Anti-inflammatory effect of erythropoietin pretreatment on cardiomyocytes with hypoxia/reoxygenation injury and the possible mechanism

Objective： To investigate the anti-inflammatory effect of erythropoietin （EPO） pretreatment on cardiomyocytes exposed to hypoxialreoxygenation injury （H/R） and explore the possible mechanism.
Methods： The cultured neonatal rats＇ ventricular cardiomyocytes were divided randomly into 4 groups, control group （C group）, EPO pretreatment group （E group）, EPO and pyrrolidine dithiocarbamate （PDTC） pretreatment group （EP group） and PDTC pretreatment group （P group）. After 24 hours＇ pretreatment, the cardiomyocytes were exposed to H/R. After pretreatment and H/R, the expression of tumor necrosis factor- α （TNF- α ） gene in all the groups was detected by RT-PCR and Western blot. The nuclear factor- κ B （NF- κB） activity was detected by electrophoretic mobility shift assay （EMSA） and the inhibitor- κB α （Ⅰ- κB α） protein level was detected by Western blot.
Results： The decrement of Ⅰ- κB a protein and the increasing NF- KB activity were found in cardiomyocytes pretreated with EPO before H/R compared to other groups （t=3.321, 4.183, P〈0.01）. However, after H/R, NF- κB activity and expression of TNF- α gene were significantly reduced, Ⅰ- κB a protein expression was increased in cardiomyocytes of E group compared to other groups （t=-3.425, 3.687, 3.454, P〈0.01）. All theses changes caused by EPO pretreatment were eliminated by the intervention of PDTC （an antagonist to NF- κB） during pretreatment.
Conclusions： EPO pretreatment can inhibit the activation of NF- κB and upregulation of TNF- α gene in cardiomyocytes exposed to H/R through a negative feedback of NF- κB signaling pathway, and thus produces the anti-inflammatory effect. This might be one of the ways EPO produces the anti-inflammatory effect.     

云南省宁蒗县不明原因猝死病例调查研究

目的探讨云南省宁蒗县不明原因猝死病例的死因。方法对云南省宁蒗县不明原因猝死病例进行现场流行病学调查,采集样本进行病理学、病毒学等相关检验及分析研究。结果猝死病例的临床表现类似阿-斯综合征发作,心电图示窦性心动过速、Q-T间期延长、ST段改变、室颤,病理检验主要以心肌间质水肿、弥漫性炎细胞浸润、心肌纤维断裂、心肌灶性坏死以及其他脏器炎细胞浸润等改变为主;同发病例的临床表现亦类似阿-斯综合征发作,心电图示Q-T间期延长、室扑,粪便标本病毒分离阴性,但是从中检测到了埃可病毒11型(ECHO11)的基因片段。结论猝死病例及同发病例与既往报道的云南地方性爆发性心肌炎类似,心肌炎性改变可能诱发快速心律失常,引起阿-斯综合征发作,最后导致发病甚至猝死。     

Three-dimensional magnetic resonance myocardial motion tracking from a single image plane.

Three-dimensional imaging for the quantification of myocardial motion is a key step in the evaluation of cardiac disease. A tagged magnetic resonance imaging method that automatically tracks myocardial displacement in three dimensions is presented. Unlike other techniques, this method tracks both in-plane and through-plane motion from a single image plane without affecting the duration of image acquisition. A small z-encoding gradient is subsequently added to the refocusing lobe of the slice-selection gradient pulse in a slice following CSPAMM acquisition. An opposite polarity z-encoding gradient is added to the orthogonal tag direction. The additional z-gradients encode the instantaneous through plane position of the slice. The vertical and horizontal tags are used to resolve in-plane motion, while the added z-gradients is used to resolve through-plane motion. Postprocessing automatically decodes the acquired data and tracks the three-dimensional displacement of every material point within the image plane for each cine frame. Experiments include both a phantom and in vivo human validation. These studies demonstrate that the simultaneous extraction of both in-plane and through-plane displacements and pathlines from tagged images is achievable. This capability should open up new avenues for the automatic quantification of cardiac motion and strain for scientific and clinical purposes.     

Cerebral Cortical Aquaporin-4 Expression in Brain Edema following Cardiac Arrest in Rats

OBJECTIVES: Brain edema occurs following clinical as well as experimental cardiac arrest (CA) and predicts a poor neurologic outcome. The objective of this study was to determine the expression of cerebral cortex aquaporin (AQP)-4, a member of a family of membrane water-channel proteins, in brain edema formation following normothermic or hypothermic CA. METHODS: Twenty-four rats were subjected to time-matched normothermic (N-Sham, 37.5 degrees C +/- 0.5 degrees C, n = 6) or hypothermic (H-Sham, 34 degrees C +/- 0.5 degrees C, n = 6) sham experiments and normothermic (N-CA, n = 6) or hypothermic (H-CA, n = 6) CA induced by asphyxiation for 8 minutes. Hypothermia was induced before CA. The animals were resuscitated with cardiopulmonary resuscitation, ventilation, and epinephrine administration. Brain edema was determined by brain wet-to-dry weight ratio at one hour of resuscitation. AQP4 immunoactivity in the cerebral cortex was determined using immunohistochemical staining and was semiquantified as an intensity of staining with an automated cell imaging system. RESULTS: Mild hypothermia in the sham experiments did not alter cerebral cortex AQP4 immunoactivity (mean +/- SD) (55.0 +/- 3.7 in H-Sham vs. 53.3 +/- 1.7 in N-Sham, p > 0.05). N-CA resulted in a significant increase in AQP4 immunoactivity (61.8 +/- 4.5) compared with N-Sham (p = 0.01) and H-Sham (p = 0.03). H-CA attenuated AQP4 compared with N-CA (53.4 +/- 1.3, p = 0.01). Brain wet-to-dry weight ratios were 4.41 +/- 0.07 in N-Sham, 4.40 +/- 0.08 in H-Sham (p > 0.05 vs. N-Sham), 4.55 +/- 0.04 in N-CA (p = 0.004 vs. N-Sham; p = 0.005 vs. H-Sham), and 4.43 +/- 0.09 in H-CA (p = 0.02 vs. N-CA; p > 0.05 vs. N-Sham and H-Sham). CONCLUSIONS: Cerebral cortical AQP4 expression is up-regulated after normothermic CA, which is attenuated by hypothermia induced before CA.     

