长达14.45秒的全心停搏一例

患者男性，73岁。因3周前无明显诱因出现眩晕于2005年7月5日入院。患者眩晕主要为体位变化和活动后发生，每次发作时间持续2～3min，休息后缓解，自发病以来，偶有打鼾，未发现睡眠呼吸暂停现象，无视物模糊，无黑嚎、意识障碍，无心悸、气促、呼吸困难，无恶心、呕吐，无肢体活动障碍。病人曾于2004年11月因头晕、胸闷，行动态心电图检查示：偶发房性早搏、偶发室性早搏、sT—T改变。冠状动脉造影示冠状动脉多支病变，行冠状动脉搭桥术。自冠状动脉塔桥术后服用：美托洛尔25mg，2次／日；地高辛0．125mg，1次／日。体格检查：心率76次／min，血压140／90mmHg（1mmHg=0．133kPa），各瓣膜区未闻及心脏杂音，双肺听诊呼吸音清。诊断：颈椎病，冠心病。行24h动态心电图检查，总心率：81244次；平均心率59次／min；最慢窦性心率24次／min（图1），最快窦性心率89次／min。〉2s的窦性停搏共799次，最长的全心停搏达14．45s（图2），发生于1：43：15睡眠时，此次停搏后恢复的第一个心搏为交界性逸搏，其后为交界性逸搏心律，窦性PP间距为24．59S；全程室性早搏30次，室上性早搏778次，短阵房性心动过速1次，ST—T水平型缺血改变，最明显时ST段压低0．20mV，长RR间距后ST—T压低无明显加重。动态心电图诊断：窦性心动过缓，窦性停搏、全心停搏，交界性逸搏心律，室性逸搏心律，频发房性早搏，短阵房性心动过速，偶发室性早搏，ST—T改变。     

Low-dose aspirin in patients recovering from myocardial infarction. Evidence for a selective inhibition of thromboxane-related platelet function

The adequacy, selectivity and long-term persistence of inhibitionin cyclooxygenase-dependent platelet function by a daily low-dose(0.45 mg kg^–1 day^–1) aspirin treatment have beenevaluated in 15 patients after a recent (less than 17 days)acute myocardial infarction. Serum thromboxane (TX) B₂, an indexof platelet TXA₂ production, was decreased by 94–98% (P<0.001)by aspirin, while urinary excretion of 6-keto-prostaglandinF^la, as an index of extraplatelet cyclooxygenase activity, remainedunchanged. Compared to placebo, aspirin induced a persistentincrease in bleeding time (% difference 45.6±21.4, mean± SD) and a decrease in platelet aggregation by ADP,epinephrine, collagen and arachidonic acid. No tendency towardsan attenuation of the effects was apparent for the period ofaspirin administration (4 weeks). Aspirin 0.45 mg kg^–1 day^–1 is adequate and selectivein the long-term inhibition of TX-related platelet functionin patients after acute myocardial infarction. The clinicaleffectiveness of such a regimen remains to be proven in clinicaltrials.     

Biotherapy for xenografted human central nervous system leukemia in mice with severe combined immunodeficiency using B43 (anti-CD19)- pokeweed antiviral protein immunotoxin

The study of central nervous system (CNS) leukemia has been hampered by the lack of a suitable animal model. We report that severe combined immunodeficiency (SCID) mice invariably develop rapidly progressive fatal CNS leukemia within 3 weeks after intravenous injection of NALM-6 pre-B acute lymphoblastic leukemia (ALL) cells. Colonization of the dura mater and subarachnoid space, usually of the distal spinal cord with occasional extension into the Virchow-Robin spaces of blood vessels subjacent to the meninges, followed involvement of bone marrow in the skull, vertebrae, and, occasionally, the appendicular skeleton. Occult CNS leukemia was detectable by polymerase chain reaction amplification of human DNA as early as 8 days postinoculation of leukemia cells. We used this in vivo model of human CNS leukemia to examine the therapeutic efficacy and toxicity of intrathecally administered B43 (anti-CD19)-pokeweed antiviral protein (PAP), an anti- B-lineage ALL immunotoxin directed against the pan-B-cell antigen CD19/Bp95. Intrathecal therapy with B43 (anti-CD19)-PAP immunotoxin at nontoxic dose levels significantly improved survival of SCID mice and was superior to intrathecal methotrexate therapy.     

