计算机X线摄影图像的静止滤线栅伪影分析

目的通过分析计算机X线摄影（CR）系统的采样频率和栅密度频率，提出尽可能有效避免滤线栅伪影出现的抑制方法。方法实际测试不同栅密度的滤线栅与不同规格的成像板（IP）匹配使用，得到不同效果的图像；模拟2种信号频率（即2种栅密度的滤线栅），采用3种采样频率[6、8、10图像空间分辨率（pixels／mm）]，得到不同的模拟图像效果。结果通过对比分析模拟图和实际图像，发现在采样频率正好等于信号频率的2倍时，可以得到正确的信号频率，图像清晰，无混淆现象。栅密度〈4LP／mm时，可较好地与14in×14in、10in×12in（1in=2．54cm）IP匹配使用。结论CR系统与普通IP匹配使用合适的采样频率和栅密度频率，可以有效避免滤线栅伪影出现。     

Mutant ryanodine receptors in catecholaminergic polymorphic ventricular tachycardia generate delayed afterdepolarizations due to increased propensity to Ca2+ waves.

AIMS: Mutations in cardiac ryanodine receptors (RyR2s) are linked to catecholaminergic polymorphic ventricular tachycardia (CPVT), characterized by risk of polymorphic ventricular tachyarrhythmias and sudden death during exercise. Arrhythmias are caused by gain-of-function defects in RyR2, but cellular arrhythmogenesis remains elusive. METHODS AND RESULTS: We recorded endocardial monophasic action potentials (MAPs) at right ventricular septum in 15 CPVT patients with a RyR2 mutation (P2,328S, Q4,201R, and V4,653F) and in 12 control subjects both at baseline and during epinephrine infusion (0.05 microg/kg/min). At baseline 3 and during epinephrine infusion, four CPVT patients, but none of the control subjects, showed delayed afterdepolarizations (DADs) occasionally coinciding with ventricular premature complexes. In order to study the underlying mechanisms, we expressed two types of mutant RyR2 (P2,328S and V4,653F) causing CPVT as well as wild-type RyR2 in HEK 293 cells. Confocal microscopy of Fluo-3 loaded cells transfected with any of the three RyR2s showed no spontaneous subcellular Ca(2+) release events at baseline. Membrane permeable cAMP analogue (Dioctanoyl-cAMP) triggered subcellular Ca(2+) release events as Ca(2+) sparks and waves. Cells expressing mutant RyR2s showed spontaneous Ca(2+) release events at lower concentrations of cAMP than cells transfected with wild-type RyR2. CONCLUSION: CPVT patients show DADs coinciding with premature action potentials in MAP recordings. Expression studies suggest that DADs are caused by increased propensity of abnormal RyR2s to generate spontaneous Ca(2+) waves in response to cAMP stimulation. Increased sensitivity of mutant RyR2s to cAMP may explain the occurrence of arrhythmias during exercise or emotional stress in CPVT.     

肺内源性和肺外源性呼吸衰竭机械通气的临床对比研究

目的探讨肺内源性和肺外源性呼吸衰竭机械通气时的肺保护性策略。方法通过25例呼吸衰竭中12例肺内源性和13例肺外源性机械通气临床资料的回顾性分析,对比研究两组呼吸力学差异时对通气模式选择、参数设置和调节的影响,以及肺保护的实施方法。结果在两组APACHE-Ⅱ评分、平均年龄和Vt设置无差异的条件(P>005)下,肺内源性组PEEP/CPAP、PSV、f的需设值均明显高于肺外源性组(P<001)。肺内源性组Pplat、PIP、Raw的监测结果大于肺外源性组,而Crs小于肺外源性组(P<001)。肺内源性组417%和肺外源性组154%因MOF而死亡(APACHE-Ⅱ评分均>20分),组间比较有显著差异(P<001)。结论肺内源性和肺外源性呼吸衰竭机械通气时,实施肺保护的方法不同。前者应首选压力预置通气模式,后者可首选容量预置通气模式。以设置中、小Vt为原则,按个体化的通气需求而设置f和加用恰当的PSV、CPAP/PEEP对减少VILI、病死率可能有益。     

