Background: The preventative effect of melatonin on the development of obesity and the progression of fatty liver under a high-fat diet (HFD) has been well elucidated through previous studies. We investigated the mechanism behind this effect regarding cholesterol biosynthesis and regulation of cholesterol levels. Methods: Mice were divided into three groups: normal chow diet (NCD); HFD; and HFD and melatonin administration group (HFD+M). We assessed the serum lipid profile, mRNA expression levels of proteins involved in cholesterol synthesis and reabsorption in the liver and nutrient transporters in the intestines, and cytokine levels. Additionally, an in vitro experiment using HepG2 cells was performed. Results: Expression of hepatic sterol regulatory element-binding protein 2 (SREBP-2), 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR), and low-density lipoprotein receptor (LDLR) demonstrated that melatonin administration significantly reduces hepatic cholesterol synthesis in mice fed an HFD. Expression of intestinal sodium-glucose transporter 1 (SGLT1), glucose transporter 2 (GLUT2), GLUT5, and Niemann-pick C1-like 1 (NPC1L1) demonstrated that melatonin administration significantly reduces intestinal carbohydrate and lipid absorption in mice fed an HFD. There were no differences in local and circulatory inflammatory cytokine levels among the NCD, HFD, and HFD+M group. HepG2 cells stimulated with palmitate showed reduced levels of SREBP, LDLR, and HMGCR indicating these results are due to the direct mechanistic effect of melatonin on hepatocytes. Conclusion Collectively, these data indicate the mechanism behind the protective effects of melatonin from weight gain and liver steatosis under HFD is through a reduction in intestinal caloric absorption and hepatic cholesterol synthesis highlighting its potential in the treatment of obesity and fatty liver disease.

The objective of this study is to analyze the shear bond strength of orthodontic buttons according to light tip distance and optic fiber diameter when an extended optic fiber was applied to the tip of a curing light unit.
In this study, 315 extracted premolar teeth were divided into 3 groups. Orthodontic buttons were attached using no optic fibers (Group I), 3.0 mm diameter optic fibers (Group II), or 5.0 mm diameter optic fibers (Group III). Each group was divided into subgroups A - C (5.0, 10.0, and 15.0 mm light tip distance), respectively. Shear bond strength was then measured while varying the light tip distance.
In group I, shear bond strength significantly decreased as the light tip distance increased. When the shear bond strength was evaluated according to the optic fiber diameter, no statistical significance was observed in group of 5.0 mm light tip distance. Compared with group IB, group IIIB showed significantly greater shear bond strength. Compared with group IC, all groups using 3.0 or 5.0 mm diameter optic fibers showed significantly greater shear bond strength.
Therefore, when a curing light unit has poor accessibility, optic fibers with a large diameter should be considered.

Understanding the developmental mechanisms of humoral immunity against intranasal antigens is essential for the development of therapeutic approaches against air-borne pathogens as well as allergen-induced pulmonary inflammation. Follicular helper T (Tfh) cells expressing CXCR5 are required for humoral immunity by providing IL-21 and ICOS costimulation to activated B cells. However, the regulation of Tfh cell responses against intranasal antigens remains unclear. Here, we found that the generation of Tfh cells and germinal center B cells in the bronchial lymph node against intranasal proteinase antigens was independent of TGF-β. In contrast, administration of STAT3 inhibitor STA-21 suppressed the generation of Tfh cells and germinal center B cells. Compared with wild-type OT-II T cells, STAT3-deficient OT-II T cells transferred into recipients lacking T cells not only showed significantly reduced frequency Tfh cells, but also induced diminished IgG as well as IgE specific for the intranasal antigens. Co-transfer study of wild-type OT-II and STAT3-deficient OT-II T cells revealed that the latter failed to differentiate into Tfh cells. These findings demonstrate that T cell-intrinsic STAT3 is required for the generation of Tfh cells to intranasal antigens and that targeting STAT3 might be an effective approach to ameliorate antibody-mediated pathology in the lung.
Allergens* ; B-Lymphocytes ; Germinal Center* ; Immunity, Humoral ; Immunoglobulin E ; Immunoglobulin G ; Immunoglobulins ; Lung ; Lymph Nodes ; Pathology ; Pneumonia ; T-Lymphocytes*

An isolated aneurysm of the iliac artery is a very rare disease that can occur as the result of atherosclerotic degeneration, mycosis, trauma, medial necrosis, fibrodysplasia, or Marfan syndrome. This abnormality is often asymptomatic, and it has a potential risk of rupture. Since patients with chronic renal failure on hemodialysis have many comorbid conditions, the risk of rupture is increased. Here, we report the case of an isolated common iliac artery aneurysm that was caused by atherosclerosis in a patient on hemodialysis, and we review the relevant literature.
Aneurysm ; Atherosclerosis ; Humans ; Iliac Aneurysm ; Iliac Artery ; Kidney Failure, Chronic ; Marfan Syndrome ; Necrosis ; Rare Diseases ; Renal Dialysis ; Renal Insufficiency ; Rupture

The expansion of allergen-specific CD4⁺ T cells is a critical step in inducing airway inflammation during allergic asthma. Such clonal expansion of T cells is initiated through the interaction between allergen-bearing dendritic cells and allergen-specific naïve T cells in the draining lymph nodes. Whether such T cell clonal expansion also occurs in the lung, the primary organ encountering inhaled allergens, remains unclear. Compared with wild-type mice, we found similar frequencies of CD4⁺ T cells in the lung of lymph node-deficient Rorgt(gfp/gfp) mice after repeated exposure to inhaled allergens. In addition, we observed an evident population of CD4⁺ T cells that underwent clonal expansion in the lung of allergen-challenged mice treated with an S1P antagonist FTY720 in an in vivo proliferation study with CFSE-labeled OT-II T cells. Moreover, the expansion of allergen-specific CD4⁺ T cells was significantly enhanced in the lungs of Rorgt(gfp/gfp) mice in comparison to that of wild-type mice. These results together demonstrate that the clonal expansion of allergen-specific CD4⁺ T cells occurs in the absence of the lymph nodes, indicating that the lung can act as a primary site of the clonal expansion of CD4⁺ T cells in response to inhaled allergens.
Allergens ; Animals ; Asthma ; Dendritic Cells ; Fingolimod Hydrochloride ; Inflammation ; Lung* ; Lymph Nodes* ; Mice ; T-Lymphocytes