Noncommunicable diseases (NCDs) are the leading causes of death globally,which kill more each year than all other causes combined.It is estimated that 63％ of global total deaths were due to NCDs.Nearly 80％ of NCD deaths occur in low- and middle-income countries.China contributes the largest number of NCD patients and deaths.NCD rates have been increasing at an alarming rate over the past two decades in China and many other countries.Population-wide interventions can help reduce NCD burden and can be cost effective.Improved health care,early detection and timely treatment are also needed for reducing the impact of NCDs.Strong government commitment,adequate investment,and extensive involvement and collaboration of multiple diverse social sectors with health sectors are critical to fight the NCD burden in all countries,especially in low- and middle-income countries.

Autophagy, which has the literal meaning of self-eating, is a cellular catabolic process executed by arrays of conserved proteins in eukaryotes. Autophagy is dynamically ongoing at a basal level, presumably in all cells, and often carries out distinct functions depending on the cell type. Therefore, although a set of common genes and proteins is involved in this process, the outcome of autophagic activation or deficit requires scrutiny regarding how it affects cells in a specific pathophysiological context. The uterus is a complex organ that carries out multiple tasks under the influence of cyclic changes of ovarian steroid hormones. Several major populations of cells are present in the uterus, and the interactions among them drive complex physiological tasks. Mouse models with autophagic deficits in the uterus are very limited, but provide an initial glimpse at how autophagy plays a distinct role in different uterine tissues. Herein, we review recent research findings on the role of autophagy in the uterine mesenchyme in mouse models.

Poor diet quality is one of strong predictors of subsequent increased mortality in hemodialysis patients. To determine diet quality and to define major problems contributing to poor diet quality in hemodialysis patients, a cross-sectional study was conducted between June 2009 and October 2010. Sixty-three hemodialysis patients (31 men, 32 women; aged 55.3 +/- 11.9 years) in stable condition were recruited from the Artificial Kidney Center in Kyung Hee University, Seoul, Korea. Three-day diet records were obtained for dietary assessment. Mean adequacy ratio (MAR) is the average of the ratio of intakes to Dietary Reference Intakes (DRI) for 12 nutrients. Index of nutritional quality (INQ) was determined as the nutritional density per 1,000 kcal of calories. Overall diet quality was evaluated using the Diet Quality Index-International (DQI-I). Statistics were used to determine diet quality, comparing dietary intake to DRI. Dietary calories (21.9 +/- 6.7 kcal/kg/day) and protein (0.9 +/- 0.3 g/kg/day) were found insufficient in the participants. The overall intake of 12 nutrients appeared to be also inadequate (0.66 +/- 0.15), but INQs of overall nutrients, except for folate (0.6) and calcium (0.8), were found relatively adequate (INQ > or = 1). As a result of diet quality assessment using DQI-I, dietary imbalance and inadequacy were found to be the most problematic in hemodialysis patients. This study suggests that the main reason for insufficient intake of essential nutrients is insufficient calorie intake. Hemodialysis patients should be encouraged to use various food sources to meet their energy requirements as well as satisfy overall balance and nutrient adequacy.
Calcium ; Cross-Sectional Studies ; Diet Records ; Diet* ; Energy Intake* ; Female ; Folic Acid ; Humans ; Kidneys, Artificial ; Korea ; Male ; Mortality ; Nutritive Value ; Recommended Dietary Allowances ; Renal Dialysis* ; Seoul

Transcription factors govern diverse aspects of cell growth and differentiation as major switches of gene expression. Etv5, a member of the E26 transformation-specific family of transcription factors, has many stories to share when it comes to reproduction. Etv5 deficient mice show complex infertility phenotypes both in males and females. In males, the infertility phenotype exhibited by Etv5 deficiency is sexually dimorphic, and it involves both somatic cells and germ cells. In Etv5-/- female mice, the problem is more complicated by hormonal involvement. This review synthesizes old and new information on this versatile transcription factor-from the inadvertent discovery of its role in the testes to its newly discovered role in maintaining spermatogonial stem cells.
Animals ; Female ; Gene Expression ; Germ Cells ; Humans ; Infertility ; Male ; Mice ; Phenotype ; Reproduction ; Stem Cells ; Testis ; Transcription Factors

Floating-Harbor syndrome (FHS) is a rare genetic disorder. This report introduced in a patient with FHS. Distinctive facial characteristics, severe skeletal class 3 malocclusion with underdeveloped maxilla and protruded mandible, congenital missing teeth, microdontia and ectopic positions of maxillary teeth were presented in the patient. In his twin sister, mild skeletal class 3 malocclusion with protruded mandible was observed but congenital missing teeth and microdontia were not observed. High-arched palate, narrow V-shaped maxillary arch compared to wide and ovoid mandibular arch and inverse relationship between the maxillary and mandibular intermolar width resulted in posterior crossbite were confirmed by model analysis of the patient. These were not observed in the twins. Behaviorally, poor cooperation during dental treatment because of mental retardation was observed in the patient.

