BACKGROUND/OBJECTIVES: While many obesity studies have pointed out the importance of meal regularity, few have conducted empirical analyses using data from food diaries. We examined the association between meal regularity (i.e., meal time regularity [MTR] and calorie intake regularity [CIR]) and weight loss. SUBJECTS/METHODS: We collected food diary data from 637 women who had participated in commercial weight loss programs for 28–168 days (4–24 weeks). This study defined “meal regularity” in terms of two concepts: MTR and CIR. MTR refers to how regularly people eat their meals (i.e., at certain times each day), whereas CIR refers to how regularly people consume a certain amount of calories at each meal. We conducted multiple regression analyses. RESULTS: MTR (model 1: β = −2,576.526, P < 0.001; model 2: β = −1511.447, P < 0.05; model 3: β = −1,721.428, P < 0.05) and CIR (model 1: β = −1,231.551, P < 0.01; model 2: β = −2,082.353, P < 0.001; model 3: β = −1,343.490, P < 0.01) turned out to be significant determinants of the amount of weight loss in breakfast, lunch, and dinner contexts. While meal regularity (i.e., MTR and CIR) was significantly associated with weight loss, daily calorie intake from meals was not significantly associated with the amount of weight loss (model 1: β = 0.13, P > 0.05; model 2: β = 0.11, P > 0.05; model 3: β = 0.14, P > 0.05). Subjects who consumed an equal amount of calories per meal throughout the day lost more weight than those who did not (model 4: β = −3,675.51, P < 0.001). CONCLUSIONS Eating each meal (i.e., breakfast, lunch, and dinner) at a certain time every day may increase weight loss success. Also, consuming the same amount of calories at each meal may help weight loss success.

Th cell lineage determination and functional specialization are tightly linked to the activation of lineage-determining transcription factors (TFs) that bind cis-regulatory elements. These lineage-determining TFs act in concert with multiple layers of transcriptional regulators to alter the epigenetic landscape, including DNA methylation, histone modification and threedimensional chromosome architecture, in order to facilitate the specific Th gene expression programs that allow for phenotypic diversification. Accumulating evidence indicates that Th cell differentiation is not as rigid as classically held; rather, extensive phenotypic plasticity is an inherent feature of T cell lineages. Recent studies have begun to uncover the epigenetic programs that mechanistically govern T cell subset specification and immunological memory. Advances in next generation sequencing technologies have allowed global transcriptomic and epigenomic interrogation of CD4+ Th cells that extends previous findings focusing on individual loci. In this review, we provide an overview of recent genome-wide insights into the transcriptional and epigenetic regulation of CD4+ T cell-mediated adaptive immunity and discuss the implications for disease as well as immunotherapies.

A 35-year-old male presented with atypical aphasia following left anterior choroidal artery infarction associated with distal internal carotid artery dissection. He presented with 1) lexical-semantic deficit without semantic impairment, 2) frequent surface errors (both surface dyslexia and dysgraphia), and 3) intact non-word reading/repetition (preserved sub-lexical route), suggesting deficit in the phonological output lexicon. Diffusion-tensor tractography analysis revealed disruption in the inferior fronto-occipital fasciculus and inferior longitudinal fasciculus, which might serve as potential subcortical neural correlates for phonological output lexicon.