Examining the Associations Between Overeating,Disinhibition, and Hunger in a Nonclinical Sample of College Women

Background

Binge eating (BE) has long been identified as a correlate of overweight and obesity. However, less empirical attention has been given to overeating with and without loss of control (LOC) in nonclinical samples.

Purpose

The goal of the present study was to examine the association of (1) established correlates of BE, namely, weight and shape concerns, dietary restraint, and negative affect, and (2) three additional correlates, disinhibition, hunger, and interoceptive awareness (IA), to overeating in a nonclinical sample of college women.

Method

Female students (n?=?1,447) aged 18 to 21 years recruited from colleges in three Canadian metropolitan areas completed self-report questionnaires in class to assess sociodemographic and anthropomorphic characteristics, overeating, LOC, dietary restraint, negative affect, weight and shape concerns, IA, disinhibition, and hunger.

Results

The established correlates of BE were significant correlates of all types of overeating and explained 33 % of the variance. Disinhibition was the most strongly associated correlate of overeating.

Conclusions

Findings suggest that established correlates of BE are associated with other types of overeating such as objective overeating (OOE), as are disinhibition and hunger.

     

Sinusoidal endothelial cell and hepatocyte death following cold ischemia-warm reperfusion of the rat liver

Cold ischemia-warm reperfusion (CI-WR) injury of the liver is characterized by marked alterations of sinusoidal endothelial cells (SECs), whereas hepatocytes appear to be relatively unscathed. However, the time course and mechanism of cell death remain controversial: early versus late phenomenon, necrosis versus apoptosis? We describe the occurrence and nature of cell death after different periods of CI with University of Wisconsin (UW) solution and after different periods of WR in the isolated perfused rat liver model. After 24- and 42-hour CI (viable and nonviable livers, respectively), similar patterns of liver cell death were seen: SEC necrosis appeared early after WR (10 minutes) and remained stable for up to 120 minutes. After 30 minutes of WR, apoptosis increased progressively with WR length. Based on morphological criteria, apoptotic cells were mainly hepatocytes within liver plates or extruded in the sinusoidal lumen. In addition, only after 42-hour CI were large clusters of necrotic hepatocytes found in areas of congested sinusoids. In these same livers, the hepatic microcirculation, evaluated by means of the multiple-indicator dilution technique, revealed extracellular matrix disappearance with no-flow areas. In conclusion, different time courses and mechanisms of cell death occur in rat livers after CI-WR, with early SEC necrosis followed by delayed hepatocyte apoptosis. These processes do not appear to be of major importance in the mechanism of graft failure because they are similar under both nonlethal and lethal conditions; this is not the case for the loss of the extracellular matrix found only under lethal conditions and associated with hepatocyte necrosis.     

A New Bioreactor for the Development of Tissue-Engineered Heart Valves

This paper reports the design, manufacturing, and characterization of a new bioreactor dedicated to the development of tissue-engineered heart valve substitutes. First, a comprehensive review of the state of the art in bioreactors is presented and a rigorous classification is put forward. The existing bioreactors found in literature are organized in three groups and discussed with respect to their quality of reproduction compared to the physiological environment. The bioreactor architecture is then decomposed into basic components which may be grouped together in different arrangements, and the well-known Windkessel approach is used to study the global behavior of the system. Then, the new design, which is based on a synthesis of the features of the most evolved systems as well as on new improvements, is explained in detail. Optimal fluid dynamics are obtained with the presented bioreactor through carefully designed components and an advanced computer-controlled actuator. This allows a very accurate reproduction of physiological parameters, namely the pulsating flow rate and pressure. Finally, experimental results of flow rate and pressure waveforms are presented, where an excellent correlation with physiological measurements can be observed.     

Sequential development of Hodgkin's disease and CD30+ diffuse large B-cell lymphoma in a patient with MALT-type lymphoma: evidence of different clonal origin of single microdissected Reed-Sternberg cells

