Emotional Eating Moderates the Relationship of Night Eating with Binge Eating and Body Mass

Night eating syndrome is marked by substantial evening or nocturnal food intake, insomnia, morning anorexia, and depressed mood. Night eating severity has been positively associated with body mass index (BMI), binge eating frequency, and emotional eating tendencies. We conducted an online questionnaire study among students (N = 729) and explored possible interactive effects between those variables. Night eating severity, binge eating frequency, BMI and emotional eating were all positively correlated with each other. Regression analyses showed that night eating severity was particularly related to more frequent binge episodes and higher BMI at high levels of emotional eating but unrelated to those variables at low levels of emotional eating. Thus, eating as a means of emotion regulation appears to be an important moderator of the relationship between night eating and both binge eating and BMI. Copyright © 2013 John Wiley & Sons, Ltd and Eating Disorders Association.     

Studying the dynamics of autonomic activity during emotional experience

Recent theories emphasize the dynamic aspects of emotions. However, the physiological measures and the methodological approaches that can capture the dynamics of emotions are underdeveloped. In the current study, we investigated whether moment‐to‐moment changes in autonomic nervous system (ANS) activity are reliably associated with the unfolding of emotional experience. We obtained cardiovascular and electrodermal signals from participants while they viewed emotional movies. We found that the ANS signals were temporally aligned across individuals, indicating a reliable stimulus‐driven response. The degree of response reliability was associated with the emotional time line of the movie. Finally, individual differences in ANS response reliability were strongly correlated with the subjective emotional responses. The current research offers a methodological approach for studying physiological responses during dynamic emotional situations.     

Relationships of diabetes-specific emotional distress,depression, anxiety,and overall well-being with HbA1c in adult persons with type 1 diabetes

Objective

Emotional problems are common in adults with diabetes, and knowledge about how different indicators of emotional problems are related with glycemic control is required. The aim was to examine the relationships of diabetes-specific emotional distress, depression, anxiety, and overall well-being with glycosylated hemoglobin (HbA_1c).

Methods

Of the 319 adults with type 1 diabetes attending the endocrinology outpatient clinic at a university hospital in Norway, 235 (74%) completed the Diabetes Distress Scale, the Problem Areas in Diabetes Survey, the Hospital Anxiety and Depression Scale, and the World Health Organization-Five Well-Being Index. Blood samples were taken at the time of data collection to determine HbA_1c. Regression analyses examined associations of diabetes-specific emotional distress, anxiety, depression, and overall well-being with HbA_1c. The relationship between diabetes-specific emotional distress and HbA_1c was tested for nonlinearity.

Results

Diabetes-specific emotional distress was related to glycemic control (DDS total: unstandardized coefficient = 0.038, P < .001; PAID total: coefficient = 0.021, P = .007), but depression, anxiety, and overall well-being were not. On the DDS, only regimen-related distress was independently related to HbA_1c (coefficient = 0.056, P < .001). A difference of 0.5 standard deviation of baseline regimen distress is associated with a difference of 0.6 in HbA_1c. No significant nonlinearity was detected in the relationship between diabetes-specific distress and HbA_1c.

Conclusions

To stimulate adequate care strategies, health personnel should acknowledge depression and diabetes-specific emotional distress as different conditions in clinical consultations. Addressing diabetes-specific emotional distress, in particular regimen distress, in clinical consultation might improve glycemic control.     

Structural insights into Helicobacter pylori oncoprotein CagA interaction with β1 integrin

Infection with the gastric pathogen Helicobacter pylori is a risk factor for the development of gastric cancer. Pathogenic strains of H. pylori carry a type IV secretion system (T4SS) responsible for the injection of the oncoprotein CagA into host cells. H. pylori and its cag-T4SS exploit α5β1 integrin as a receptor for CagA translocation. Injected CagA localizes to the inner leaflet of the host cell membrane, where it hijacks host cell signaling and induces cytoskeleton reorganization. Here we describe the crystal structure of the N-terminal ∼100-kDa subdomain of CagA at 3.6 Å that unveils a unique combination of folds. The core domain of the protein consists of an extended single-layer β-sheet stabilized by two independent helical subdomains. The core is followed by a long helix that forms a four-helix helical bundle with the C-terminal domain. Mapping of conserved regions in a set of CagA sequences identified four conserved surface-exposed patches (CSP1–4), which represent putative hot-spots for protein–protein interactions. The proximal part of the single-layer β-sheet, covering CSP4, is involved in specific binding of CagA to the β1 integrin, as determined by yeast two-hybrid and in vivo competition assays in H. pylori cell-culture infection studies. These data provide a structural basis for the first step of CagA internalization into host cells and suggest that CagA uses a previously undescribed mechanism to bind β1 integrin to mediate its own translocation.     

牙龈蛋白酶及其致病作用

牙龈卟啉单胞菌是引起和加重牙周炎的重要致病菌,其分泌的牙龈蛋白酶是其主要的毒力因子之一。本文就牙龈卟啉单胞菌牙龈蛋白酶以及牙龈蛋白酶对细菌生长和黏附的影响、对组织的破坏作用、对宿主防御机制的作用等研究进展作一综述。     

Different levels of implicit emotional recognition in posterior cortical atrophy (PCA)

Previous single-case reports in posterior cortical atrophy (PCA) have shown preserved nonconscious visual recognition despite the absence of explicit recognition. In this study, we investigated three levels of visual recognition in both a female patient with PCA and a control group during the presentation of neutral, positive, and negative affective stimuli. Our results confirmed the profile of impaired explicit recognition and intact psychophysiological responses in the patient. In addition, she was able to implicitly recognize the valence and intensity of arousal of these stimuli. We suggest that implicit emotional awareness may mediates explicit and psychophysiological recognition in PCA.     

Characterization of recovery and neuropsychological consequences of orbitofrontal lesion: A case study

We present a case study of a patient with acquired prefrontal lesion involving mainly ventromedial and orbital structures (VM-PFD). The patient showed behavioral and emotional disturbances one year after the injury. In a follow-up examination seven years later, we evaluated her performance in tasks found theoretically to be sensitive to orbital and medial lesions. In contrast to our hypothesis, her performance was in the normal range. We suggest that a possible explanation for her magnificent recovery may include a high cognitive reserve and the specific characteristics of her injury.     

Dysfunctional Facial Emotional Expression and Comprehension in a Patient with Corticobasal Degeneration

Patients with corticobasal degeneration (CBD) frequently develop orofacial apraxia but little is known about CBD's influence on emotional facial processing. We describe a patient who developed a facial apraxia including an impaired ability to voluntarily generate facial expressions with relative sparing of spontaneous emotional faces. Her ability to interpret the facial expressions of others was also severely impaired. Despite these deficits, the patient had normal affect and normal speech, including expressive and receptive emotional prosody. As patients with corticobasal degeneration are known to manifest both orofacial apraxia and visuospatial dysfunction this patient's expressive and receptive deficits may be independent manifestations of the same underlying disease process. Alternatively, these functions may share a common neuroanatomic substrate that degenerates with CBD.