Objective To investigate the occupational hazards of nurses in the supply room,to determine what kind of occupational hazards is most dangerous,and accordingly put forward some suggestions of protective measures.Methods Totally 208 nurses from supply rooms of 4 general hospitals were surveyed with questionnaires.The data of occupational hazards were analyzed.Results Various kinds of occupational hazards happened among nurses in the supply room,and among all occupational hazards,physical damage was the most frequently happened.Conclusions The occupational protection awareness of nurses is relatively weak.They can not properly handle damages caused by occupational hazards,so sufficient attention should be given to it.

Waste plastics in the environment is called"gray pollution"as a result of difficult degradation and when dis-posed by incineration,secondary pollutants are released.In this paper the formation mechanism and path of some persistent or-ganic pollutants in the process of waste plastic incineration disposal and their potential hazards to the ecological system,even to human beings are briefly reviewed,and valuable references and suggestions are given.Some of effective measures which should be taken to inhibit the formation of these toxic organic compounds during waste disposal and reduce their negative effect on mankind.

Objective To study the effects of embryonic neural stem cells transplantion on trauma of red nucleus neu-rons of the rats with spinal cord injury.Methods NSCs in logarithmic phage were labeled with BrdU,a Sprague Dawley rat mode of spinal cord injury (SCI) was developed with electrocircuit control spinal cord injuring device.Thirty SD rats were randomly divided into three groups: sham group,SCI group and NSC group.The NSCs were trans-planted into injured site three days after SCI.Then NSCs labeled with Brdu were detected by immunohistochemisty,rubrospinal tract (RST) neurons were labeled by retrograde transport of the horseradish peroxidase (HRP) from the lesion site,which were taken by damaged axons and remained in the neurons,then the labeled red nucleus (RN) neurons were counted.Hind limb function of experimental rats was evaluated by a blinder observer using BBB open field locomotion rating score.Results BrdU positive NSCs were detected in the spinal cord after transplantation,the number of RST neurons labeled by HRP in NSC group was more than that in SCI group (P <0.01),the BBB score of NSC group was higher than SCI group (P <0.01).Conclusion The transplanted NSCs can survive in the injured site of spinal cord and protect RN,then promote more remarkably functional recovery after SCI.

Objective To analyze the relationship between CT characteristics of chronic subdural hematoma (CSDH) and its recurrence, as well as relevant pathological mechanism. Methods The study involved 178 patients with CSDH who underwent surgery, of whom 38 patients (40 lesions) experienced recurrence of CSDH. Univariate and multivariate logistic analyses were performed to assess the correlation among CT characteristics ( including side, density, width, subtype and midline shift of the hematoma) and CSDH recurrence. Results ( 1 ) The width of hematoma, midline shift, type of hematoma were found to be correlated with the recurrence of CSDH in the univariate analysis. The odds ratio (OR)and 95% confidence interval (CI) value of patients with hematoma width ＞30 mm, midline shift ＞10 mm and the separated type were 18. 400 (2.024-167. 301 ), 4. 643 ( 1. 815-11. 877 ) and 14. 385 (3. 601-57.467 ), respectively. (2) The midline shift and type of hematoma were found to be correlated with the recurrence of CSDH in the multivariate analysis, when the OR and 95% CI value of patients with hematoma midline shift ＞ 10 mm and separated type were 5. 280 ( 1. 339-20. 823) and 19. 125 (4. 175-87.619), the OR and 95% CI value of patients with hematoma width ＞30 mm was 14. 838 ( 1. 353-162.698). Conclusions Type of hematoma and midline shift are found to be independently correlated with the recurrence of CSDH, and the width of hematoma is also related with its recurrence.

