应用通气阈控制男性肥胖型高血压患者的运动强度

目的:利用通气阈,观察男性肥胖高血压患者的适宜运动强度。方法:2004年从江西高校选取41例男性肥胖高血压者为观察对象。他们除了发现血压高、体质量指数超标外,无其他慢性病,平时不参加体育锻炼,受试者均知情同意。①运动处方的制定:以通气阈作为运动强度(相当于60%最大心率),让受试者进行为期1年的快走锻炼,运动时间为60min/次,隔日1次。每周三四次。②分别在实施运动处方前后按常规方法,各测定1次安静状态下的收缩压、舒张压、平均动脉压、心率和体成分、体质量、体质量指数、腰围、臀围、体脂、皮下脂肪面积、内脏脂肪面积。③要求受试者进行有氧运动,在达到通气阈时,记录下吸氧量、功率、心率、心率差、最高心率百分比、心率贮备百分比、主观运动强度、收缩压、平均动脉压、舒张压。结果:41例受试者全部进入结果分析。①实施运动处方前、后安静状态时各指标变化:体质量[(83.5±11.4),(78.1±7.4)kg]、体质量指数[(28.9±3.5),(27.2±2.3)kg/m2]、腰围[(95.4±8.3),(89.3±5.7)cm]、臀围[(100.6±5.9),(98.3±4.3)cm]、腰臀围比(0.95±0.05,0.91±0.04)、体脂百分比[(29.8±4.5)%,(26.6±4.3)%]、皮下脂肪面积[(147.8±35.1),(123.4±43.4)cm2];内脏脂肪面积[(109.8±57.2),(82.7±42.6)cm2]、内脏脂肪面积/皮下脂肪面积(0.80±0.51,0.72±0.39)、收缩压[(153.3±11.9),(127.0±12.1)mmHg]、舒张压[(97.0±12.6),(80.1±7.7)mmHg]和平均动脉压[(115.8±10.4),(95.7±8.7)mmHg]都有显著性改善(t=4.956～6.772,P<0.05或0.01)。②实施运动处方前、后,在通气阈时各指标变化:吸氧量[(13.5±2.1),(16.3±2.4)mL/(kg·min)]、功率[(75.1±16.5),(102.4±17.0)W],收缩压[(172.9±22.3),(149.3±15.9)mmHg]、舒张压[(100.1±16.4),(86.8±6.6)mmHg]及平均动脉压[(124.4±17.0),(107.7±7.0)mmHg]都有显著性改善(t=4.112～5.223,P<0.05);心率、心率差、最高心率百分比、心率贮备百分比以及主观强度感觉也都有改善。结论:对于男性肥胖高血压患者,可以采用通气阈确定其适宜运动强度,即运动强度是60%最高心率、30%心率贮备和主观运动强度12。     

The differentiation of delayed hemolytic and delayed serologic transfusion reactions: incidence and predictors of hemolysis

BACKGROUND: After differentiation of the entities of clinically detectable delayed hemolytic (DHTR) and delayed serologic transfusion reactions (DSTR), previous investigators calculated a DHTR:DSTR incidence ratio of 18:72 from a retrospective review of patients with serologic evidence of DHTR or DSTR. There are no published data on factors that may influence the occurrence of DHTR versus DSTR in a given patient. STUDY DESIGN AND METHODS: Retrospective review was conducted of 292 patients at the Mayo Clinic who, between 1980 and 1992, received a clinical diagnosis of DHTR or DSTR concurrently with a serologic diagnosis. Red cell alloantibody specificity, the activity of the patient's reticuloendothelial system, and concurrent immunosuppression were evaluated as potential predictors of the occurrence of DHTR versus DSTR in different patients. RESULTS: The incidence of DHTR or DSTR was 1 in 1899 allogeneic red cell units transfused, with a DHTR:DSTR ratio of 36:64. Alloantibody specificity was the only variable that affected the occurrence of DHTR versus DSTR at the clinical level, with the anti-Jka and anti-Fya specificities, as well as multiple coexisting specificities, significantly associated with detectable hemolysis (p < 0.05). CONCLUSION: Clinically detectable DHTRs are found to occur more commonly than previously believed when the clinical and serologic diagnoses are made concurrently and appropriate work-ups for hemolysis are ordered. The association of certain alloantibody specificities with detectable DHTRs may have implications for clinical transfusion practice.     

