Pacemaker Inhibition by Myopotentials Detected by Holter Monitoring

Ambulatory eiectrocardiography revealed myopoiential inhibition of a demand ventricular pacemaker in each of two patients. Although it was first regarded as artifact, fine baseline osciliations observed during apparent pacemaker malfunction actualiy signalled skeletal muscie-induced pacemaker inhibition. Though not widely recognized, myopotential inhibition may be a common occurrence in unipolar lead systems. As greater numbers of patients undergo ambulatory monitoring, awareness of this phenomenon should become more widespread     

嗜铬细胞瘤切除术中麻醉处置不当并发脑梗死

1 病例资料 女,68岁.体检时B超发现结石性胆囊炎、右肾上腺实质性占位病变,考虑嗜铬细胞瘤,以结石性胆囊炎,右肾上腺占位病变收入院.既往有高血压病、糖尿病2年,曾口服依那普利、格列齐特,血压控制在130～140/90～80 mmHg,血糖6.0 mmol/L;1年前曾发生脑梗死,治疗后好转.     

5，7-DHT诱导5-HT神经元毁损致小鼠抑郁表现

目的：通过侧脑室注射5-HT（5-羟色胺，5-Hydroxytryptamine）类似物5,7-DHT（5，7-双羟色胺．5,7-dihydroxytryptamine），毁损中缝背核的5-HT能神经元，通过行为学评估研究其是否导致小鼠抑郁样症状，探讨5-HT在抑郁发病机制中的作用。方法：C57BL/6J小鼠经脑室注射5，7-DHT后14天，观察体重变化，并使用强制游泳实验、悬尾实验评估其是否出现抑郁症状，并用免疫组织化学方法观察中缝背核5-HT神经元的残存情况。结果：侧脑室中注射5，7-DHT后14天，脑中中缝背核的5-HT能神经元几乎完全消失，被GFAP阳性的星形胶质细胞所代替，小鼠体重几乎不增加、强制游泳实验和悬尾实验中的“无动时间”均明显延长，表现出明显的抑郁症状。结论：5，7-DHT可以毁损5-HT神经元，引起抑郁症状，提示5-HT在抑郁症的发病机制中发挥着-定作用。a     

Modulation of emotion by cognition and cognition by emotion

In this study, we examined the impact of goal-directed processing on the response to emotional pictures and the impact of emotional pictures on goal-directed processing. Subjects (N=22) viewed neutral or emotional pictures in the presence or absence of a demanding cognitive task. Goal-directed processing disrupted the BOLD response to emotional pictures. In particular, the BOLD response within bilateral amygdala and inferior frontal gyrus decreased during concurrent task performance. Moreover, the presence of both positive and negative distractors disrupted task performance, with reaction times increasing for emotional relative to neutral distractors. Moreover, in line with the suggestion of the importance of lateral frontal regions in emotional regulation [Ochsner, K. N., Ray, R. D., Cooper, J. C., Robertson, E. R., Chopra, S., Gabrieli, J. D., et al. (2004). For better or for worse: neural systems supporting the cognitive down-and up-regulation of negative emotion. NeuroImage, 23(2), 483-499], connectivity analysis revealed positive connectivity between lateral superior frontal cortex and regions of middle frontal cortex previously implicated in emotional suppression [Beauregard, M., Levesque, J., and Bourgouin, P. (2001). Neural correlates of conscious self-regulation of emotion. J. Neurosci., 21 (18), RC165.; Levesque, J., Eugene, F., Joanette, Y., Paquette, V., Mensour, B., Beaudoin, G., et al. (2003). Neural circuitry underlying voluntary suppression of sadness. Biol. Psychiatry, 53 (6), 502-510.; Ohira, H., Nomura, M., Ichikawa, N., Isowa, T., Iidaka, T., Sato, A., et al. (2006). Association of neural and physiological responses during voluntary emotion suppression. NeuroImage, 29 (3), 721-733] and negative connectivity with bilateral amygdala. These data suggest that processes involved in emotional regulation are recruited during task performance in the context of emotional distractors.