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Objective: Studies have indicated that weight regain following weight loss predisposes obese individuals to metabolic disorders; however, the molecular mechanism of this potential adverse effect of weight regain is not fully understood. Here we investigated global transcriptome changes and the immune response in mouse white adipose tissue caused by weight regain. Design: We established a diet switch protocol to compare the effects of weight regain with those of weight gain without precedent weight loss, weight loss maintenance and chow diet. We conducted a time course analysis of global transcriptome changes in gonadal white adipose tissue (gWAT) during the weight fluctuation. Co-expression network analysis was used to identify functional modules associated with the weigh regain phenotype. Immune cell populations in gWAT were characterized by flow-cytometric immunophenotyping. Metabolic phenotypes were monitored by histological analysis of adipose tissue and liver, and blood-chemistry and body weight/composition analyses. Results: In total, 952 genes were differentially expressed in the gWAT in the weight regain vs the weight gain group. Upregulated genes were associated with immune response and leukocyte activation. Co-expression network analysis showed that genes involved in major histocompatibility complex I and II-mediated antigen presentation and T-cell activation function were upregulated. Consistent with the transcriptome analysis results, flow cytometry demonstrated significant increases in subsets of T cells and proinflammatory M1 macrophages in the gWAT in the weight regain as compared to the weight gain group. In addition, upregulation of adaptive immune responses was associated with high incidence of adipocyte death and upregulation of high mobility group box 1, a well-known component of damage-associated molecular patterns. Conclusions: Our global transcriptome analysis identified weight regain-induced activation of adaptive immune responses in mouse white adipose tissue. Results suggest that activation of adipocyte death-associated adaptive immunity in adipose tissue may contribute to unfavorable metabolic effects of weight regain following weight loss.

Genetically engineered mouse models are used in high-throughput phenotyping screens to understand genotype-phenotype associations and their relevance to human diseases. However, not all mutant mouse lines with detectable phenotypes are associated with human diseases. Here, we propose the “Target gene selection system for Genetically engineered mouse models” (TarGo). Using a combination of human disease descriptions, network topology, and genotype-phenotype correlations, novel genes that are potentially related to human diseases are suggested. We constructed a gene interaction network using protein-protein interactions, molecular pathways, and co-expression data. Several repositories for human disease signatures were used to obtain information on human disease-related genes. We calculated disease- or phenotype-specific gene ranks using network topology and disease signatures. In conclusion, TarGo provides many novel features for gene function prediction.

Diet-induced weight loss and regain leads to physiological and metabolic changes, some of which are potentially harmful. However, the specific metabolic processes and dysfunctions associated with weight regain, and how they differ from initial weight gain, remain unclear. Thus, we examined the metabolic profiles of mice following weight regain compared to initial weight gain. Mice were fed a normal diet or a high-fat diet or were cycled between the two diets to alternate between obese and lean states. Liver samples were collected and hepatic metabolites were profiled using nuclear magnetic resonance (NMR). The identified metabolites associated with weight regain were quantified using gas chromatography/mass spectrometry (GC/MS) and lipid profiles were assessed using ultra-high-performance liquid chromatography-quadrupole time-of-flight MS (UPLC-QTOF-MS). In addition, changes in expression of pro-inflammatory cytokines and gluconeogenic enzymes were investigated using polymerase chain reaction (PCR) and western blotting, respectively. Hepatic levels of several amino acids were reduced in mice during weight regain compared with initial weight gain. In addition, gluconeogenic enzyme levels were increased following weight regain, indicating an up-regulation of gluconeogenesis. Lipidomic profiling revealed that levels of ceramide and sphingomyelin, which are related to obesity-induced inflammation, were significantly increased during weight regain compared to initial weight gain. Moreover, tumor necrosis factor-α (TNF-α) and transforming growth factor-β1 (TGF-β1) levels were significantly up-regulated during weight regain. In this study, weight regains lead to an up-regulation of gluconeogenesis and aggravated inflammation. Additionally, weight regain can worsen the metabolic dysfunction associated with obesity.

The palmaris longus (PL) is a slender, spindle-shaped weak flexor of the wrist. Congenital absence of the PL is estimated to occur in 15% among individuals worldwide. However, the frequency of its absence varies considerably among different population groups and with different detection techniques. In the present study, the presence of the PL tendon was examined in a Korean population (n=269) using three clinical tests, namely the Traditional Test, Mishra's Test II, and the Gangata Test. We classified subjects into six types based on whether inspection or palpation was required to determine the presence of the PL and flexor carpi radialis. The most reliable test was determined using Kendall's coefficient of concordance. Our results showed that the PL tendon was absent in 4.1% of the subjects in our study, and bilateral and unilateral absences were 2.2% and 1.8%, respectively. Statistical analysis revealed that these tests had similar reliability for assessing the PL tendon, and the Traditional Test showed the highest effectiveness, at 93%. Therefore the Traditional Test was found to be the most effective for revealing the PL in this Korean population.

The axillary vein is a large-blood vessel that lies on the medial side to the axillary artery. The veins of the axilla are more abundant than the arteries and their variations were extremely common. During educational dissection, a rare form of the axillary vein accompanying arterial variation was founded in left arm of 70-year-old female cadaver. The axillary vein was divided into two large veins, anterior and posterior axillary veins according to their anatomical position. The lateral-thoracic artery arose from the second part of the axillary artery and passed through the gap of duplicated axillary vein. Before the lateral-thoracic artery passed through the gap of duplicated axillary vein, the lateral-thoracic artery gave-off an additional branch, which descended superficial to the anterior axillary vein. It surrounded the anterior axillary vein as annular form and the diameter of surrounded part of the anterior axillary vein became narrow. This novel case was reported and its clinical implications of such a variant were discussed.

The digastric muscle, as the landmark in head and neck surgery, has two bellies, of which various variations have been reported. In the submental region of a 72-year-old Korean male cadaver, bilateral variations were found in the anterior belly of the digastric muscle. Two accessory bellies, medial to the two normal anterior bellies of the digastric muscle, ran posterior and medially, merging and attaching at the mylohyoid raphe of the mylohyoid muscle. The 3rd accessory belly originated from the right intermediate tendon and ran horizontally, merging the right lower bundle of the right accessory belly and inserted together. These accessory bellies had no connection with the left anterior belly. This unique variation has not been reported in the literature previously, and this presentation will guide clinicians during surgical interventions and radiological diagnoses.