5分钟短时心率变异性自回归模型频域分析的临床应用价值

目的:基于自回归模型5min心率变异性频域分析的临床价值,检验糖尿病患者5min短时心率变异性自回归模型分析频域指标的变化。方法:实验对象为50岁以上糖尿病患者9例和正常人7例,糖尿病史>6年7例,糖尿病史<3年2例。被试者采用坐姿,静息状态,测试30min的ECG信号,采样率为1000Hz。对每个样本取第10～15分钟的时长5min的RR间期作为心率变异性信号,进行基于自回归模型的频域分析。依据功率谱估计计算16例受试者的总能量,低频段能量,高频段能量,低频段高频段能量比值等指标参数。结果:通过对5min心率变异性自回归模型计算结果得出,糖尿病史>6年患者总能量、低频段能量、高频段能量低于正常人,差异有显著性意义(t=2.4952,2.7027,1.7299,P<0.05)。糖尿病史<3年患者总能量、低频段能量、高频段能量与正常人差异不明显。两类糖尿病患者与正常人低频段高频段能量比值无明显差异。结论:5min短时心率变异性自回归模型分析能够有效反映糖尿病患者自主神经的病变,可能成为检测自主神经病变的方法。     

Diagnosis,treatment and complications of radial head and neck fractures in the pediatric patient

Radial head and neck fractures represent up to 14% of all pediatric elbow fractures and can be a difficult challenge in the pediatric patient. In up to 39% of proximal radius fractures, there is a concomitant fracture, which can easily be overlooked on the initial standard radiographs. The treatment options for proximal radius fractures in children range from non-surgical treatment, such as immobilization alone and closed reduction followed by immobilization, to more invasive options, including closed reduction with percutaneous pinning and open reduction with internal fixation. The choice of treatment depends on the degree of angulation and displacement of the fracture and the age of the patient; an angulation of less than 30 degrees and translation of less than 50% is generally accepted, whereas a higher degree of displacement is considered an indication for surgical intervention. Fractures with limited displacement and non-surgical treatment generally result in superior outcomes in terms of patient-reported outcome measures, range of motion and complications compared to severely displaced fractures requiring surgical intervention. With proper management, good to excellent results are achieved in most cases, and long-term sequelae are rare. However, severe complications do occur, including radio-ulnar synostosis, osteonecrosis, rotational impairment, and premature physeal closure with a malformation of the radial head as a result, especially after more invasive procedures. Adequate follow-up is therefore warranted.     

Comparison of bleeding tendency, factor XI coagulant activity, and factor XI antigen in 25 factor XI-deficient kindreds

The relationship of clinical bleeding tendency and factor XI antigen (XI:Ag) in factor XI deficiency was studied in 78 members of 25 factor XI-deficient kindreds. Factor XI:Ag was measured in a competitive radioimmunoassay, using monospecific, heterologous anti-factor XI antibody. 125I-labeled factor XI, and staphylococcal protein A as the precipitating agent. Deficiency of factor XI clotting activity (XI:C), less than 0.62 U/mL, occurred in 48 individuals, 22 of whom experienced postoperative or posttraumatic bleeding: Their mean factor XI:C was 0.21 +/- 0.04 U/mL (SEM), and factor XI:Ag was 0.23 +/- 0.04 U/mL. The remaining 26 had no clinical bleeding, many despite surgical challenge: Their mean factor XI:C was 0.30 +/- 0.04 U/mL, and factor XI:Ag was 0.34 +/- 0.05 U/mL. In all, 13 kindreds had between 1 and 11 members with bleeding; the other 12 had none with deficient hemostasis. Two heterozygous factor XI-deficient individuals appeared to be positive for cross-reacting material (CRM+). The slope of the regression line for factor XI:C and factor XI:Ag data points in the 78 individuals tested did not differ from control, and all points fell within 95% confidence limits derived from control. In conclusion, bleeding tendency appears to be consistent within a given kindred and is not determined exclusively by factor XI:C or factor XI:Ag levels.     