中药高臀位灌肠治疗慢性肾功能衰竭疗效观察

目的 观察中药高臀位灌肠治疗慢性肾功能衰竭(chronic renal failure,CRF)的临床疗效.方法 将100例CRF患者随机分为两组,治疗组70例采用中药高臀化灌肠治疗,对照组30例口服活性炭治疗.结果 治疗组总有效率为88.6%,对照组总有效率为50.0%.结论 中药高臀位灌肠治疗CRF有效.     

Cardiac metastasis of renal pelvic cancer

Abstract:   A 66-year-old man was referred to our hospital with chest discomfort and shortness of breath. Seven months previously he had undergone a laparoscopic left nephroureterectomy for a left renal pelvic tumor and was given two cycles of adjuvant chemotherapy (methotrexate, epirubicin and cisplatin). Echocardiogram showed an 8-mm sized mass extending from the right atrium into the right ventricle. On computed tomography, multiple lung tumors, as well as the right atrial and ventricular mass, were seen. The patient died of acute heart failure caused by right ventricular outflow obstruction. On autopsy, a right atrial and ventricular metastasis of the initial transitional cell carcinoma was found. The patient's cause of death was acute heart failure as a result of cardiac metastasis of his initial renal pelvic carcinoma.     

生脉注射液对慢性心力衰竭患者凝血功能的影响

目的研究大剂量生脉注射液对慢性心功能衰竭（简称心衰）患者凝血功能的影响。方法将60例慢性心衰患者随机分为治疗组（即生脉注射液组）和对照组，每组各30例，治疗组给予生脉注射液加西药常规治疗，对照组仅西药常规治疗，观察用药前后心功能改善程度及血浆P-选择素、血管性血友病因子（vWF）和D-二聚体水平的变化。结果治疗组临床显效率与总有效率明显高于对照组。心是患者血浆P-选择素、vWF和D-二聚体水平明显高于健康人，治疗后两组患者血浆P-选择素、vWF和D-二聚体水平均下降，治疗组优于对照组。结论慢性心衰患者，体内存在着高凝状态，大剂量生脉注射液可改善慢性心衰患者的凝血功能，可能在一定程度上减少心衰患者血栓事件的发生和发展？     

Sudden Death and Staged Therapy for Hemodynamic Stabilization in Patients Enrolled in a Heart Transplantation Program

To investigate the impact of staged therapy for advanced heart failure on therapeutic endpoints, 236 consecutive patients (coronary artery disease/dilated cardiomyopathy in 61/175 patients, left ventricular ejection fraction 14%± 5%, New York Heart Association Class IIl/IIIIV in 102/79/55 patients, respectively) with advanced heart failure were prospectively followed. One hundred thirtyseven patients enrolled from January 1989 to December 1991 were treated conventionally with digoxin, furosemide, and low dose angiotension converting enzyme (ACE) inhibition. Patients refractory to this therapy underwent urgent heart transplantation. Ninetynine patients enrolled from January 1992 to August 1993 underwent staged therapy: stage 1: maximal tolerated ACE inhibition; stage 2: therapy with PGE₁ for preand afterload reduction to achieve hemodynamic stabilization; or stage 3: refractory patients bridged to heart transplantation with continuous outpatient dobutamine. Sudden death was defined as death within 1 hour of symptoms if heart failure symptoms remained stable over the previous 7 days. Conventionally treated patients were followed for 10 ± 9 months; patients who underwent staged therapy for 9 ±5 months. In the group of patients that underwent standard therapy, 39 of 137 (28%) patients died: 5 (13%) deaths occurred suddenly, and death due to progressive pump failure occurred in the remaining 34 (87%) patients. In the group of patients that underwent staged therapy, 25 of 99 (25%) patients died: 13 (52%) deaths occurred suddenly, and 12 (48%) deaths occurred due to progressive pump failure. Thus, patients who underwent staged therapy were at increased risk for sudden death (P = 0.01, relative risk 3.4, 95% confidence interval 1.2–9.7) but were at lower risk for death from pump failure (P = 0.009, relative risk 0.44, 95% confidence interval 0.22–0.84). In patients who underwent therapy with continuous outpatient PGE₁ (n = 7) or dobutamine (n= 21), risk for sudden death (P = NS by log rank test) did not increase. In conclusion, staged therapy significantly reduced death from pump failure; however, patients who could be stabilized and considered too well for heart transplantation were at increased risk for sudden death. Thus, overall survival did not improve. Of note, outpatient dobutamine did not increase the risk for sudden death.     

