醒脑静在重症一氧化碳中毒抢救中的临床应用

目的　探讨醒脑静对急性重症一氧化碳 (CO)中毒的催醒作用。方法　在急性重症CO中毒常规综合抢救中加入醒脑静并与常规方法进行对比研究。结果　醒脑静治疗组较常规治疗组清醒时间明显缩短 (P <0 .0 1)。结论　醒脑静可作为急性重症CO中毒病人综合抢救中常规用药。     

乳腺髓样癌的超声检查与组织病理的相关性分析

目的:探讨超声检查在诊断乳腺典型髓样癌中的临床意义。方法:按严格的病理诊断学标准将病例重新分类为乳腺典型髓样癌和非典型髓样癌,比较两者间声像学特征的异同。结果:32例中有13侧重新诊断为乳腺典型髓样癌;另外19例为非典型髓样癌。13例典型髓样癌患者中的10例边界整齐光滑;全部19例非典型髓样癌病人没有一例边界光滑,或者边界呈锯齿状(16例),或者边界光滑伴局部不规则(3例)。非典型与典型髓样癌间肿瘤边界的规则性有明显的差异。结论:如果超声检查提示肿瘤边界呈锯齿状或肿瘤边界光滑伴局部不规则,应行整个肿瘤的病理评估防止典型髓样癌的过诊断。     

电磁辐射对小鼠神经系统超微结构影向的分析

目的探讨移动电话的电磁辐射对生物体的影响.方法用大众常用移动电话作为辐射源,工作频率为900MHz,功率密度为1190μW/cm2,在一定范围对小鼠辐射2h/d,30d后把小鼠断颈处死,取出大脑皮层、海马和小脑进行电镜观察分析.结果电镜所见,处理组与对照组小鼠的神经系统的细胞超微结构未见明显异常.结论一定时间内,移动电话的电磁辐射,对小鼠神经系统的细胞超微结构并没有明显影响.     

Dark Tea: A popular beverage with possible medicinal application

Tea is a famous beverage that is produced from leaves of Camellia sinensis. Amongst the six major tea categories in China, dark tea is the only one that involves microbial fermentation in the manufacturing process, which contributes unique flavors and functions for the tea. In the recent decade, the reports about the biofunctions of dark teas have increased rapidly. Therefore it may be the proper time to consider dark tea as one potential homology of medicine and food. In this viewpoint, our current understanding of the chemical constituents, biological activities and possible health beneficial effects of dark teas were introduced. Some future directions and challenges to the development perspectives of dark teas were also discussed.     

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.     

磷酸钛钾激光声带切除术不同术式的临床特点

目的 探讨支撑喉镜下磷酸钛钾（ｐｏｔａｓｉｕｍ ｔｉｔａｎｉｕｍ ｐｈｏｓｐｈａｔｅ,ＫＴＰ）激光声带切除术不同术式的选择及愈合过程中的临床特点。方法 选择７６例早期声门型喉癌行ＫＴＰ激光声带切除术,对不同术式术后喉内结构恢复过程、音质变化等进行随访观察记录。结果 Ⅰ型术式１１例,３个月后恢复喉的正常结构及功能;Ⅱ型术式５０例,３个月后有声带样粘膜皱襞（以下称新声带）形成,基本恢复喉的结构;Ⅲ型术     

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.