The modulated expression of Mo5, a human myelomonocytic plasma membrane antigen

Mo5 is a 94-kd protein antigen expressed by human peripheral blood monocytes, neutrophils, and by all bone marrow myeloperoxidase-positive myeloid precursors (promyelocytes, myelocytes, metamyelocytes, and bands). Mo5 is borne by the malignant cells of 74% of patients (N = 27) with acute monocytic leukemia (French-American-British [FAB] group M4, M5), and 50% of patients (N = 38) with acute granulocytic leukemia (FAB M1, M2, and M3). Nonmyeloid cells in peripheral blood and bone marrow are Mo5-negative. The surface expression of Mo5 by myeloid cells is modulated by several experimental conditions: Exposure of neutrophils to calcium ionophore (1 mumol/L, 37 degrees C, ten minutes) under conditions resulting in degranulation of specific granules produces a three- to fourfold increase in the plasma membrane density of Mo5 antigen. This suggests that, in neutrophils, there is an intracellular pool of Mo5 antigen, which may be associated with specific granules, and that granule-associated Mo5 is translocated to the plasma membrane upon degranulation. Conversely, incubation of monocytes, neutrophils, U- 937, and Mo5-positive leukemia cells in medium containing anti-Mo5 monoclonal antibody results in a significant decrease in surface Mo5 expression. This loss of surface Mo5 is a rapid, temperature-dependent process (occurring within 30 minutes at 37 degrees C) that is produced by divalent anti-Mo5 immunoglobulin [F(ab')2 but not F(ab)]. After down- modulation, Mo5 is reexpressed by monocytes within 48 hours. Mo5 is therefore a human myelomonocytic differentiation antigen whose expression is modulated up or down depending on the nature of extracellular stimuli.     

Intensive cytotoxic therapy followed by autologous bone marrow transplantation for non-Hodgkin's lymphoma of high-grade malignancy

Fourteen patients with non-Hodgkin's lymphoma (NHL) of high-grade malignancy were treated with cyclophosphamide and total body irradiation followed by autologous bone marrow transplantation (ABMT). All patients were pretreated with conventional chemotherapy. Three of four patients with drug-resistant disease achieved complete remission (CR), but relapse occurred within six months. Four patients in partial remission (PR) achieved CR; one died because of sepsis, two relapsed within six months, and one is still in CR 28+ months later. Six were treated in CR, five in first CR, and one in second CR. From these six patients (who received this treatment as consolidation therapy), five are in unmaintained CR seven to 31+ months after ABMT (one patient died of a secondary illness). There were two therapy-related deaths, both in patients with a poor clinical condition. Toxicity of this treatment was mild for those receiving transplants who were in better condition. These preliminary results suggest that intensive cytoreductive therapy followed by ABMT may improve disease-free survival in patients in NHL of high-grade malignancy in CR.     

A monoclonal antibody that inhibits activation of human Hageman factor (factor XII)

A monoclonal antibody to human Hageman factor (HF, factor XII) was derived from BALB/c mouse spleen cells fused with NS-1 mouse myeloma cells. This antibody, purified from ascites fluid, reacted with HF to inhibit the activation of HF, purified or in normal pooled plasma, as measured by a coagulation assay. The antibody did not inhibit the coagulant activity of activated HF. The antibody also inhibited the generation of amidolytic activity in HF-ellagic acid mixtures, but failed to inhibit the amidolytic properties of the carboxy-terminal fragment of HF (HFf). Amidolytic activity, absent in an HF-monoclonal antibody mixture, was generated upon treatment with insoluble trypsin. Monoclonal antibody, bound to CNBr Sepharose 4B gel (Pharmacia Fine Chemicals, Piscataway, NJ), reversibly bound HF in plasma or in buffer, without activating it. HF was then eluted with 4 mol/L guanidine HCI. The passage of 125I-labeled HF enzymatically cleaved by trypsin through a column of monoclonal antibody-CNBr Sepharose 4B gel resulted in flow- through of HFf with a molecular weight (mol wt) of 30,000 and HF fragments of mol wt 12,000. Elution with 4 mol/L guanidine HCI yielded several HF fragments (mol wt 80,000, 52,000, and 40,000) but not HFf. These data suggest that the single determinant recognized by the murine monoclonal antibody is not on HFf, but rather on the amino-terminal fragment thought to be involved in the binding activity of HF. The monoclonal anti-HF bound to CNBr-activated Sepharose 4B gel could be used to artificially deplete plasma samples of HF.     

