with K562-DC fusion vaccines stimulated CIK/NK cells died at the 65th day, the anti-tumor response rate was 87.5%. Two of the leukemia mice treated with CIK/NK cells died at the 56th and 65th day respectively, the anti-tumor response rate was 75%. There was no significant difference in survival time between these two groups, and both survivals were longer than that of the control group. There was no significant difference in CD13 positive cells in the survival mice between these two groups, and both of that were less than that of the control mice. There was no significant difference in CD56 positive cells between the two treated groups and the control group.

CONCLUSIONSCord blood derived CIK/ NK cells stimulated by inactivated tumor cells retain the cytotoxicity and do not develop tumor in vivo.

Animals ; Cancer Vaccines ; immunology ; Cytokine-Induced Killer Cells ; immunology ; Cytotoxicity, Immunologic ; Dendritic Cells ; immunology ; Humans ; K562 Cells ; Killer Cells, Natural ; immunology ; Leukemia, Erythroblastic, Acute ; immunology ; Mice ; Mice, Inbred NOD ; Mice, SCID