The effects of brisk walking on markers of bone and calcium metabolism in postmenopausal women

Weight-bearing exercise has been shown to maintain or increase bone mass in younger as well as older individuals but the mechanisms by which mechanical loading affects bone metabolism are not known in detail. Twelve postmenopausal women participated in a single bout of brisk walking (50% of VO_{2 max}) for 90 minuttes. Calciotropic hormones and markers of type I collagen formation (PICP) and degradation (ICTP) were measured before the exercise, and 1, 24, and 72 hours following the exercise. Total body bone mineral content (BMC) and density (BMD) were measured by dual energy X-ray absorptiometry (DXA). Brisk walking did not induce any significant changes in the concentrations of ionized calcium, parathyroid hormone (PTH), calcitonin, or osteocalcin. A significant increase of PICP was noted 24 and 72 hours (P<0.01) after exertion and a significant decrease in the concentration of serum ICTP at 1 hour (P<0.05) was followed by an increase at 72 hours (P<0.001). There was no significant difference between the increases in the concentrations of PICP and ICTP at 72 hours. Strong inverse correlations between the basal levels of PTH and BMD (r=−0.78;P<0.01) as well as between osteocalcin and BMD (r=−0.83;P<0.01) were noticed. The changes in serum levels of bone collagen markers indicate an altered bone collagen turnover due to this moderate endurance exercise. The results also support the fact that serum levels of PTH as well as those of osteocalcin are associated with total body BMD in postmenopausal women.     

Effect of haemodialysis on serum levels of tumour markers in patients with end-stage renal failure

SUMMARY: We studied the effect of haemodialysis on the serum levels of tumour markers in 78 patients, 49 men and 29 women with a mean age of 61 ± 2 years, who had been undergoing haemodialysis for 39 ± 10 months. No patient had any clinical evidence of malignancy. Serum values of carcinoembryonic antigen (CEA), alpha-fetoprotein (AFP), squamous-cell-carcinoma-related antigen (SCC), neuron-specific enolase (NSE), tissue polypeptide antigen (TPA), CA 15-3, CA 19–9, and among males prostate-specific antigen (PSA) were determined before and after dialysis. Postdialysis values, after being corrected for haemoconcentration, were compared with predialysis values. A significant increase of 32% was observed in NSE levels ( P <0.001) and of 21% in CA 15-3 ( P <0.001) after haemodialysis. A lesser, but still statistically significant, increase (8-12%) was observed in SCC, AFP and CEA levels ( P <0.05), while the values of the remaining three markers remained unchanged. In conclusion, an increase in some tumour markers was found in our patients after dialysis, a finding which requires further investigation.     

联合检测肿瘤标志物对良恶性胸腔积液的诊断价值

目的:探讨联合检测肿瘤标志物ProGRP、CEA、CYFRA21-1、NSE、SCC对良恶性胸腔积液的诊断价值。方法:收集2020年1月-2021年1月在包头医学院第一附属医院收治的确诊为良性胸腔积液(BPE,87例)和恶性胸腔积液(MPE,44例)患者,共131例。应用化学发光法检测患者胸腔积液中ProGRP、CEA、CYFRA21-1、NSE以及SCC的浓度,比较良恶性胸腔积液中肿瘤标志物的水平,将5种肿瘤标志物以不同的方式组合,通过受试者工作特征(ROC)曲线分析比较不同联合方式的诊断价值。结果:ProGRP+CEA+CYFRA21-1+NSE联合方式对应的ROC曲线下面积(AUC)最大(0.841),其约登指数最大时,灵敏度77.3%,特异度85.1%,阳性似然比5.188,阴性似然比0.267,诊断价值最高。结论:通过联合检测不同组合的肿瘤标志物发现,ProGRP+CEA+CYFRA21-1+NSE的组合形式在诊断效能、特异度、灵敏度、阳性似然比、阴性似然比等方面优于其他组合,在鉴别诊断胸腔积液性质方面有重要参考价值。     

维持性血液透析患者血栓前状态标志物变化及临床意义

目的:探讨终末期肾衰竭维持性血液透析患者血栓前状态标志物的变化.方法:59例维持性血液透析患者,血液透析前采静脉血4.5ml,30名健康志愿者作为对照组,清晨空腹采静脉血4.5ml,用ELISA测定血浆凝血酶-抗凝血酶复合物(TAT)、纤维蛋白肽A(FPA)、蛋白C(PC)、血管性血友病因子(vWF)、P-选择素(P-Selectin)、血栓前体蛋白(TpP)、D-二聚体(DD)含量.结果:与健康对照组相比,维持性血液透析患者组血浆TpP、TAT、vWF、FPA、DD显著升高(P＜0.05);P-选择素、PC显著下降(P＜0.01).结论:终末期肾衰竭维持性血液透析患者存在血栓前状态标志物异常,提示可能存在血栓前状态.     

