Objective To meet an emergency of film development by automatic-manual X-ray film development machine when malfunction or power failure occurs.Methods The field dark room was made along with development and fixing baths.The film was developed artificially.Results Satisfactory films for limbs and chest were developed.Conclusion The equipment is easy to load,spread and operate.It can be used not only as assistant field film development equipment,but also as training equipment for field hygiene unit that isn't allotted automatic-manual X-ray film development machine.

Objective To study the concentrations of endocrine disrupting compounds in reclaimed water samples. Methods A solid-phase extraction (SPE)-gas chromatography (GC)-mass spectrometry (MS) analytical method was used for the separation and determination of endocrine disrupting compounds (EDCs) from water samples. The water samples were collected from each process of the reclaimed water plant of Tianjin, China. Important and contrasting EDCs including estrone (E1), 17?-estradiol (E2), 17?-ethynylestradiol (EE2), 4-tert-octylphenol (OP), 4-nonylphenol (NP), bisphenol A (BPA), di-n-butyl phthalate (DnBP), diisobutyl phthalate (DIBP), and di (2-ethylhexyl) phthalate (DEHP) were selected as the target compounds. C-18 solid-phase extraction (SPE) technique was used for the extraction recoveries of target compounds from water samples while ethyl acetate was efficient in eluting EDCs from SPE cartridges. After elution from the SPE column, the t-butyldimethylsilyl (TBS) derivatives of EDCs with N-methyl-N-(tertbutyldimethylsilyl) trifluoroacetamide (MTBSTFA) were analyzed by GC-MS in the selected ion mode (SIM). Results Concentrations of steroid hormones, phenolic compounds and phthalate esters ranged from not detected to 7.01 ng/L, 4.85 ng/L, and 0.03 ?g/L to 23.82 ?g/L, respectively. Conclusion Environmental endocrine disrupting compounds are not completely removed in the process of reclaimed water treatment and will be carried over into the general aquatic environment as it will be reused.

BACKGROUND: Previous studies suggest that vascular endothelial growth factor 121 may be an optimal target gene for thetreatment of acute myocardial infarction.OBJECTIVE: To investigate effect of direct myocardial injection of adenovirus recombinant human vascular endothelial growthfactor 121 gene (Ad-hVEGF121) on myocardial infracted rat heart structure, function and angiogenesis.METHODS: Totally 78 male SD rats were randomly divided into the sham-surgery (n=18), acute myocardial infarction (n=24),Ad-VEGF121 (n=19) and normal saline (n=17) groups. Among them, left anterior descending coronary arteries of the latter threegroups were ligated to prepare acute myocardial infarction models and rats were randomly selected to receive Ad-hVEGF12 ornormal saline via three points in the cardiac muscle at the 10-15 minutes after ligation. The chest was exposed without ligation inthe sham-surgery group.RESULTS AND CONCLUSION: At 2 weeks after injection, cardiac ultrasound showed that, compared with the sham-surgerygroup, the number of new capillaries, body weight and left ventricular mass / body weight of the acute myocardial infarction,Ad-hVEGF121 and normal saline groups were obviously increased (P < 0.05 or P < 0.01), especially those received transfectedrAd-hVEGF12, had higher density of blood capillaries than those of the normal saline and acute myocardial infarction groups.However, there were no obviously differences between each group in infarct size, cardiac structure or functions. The directmyocardial injection of Ad-VEGF121 can significantly promote the formation of new blood vessels within the myocardium.

OBJECTIVETo investigate the levels of IL-18 in the bone marrow of both normal subjects and patients with hematological diseases and to determine the possible significance of IL-18 in pathogenesis of some hematological malignancies.

METHODSThe IL-18 mRNA levels in the bone marrow of 140 patients with hematological diseases and 15 normal donors were determined by the semi-quantitative reverse transcriptase polymerase chain reaction (RT-PCR). Immunohistochemical method was used to detect IL-18 protein in 12 patients with acute myeloid leukemia (AML). The possible regulation of IL-18 for proliferation of some leukemia cells was investigated using antisense techniques.

RESULTSIL-18 mRNA levels were obviously higher in the patients with leukemia or other malignant hematological diseases (OMHD) than in normal donors. However, no significant difference was found in the level of transcription between patients with iron deficiency anemia (IDA) and normal controls. Immunohistochemical method confirmed the presence of IL-18 protein in 10 out of 12 AML cases with positive transcription. By 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay, IL-18 antisense oligodeoxynucleotides (ASON) clearly inhibited the growth of J6-1 and HL-60 cells (42% and 12% inhibited, respectively) in a dose-dependent manner.

CONCLUSIONSIL-18 was detected at elevated levels in the bone marrow of patients with some hematological malignancies, and might be involved in the proliferation of certain leukemic cells in vivo through an autocrine mechanism.

