Low-artifact intravascular devices: MR imaging evaluation

Flow-phantom magnetic resonance (MR) imaging, with use of both spin-echo (SE) and gradient-echo (GRE) techniques at 1.5 T, was performed on the percutaneous Greenfield (beta-III titanium alloy [TMA wire]), Amplatz (MP32-N alloy), and Simon nitinol filters and TMA wire facsimiles of the bird's nest, Gunther, new retrievable, and Amplatz vena caval filters. SE imaging allowed detection of thrombi as small as 5 X 5 mm trapped within the percutaneous Greenfield, Simon nitinol, and TMA-wire facsimile filters; with the MP32-N Amplatz filter, a larger volume of thrombus (10 X 20-mm clots) was necessary for clot detection. GRE imaging allowed detection of intraluminal tilting of the percutaneous Greenfield and facsimile Amplatz (TMA-wire) filters. GRE imaging was useful for demonstrating postfilter turbulence due to clots, which was greatest for the Amplatz filter. Imaging of facsimile vascular devices made of tantalum or TMA wire did not cause the severe "black-hole" MR artifacts typical of the stainless-steel devices. SE and GRE imaging were very useful for determining caval patency in two patients with previously placed Mobin-Uddin filters. Noninvasive MR evaluation of blood vessels in the presence of a variety of low-artifact intravascular devices appears feasible.     

Plasma endothelin-1 release during acute stress: role of ethnicity and sex

OBJECTIVES: The purposes of this study were to examine possible ethnic and sex differences in plasma ET-1 levels at rest and in response to acute stress and to examine relationships between ET-1 and vasoconstrictive-mediated BP reactivity to stress. METHODS: Two hundred twenty-two adolescents (mean age = 18.5 +/- 2.8 years; 130 [70 males] EAs and 92 [48 males] AAs) completed two stressors (video game, forehead cold). Hemodynamic measures and blood samples were collected at catheter insertion and before and immediately after the two stressors, separated by 20-minute rest periods. RESULTS: AAs and males exhibited higher levels of SBP and DBP and of TPRI and ET-1 at each sampling point compared with EAs and females, respectively (p values <.001). AAs and males exhibited greater increases in SBP, TPRI, and ET-1 in response to each stressor (p values <.05). Intraindividual correlations between ET-1 and hemodynamic parameters revealed that most individuals exhibited a positive association between ET-1, BP, and TPRI. However, some individuals exhibited a negative association between ET-1 and the above-mentioned hemodynamics, suggesting a compensatory vasodilation mechanism. CONCLUSION: The findings demonstrate significant sex and ethnicity differences in stress-induced vasoconstrictive peptide release and support the hypothesis that these differences may be important in explaining the ethnicity and sex differences in the prevalence of cardiovascular disease.     

Association of tuberculin-boosted antibody responses with pathology and cell-mediated immunity in cattle vaccinated with Mycobacterium bovis BCG and infected with M. bovis

Vaccine development and our understanding of the pathology of bovine tuberculosis in cattle would be greatly facilitated by definition of the immunological correlates of protection and/or pathology. In this study we analyzed humoral immune responses in Mycobacterium bovis BCG-vaccinated and control cattle (in particular, the relationship between the intradermal comparative tuberculin skin test and serum immunoglobulin G [IgG] responses) against a range of mycobacterial antigens (MPB59, MPB64, MPB70, MPB83, ESAT-6, CFP-10, Acr1, and PstS-1) by multiantigen print immunoassay and conventional enzyme-linked immunosorbent assay. Following M. bovis infection, the comparative tuberculin skin test strongly boosted IgG, IgG1, and IgG2 antibody responses, particularly against MPB83 and MPB70, in unvaccinated cattle but failed to boost these responses, or did so only weakly, in BCG-vaccinated calves. In addition, the skin test-induced increases in MPB83-specific IgG responses correlated positively with bacterial loads and ESAT-6-induced in vitro gamma interferon responses. In conclusion, both the negative correlation of skin test-enhanced MPB83-specific antibody responses with BCG-induced protection and their positive correlation with bacterial loads can serve as useful markers for vaccine efficacy after challenge.     