Objective To observe the effect of adenosine A1 receptor (A1AR) on the megalin defect in type 1 diabetic mice with early kidney disease.Methods 7-8 week-old,baseline body weight and fasting blood glucose matched wild type (WT) C57BL/6J mice were selected,and randomly divided into two groups:control group (n=6) and WT DM group (n=6).In the same way,male A1AR knock-out C57BL/6J mice were selected as A1AR-/-DM group (n=6).DM model was established by intraperitoneal injection of streptozocin.The blood glucose (BG),body weight (BW),kidney weight (KW),24 h proteinuria (24hUP) and albumin creatine ratio (ACR) were measured at 4 weeks.The renal pathological lesion was observed and the expression of megalin in proximal tubules was examined by immunohistochemistry.The expression of caspase-1,IL-18 and A1AR were detected by Western blotting.Results At 4th week,compared with WT control mice,the BG,BW,KW and 24hUP of WT DM mice were increased significantly (n=6,P ＜ 0.01),with the pathological glomerular enlargement,mesangial cell proliferation,extracellular matrix accumulation and renal tubule hypertrophy being observed.Immunohistochemistry revealed decreased expression of megalin,an important multiligand protein receptor on the brush border of proximal tubular epithelial cells in WT DM mice,which was correlated with 24hUP (r=-0.645,P ＜ 0.01).Compared with the control mice,the expressions of caspase-1,IL-18 and A1AR were significantly increased in WT DM mice (P ＜ 0.05).For A1AR-/-DM mice,more serious pathological lesion and megalin defect,together with increasing of casapase-1 and heavier proteinuria were observed than those in WT DM mice.Conclusion A1AR may play a protective role in megalin expression of diabetic mice with early kidney disease,in which the mechanism may be associated with caspase-1 related pyroptosis pathway.The details need further exploration.

Objective To investigate the genotype and mutation frequency of thalassemia in child patients of Shenzhen region so as to provide evidences for the gene diagnosis and genetic counseling of thalassemia.Methods A total of 1 206 child patients suspected with thalassemia were retrospectively analyzed.The gene deletion of α-thalassemia was detected by Gap-PCR.The point mutations of α-thalassemia and β-thalassemia were determined by reverse dot blot(RDB)-PCR.The specimens suspected with HKαα and rare gene mutations were determined with nested PCR and gene sequencing,respectively.Results The detection rate of thalassemia was 76.9％ (927/ 1 206).Among them,α-thalassemia accounted for 40.5％ (489/1 206),and--SEA/αα was the most common gene mutation(75.1％);β-thalassemia accounted for 33.7％ (406/1 206),and the main IVS-2-654 (C→T) and CDM1-42 (-TCTT) heterozygous mutations accounted for 35％ and 32.5％,respectively.In addition,there were 32(2.7％) β-thalassemia patients with α-thalassemia mutation,1 patient with HKαα/ααQS,1 α-thalassemia patient with CD61 (AAG→TAG)/--SEA and 1 β-thalassemia patient with CD5 (CCT→C).Conclusion The are complicated gene mutation types and rare gene mutations of thalassemia in child patients of Shenzhen region.

Objective To establish a method for determination of atractylodin in essential oil of Jingfukang preparations by GC and analyze its stability in different solutions. Methods Using HP-5 quartz capillary column (30 m×0.32 mm), programmed temperature was conducted with the FID as detector. The content of atractylodin was determined both at room temperature and 4 ℃ in 20 days. Results The linear range of atractylodin was 4.172-41.72 μg/mL (r=0.999 7). The stability of atractylodin in essential oil of atractylodes was better than in anhydrous alcohol solution or in essential oil of Jingfukang preparation. Conclusion This method is suitable for the quality control of atractylodin in essential oil of Jingfukang preparations. Low temperature is helpful to the stability of atractylodin. The storage period of essential oil of Jingfukang preparations should not be too long.

Objective To evaluate combined effect on different population through 2 459 data of SAA,hs-CRP and PCT from 8 three-level hospitals in Guangdong region.Methods Subjects were divided into five groups by ages,and every group had bacterial and virus type.In order to confirm diagnostic effect on infection,methods were performed including in tendency of SAA and hs-CRP,Paired t test between bacterial and virus group,efficiency of 3 indexes in judging infection depending on ROC and parameters,multiple logistic regression,consistency between positive bacterial infection and bacterial culture.Re-sults There were statistically significant differences in SAA and hs-CRP between bacterial and virus in infants and children (P <0.001).SAA had the biggest AUC area 0.824 with sensibility 71.8% and specificity 82.6% in younger group.Corre-sponding,hs-CRP had the biggest area 0.806 with sensibility 84%.There was the accuracy of 78.8% for differential diagno-sis in younger group,while 65.1% in elder group.AUC of SAA was 0.883 for positive bacterial culture with sensibility 71.2% and specificity 90.7%,accuracy of 95.2% for differential diagnosis.Conclusion There was obvious trend of age in SAA and hs-CRP,3 indexes could be used for differential diagnosis alone or combined,especially in younger group.SAA is the best index as a separated index.There is less value at ratio of SAA and hs-CRP.

