Risk of eating disorders and the relationship with interest in modern culture among young female students in a university in Bangladesh: a cross-sectional study.

BACKGROUND: Eating disorders (EDs) emerge most often in adolescent girls. While the basic neural and psychiatric mechanisms of ED development remain unknown, their incidence has increased with sociocultural modernization. To determine what aspects of modern culture are related to EDs, we examined the relationship between predisposition to EDs and interest in several modern cultural factors among young female university students in Bangladesh. METHODS: A cross-sectional study was conducted in a population of 196 female students aged 18-29 years in a university in Bangladesh. Their predisposition to EDs was examined using the Eating Attitudes Test-26 (EAT-26), and their interest in modern culture was evaluated by grading interest in fashionable clothes, Indian TV shows/serials, luxury food and social network activities, and by examining involvement in cultural activities such as playing, dancing, parties and singing. The relationship between predisposition to EDs and interest in modern culture was then examined. The relation between EAT-26 score and body mass index (BMI) was also examined. RESULTS: The EAT-26 revealed that 37% of the participants were at risk of developing an ED. Correlation analyses showed that a high EAT-26 score was correlated with a high interest in fashionable clothes and Indian TV shows/serials, but not with a high interest in luxury food or social network activities, or involvement in cultural activities, such as playing, dancing, parties and singing. Further, EAT-26 questions in the dieting category and oral control category, but not the bulimia and food preoccupation category, were correlated with interest in cultural factors. EAT-26 score showed no significant correlation with BMI. CONCLUSIONS: The results of this study indicate that the risk of EDs is related to an interest in several facets of modern culture. Monitoring the cultural interests of adolescent females, who are continually exposed to modern culture and highly susceptible to EDs, will contribute to the prevention of EDs.

Expression of feeding-related neuromodulatory signalling molecules in the mouse central olfactory system.

Various neural systems cooperate in feeding behaviour, and olfaction plays crucial roles in detecting and evaluating food objects. While odour-mediated feeding behaviour is highly adaptive and influenced by metabolic state, hedonic cues and learning processes, the underlying mechanism is not well understood. Feeding behaviour is regulated by orexigenic and anorexigenic neuromodulatory molecules. However, knowledge of their roles especially in higher olfactory areas is limited. Given the potentiation of feeding behaviour in hunger state, we systemically examined the expression of feeding-related neuromodulatory molecules in food-restricted mice through quantitative PCR, in the olfactory bulb (OB), olfactory tubercle (OT), and remaining olfactory cortical area (OC). The OT was further divided into attraction-related anteromedial, aversion-related lateral and remaining central regions. Examination of 23 molecules including neuropeptides, opioids, cannabinoids, and their receptors as well as signalling molecules showed that they had different expression patterns, with many showing elevated expression in the OT, especially in the anteromedial and central OT. Further, in mice trained with odour-food association, the expression was significantly altered and the increase or decrease of a given molecule varied among areas. These results suggest that different olfactory areas are regulated separately by feeding-related molecules, which contributes to the adaptive regulation of feeding behaviour.

Keratinocyte differentiation induces APOBEC3A, 3B, and mitochondrial DNA hypermutation.

Mitochondrial DNA (mtDNA) mutations are found in many types of cancers and suspected to be involved in carcinogenesis, although the mechanism has not been elucidated. In this study, we report that consecutive C-to-T mutations (hypermutations), a unique feature of mutations induced by APOBECs, are found in mtDNA from cervical dysplasia and oropharyngeal cancers. In vitro, we found that APOBEC3A (A3A) and 3B (A3B) expression, as well as mtDNA hypermutation, were induced in a cervical dysplastic cell line W12 when cultured in a differentiating condition. The ectopic expression of A3A or A3B was sufficient to hypermutate mtDNA. Fractionation of W12 cell lysates and immunocytochemical analysis revealed that A3A and A3B could be contained in mitochondrion. These results suggest that mtDNA hypermutation is induced upon keratinocyte differentiation, and shed light on its molecular mechanism, which involves A3s. The possible involvement of mtDNA hypermutations in carcinogenesis is also discussed.

APOBEC3A and 3C decrease human papillomavirus 16 pseudovirion infectivity.

Apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like (APOBEC) proteins are cellular DNA/RNA-editing enzymes that play pivotal roles in the innate immune response to viral infection. APOBEC3 (A3) proteins were reported to hypermutate the genome of human papillomavirus 16 (HPV16), the causative agent of cervical cancer. However, hypermutation did not affect viral DNA maintenance, leaving the exact role of A3 against HPV infection elusive. Here we examine whether A3 proteins affect the virion assembly using an HPV16 pseudovirion (PsV) production system, in which PsVs are assembled from its capsid proteins L1/L2 encapsidating a reporter plasmid in 293FT cells. We found that co-expression of A3A or A3C in 293FT cells greatly reduced the infectivity of PsV. The reduced infectivity of PsV assembled in the presence of A3A, but not A3C, was attributed to the decreased copy number of the encapsidated reporter plasmid. On the other hand, A3C, but not A3A, efficiently bound to L1 in co-immunoprecipitation assays, which suggests that this physical interaction may lead to reduced infectivity of PsV assembled in the presence of A3C. These results provide mechanistic insights into A3s' inhibitory effects on the assembly phase of the HPV16 virion.