生物学疗法在亚洲炎症性肠病患者中的应用前景

在不断揭秘炎症性肠病(IBD)发病机制的过程中,发现越来越多的具有治疗干预作用的靶点[1.2].目前一般认为溃疡性结肠炎(UC)与克罗恩病(CD)均是肠道对尚未明确的环境触发因素发生过度免疫反应所致.这一概念开启了发展针对肠道微观生物医学(the intestinal microbiome)进行干预治疗的设想.此外,针对抗原处理与递呈、T细胞激活、抑制促炎细胞因子/趋化因子、刺激抗炎细胞因子、抑制血液循环中炎症细胞募集、游走与粘附、抑制炎性细胞及其产物(如自由基)及刺激上皮细胞修复与重建等的治疗干预措施也得到了发展或应用.     

Nonrandom involvement of the 12p12 breakpoint in chromosome abnormalities of childhood acute lymphoblastic leukemia

We studied the presenting clinical and biologic features of 23 children with acute lymphoblastic leukemia (ALL) whose leukemic marrow karyotypes contained abnormalities involving the short arm of chromosome 12. Nineteen of the abnormalities were assigned to the 12p12 breakpoint. The median age of the children was 5 years (range 2 to 13 years) and their initial leukocyte counts ranged from 1,800 to 424,000/microL (median 30,000/microL). Twenty-one patients (91%) had common phenotype ALL (CALLA+, HLA-DR+), including three cases with a pre-B cell phenotype (CIg+). The remaining two cases were T cell in origin. The French-American-British (FAB) morphologic type of lymphoblastic leukemia was L1 in all cases but one. With a median follow-up of 11 months, four patients have relapsed and another failed induction therapy. The modal chromosome number in all cases was less than 50. Three distinct cytogenetic patterns, with apparently similar clinical manifestations, were noted: terminal deletions of chromosome 12 in 10 cases, apparently balanced reciprocal translocations in 6, and unbalanced translocations in 7. All translocations were between the 12p arm and different donor chromosomes except for chromosomes 7, 9, and 17, which participated twice. Only two patients had identical translocations: t(7;12)(q11;p12). This unusual variation in donor chromosomes and breakpoints suggests that translocations involving the 12p are specific with respect to only one member of the translocation pair, namely chromosome 12. The relatively high frequency of the 12p abnormalities in this study (10% of all completely banded cases seen over a 35-month period) warrants further investigation.     

Serum levels of CD8 antigen in childhood lymphoid malignancies: a possible indicator of increased suppressor cell activity in poor-risk patients

Serum concentrations of CD8 antigen were measured at diagnosis with an enzyme-linked immunoassay in children with acute lymphoblastic leukemia (n = 344) or non-Hodgkin's lymphoma (n = 65). All patients had detectable levels of the serum antigen, which in its soluble nonreduced form appeared to be a 52-Kd homodimer as compared with the 66-Kd surface membrane component on most thymocytes and on a subset of functionally distinct T cells (suppressor/cytotoxic). Increased serum levels of CD8 in leukemia patients were significantly related to recognized high-risk prognostic features: high leukocyte count, large liver and spleen size, high serum lactic dehydrogenase level, T-cell immunophenotype, presence of a mediastinal mass, pseudodiploid karyotype, DNA index less than 1.16, and chromosomal translocation. Children with serum CD8 levels greater than or equal to 450 U/mL were more likely to fail treatment than were those with lower levels (P = .002), even in the group with non-T-cell leukemia (P = .003). In a multivariate analysis, serum CD8 antigen contributed independent prognostic information beyond that conveyed by age, leukocyte count, and race (P = .02). High serum CD8 antigen levels also correlated with advanced stages of disease in children with non-Hodgkin's lymphoma or B- cell leukemia. Children with higher serum CD8 antigen levels (greater than or equal to 700 U/mL) had a poorer treatment outcome (P = .003), even after results were adjusted for disease stage and serum lactic dehydrogenase level (P = .05). Measurement of serum levels of CD8 antigen not only has important prognostic value in childhood lymphoid malignancies but also could be useful in assessing the immunoregulatory role of T cells in patients with cancer.     