Objective To investigate the effects of p300/CBP on histone acetylation of Foxp3 gene and its roles in the immunological pathogenesis of Kawasaki disease (KD).Methods Forty-six children with KD and twenty-eight age-matched health children were consented to participate in this study.Co-immunoprecipitation and real-time PCR were performed to detect Foxp3-associated acetylation levels of histone H4 and binding abilities of p300, CBP, pSmad3 (phosphorylated mothers against decapentaplegic homolog 3) and NF-AT (nuclear factor of activated T cells) with Foxp3 gene in CD4+ T cells.The percentages of CD4+CD25high Foxp3+ cells (Treg) and the expression of Foxp3, CTLA4 (cytotoxic T-lymphocyte-associated protein 4), p300, CBP, TGF-βRⅡ (transforming growth factor β receptor Ⅱ) and pLAT1 at protein level were analyzed by flow cytometry.Quantitative real-time PCR was used to measure the expression of Foxp3, IL-10, TGF-β, TGF-βRⅠ, Egr-1 (early growth response protein 1), RARα (retinoic acid receptor α) and PLCγ1 (phospholipase C-γ1) in Treg cells at mRNA level.Plasma concentrations of TGF-β and retinol acid (RA) were measured by enzyme-linked immunosorbent assay.Results (1) The percentages of Treg cells, levels of Foxp3 and molecules associated with suppressive function of Treg cells (TGF-β, IL-10 and CTLA4), acetylation levels of histone H4 associated with promoter, conserved non-coding DNA sequence 1 (CNS1) and CNS2 of Foxp3 gene decreased remarkably during acute KD (P<0.05), but were restored after IVIG therapy (P<0.05).Meanwhile, all of the aforementioned items in KD patients with coronary artery lesions (KD-CAL+) were lower than those without coronary artery lesions (KD-CAL-) (P<0.05).No significant differences in histone H4 acetylation associated with CNS3 were found among different groups (P>0.05).(2) The levels of p300 and CBP in Treg cells and their binding abilities with Foxp3 gene were down-regulated significantly during acute KD (P<0.05), but were restored to some extent after IVIG treatment (P<0.05).The Foxp3-associated histone acetylation was positively correlated with the expression of p300 and CBP at mRNA level during acute KD (r=0.65, 0.42, P<0.05).Furthermore, the expression of p300 and CBP and their binding abilities with Foxp3 gene in KD-CAL+ group were lower than those in KD-CAL-group (P<0.05).(3) Compared with healthy subjects, plasma concentrations of TGF-β and RA and the expression of TGF-βRⅠ/Ⅱ/Egr-1, RARα and pLAT1/PLCγ1 were down-regulated during acute KD (P<0.05);the binding abilities of pSmad3 and NFAT with Foxp3 gene were reduced remarkably in patients with acute KD (P<0.05).All the items mentioned above were restored after IVIG treatment (P<0.05).Moreover, the ten items aforementioned in KD-CAL+ group were lower than those in KD-CAL-group (P<0.05).(4) Higher acetylation levels of histone H4 associated with promoter, CNS1 and CNS2, and enhanced binding abilities of p300 and CBP with Foxp3 gene were found in CD4+ T cells isolated from patients with acute KD after co-stimulation with TGF-β, RA and anti-CD3/CD28 antibodies as compared with those in CD4+ T cells without stimulation (P<0.05).However, no statistical difference in the acetylation level of histone H4 associated with CNS3 was found between the two groups (P>0.05).Conclusion Hypoacetylation of histone H4 associated with Foxp3 gene caused by insufficient expression of p300/CBP and their impaired binding abilities might be involved with immune dysfunction in KD.IVIG therapy regulates the expression of p300/CBP and their binding abilities with Foxp3 gene through up-regulating TGF-β signal.

