Occurrence,Human Exposure,and Risk Assessment of Polybrominated Dibenzo-p-Dioxins and Dibenzofurans,Polychlorinated Naphthalenes,and Metals in Atmosphere Around Industrial Parks in Jiangsu,China

Air samples were collected around industrial parks in Jiangsu, China, to allow the concentrations, profiles, and risk assessment of polybrominated dibenzo-p-dioxins and dibenzofurans (PBDD/Fs), polychlorinated naphthalenes (PCNs), and metals to be investigated. The concentrations of ΣPBDD/Fs and ΣPCNs were 1324.26–2080.98 fg/m³ (11.35–42.57 fg I-TEQ/m³) and 10,404.9–29,322.9 fg/m³ (1.32–7.19 fg I-TEQ/ m³), respectively. The highest concentration of ΣPBDD/Fs and ΣPCNs were observed at site C. PBDD/Fs were mainly dominated by PBDFs. The main contributor to the ΣPBDD/Fs in all samples was 1,2,3,4,6,7,8-HpBDF, which accounted for 25.75%–39.4%. For PCNs, the predominating homologues were tetra-, tri- and penta-CNs, which contributed 30.7%–43.3%, 24.7%–31.0%, and 10.6%–21.6%, respectively. As for metals, the pollution of As, Mn, Cr, and Ni in most samples exceeded National Ambient Air Quality Standards of China. Assessing the risk of inhalation exposure showed that there were potential carcinogenic risks to local residents.

     

五种免疫相关性心血管疾病的免疫学研究

对扩张型心肌病、风湿性心脏病，原发性高血压，冠心病及肥厚型心肌病进行外周血清可溶性白细胞介素２受体，Ｔ淋巴细胞亚群及自然杀伤细胞活性的检测，并与健康对照组比较，结果显示：ＤＣＭ组，ＲＨＤ组及ＥＨＴ组的ｓＩＬ－２Ｒ明显高于ＮＣ组，而ＤＣＭ、ＲＨＤ风湿活动组的ＮＫ活性低于ＮＣ组，ＥＨＴ组ＮＫ活性高于ＮＣ组。     

The neuroprotective effects of K252a through inhibiting MLK3/MKK7/JNK3 signaling pathway on ischemic brain injury in rat hippocampal CA1 region

It has been well documented that the activation of c-Jun N-terminal protein kinase (JNK) pathway and caspase-3 signal are involved in the delayed neuronal cell death in cerebral ischemia. In this study, we first detected the activation pattern of JNK signaling including mixed lineage kinase (MLK)3, mitogen-activated protein kinase kinase (MKK)7 and JNK3 in hippocampal CA1 and CA3/DG regions at various time points after 15 min of ischemia. These results indicated that cerebral ischemia induced the continuous activation of MLK3/MKK7/JNK3 cascade, which all had two active waves only in the CA1 region. We also detected the phosphorylation of JNK substrates c-Jun and Bcl-2, and the activation of a key protease of caspase-3 in CA1 region, which only had one active peak, respectively. Because K252a has recently been shown to be a potent inhibitor of MLK3 activity both in vivo and in vitro, we further examined the possible effects and mechanism of this interesting drug in cerebral ischemia. In our present paper, we found that administration of K252a 20 min prior to ischemia inhibited MLK3/MKK7/JNK3 signaling, Bcl-2 phosphorylation, the activation of c-Jun and caspase-3, but had no significant effects on these protein expressions. Additionally, pretreatment of K252a significantly increased the number of the surviving CA1 pyramidal cells at 5 days of reperfusion. Our results suggest that K252a play a neuroprotective role in ischemic injury via inhibition of the JNK pathway, involving the death effector of caspase-3. Thus, JNK signaling may eventually emerge as a prime target for novel therapeutic approaches to treatment of ischemic stroke, and K252a may serve as a potential and important neuroprotectant in therapeutic aspect in ischemic stroke.     

Microsomal casein kinase II in endoplasmic reticulum- and Golgi apparatus-rich fractions of ROS 17/2.8 osteoblast-like cells: An enzyme that modifies osteopontin

Osteopontin is an acidic phosphoprotein containing casein kinase II (CKII) phosphorylatable sites and an acidic amino acid cluster. The metabolically ³²P-labelings of both serines and threonines in vitro in osteopontin immunoprecipitated from rat osteoblast-like ROS 17/2.8 cells may suggest that casein kinase II catalyzes this modification. The enzyme occurs in microsomal fractions of rat osteoblast-like ROS 17/2.8 cells. Subcellular fractions containing endoplasmic reticulum and Golgi apparatus were isolated by differential centrifugation and were identified according to their ultrastructures and the presence of marker enzymes such as glucose-6-phosphatase and thiamine pyrophosphatase, respectively. Both fractions phosphorylated the partially dephosphorylated osteopontin and the specific substrate peptide RRREEETEEE. Endoplasmic reticulum-catalyzed peptide phosphorylation was 2.7 times lower than that of Golgi although both endoplasmic reticulum- and Golgi-catalyzed peptide reactions were 50% inhibited by 20 and 100 ng/ml heparin, respectively. Western blot analysis revealed that both fractions contained osteopontin and microsomal CKII. Furthermore, microsomal CKII was immunogold-labeled in endoplasmic reticulum and Golgi apparatus. Heparin inhibition and utilization of [-³²P]GTP as a phosphate donor by both fractions confirmed their capacity to phosphorylate osteopontin. The results suggest that microsomal CKII modifies the acidie matrix proteins during transportation. These matrix phosphoproteins may participate in the mineralization process of hard tissues.     

医疗机构产权制度改革及其监管

本文从产权的角度出发,对当前的医疗机构改革进行了分析,并对医疗机构自主经营、企业化经营过程中可能出现的一些问题,提出了政府作为财产的最终所有者应加强对医疗机构经营状况的监管。     

测定尿红细胞平均体积和分布曲线鉴别血尿来源的临床价值

目的观察尿红细胞平均体积（ＭＣＶ）和尿红细胞分布曲线鉴别血尿来源和性质。方法用ＣＯＵＬＴＥＲ－ＪＴ全自动血球计数仪检测４０例肾小球性血尿、４０例非肾小球性血尿ＭＣＶ和分布曲线。结果肾小球肾炎ＭＣＶ为６１±１４ｆｌ,非肾小球肾炎ＭＣＶ为８９±１８ｆｌ,以ＭＣＶ＜８０ｆｌ鉴别为肾小球性血尿,敏感性和特异性分别为９７．５％和８８．２％。分布曲线的特点不同,峰值差异很大。结论测定尿ＭＣＶ及分布曲线对鉴别血尿来源和性质有重要意义。     

联合内分泌治疗对前列腺和睾丸的影响

目的 探讨抑那通和缓退瘤联合治疗对正常前列腺,增生的前列腺（ＢＰＨ）和前列腺癌以及睾丸的作用。方法 对１６例接受联合内分泌治疗至少３个月且有治疗前后病理资料的前列腺癌患者的标本进行了系统的病理学检查。对内分泌治疗后的睾丸标本与同龄未接受治疗的进行对照研究。结果 １４例内分泌治疗后的前列腺标本２例未见残存癌灶,９例对治疗有明显的反应;３例对治疗反应差,治疗并未降低前列腺癌的病理分期。３例内分泌治疗后