De novo proximal interstitial deletions of 14q: Cytogenetic and molecular investigations

We report on 2 unrelated patients who had chromosome analysis performed because of psychomotor delay, Failure to thrive, and minor anomalies. Each patient had a novel proximal 14q deletion (q11.2 to q21.1 in patient 737 and q12 to q22 in patient 777). Polymorphic (C-A)_n microsatellite markers distributed along the length of chromosome 14q were examined in both patients and their parents in order to determine which marker loci were deleted. The deletion in patient 737 was found to be paternal in origin, based on the analysis of 2 marker loci (D14S54 and D14S70), thus assigning these loci to the deleted interval q11.2 q21.1. Furthermore, 3 loci were not deleted (TCRD, D14S50, and D14S80), suggesting that they are within or proximal to 14q11.2. In the other family (patient 777), none of the markers were fully informative, but the deleted chromosome was determined to be paternally derived based on cytogenetic heteromorphisms. Despite having overlapping proximal 14q deletions, these 2 patients shared few phenotypic similarities except for failure to thrive, micrognathia, and hypoplasia of the corpus callosum. Therefore, a distinct proximal 14q deletion syndrome is not yet apparent. However, the molecular analyses facilitated the localization of several 14q DNA markers to the deletion regions in these 2 patients, while excluding other markers from each deletion. © 1994 Wiley-Liss, Inc.     

A longitudinal study of the IgG antibody response to HIV-1 p17 gag protein in HIV-1+ patients with haemophilia: titre and avidity.

The IgG response to HIV-1 p17 gag protein was studied for up to 6 years in 12 HIV-1-infected patients with haemophilia, who had seroconverted between 1982 and 1985. To assess any prognostic value, p17 IgG titres were compared with p24 IgG titres, CD4 cell counts and p24 antigenaemia. p17 IgG avidity index was also examined. A strong similarity was found between the IgG titre to HIV-1 p17 and that to p24. In patients who developed AIDS the decline in p17 IgG titres could precede by several years the drop in CD4 cells to under 200 cells/microliters; whereas some long-term asymptomatic patients (CDCII) had increasing p17 IgG titres and stable CD4 cell counts. Declining p17 and p24 IgG titres were not always associated with an increase in p24 antigenaemia. IgG titres were found to be better predictors of disease progression than CD4 cell counts or p24 antigenaemia. Patients who developed AIDS during the study were also characterized by a lower p17 IgG avidity than patients who remained asymptomatic. This result suggests that IgG avidity could have prognostic relevance and be of importance for host resistance to AIDS onset.     

Demonstration of T4, T8, M1 and B7 determinants on human T cells with a rosette test: implications for the assay specificity of monoclonal antibodies

Under optimal test conditions significantly more freshly isolated human T cells reacted with OKT4, OKT8, OKM1 and OKB7 monoclonal antibodies (Mabs) in the indirect antiglobulin rosetting reaction (IARR) than by indirect immunofluorescence. Rabbit erythrocytes (E) coated with anti-mouse immunoglobulin were more sensitive indicator cells in the IARR than similarly coated sheep E. Treatment of T cells with neuraminidase further enhanced T cell reactivity in the IARR with each Mab so that an average of 60% or more of T cells were T4+, T8+ and M1+ and at least 40% had the T4+ T8+ phenotype. The various findings suggest that the rosette assay detects determinants on T cells that are expressed below the detection threshold of immunofluorescence. Moreover, these findings indicate that the cellular specificities of a particular Mab may change when one assay system is substituted for another or when the protocol of a particular assay is altered.     

Simultaneous Detection of ACP1 and GC Genotypes Using PCR/SSCP

The classical enzyme and protein markers ACP1 and GC have gained new importance because of the biological functions of their gene products. ACP1 encodes a low molecular weight enzyme which is now recognized as a phosphotyrosine phosphatase with a role in the regulation of signal transduction pathways, and GC‐globulin acts both as a transporter of vitamin D and as a plasma actin scavenger and plays a role in macrophage activation. These two polymorphisms were phenotyped for decades on the basis of electrophoretic isozyme or protein patterns; the gene structures are now known. Nucleotide substitutions determining the common alleles are close enough at each locus to be contained in one short PCR product. We have developed a simple, rapid and reliable multiplex method based on PCR and SSCP which allows the simultaneous determination of the common ACP1 and GC genotypes.     

Elevation of activated gamma delta T cell receptor bearing T lymphocytes in patients with autoimmune chronic liver disease.

To study the possible role of T cells bearing the gamma delta T cell receptor (TCR) heterodimer in the pathogenesis of autoimmune chronic active hepatitis (AI-CAH) and primary sclerosing cholangitis (PSC) in children, we measured levels of gamma delta+ T cells in the peripheral blood, assessed the proportion of cells bearing the disulphide-linked (BB3+) and non-disulphide-linked (A13+) subtypes of the receptor, and studied the co-expression of TCR-gamma delta and the activation markers HLA-DR and IL-2 receptor (IL-2R), and the memory cell marker CD45RO. Percentage levels and absolute numbers of gamma delta +T cells were higher in both groups of patients than in controls (P less than 0.01), mainly as a result of an increase in both percentage levels and absolute numbers of the A13+ subtype (P less than 0.001). Co-expression of IL-2R and TCR-gamma delta was not found in controls but was present in some patients with AI-CAH (four out of 17) and PSC (six out of 12) at low levels (median 2.3%, range 1.7-5.0%). Expression of HLA-DR on gamma delta+ T cells was similar in both groups of patients and controls. The majority of gamma delta+ T cells in children with AI-CAH and PSC also expressed CD45RO (74.7 +/- 18.4% and 79.8 +/- 24.3%, respectively) at levels significantly higher than in controls (53.3 +/- 17.2%, P less than 0.01). These results suggest that autoimmune liver diseases in children are associated with an expansion and activation of gamma delta+ T cells in the peripheral blood, which may be important in the pathogenesis of these disorders.