335例退行性骨关节病直流感应电康复总结

报告335例退行性骨关节病变,均经 x 线摄影证实,用直流感应电治疗。痊愈62例,占18.51%;显效115例,占34.33%;好转139例,占41.49%;无效19例;占5.67%。总有效率94.33%。有复发者再经治疗仍可收到效果。并对作用机制进行了探讨。     

Correlation between gene expression of aryl hydrocarbon receptor (AhR), hydrocarbon receptor nuclear translocator (Arnt), cytochromes P4501A1 (CYP1A1) and 1B1 (CYP1B1), and inducibility of CYP1A1 and CYP1B1 in human lymphocytes.

The relationships between gene expression of aryl hydrocarbon receptor (AhR), aryl hydrocarbon receptor nuclear translocator (Arnt), cytochromes P4501A1 (CYP1A1), 1B1 (CYP1B1), CYP1A1, and the inducibility of CYP1A1 and CYP1B1 were determined in 32 cultivated human lymphocytes. Cytochrome P450 induction was performed by incubating lymphocytes with benzanthracene. The relative gene expression levels were determined by quantitative real-time RT-PCR assay. We found that gender is an important confounding factor for gene expression in cultivated lymphocytes. AhR, CYP1A1 and CYP1B1 levels in noninduced lymphocytes were significantly higher in female nonsmokers than in male nonsmokers (p < 0.05). Nevertheless, CYP1A1 and CYP1B1 inducibility was lower in female nonsmokers. CYP1A1 inducibility was higher in male smokers than in male nonsmokers (p < 0.05). After controlling for gender and cigarette smoking, AhR levels positively correlated with CYP1B1 levels and CYP1A1 inducibility (p < 0.01 and p = 0.03, respectively). Arnt levels also correlated with CYP1B1 levels in induced lymphocytes (p < 0.01). However, AhR levels were negatively correlated with CYP1B1 inducibility. These data indicate that AhR expression associates with individual variation of CYP1A1 inducibility and CYP1B1 expression in cultivated lymphocytes. Furthermore, gender and cigarette smoking are important confounding factors for gene expression levels in cultivated lymphocytes.     

发热门诊基于Kaiser模型的灾害脆弱性分析及干预

目的 分析发热门诊可能存在的灾害脆弱性事件,并采取针对性防控策略,减少安全隐患。 方法 基于Kaiser模型制订发热门诊可能存在的35个灾害事件风险评估指标,对20名医护人员进行调查,针对风险值排在前10位的指标进行针对性干预。 结果 风险值排名前10位的是患者突发心脏骤停（0.407）、医生防护知识不足（0.389）、工勤人员防护知识培训不到位（0.333）、药房药品短缺（0.333）、外来工作人员防护不到位（0.315）、工勤人员手卫生依从性低（0.287）、错误的垃圾收运方式（0.278）、医疗纠纷（0.259）、医务人员手卫生依从性低（0.250）、护理人员配备不足（0.213）。针对上述10项风险进行针对性干预,干预后其中９项风险值显著低于干预前,门诊医生防护知识理论考核成绩显著高于实施前（均P＜0.05）。 结论 发热门诊存在不同程度的管理风险,基于Kaiser模型的灾害脆弱性分析及干预,有利于降低风险值,保障患者安全。     

Establishment of a bilateral femoral large segmental bone defect mouse model potentially applicable to basic research in bone tissue engineering

Background

To understand the cellular mechanism underlying bone defect healing in the context of tissue engineering, a reliable, reproducible, and standardized load-bearing large segmental bone defect model in small animals is indispensable. The aim of this study was to establish and evaluate a bilateral femoral defect model in mice.

Materials and methods

Donor mouse bone marrow mesenchymal stem cells (mBMSCs) were obtained from six mice (FVB/N) and incorporated into partially demineralized bone matrix scaffolds to construct tissue-engineered bones. In total, 36 GFP⁺ mice were used for modeling. Titanium fixation plates with locking steel wires were attached to the femurs for stabilization, and 2-mm–long segmental bone defects were created in the bilateral femoral midshafts. The defects in the left and right femurs were transplanted with tissue-engineered bones and control scaffolds, respectively. The healing process was monitored by x-ray radiography, microcomputed tomography, and histology. The capacity of the transplanted mBMSCs to recruit host CD31⁺ cells was investigated by immunofluorescence and real-time polymerase chain reaction.

Results

Postoperatively, no complication was observed, except that two mice died of unknown causes. Stable fixation of femurs and implants with full load bearing was achieved in all animals. The process of bone defect repair was significantly accelerated due to the introduction of mBMSCs. Moreover, the transplanted mBMSCs attracted more host CD31⁺ endothelial progenitors into the grafts.