Objective To investigate the effects of SMYD3 and MLL5 on histone methylation of Transcription factor forkhead box protein 3 (Foxp3) gene and its roles in the immunological pathogenesis of Kawasaki disease (KD). Methods Forty-two children with KD and 26 age-matched healthy children were consented to participate in this study. Co-Immunoprec-ipitation and real-time polymerase chain reaction (PCR) was performed to determine Foxp3-associated histone methylation levels of H3K4me3 and H3K27me3, and binding levels of SMYD3 and MLL5 with Foxp3 gene in CD4+T cells. The proportion of CD4+CD25high Foxp3+cells (Treg) and protein levels of Foxp3, cytotoxic T lymphocyte associated antigen-4 (CTLA4), TGF-βRⅡand pSmad3 were analyzed by flow cytometry. Quantitative real-time PCR was used to evaluate levels of Foxp3, interleukin (IL)-10, GITR, TGF-βRⅠand RARαmRNA in CD4+T cells. Plasma concentrations of TGF-βand retinol acid (RA) were measured by enzyme-linked Immunosorbent assay. Independent-samples t-test was used as the statistical method in this study. Results ① The proportion of Treg, expression levels of Foxp3 and molecules associated with suppressive function of Treg cells(IL-10, GITR and CTLA4), and histone methylation levels of H3K4me3 associating with promoter, conserved non-coding DNA sequence (CNS) 1 and CNS2 of Foxp3 gene decreased remarkably during acute KD [Promoter:(5.4±1.8)%vs (9.1±2.2)%;CNS1:(2.6±0.9)% vs (3.8±1.1)%; CNS2: (2.4±0.8)% vs (4.2±1.0)%; t=5.50, 6.02, 9.56, 7.92, 7.97, 4.76, 7.73, 5.01, 8.66; P<0.05], and restored after intravenous immunoglobulins (IVIG) therapy [Promoter: (7.2 ±2.1)% vs (5.4 ±1.8)%; CNS1:(3.6±1.4)% vs (2.6±0.9)%; CNS2: (3.6±1.4)% vs (2.4±0.8)%; t=5.56, 4.59, 7.01, 6.04, 5.89, 4.83, 4.45, 4.00, 5.12; P<0.05]. Meanwhile, the nine former items in KD patients with coronary artery lesions (KD-CAL+) were lower than those without coronary artery lesions (KD-CAL-) [Promoter: (4.11±1.45)% vs (6.16±1.93)%; CNS1:(1.99±0.87)%vs (2.96±1.10)%;CNS2: (1.75±0.63)%vs (2.72±1.16)%;t=6.28, 3.24, 4.56, 3.69, 3.38, 4.40, 3.65, 3.00, 3.51; P<0.05]. No significant difference of H3K4me3 associated with CNS3 and H3K27me3 were found among the groups (t=1.03, 0.91, 1.48 and 0.79, 0.82, 1.53; P>0.05). ② Binding levels of SMYD3 and MLL5 with Foxp3 gene in CD4+T cells were down-regulated significantly during acute KD (t=6.63, 6.15; P<0.05), and restored to some extent after IVIG treatment (t=5.36, 4.56; P<0.05). Positive correlations between binding levels of SMYD3 and MLL5 and expression level of Foxp3 mRNA were detected in patients with acute KD (r=0.62、0.45, P<0.05). Furthermore, Binding levels of SMYD3 and MLL5 with Foxp3 gene in KD-CAL+group were lower than those in KD-CAL- group (t=4.11, 4.31; P<0.05). ③ Compared with healthy controls, plasma concentration of TGF-β and RA, and expressions of TGF-βRⅡ, TGF-βRⅠ, pSmad3 and RARα were down-regulated during acute KD (t=11.54, 12.81, 7.43, 16.10, 8.25, 12.06; P<0.05), and elevated remarkably after IVIG treatment (t=8.40, 6.24, 5.94, 11.78, 6.27, 8.30; P<0.05). Simultaneously, all the items aforementioned in KD-CAL+ group were found to be lower than those in KD-CAL-group (t=3.58, 3.30, 3.82, 5.27, 4.71, 3.78; P<0.05). Conclusion Hypomethylation of H3K4me3 associated with Foxp3 gene caused by insufficient binding levels of SMYD3/MLL5 may be involved with immune dysfunction in Kawasaki disease.