脑缺血时皮层扩布性抑制与心功能障碍

目的 :研究树 鼠句脑缺血时单胺氧化酶 (MAO)活化在脑缺血时心功能障碍以及扩布性抑制中的可能作用。方法 :采用光化学法诱导树 鼠句血栓性脑缺血 ,测定缺血区及血清MAO活性、多巴胺及去甲肾上腺素 (NA)水平 ,经电镜观察脑及肾上腺的超微结构。记录仪检测心率(HR)、左室收缩压峰值 (LVSP) ,左室瞬间收缩与舒张最大速率 (±dp/dtmax) ,左室舒张末期压力 (LVEDP) ,平均动脉压 (MAP)。结果 :树鼠句脑缺血过程中血清NA先升高 (由 11.60± 0 .73ng/ml升高至18.46± 0 .3 9ng/ml,P <0 .0 1) ,72h后降至 8.3 2± 1.86ng/ml;血清MAO活性逐渐升高 ,达 2 10 .1± 2 6.67U/ml(P <0 .0 1) ,72h降低至对照水平 ;心功能指标 (±dp/dtmax,LVSP ) ,尤其是HR明显降低 ,由3 17.0± 98.0 1beat/min降至 2 3 7.4± 3 1.90beat/min(P <0 .0 1) ,于2 4h恢复至对照水平。结论 :血栓性脑缺血时血清NA水平明显取决于MAO活性的变化 ,后者对脑缺血时心脏舒缩功能可能具有调节作用。     

The RNA helicase, nucleotide 5'-triphosphatase, and RNA 5'-triphosphatase activities of Dengue virus protein NS3 are Mg2+-dependent and require a functional Walker B motif in the helicase catalytic core

The nonstructural protein 3 (NS3) of Dengue virus (DV) is a multifunctional enzyme carrying activities involved in viral RNA replication and capping: helicase, nucleoside 5'-triphosphatase (NTPase), and RNA 5'-triphosphatase (RTPase). Here, a 54-kDa C-terminal domain of NS3 (DeltaNS3) bearing all three activities was expressed as a recombinant protein. Structure-based sequence analysis in comparison with Hepatitis C virus (HCV) helicase indicates the presence of a HCV-helicase-like catalytic core domain in the N-terminal part of DeltaNS3, whereas the C-terminal part seems to be different. In this report, we show that the RTPase activity of DeltaNS3 is Mg2+-dependent as are both helicase and NTPase activities. Mutational analysis shows that the RTPase activity requires an intact NTPase/helicase Walker B motif in the helicase core, consistent with the fact that such motifs are involved in the coordination of Mg2+. The R513A substitution in the C-terminal domain of DeltaNS3 abrogates helicase activity and strongly diminishes RTPase activity, indicating that both activities are functionally coupled. DV RTPase seems to belong to a new class of Mg2+-dependent RTPases, which use the active center of the helicase/NTPase catalytic core in conjunction with elements in the C-terminal domain.     

^32磷简易敷贴药膜治疗小儿皮肤血管瘤2450例疗效分析

目的　评价3 2 磷简易敷贴药膜治疗小儿皮肤血管瘤的效果 .方法　 2 4 5 0例不同年龄的血管瘤小儿接受3 2 磷简易敷贴药膜治疗 ,治疗次数为 1～ 9次 ,平均 3.5次 ;每次间隔 2个月 ,按不同年龄给不同的照射量 ,以治疗时间换算 ,每次治疗剂量为 0 .92 5MBq/cm2 × ( 12～ 4 2 )h .结果　血管瘤和血管痣治愈率 71.7% ,部分治愈 2 2 .5 % ,总有效率 94 .2 % ,无效者 5 .8% .其中血管瘤效果明显优于血管痣 (p<0 .0 1) ,并且年龄越小效果越明显 (p<0 .0 1) .结论　3 2 磷简易敷贴药膜治疗小儿皮肤血管瘤是一种治疗简便、疗效确切的方法 ,尽早治疗效果更明显     

Development of acute autoimmune encephalomyelitis in mice: Factors regulating the effector phase of the disease

The development of acute experimental autoimmune encephalomyelitis (EAE) in mice is potentiated by the use of Bordetella pertussis vaccine as an adjuvant. Histamine sensitizing factor (HSF) extracted from B. pertussis is the active adjuvant agent and causes a mild increase in cerebrovascular permeability. During the development of EAE, there is an additional increase in vascular permeability of the brain and spinal cord. The adjuvant action of B. pertussis HSF does not appear to mimic a generalized beta-adrenergic blockade, since the course of EAE is not potentiated by adrenalectomy. The cerebrovascular permeability changes observed in EAE are probably mediated by vasoactive amines, since the expression of EAE can be blocked by vasoactive amine antagonists.     