Conclusions

The present study established a feasible, reproducible, and clinically relevant bilateral femoral large segmental bone defect mouse model. This model is potentially suitable for basic research in the field of bone tissue engineering.     

Persistent elevation of blood pressure by ambient coarse particulate matter after recovery from pulmonary inflammation in mice

Exposure to ambient particulate matter (PM) is associated with hypertension and cardiovascular diseases. Recently, we reported that exposure to fine and coarse PM caused pulmonary inflammation and pulmonary small arterial remodeling in mice, and osteopontin (OPN) level was elevated following PM exposure. However, in the present study, cotreatment with 5‐methoxytryptophan for 4 weeks partially reduced coarse PM‐induced pulmonary inflammation without reducing pulmonary OPN secretion or recovery from pulmonary arterial remodeling in mice. Persistent vascular dysfunction may lead to vascular remodeling. Therefore, we further compared the relationship between coarse PM‐induced inflammation and vascular dysfunction by exposing mice to PM before and after cessation of PM exposure. Oropharyngeal aspiration of PM for 8 weeks induced pulmonary inflammation and pulmonary small artery remodeling in mice, as well as increased serum C‐reactive protein and OPN concentrations and systolic blood pressure (SBP). After the cessation of PM exposure for another 8 weeks, lung inflammation had recovered and vascular remodeling had partially recovered. Elevation of OPN, metalloproteinases (MMPs), and cytokines in bronchioalveolar lavage were significantly reduced. However, PM‐induced systemic responses did not recover after the cessation of PM exposure. Notably, not only serum OPN and SBP remained significantly elevated; also, serum endothelin‐1, MMP‐9, and keratinocyte‐derived chemokine concentrations were significantly increased after cessation of PM exposure for another 8 weeks. These data suggested that systemic inflammation and systemic vascular dysfunction might be important in PM‐induced elevation of SBP. Furthermore, SBP elevation was persistent after cessation of PM exposure for 8 weeks.     

Trans, Trans-2,4-Decadienal, a Product Found in Cooking Oil Fumes, Induces Cell Proliferation and Cytokine Production Due to Reactive Oxygen Species in Human Bronchial Epithelial Cells

Dienaldehydes are by-products of peroxidation of polyunsaturatedlipids and commonly found in many foods or food-products. BothNational Cancer Institute (NCI) and NTP have expressed greatconcern on the potential genotoxicity and carcinogenicity ofdienaldehydes. Trans, trans-2,4-decadienal (tt-DDE or 2,4-De),a specific type of dienaldehyde, is abundant in heated oilsand has been associated with lung adenocarcinoma developmentin women due to their exposure to oil fumes during cooking.Cultured human bronchial epithelial cells (BEAS-2B cells) wereexposed to 0.1 or 1.0 µM tt-DDE for 45 days, and oxidativestress, reactive oxygen species (ROS) production, GSH/GSSG ratio,cell proliferation, and expression of TNF and IL-1ßwere measured. The results show that tt-DDE induced oxidativestress, an increase in ROS production, and a decrease in GSH/GSSGratio (glutathione status) in a dose-dependent manner. Treatmentof BEAS-2B cells with 1.0 µM tt-DDE for 45 days increasedcell proliferation and the expression and release of pro-inflammatorycytokines TNF and IL-1ß. Cotreatment of BEAS-2B cellswith antioxidant N-acetylcysteine prevented tt-DDE-induced cellproliferation and release of cytokines. Therefore, these resultssuggest that tt-DDE-induced changes may be due to increasedROS production and enhanced oxidative stress. Since increasedcell proliferation and the release of TNF- and IL-1ßare believed to be involved in tumor promotion, our resultssuggest that tt-DDE may play a role in cancer promotion. Previousstudies on dienaldehydes have focused on their genotoxic orcarcinogenic effects in the gastrointestinal tract; the presentstudy suggests a potential new role of tt-DDE as a tumor promoterin human lung epithelial cells.     