63例重症急性胆管炎的救治体会

作者报道15年间由胆石症导致的重症急性胆管炎（ACST）63例的救治，指出胆石症导致的重症急性胆管炎（ACST）并发多器官功能衰竭（MSOF）是良性胆道疾病最重要、最直接的死亡原因，强调一旦发生多器官功能衰竭，要给予强有力的“四大一支持”综合疗法。该疗法有助于ACST病人渡过手术关，在致死性的触发病因去除后，促进器官功能发生逆转，最终使患者获得痊愈。     

Multiple Cerebral Haematomata and Peripheral Nerve Palsies Associated with a Case of Juvenile Diabetic Ketoacidosis

A 15-year-old girl presented de novo in diabetic ketoacidosis having been comatose for 24 h (day 1). A CT scan and lumbar puncture performed on admission were normal and her conscious level slowly improved over several days. On day 7 she had central neurological signs of bilateral knee clonus and an extensor plantar response. In addition, she had developed lower motor neurological signs of an ulnar nerve palsy of the left forearm, and ulnar, median, and radial nerve palsies of the right forearm. Magnetic resonance imaging (MRI), performed on day 12, showed multiple small cerebral haematomata with appearances at least several days of age. The scattered lesions were localized particularly to the parieto-occipital region, with sparing of the basal ganglia and without cerebral oedema, a novel feature not previously described in juvenile ketoacidosis. Four months later there was minimal residual disability of her right arm. The clinical findings together with the MRI images suggested that the peripheral nerve and central lesions were temporally related, suggesting a common aetiology. However, it is likely that MRI showed cerebral lesions which may have been missed by the conventional CT scanning performed initially.     

Regeneration of kidney tubular epithelial cells

Conclusion The mechanisms that regulate regeneration of kidney epithelial cells after acute tubular necrosis are poorly understood. Repair of the nephron can take place in the adverse systemic metabolic setting caused by failure of renal function. This clinical observation suggests that factors released at the site of the tubular insult can mediate repair. Studies carried out in this and other laboratories show that kidney epithelial cells can release and respond to polypeptide growth factors which may thereby contribute to renal regeneration by autocrine and paracrine mechanisms. Specific growth factors secreted by cells and deposited in the tubular basement membrane prior to injury may subsequently participate in nephron repair. In addition, adenine nucleotides released from injured or dying cells at the injury site or provided exogenously could stimulate surviving renal epithelial cells at the edges of the wound to migrate along the basement membrane to rapidly reepithelialize the nephron and subsequently initiate mitogenesis to replace cells lost by necrosis.The nephrotoxic effect of many agents used in cancer chemotherapy and the older age of patients undergoing complicated surgical procedures has increased the incidence of ARF, whereas the mortality rate has not changed since the early 1950s [22]. Thus there is considerable need for innovative therapeutic strategies. An important goal of future research efforts is to identify new growth factors that facilitate migration, differentiation, and proliferation of renal epithelial cells at sites of tubular necrosis. Isolation and use of these agents in combination with dialysis and nutritional support could speed renal regeneration and thereby improve the outcome in patients with this condition.Abbreviations ARF acute renal failure - ECM extracellular matrix - EGF epidermal growth factor - FGF fibroblast growth factor - IGF insulin-like growth factor - MGSA melanocyte growth-stimulating activity - PDGF platelet-derived growth factor - IGF transforming growth factor