Accelerating cardiac cine 3D imaging using k-t BLAST.

By exploiting spatiotemporal correlations in cardiac acquisitions using k-t BLAST, gated cine 3D acquisitions of the heart were accelerated by a net factor of 4.3, making single breathhold acquisitions possible. Sparse sampling of k-t space along a sheared grid pattern was implemented into a cine 3D SSFP sequence. The acquisition of low-resolution training data, which was required to resolve aliasing in the k-t BLAST method, was either interleaved into the sampling process or obtained in a separate prescan to allow for shorter breathhold durations in patients with heart disease. Volumetric datasets covering the heart with 20 slices at a spatial resolution of 2 x 2 x 5 mm3 were recorded with 20 cardiac phases in a total breathhold duration of 25-27 sec, or 18 sec if partial Fourier sampling was additionally employed. The feasibility of the method was demonstrated on healthy volunteers and on patients. The comparison of endocardial area derived from single slices of the 3D dataset with values extracted from separate single-slice acquisitions showed no significant differences. By shortening the acquisition substantially, k-t BLAST may greatly facilitate volumetric imaging of the heart for evaluation of regional wall motion and the assessment of ventricular volume and ejection fraction.     

补益中药对老龄雄性大鼠下丘脑神经递质——甲状腺轴机能作用的研究

本文通过对3月龄、18月龄、24月龄雄性大鼠下丘脑去甲肾上腺素(NE)、多巴胺(DA)、5-羟色胺(5-HT)、5-羟吲哚乙酸(5-HIAA),和下丘脑垂体促甲状腺释放激素(TRH)、垂体、血甲状腺释放激素(TSH)、血甲状腺激素(T_3、T_4)的测定,研究了大鼠下丘脑神经递质与甲状腺轴机能的增龄性变化,并在此基础上探讨了补益中药对老龄大鼠下丘脑—垂体—甲状腺机能的作用。结果提示:老龄大鼠下丘脑机能的减退是甲状腺轴机能减退的重要原因;补益中药可能改善了老龄大鼠下丘脑的调控机能,进而延缓了甲状腺轴机能的老年性变化。     

猪心肌球蛋白及其轻,重链亚基的纯化和鉴定

采用一种改进的方法，从１００ｇ猪心室肌中提取心肌肌球蛋白３７０ｍｇ，并进一步分离和纯化其亚基成分，分别得到肌球蛋白轻链２４ｍｇ和重链２１０ｍｇ，核酸含量＜１％，不含有肌动蛋白、原肌球蛋白、肌钙蛋白及其它杂蛋白；ＳＤＳＰＡＧＥ显示，猪心肌球蛋白重链为２００～２２０ＫＤ一条带，肌球蛋白轻链则为２７ｋｄ、２１．４ｋｄ、１９ｋｄ三条带；纯化猪心肌球蛋白的Ｃａ２＋激活ＡＴＰ酶活性为０．２４μｍｏｌＰｉ／（ｍｇ·ｍｉｎ），但其分离后的亚基则无此活性。     

火器伤后胸心异物存留

目的：探讨火器伤后胸心异物存留摘除的指征、时机、方法及结果。方法：回顾性分析了３９例火器伤后胸心异物存留摘除者的一般资料、临床表现、不同处理方法的选择及效果。结果：１９例患者早期因凝固性血胸及肺持续漏气伴异物存留或异物存留伴胸腔及心包腔化脓性感染，在开胸清创时做了异物摘除；另２０例患者为胸伤伤情恢复后单纯异物存留，因异物位于肺门、心脏及大血管旁或远期并发症等，而后期开胸异物摘除。结论：火器性胸部穿透伤后，因异物本身或其他原因所致早期并发症者，应在开胸清创的同时摘除异物；胸伤伤情恢复而单纯胸心异物存留，应选择性摘除或因并发远期并发症而摘除。     

Abnormal cardiac histology in severe intrauterine growth retardation infants

Four infants with severe intrauterine growth retardation (IUGR) weighing less than 1000 g at birth developed heart failure and died in our unit, where heart failure of IUGR infants is the main reason of death in extremely low birth-weight infants. The causes of their heart failure are one of the main themes in current neonatal medicine. The subjects of this study were four small for gestational age infants; all died due to heart failure 5 to 10 days after birth. Microscopic specimens of hearts from autopsies were evaluated with respect to the following characteristics: thickness of myocardial fibers, maturation of nuclei, presence of dysgenesis or necrosis in myocardium, and amount of glycogen in the heart. Neither dysgenesis nor infarction of the heart was found but hypoplasia in myocardial fibers and decreased glycogen levels were observed. Maturation delay in myocytes' nuclei did not appear to be severe. We conclude that these infants' hearts failed to adapt to postnatal hemodynamic changes because of inadequate myocardial function and inadequate glycogen reserves.