Generation of CD8(+) T-cell responses to Mycobacterium bovis and mycobacterial antigen in experimental bovine tuberculosis

Protective immunity against tuberculosis is considered to be essentially cell mediated, and an important role for CD8(+) T lymphocytes has been suggested by several studies of murine and human infections. The present work, using an experimental model of infection with Mycobacterium bovis in cattle, showed that live M. bovis elicits the activation of CD8(+) T cells in vitro. However, a sonic extract prepared from M. bovis (MBSE) and protein purified derivative (PPDb) also induced a considerable degree of activation of the CD8(+) T cells. Analysis of proliferative responses of peripheral blood mononuclear cells, purified CD8(+) T cells, and CD8(+) T-cell clones to M. bovis and to soluble antigenic preparations (MBSE, PPDb) showed that the responses of all three types of cells were always superior for live mycobacteria but that strong responses were also obtained with complex soluble preparations. Furthermore, while cytotoxic capabilities were not investigated, the CD8(+) T cells were found to produce and release gamma interferon in response to antigen (live and soluble), which indicated one possible protective mechanism for these cells in bovine tuberculosis. Finally, it was demonstrated by metabolic inhibition with brefeldin A and cytochalasin D at the clonal level that an endogenous pathway of antigen processing is required for presentation to bovine CD8(+) cells and that presentation is also dependent on phagocytosis of the antigen.     

Time course for strength and muscle thickness changes following upper and lower body resistance training in men and women

 The purpose of this study was to investigate the time course of skeletal muscle adaptations resulting from high-intensity, upper and lower body dynamic resistance training (WT). A group of 17 men and 20 women were recruited for WT, and 6 men and 7 women served as a control group. The WT group performed six dynamic resistance exercises to fatigue using 8–12 repetition maximum (RM). The subjects trained 3 days a week for 12 weeks. One-RM knee extension (KE) and chest press (CP) exercises were measured at baseline and at weeks 2, 4, 6, 8, and 12 for the WT group. Muscle thickness (MTH) was measured by ultrasound at eight anatomical sites. One-RM CP and KE strength had increased significantly at week 4 for the female WT group. For the men in the WT group, 1 RM had increased significantly at week 2 for KE and at week 6 for CP. The mean relative increases in KE and CP strength were 19% and 19% for the men and 19% and 27% for the women, respectively, after 12 weeks of WT. Resistance training elicited a significant increase in MTH of the chest and triceps muscles at week 6 in both sexes. There were non-significant trends for increases in quadriceps MTH for the WT groups. The relative increases in upper and lower body MTH were 12%–21% and 7%–9% in the men and 10%–31% and 7%–8% in the women respectively, after 12 weeks of WT. These results would suggest that increases in MTH in the upper body are greater and occur earlier compared to the lower extremity, during the first 12 weeks of a total body WT programme. The time-course and proportions of the increase in strength and MTH were similar for both the men and the women. Accepted: 6 September 1999     

Defects in neurofibromatosis 2 protein function can arise at multiple levels

Neurofibromatosis 2 (NF2) is an inherited cancer syndrome resulting from mutations in the NF2 tumor suppressor gene. Analysis of NF2 mutations has revealed some general genotype-phenotype correlations. Severe disease has been associated with mutations that produce a premature termination while more mild disease has been associated with missense mutations. Here, we provide experimental proof for these genotype-phenotype correlations by demonstrating that nonsense mutations fail to produce stable merlin protein while missense mutations result in the generation of merlin proteins defective in negative growth regulation. This inability to suppress cell growth may result from defects in the function of merlin at several levels, including failure to form an intramolecular complex. Based on these findings, we propose a model for merlin growth suppression that provides a framework for analyzing NF2 patient mutations and merlin function.