Glycine N-methyltransferase tumor susceptibility gene in the benzo(a)pyrene-detoxification pathway

Glycine N-methyltransferase (GNMT) affects genetic stability by (a) regulating the ratio of S-adenosylmethionine to S-adenosylhomocystine and (b) binding to folate. Based on the identification of GNMT as a 4 S polyaromatic hydrocarbon-binding protein, we used liver cancer cell lines that expressed GNMT either transiently or stably in cDNA transfections to analyze the role of GNMT in the benzo(a)pyrene (BaP) detoxification pathway. Results from an indirect immunofluorescent antibody assay showed that GNMT was expressed in cell cytoplasm before BaP treatment and translocated to cell nuclei after BaP treatment. Compared with cells transfected with the vector plasmid, the number of BaP-7,8-diol 9,10-epoxide-DNA adducts that formed in GNMT-expressing cells was significantly reduced. Furthermore, the dose-dependent inhibition of BaP-7,8-diol 9,10-epoxide-DNA adduct formation by GNMT was observed in HepG2 cells infected with different multiplicities of infection of recombinant adenoviruses carrying GNMT cDNA. According to an aryl hydrocarbon hydroxylase enzyme activity assay, GNMT inhibited BaP-induced cytochrome P450 1A1 enzyme activity. Automated BaP docking using a Lamarckian genetic algorithm with GNMT X-ray crystallography revealed a BaP preference for the S-adenosylmethionine-binding domain of the dimeric form of GNMT, a novel finding of a cellular defense against potentially damaging exposures. In addition to GNMT, results from docking experiments showed that BaP binds readily with other DNA methyltransferases, including HhaI, HaeIII, PvuII methyltransferases and human DNA methyltransferase 2. We therefore hypothesized that BaP-DNA methyltransferase and BaP-GNMT interactions may contribute to carcinogenesis.     

Using a combination of cytochrome P450 1B1 and β-catenin for early diagnosis and prevention of colorectal cancer

Background: Although fecal occult blood test and invasive endoscopic examination are common used to detect colorectal adenomas and cancers, non-invasive and specific biomarkers are still under investigation. The objective is to evaluate the biomarker CYP1B1 alone or in combination with aryl hydrocarbon receptor (AhR), nuclear β-catenin, p53 or bcl-2 for early diagnosis and prevention of colorectal cancer. Methods: These biomarkers were analyzed semi-quantified across 231 colonic tissues including 97 adenocarcinomas, 85 adenomas and 49 non-neoplastic colons using immunohistochemistry. In order to differentiate non-neoplastic colons from colorectal neoplasms (adenoma and carcinoma), the values for CYP1B1, AhR, nuclear β-catenin, p53 and bcl-2 expressions were subjected to discrimination analysis, then the cross-validation, sensitivity and specificity of these models were calculated. Results: Expressions of CYP1B1, p53, nuclear β-catenin and bcl-2 were significantly associated with colorectal carcinogenesis (p < 0.01 for the trend test). The overexpression rates for CYP1B1, p53, nuclear β-catenin and bcl-2 were significantly higher in the adenoma and carcinoma groups than in the non-neoplastic colon group (p < 0.05). The discrimination models showed that a combination of two biomarkers was better than a single biomarker, and provided specificity ranging from 39% to 100% and sensitivity ranging from 43% to 82% for colorectal carcinoma. Conclusions: The increase in expression of CYP1B1 occurred not only in colorectal carcinoma and but also in adenoma. Moreover, a screening panel of CYP1B1 in combination with nuclear β-catenin was the most suitable marker pair to screen for colorectal carcinoma based on this study.     

4-Methoxyestradiol-induced oxidative injuries in human lung epithelial cells

Epidemiological studies indicated that people exposed to dioxins were prone to the development of lung diseases including lung cancer. Animal studies demonstrated that 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) increased liver tumors and promoted lung metaplasia in females. Metabolic changes in 17beta-estradiol (E(2)) resulted from an interaction between TCDD and E(2) could be associated with gender difference. Previously, we reported that methoxylestradiols (MeOE(2)), especially 4-MeOE(2), accumulated in human lung cells (BEAS-2B) co-treated with TCDD and E(2). In the present study, we demonstrate unique accumulation of 4-MeOE(2), as a result of TCDD/E(2) interaction and revealed its bioactivity in human lung epithelial cell line (H1355). 4-Methoxyestradiol treatment significantly decreased cell growth and increased mitotic index. Elevation of ROS and SOD activity, with a concomitant decrease in the intracellular GSH/GSSG ratio, was also detected in 4-MeOE(2)-treated cells. Quantitative comet assay showed increased oxidative DNA damage in the 4-MeOE(2)-treated H1355 cells, which could be significantly reduced by the anti-oxidant N-acetylcysteine (NAC). However, inhibition of cell growth and increase in mitotic arrest induced by 4-MeOE(2) were unaffected by NAC. We concluded that 4-MeOE(2) accumulation resulting from TCDD and E(2) interaction would contribute to the higher vulnerability on lung pathogenesis in females when exposed to TCDD.