Adolescent ; Adult ; Bone Marrow ; metabolism ; Cell Division ; drug effects ; Dose-Response Relationship, Drug ; Female ; Humans ; Immunohistochemistry ; Interleukin-18 ; analysis ; antagonists & inhibitors ; genetics ; Leukemia ; drug therapy ; metabolism ; pathology ; Male ; Middle Aged ; Oligonucleotides, Antisense ; pharmacology ; RNA, Messenger ; analysis

Objective To clarify the role of nuclear factor κB(NF-κB) signaling pathway in pathogenesis of Kashin-Beck disease(KBD) by observing the expression of NF-κB p65 in the whole blood samples of patients with KBD and controls,and the expression of NF-κB p65 in C28/I2 chondrocyte, and to analyze the role of NF-κB p65 molecule in chondrocyte apoptosis. Methods Through a case-control study, 161 patients with KBD (KBD group) were selected from Xunyi, Yongshou, Changwu, Linyou, Qianyang and Long counties in KBD endemic areas and 312 healthy people(control group) were matched by age and sex in Shaanxi Province. Venous blood samples were collected from patients and healthy controls, which were anticoagulated and used for determination of NF-κB p65 protein.According to the group design,the model of C28/I2 chondrocyte oxidative damage was established.The experiments were divided into 4 groups including control group(C), tBHP injury group (O, tBHP 300.00 μmol/L), low selenium pre-protection group (OS1, 0.05 mg/L Na2SeO3+ 300.00 μmol/L tBHP), and middle selenium pre-protection group(OS2, 0.10 mg/L Na2SeO3+ 300.00 μmol/L tBHP). Then, cell apoptosis was detected by Hoechst 33342 and reactive oxygen species (ROS) was detected by dichlorfluorescein(DCF) method. The protein was extracted by Trizol method, then protein expression level of NF-κB p65 molecule was detected by Western blotting in whole blood samples and C28/I2 chondrocyte. Results The differences in age and sex were not statistically significant between KBD group and control group (t = 0.336, P > 0.05; χ2= 0.407, P > 0.05). The protein expression level of NF-κB p65 in KBD group was 1.835 times as high as that of control group (KBD:0.167 ± 0.026, control: 0.091 ± 0.014, t = 5.147, P < 0.01). Under the fluorescence microscope, chondrocyte showed strong blue fluorescence in tBHP group and the level of ROS(1.219 ± 0.104) was higher than those of low and middle selenium pre-protection groups(0.832 ± 0.077, 0.635 ± 0.070, P < 0.05).The protein expression level of NF-κB p65 in tBHP group (1.563 ± 0.351) was higher than that of control group (0.451 ± 0.069, P < 0.05), and protein levels of NF-κB p65 had a decreasing tendency in low and middle selenium pre-protection groups compared to tBHP group. Conclusion The NF-κB signaling pathway is up-regulated in KBD patients, moreover, chondrocyte experiments show that cell apoptosis is mediated via upregulation of NF-κB p65,which suggests NF-κB signaling pathway may play an important role in pathogenesis of KBD.

Objective To explore the effects of oxidative damage and selenium on the apoptosis of articular chondrocytes and the expression of selenoprotein genes.Methods C28/I2 chondrocytes were preincubated for 24 h,using sodium selenite (Na2SeO3) or t-butyl hydroperoxide (tBHP) for 24 h.The experiment was divided into six groups,including control group (C,0.00 mg/L Na2,SeO3 + 0.00 μmol/L tBHP),selenium beforehand protection group (S2,0.10 mg/L Na2SeO3),oxidative damage group (O,150.00 μmol/L tBHP),low dose selenium protection group (OS 1,0.05mg/L Na2SeO3 + 150.00 μmol/L tBHP),medium dose selenium protection group (OS2,0.10 mg/L Na2SeO3 + 150.00 μmol/L tBHP),and high dose selenium protection group (OS3,0.15 mg/L Na2SeO3 + 150.00 μmol/L tBHP).After 24 h,Hoechst 33342 staining method was used to observe apoptosis,mRNA expression of glutathione peroxidase 1 (GPX1),GPX4,deiodinase 2 (DIO2),DIO3,selenoprotein P (SEPP1),thioredoxin reductase 1 (TrxR-1) and selenoprotein W(Sel W) was detected by Real-time PCR,both experiments were done three times.Results Apoptotic rates of C,S2,O,OS1,OS2,OS3 groups [(0.78 ± 0.06)％,(13.61 ± 7.11)％,(92.27 ± 3.44)％,(71.38 ± 5.22)％,(44.31 ± 9.16)％,(72.46 ± 4.69)％] were compared between groups,the differences were statistically significant (F =120.10,P ＜ 0.01).The apoptotic rates of O group was significantly higher than that of C group (P ＜ 0.05);compared to O group,the apoptotic rates of OS1,OS2,OS3 groups decreased significantly (P＜ 0.05),OS2 group was the most obvious.DIO2,SEPP1,GPX1,GPX4,TrxR-1,Sel W mRNA levels were compared in the six groups,the differences were statistically significant (F =24.60,14.53,127.60,30.60,637.10,59.64,P ＜ 0.01).Compared to C group (1.00 ± 0.00),the mRNA levels of GPX1 (0.10 ± 0.05),GPX4 (0.43 ± 0.09),TrxR-1 (0.11 ± 0.05) and Sel W (0.72 ± 0.15) in O groups were decreased significantly (P ＜ 0.05);compared to 0 group,the mRNA levels of GPX1 in OS1 (0.20 ± 0.03),OS2 (0.74 ± 0.10),and OS3 (0.30 ± 0.07) were increased significantly (P ＜ 0.05).Conclusion Down-regulated expression of selenoprotein genes are involved in the regulation process of articular cartilage apoptosis caused by oxidative stress,selenium also has a regulatory role in selenoprotein gene expression in articular chondrocytes.