Von Willebrand factor in the vessel wall mediates platelet adherence

A monoclonal antibody directed against the von Willebrand factor moiety (vWF) of factor VIII-von Willebrand factor (FVIII-vWF), which blocks ristocetin-induced platelet aggregation as well as the binding of FVIII- vWF to platelets in the presence of ristocetin, inhibited platelet adherence to human artery subendothelium when present in normal flowing blood. This monoclonal antibody, CLB-RAg 35, inhibited platelet adherence as a function of the shear rate. At wall shear rates below 500 s-1, platelet adherence was not affected, but at higher shear rates platelet adherence was gradually inhibited, reaching an average of 11% of the normal value at 2,500 s-1. Indirect immunofluorescence established the reactivity of CLB-RAg 35 with vWF present in artery subendothelium. Pretreatment of normal vessel walls with this antibody inhibited adherence of platelets in blood from a patient with severe homozygous von Willebrand's disease and in blood from normal individuals. The inhibition was shear-rate dependent and significant at high shear rates (2,500 s-1). By adding increasing amounts of purified FVIII-vWF to normal blood, the inhibition was gradually overcome. These data indicate that vWF present in the vessel wall contributes appreciably to platelet adherence. At high wall shear rates, platelet adherence is mediated virtually completely by both plasma FVIII-vWF and vWF in the vessel wall. At low wall shear rates (below 500 s-1), platelet adherence occurs independent of FVIII-vWF in plasma and vWF in the vessel wall.     

Amphotericin B-induced injury in stored human platelets

Administration of intravenous amphotericin B is a major factor in the reduction of the recovery of transfused platelet concentrates (PCs). For the study of possible drug-induced platelet lesions, fresh platelets and stored PCs were incubated with therapeutic concentrations of amphotericin B (10-50 micrograms/mL) and examined for membrane changes by scanning electron microscopy. Stored platelets demonstrated the formation of "pits" on the surface membrane, which were maximal immediately after preparation and gradually decreased with storage. The number of pits was significantly higher after exposure to amphotericin B. No increase was detected in fresh platelets following exposure to amphotericin B. The maximal effect of the drug was seen after 5 days of storage as PCs. Amphotericin B did not affect platelet shape or the number of pseudopodia. There was no correlation between pit formation and the pH, pO2, or pCO2 of the concentrates. Amphotericin B did not release 51Cr from prelabeled stored platelets after 2 hours' incubation at 37 degrees C. Thus, amphotericin B appears to exacerbate a membrane lesion induced by the preparation and storage of PCs.     

Thymus in the superior mediastinum simulating adenopathy: appearance on CT

A soft-tissue nodule was identified in the mediastinum superior to the left brachiocephalic vein in six patients undergoing computed tomography (CT) of the chest. In one case, biopsy of the mass showed that it was thymic tissue. In the remaining cases, the nodule was identified as thymus on the basis of the CT findings. The findings include equal density of the superior mediastinal nodule and the thymic lobes anterior to the ascending aorta, no displacement or narrowing of adjacent arteries, absence of a fat plane between the nodule and the thymic lobes, and parallel reduction in size of the nodule and the rest of the thymus. Two patients were examined with magnetic resonance (MR) imaging. Sagittal MR images demonstrated continuity of the superior mediastinal nodule with the more caudal portion of the thymus. Recognition of this normal variant in children is important in order to avoid unnecessary mediastinal biopsies or overstaging of malignancies.