We observed in the same patient the development of a tonsil mucosa-associated lymphoid tissue-type lymphoma in 1994, a mediastinal Hodgkin's disease in 1998, and a colonic CD30+ anaplastic diffuse large B-cell lymphoma in 2000. A same-sized FR3-JH fragment was demonstrated by polymerase chain reaction, both at the level of total DNA and of single micromanipulated cells, showing monocytoid, Reed-Sternberg, or anaplastic morphology. Moreover, an identical IgH nucleotide sequence was detected in mucosa-associated lymphoid tissue-type lymphoma and colonic CD30+ anaplastic diffuse large B-cell lymphoma, whereas mediastinal Hodgkin's disease IgH rearrangement involved different VH and JH genes. CD30+ Reed-Sternberg and diffuse large B-cell lymphoma cells contained Epstein-Barr virus EBER sequences that were not observed at the level of mucosa-associated lymphoid tissue-type lymphoma. Therefore, Epstein-Barr virus infection may have played a role in diffuse large B-cell lymphoma transformation of mucosa-associated lymphoid tissue-type lymphoma and in the lymphomagenesis of Hodgkin's disease. In addition to their different clonal origin, Reed-Sternberg cells of Hodgkin's disease expressed a CD15+, CD20+ (rare cells), CD30+, Oct-2-, EBNA2-, LMP1+ phenotype, whereas anaplastic and Reed-Sternberg-like cells of diffuse large B-cell lymphoma were CD15-, CD20+, CD30+, Oct-2+, EBNA2+, and LMP1+. Interestingly, we also detected scattered CD30+ Epstein-Barr virus- large cells with prominent nucleoli in the initial tonsil mucosa-associated lymphoid tissue-type lymphoma, suggesting that these cells could be prone to Epstein-Barr virus infection and/or large cell transformation.     

Loss of chloride channel ClC-5 impairs endocytosis by defective trafficking of megalin and cubilin in kidney proximal tubules

Loss of the renal endosome-associated chloride channel, ClC-5, in Dent's disease and knockout (KO) mice strongly inhibits endocytosis of filtered proteins by kidney proximal tubular cells (PTC). The underlying mechanism remains unknown. We therefore tested whether this endocytic failure could primarily reflect a loss of reabsorption by the multiligand receptors, megalin, and cubilin, caused by a trafficking defect. Impaired protein endocytosis in PTC of ClC-5 KO mice was demonstrated by (i) a major decreased uptake of injected 125I-beta 2-microglobulin, but not of the fluid-phase tracer, FITC-dextran, (ii) reduced labeling of endosomes by injected peroxidase and for the endogenous megalin/cubilin ligands, vitamin D- and retinol-binding proteins, and (iii) urinary appearance of low-molecular-weight proteins and the selective cubilin ligand, transferrin. Contrasting with preserved mRNA levels, megalin and cubilin abundance was significantly decreased in kidney extracts of KO mice. Percoll gradients resolving early and late endosomes (Rab5a, Rab7), brush border (villin, aminopeptidase M), and a dense peak comprising lysosomes (acid hydrolases) showed a disappearance of the brush border component for megalin and cubilin in KO mice. Quantitative ultrastructural immunogold labeling confirmed the overall decrease of megalin and cubilin in PTC and their selective loss at the brush border. In contrast, total contents of the rate-limiting endocytic catalysts, Rab5a and Rab7, were unaffected. Thus, impaired protein endocytosis caused by invalidation of ClC-5 primarily reflects a trafficking defect of megalin and cubilin in PTC.     

Histopathologic evaluation of cutaneous squamous cell carcinoma: results of a survey among dermatopathologists

BACKGROUND: There are numerous histopathologic features related to prognosis in cutaneous squamous cell carcinoma (CSCC). We hypothesize that there is no uniform approach toward the reporting of these features. This may be related to differing opinions on their prognostic use. METHODS: A written survey concerning the microscopic evaluation of CSCC was sent to 120 dermatopathologists in the United States and Canada. Respondents were asked whether they comment on specific microscopic features of CSCC, and whether they believe that each specific feature can predict prognosis. RESULTS: The response rate was 78%. Histologic type, and the presence of perineural or vascular/lymphatic invasion, is reported by most dermatopathologists (90%, 96%, and 95%, respectively). These features are also thought to predict prognosis by the majority of respondents. Only 54% report histologic grade, and 49% think grade predicts prognosis. Depth is reported anatomically by 63%, but by only 8% in actual millimeters of invasion. However, 55% think tumor depth predicts prognosis. A total of 43% report the presence of an associated actinic keratosis, although very few (16%) think it predicts prognosis. Very few comment on the presence of inflammation. CONCLUSIONS: Histopathologic reporting of CSCC is not uniform among dermatopathologists. Also, there appears to be differing opinions on the use of certain histopathologic features for predicting prognosis.