Direct evidence for modified solvent structure within the hydration shell of a hydrophobic amino acid.

Neutron scattering experiments are used to determine scattering profiles for aqueous solutions of hydrophobic and hydrophilic amino acid analogs. Solutions of hydrophobic solutes show a shift in the main diffraction peak to smaller angle as compared with pure water, whereas solutions of hydrophilic solutes do not. The same difference for solutions of hydrophobic and hydrophilic side chains is also predicted by molecular dynamics simulations. The neutron scattering curves of aqueous solutions of hydrophobic amino acids at room temperature are qualitatively similar to differences between the liquid molecular structure functions measured for ambient and supercooled water. The nonpolar solute-induced expansion of water structure reported here is also complementary to recent neutron experiments where compression of aqueous solvent structure has been observed at high salt concentration.     

T cell-mediated immunity in murine malaria. II. Induction of protective immunity to P. chabaudi by antigen fed macrophages and antigen educated lymphocytes

We previously described assay systems for generating antigen specific proliferating T cells to P. chabaudi antigens. In the present study we examine whether the various sensitization approaches confer immunity against a cloned virulent strain IP-PCI of P. chabaudi. We present data indicating that effective specific protective immunity can be induced through P. chabaudi antigen fed macrophages and antigen educated spleen cells (initiator lymphocytes). The expression of this protective immunity is proposed to depend on (a) antigen presentation and/or accessory function of macrophages and (b) the subsequent activation of T cell functions related to protection. Indeed analysis of different macrophage populations revealed a correlation between the expression of Ia molecules and IL-1 secretion with their capacity to induce antigen specific T cells in vivo and subsequent protective immune mechanisms. Thus these results emphasize the critical functions of accessory cells in determining the outcome of malaria infections.     

Molecular basis of altered red blood cell membrane properties in Southeast Asian ovalocytosis: role of the mutant band 3 protein in band 3 oligomerization and retention by the membrane skeleton

Southeast Asian ovalocytosis (SAO) is an asymptomatic trait characterized by rigid, poorly deformable red cells that resist invasion by several strains of malaria parasites. The underlying molecular genetic defect involves simple heterozygous state for a mutant band 3 protein, which contains a deletion of amino acids 400 through 408, linked with a Lys 56-to-Glu substitution (band 3-Memphis polymorphism). To elucidate the contribution of the mutant SAO band 3 protein to increased SAO red blood cell (RBC) rigidity, we examined the participation of the mutant SAO band 3 protein in increased band 3 attachment to the skeleton and band 3 oligomerization. We found first that SAO RBC skeletons retained more band 3 than normal cells and that this increased retention preferentially involved the mutant SAO band 3 protein. Second, SAO RBCs contained a higher percentage of band 3 oligomer-ankyrin complexes than normal cells, and these oligomers were preferentially enriched by the mutant SAO protein. At the ultrastructural level, the increased oligomer formation of SAO RBCs was reflected by stacking of band 3-containing intramembrane particles (IMP) into longitudinal strands. The IMP stacking was not reversed by treating SAO RBCs in alkaline pH (pH 11), which is known to weaken ankyrin-band 3 interactions, or by removing the cytoplasmic domain of band 3 from SAO membranes with trypsin. Finally, we found that band 3 protein in intact SAO RBCs exhibited a markedly decreased rotational mobility, presumably reflecting the increased oligomerization and the membrane skeletal association of the SAO band 3 protein. We propose that the mutant SAO band 3 has an increased propensity to form oligomers, which appear as longitudinal strands of IMP and exhibit increased association with membrane skeleton. This band 3 oligomerization underlies the increase in membrane rigidity by precluding membrane skeletal extension, which is necessary for membrane deformation.