Negative affective stress reactivity: The dampening effect of snacking

The present study sets out to further elucidate the complex relationship between daily hassles, snacking, and negative affect (NA). The aim of the present study was to examine whether or not moment‐to‐moment energy intake from snacks moderates the association between momentary stress and NA. And, if so, can this moderating effect be replicated by using the amount of macronutrient intake (i.e., carbohydrates, fat, and protein) as moderator on the association between momentary stress and NA? Adults (N = 269), aged 20–50 years, participated in this study. Stress, NA, and snack intake were assessed 10 times a day for 7 consecutive days in daily life with an experience sampling smartphone application. Multilevel regression analyses were performed to assess the hypothesized associations. Our study revealed a dampening effect of snacking on negative affective stress reactivity. However, this dampening effect could not be replicated by the amount of macronutrient intake from snacks. On the contrary, the amount of carbohydrates has an enhancing effect on negative affective stress reactivity. In the end, our study suggests that the critical question is which mechanisms are decisive in the dampening role of snacking on stress reactivity. A multidisciplinary approach may provide a full perspective.     

Multicentre evaluation of a new point-of-care test for the determination of NT-proBNP in whole blood.

BACKGROUND: The Roche CARDIAC proBNP point-of-care (POC) test is the first test intended for the quantitative determination of N-terminal pro-brain natriuretic peptide (NT-proBNP) in whole blood as an aid in the diagnosis of suspected congestive heart failure, in the monitoring of patients with compensated left-ventricular dysfunction and in the risk stratification of patients with acute coronary syndromes. METHODS: A multicentre evaluation was carried out to assess the analytical performance of the POC NT-proBNP test at seven different sites. RESULTS: The majority of all coefficients of variation (CVs) obtained for within-series imprecision using native blood samples was below 10% for both 52 samples measured ten times and for 674 samples measured in duplicate. Using quality control material, the majority of CV values for day-to-day imprecision were below 14% for the low control level and below 13% for the high control level. In method comparisons for four lots of the POC NT-proBNP test with the laboratory reference method (Elecsys proBNP), the slope ranged from 0.93 to 1.10 and the intercept ranged from 1.8 to 6.9. The bias found between venous and arterial blood with the POC NT-proBNP method was < or =5%. All four lots of the POC NT-proBNP test investigated showed excellent agreement, with mean differences of between -5% and +4%. No significant interference was observed with lipaemic blood (triglyceride concentrations up to 6.3 mmol/L), icteric blood (bilirubin concentrations up to 582 micromol/L), haemolytic blood (haemoglobin concentrations up to 62 mg/L), biotin (up to 10 mg/L), rheumatoid factor (up to 42 IU/mL), or with 50 out of 52 standard or cardiological drugs in therapeutic concentrations. With bisoprolol and BNP, somewhat higher bias in the low NT-proBNP concentration range (<175 ng/L) was found. Haematocrit values between 28% and 58% had no influence on the test result. Interference may be caused by human anti-mouse antibodies (HAMA) types 1 and 2. No significant influence on the results with POC NT-proBNP was found using volumes of 140-165 muL. High NT-proBNP concentrations above the measuring range of the POC NT-proBNP test did not lead to false low results due to a potential high-dose hook effect. CONCLUSIONS: The POC NT-proBNP test showed good analytical performance and excellent agreement with the laboratory method. The POC NT-proBNP assay is therefore suitable in the POC setting.     

T cell early activation antigens expressed by peripheral lymphocytes in Crohn's disease

We studied the expression of early activation antigens (4F2, transferrin receptor, IL-2 receptor) on peripheral lymphocytes (PBL) of patients with Crohn's Disease. We have found that the proportion of PBL expressing these antigens was significantly higher in patients than in controls. The expression of the 4F2 antigen was more pronounced than that of other activation antigens directly involved in promoting cell growth (e.g. transferrin receptor, IL-2 receptor). These results indicate that CD patients have an increased number of T cells in a very early phase of activation.     