AMPK as a metabolic switch in rat muscle,liver and adipose tissue after exercise

An increasing body of evidence has revealed that activation of adenosine monophosphate (AMP)‐activated protein kinase (AMPK)‐activated protein kinase increases fatty acid oxidation by lowering the concentration of malonyl coenzyme A (CoA), an inhibitor of carnitine palmitoyl transferase 1. Studies carried out primarily in skeletal muscle suggest that AMPK modulates the concentration of malonyl CoA by concurrently phosphorylating and inhibiting acetyl CoA carboxylase (ACC), the rate limiting enzyme in malonyl CoA synthesis, and phosphorylating and activating malonyl CoA decarboxylase (MCD), an enzyme involved in its degradation. We have recently observed that AMPK and MCD activities are increased and ACC activity diminished in skeletal muscle, liver and, surprisingly, in adipose tissue 30 min following exercise (treadmill run) in normal rats. In liver and adipose tissue these changes were associated with a decrease in the activity of glycerol‐3‐phosphate acyltransferase (GPAT), which catalyses the first committed reaction in glycerolipid synthesis and, which like ACC, is phosphorylated and inhibited by AMPK. Similar changes in ACC, MCD and GPAT were observed following the administration of 5‐aminoimidazole 4‐carboxamide‐riboside (AICAR), further indicating that the exercise‐induced alterations in these enzymes were AMPK‐mediated. Conclusions: (1) AMPK plays a major role in regulating lipid metabolism in multiple tissues following exercise. (2) The net effect of its activation is to increase fatty acid oxidation and diminish glycerolipid synthesis. (3) The relevance of these findings to the regulation of muscle glycogen repletion in the post‐exercise state and to the demonstrated ability of AMPK activation to decrease adiposity and increase insulin sensitivity in rodents remains to be determined.     

汉族人群载脂蛋白CII基因二核苷酸串联重复序列(TG)n(AG)m及(AG)m多态性

采用套式聚合酶链反应结合变性聚丙烯酰胺凝胶电泳和银染技术，并构建载脂蛋白CII（ApoCII)基因二核苷酸串联重复序列（TG）n(AG)m及（AG）m序列等位基因梯阶标准；检测正常汉族人群基因型和等位基因频率分布，检出36种（TG）n(AG)m序列基因型、12种等位基因。等位基因为17、18、26－35，其频率分别为0．061、0．011、0．002、0．002、0．054、0．255、0．372、0．084、0．026、0．039、0．052、0．041。检出7种（AG）m序列基因型、4种等位基因。等位基因为6、7、8、9，其频率分别为0．002、0．152、0．812、0．034。与欧洲白种人比较，ApoCII基因二核苷酸串联重复序列（TG）n(AG)m及（AG）m序列等位基因频率分布均具有明显的种族差异性（P＜0．01，P＜0．01）。     

Neck masses due to internal jugular vein phlebectasia: Frequency in Menkes disease and literature review of 85 pediatric subjects

Classic Menkes disease is a rare X‐linked recessive disorder of copper metabolism caused by pathogenic variants in the copper transporter gene, ATP7A. Untreated affected individuals suffer failure to thrive and neurodevelopmental delays that begin at 6–8 weeks of age and progress inexorably to death, often within 3 years. Subcutaneous injections of Copper Histidinate (US Food and Drug Administration IND #34,166, Orphan product designation #12‐3663) are associated with improved survival and neurological outcomes, especially when commenced within a month of birth. We previously identified internal jugular vein phlebectasia (IJP) in four Menkes disease subjects. This feature and other connective tissue abnormalities appear to be consequences of deficient activity of lysyl oxidase, a copper‐dependent enzyme. Here, we report results from a prospective study of IJP based on 178 neck ultrasounds in 66 Menkes subjects obtained between November 2007 and March 2018. Nine patients met the criterion for IJP (one or more cross‐sectional area measurements exceeding 2.2 cm²) and five subjects had clinically apparent neck masses that enlarged over time. Our prospective results suggest that IJP occurs in approximately 14% (9/66) of Menkes disease patients and appears to be clinically benign with no specific medical or surgical actionability. We surveyed the medical literature for prior reports of IJP in pediatric subjects and identified 85 individuals and reviewed the distribution of this abnormality by gender, sidedness, and underlying etiology. Taken together, Menkes disease accounts for 16% (15/94) of all reported IJP individuals. Neck masses from IJP represent underappreciated abnormalities in Menkes disease.     

医用磷酸钙骨水泥的制备及性能的实验研究

探索了磷酸四钙（Ca4（PO4）2O，TTCP）的制备，并合成了磷酸钙骨水泥（CPC），对CPC固化时间、引起浸泡液pH值的变化、抗压强度、产物物相组成及微观结构进行了研究。结果表明：在真空条件下、1500℃下煅烧6h可制得TTCP，并含有少量CaO。CPC初凝时间为4min、终凝时间为15min，浸泡1d和7d后的抗压强度分别为20MPa和35MPa，浸泡液的pH值在6．4～8．9之间变化，这些性能均符合临床用CPC的性能要求。CPC水化产物为片状或针状羟基磷灰石（Ca5（PO4）3OH，HA），相互交错呈连续分布的网状结构，这种结构有利于材料强度的提高。实验研制的CPC材料可用于骨缺损的修复治疗。     

The effects of reverse monocular deprivation in monkeys II. Electrophysiological and anatomical studies

Summary Monkeys had one eye closed at about 30 days of age for 14, 30, 60, or 90 days, then opened, and the fellow eye closed for another 120 days. The animals then had at least 10 months of binocular visual experience before extensive behavioral training and testing were carried out. In terminal experiments concluded more than 18 months later, microelectrode investigations of the striate cortex demonstrated that there was almost a complete absence of binocular neurons in all animals. The initially deprived eyes (IDEs) dominated the majority of cortical neurons, even when soma size measurements of lateral geniculate neurons indicated that the LGN cells driven by the IDE had not regained their normal size. The monkeys which had significant interocular differences in spatial vision also exhibited abnormalities in the distribution of the metabolic enzyme, cytochrome oxidase (CO), within the striate cortex. These results demonstrate that many of the severe alterations in cortical physiology and eye dominance produced by early monocular form deprivation can be reversed, with recovery of normal cortical function, via the reverse-deprivation procedure.Supported by National Eye Institute grants R01 EY01120, R01 EY03611, R01 EY01139, and EY02520