Cytokine-specific regulation of urokinase receptor (CD87) expression by U937 mononuclear phagocytes

Mononuclear phagocytes concentrate urokinase-type plasminogen activator (uPA) at the cell surface by expressing membrane uPA receptors (uPAR). This study examines the ability of exogenous cytokines to alter expression of membrane-associated uPA and uPAR in U937 mononuclear phagocytes. Cells were stimulated with recombinant interferon gamma (IFN gamma) or tumor necrosis factor alpha (TNF alpha), followed by immunolabeling for uPA or uPAR and flow cytometry. IFN gamma increased surface uPA 2.2-fold relative to unstimulated controls (P < .001), whereas TNF alpha had no significant effect. Likewise, maximal uPA binding capacity was increased 2.8-fold by IFN gamma (P < .02), but was not affected by TNF alpha. In unstimulated cells, 50% of receptors were occupied by endogenously generated uPA, and this proportion was not affected by either cytokine. IFN gamma upregulated uPAR 2.1-fold relative to unstimulated controls (P < .001), whereas TNF alpha had no effect. In contrast to effects on surface protein, TNF alpha induced a substantial increase in uPAR mRNA, equaling the effect of IFN gamma. In addition, both cytokines doubled the intracellular uPAR pool (P < .01). By contrast, TNF alpha induced a 2.5-fold increase in the level of uPAR protein released into conditioned medium (compared with unstimulated cells), whereas IFN gamma had no effect. These results indicate that uPAR expression is regulated in a cytokine-specific fashion. Some stimuli, such as TNF alpha, may increase uPAR synthetic activity without a corresponding change in membrane expression, because of enhanced release of uPAR from the cell. Cytokine-specific modulation of uPAR may be important in regulating the function of mononuclear phagocytes in inflammation and tissue repair.     

Cytogenetic features and serum lactic dehydrogenase level predict a poor treatment outcome for children with pre-B-cell leukemia

Leukemic cells from 89 (24%) of 369 children with newly diagnosed acute lymphoblastic leukemia (ALL) were found to have a pre-B immunophenotype. By comparison with blasts having the common ALL phenotype, the pre-B cells were more likely to have a DNA index less than 1.16 (P = 0.02), a pseudodiploid karyotype (P less than 0.001), and a chromosomal translocation (P = 0.001). Increased serum lactic dehydrogenase levels (P = 0.001) were also characteristic of pre-B ALL; otherwise, the clinical and laboratory features of the two groups were similar. A nonrandom chromosomal translocation, t(1;19)(q23;p13.3), was identified in blast cells from 16 (23%) of the 70 patients with pre-B ALL and adequate chromosome banding studies; different translocations were found in 11 of the remaining patients. The presence of any chromosomal translocation in the pre-B group was significantly related to a higher leukocyte count, an increased level of serum lactic dehydrogenase, an increased percentage of S-phase cells, black race, and a blast cell DNA index less than 1.16. Four presenting features were found to confer an increased risk of treatment failure among pre-B patients: pseudodiploidy, chromosomal translocation, black race, and higher serum lactic dehydrogenase level. In a multivariate analysis, pseudodiploidy emerged as the strongest factor for predicting relapse in pre-B ALL. The frequent association of chromosomal abnormalities of known adverse prognostic significance and high serum lactic dehydrogenase levels with pre-B-cell ALL explains, at least in part, the poor treatment outcome reported for children with this subtype of leukemia.