Remarkably similar antigen receptors among a subset of patients with chronic lymphocytic leukemia

Studies of B cell antigen receptors (BCRs) expressed by leukemic lymphocytes from patients with B cell chronic lymphocytic leukemia (B-CLL) suggest that B lymphocytes with some level of BCR structural restriction become transformed. While analyzing rearranged V(H)DJ(H) and V(L)J(L) genes of 25 non-IgM-producing B-CLL cases, we found five IgG(+) cases that display strikingly similar BCRs (use of the same H- and L-chain V gene segments with unique, shared heavy chain third complementarity-determining region [HCDR3] and light chain third complementarity-determining region [LCDR3] motifs). These H- and L-chain characteristics were not identified in other B-CLL cases or in normal B lymphocytes whose sequences are available in the public databases. Three-dimensional modeling studies suggest that these BCRs could bind the same antigenic epitope. The structural features of the B-CLL BCRs resemble those of mAb's reactive with carbohydrate determinants of bacterial capsules or viral coats and with certain autoantigens. These findings suggest that the B lymphocytes that gave rise to these IgG(+) B-CLL cells were selected for this unique BCR structure. This selection could have occurred because the precursors of the B-CLL cells were chosen for their antigen-binding capabilities by antigen(s) of restricted nature and structure, or because the precursors derived from a B cell subpopulation with limited BCR heterogeneity, or both.     

Dysferlin-mediated membrane repair protects the heart from stress-induced left ventricular injury

Dilated cardiomyopathy is a life-threatening syndrome that can arise from a myriad of causes, but predisposition toward this malady is inherited in many cases. A number of inherited forms of dilated cardiomyopathy arise from mutations in genes that encode proteins involved in linking the cytoskeleton to the extracellular matrix, and disruption of this link renders the cell membrane more susceptible to injury. Membrane repair is an important cellular mechanism that animal cells have developed to survive membrane disruption. We have previously shown that dysferlin deficiency leads to defective membrane resealing in skeletal muscle and muscle necrosis; however, the function of dysferlin in the heart remains to be determined. Here, we demonstrate that dysferlin is also involved in cardiomyocyte membrane repair and that dysferlin deficiency leads to cardiomyopathy. In particular, stress exercise disturbs left ventricular function in dysferlin-null mice and increases Evans blue dye uptake in dysferlin-deficient cardiomyocytes. Furthermore, a combined deficiency of dystrophin and dysferlin leads to early onset cardiomyopathy. Our results suggest that dysferlin-mediated membrane repair is important for maintaining membrane integrity of cardiomyocytes, particularly under conditions of mechanical stress. Thus, our study establishes what we believe is a novel mechanism underlying the cardiomyopathy that results from a defective membrane repair in the absence of dysferlin.     

Induction of lymphocyte apoptosis by tumor cell secretion of FasL-bearing microvesicles

The hypothesis that FasL expression by tumor cells may impair the in vivo efficacy of antitumor immune responses, through a mechanism known as 'Fas tumor counterattack,' has been recently questioned, becoming the object of an intense debate based on conflicting results. Here we definitely show that FasL is indeed detectable in the cytoplasm of melanoma cells and its expression is confined to multivesicular bodies that contain melanosomes. In these structures FasL colocalizes with both melanosomal (i.e., gp100) and lysosomal (i.e., CD63) antigens. Isolated melanosomes express FasL, as detected by Western blot and cytofluorimetry, and they can exert Fas-mediated apoptosis in Jurkat cells. We additionally show that melanosome-containing multivesicular bodies degranulate extracellularly and release FasL-bearing microvesicles, that coexpress both gp100 and CD63 and retain their functional activity in triggering Fas-dependent apoptosis of lymphoid cells. Hence our data provide evidence for a novel mechanism potentially operating in Fas tumor counterattack through the secretion of subcellular particles expressing functional FasL. Such vesicles may form a sort of front line hindering lymphocytes and other immunocompetent cells from entering neoplastic lesions and exert their antitumor activity.     

Importance of physical rehabilitation before and after cardiac transplantation in a patient with myotonic dystrophy: a case report

Patients with muscular dystrophy and concomitant cardiomyopathy are only reluctantly accepted for heart transplantation because of the perioperative risk secondary to respiratory muscle weakness. We describe a man with Steinert's disease (myotonic dystrophy) who received a cardiac allograft because of end-stage dilated cardiomyopathy. This case shows the importance of uninterrupted physiotherapeutic training and assistance to minimize respiratory infections and ventilatory insufficiency in patients with muscle diseases under high-dose immunosuppression. To our knowledge, this is the first heart transplantation reported in a patient with Steinert's disease who has clinically overt muscular impairment.