The purpose of this study was to analyze treatment methods, results, timings and clinical signs and symptoms in failed cases of each treatment method of dens evaginatus on the premolar areas. In this study, 151 patients and 417 teeth were included. Resin restoration and direct pulp capping as preventive treatment and pulp revascularization, apexification and conventional endodontic treatment as endodontic treatment were included for treatment methods. In the preventive resin restoration, successful results were shown in the intact tubercles and also effective when the tubercles were fractured. In the direct pulp capping, resolved clinical symptoms and growth of the roots were shown when there was only pain during chewing without apical lesion. Apical lesion was the most common pretreatment signs and symptoms of the pulp revascularization, apexification and conventional endodontic treatment. In the pulp revascularization, successful results was obtained in most cases. But in some cases, root length or root wall thickness was not increased. Effective results were shown both of the apexification and conventional endodontic treatment. In order to increase success rate of preventive treatment of dens evaginatus, resin restoration was required to be done when tubercle did not occluded or in the presence of intact tubercles. When tubercle was fractured, root development stage and pulp condition should be considered for successful treatment.

Objective: Autophagy is highly active in ovariectomized mice experiencing hormone deprivation, especially in the uterine mesenchyme. Autophagy is responsible for the turnover of vasoactive factors in the uterus, which was demonstrated in anti-Müllerian hormone receptor type 2 receptor (Amhr2)-Cre-driven autophagy-related gene 7 (Atg7) knockout (Amhr-Cre/Atg7f/f mice). In that study, we uncovered a striking difference in the amount of sequestosome 1 (SQSTM1) accumulation between virgin mice and breeder mice with the same genotype. Herein, we aimed to determine whether repeated breeding changed the composition of mesenchymal cell populations in the uterine stroma. Methods: All female mice used in this study were of the same genotype. Atg7 was deleted by Amhr2 promoter-driven Cre recombinase in the uterine stroma and myometrium, except for a triangular stromal region on the mesometrial side. Amhr-Cre/Atg7f/f female mice were divided into two groups: virgin mice with no mating history and aged between 11 and 12 months, and breeder mice with at least 6-month breeding cycles with multiple pregnancies and aged around 12 months. The uteri were used for Western blotting and immunofluorescence staining. Results: SQSTM1 accumulation, representing Atg7 deletion and halted autophagy, was much higher in virgin mice than in breeders. Breeders showed reduced accumulation of several vasoconstrictive factors, which are potential autophagy targets, in the uterus, suggesting that the uterine stroma was repopulated with autophagy-intact cells during repeated pregnancies. Conclusion Multiple pregnancies seem to have improved the uterine environment by replacing autophagy-deficient cells with autophagy-intact cells, providing evidence of cell mixing.

Objective: Autophagy is a major intracellular catabolic pathway governed by the sequential actions of proteins encoded by autophagy-related genes (Atg). ATG9, the only transmembrane protein involved in this process, regulates phospholipid translocation to autophagosomes during the early phases of autophagy. In mammals, two Atg9 isoforms have been reported: Atg9a and Atg9b. In this study, we examined whether the molecular and cellular characteristics of these two isoforms differed in mice. Methods: Whole uteri were collected on days 1, 4, and 8 of pregnancy and from ovariectomized mice injected with vehicle, progesterone, or 17β-estradiol. Cells from reproductive tissues, such as granulosa cells, uterine epithelial cells (UECs), uterine stromal cells (USCs), and oocytes were collected. Two human uterine cell lines were also used in this analysis. Reverse transcription-polymerase chain reaction tests, Western blotting, and immunofluorescence staining were performed. Serum starvation conditions were used to induce autophagy in primary cells. Results: Atg9a and Atg9b were expressed in multiple mouse tissues and reproductive cells. Neither Atg9A nor Atg9B significantly changed in response to steroid hormones. Immunofluorescence staining of the UECs and USCs showed that ATG9A was distributed in a punctate-like pattern, whereas ATG9B exhibited a pattern of elongated tubular shapes in the cytoplasm. In human cancer cell lines, ATG9B was undetectable, whereas ATG9A was found in all cell types examined. Conclusion The Atg9 isoforms exhibited distinct subcellular localizations in UECs and may play different roles in autophagy. Notably, human uterine cells exhibited reduced ATG9B expression, suggesting that this suppression may be due to epigenetic regulation.

Objective: Autophagy is a major intracellular catabolic pathway governed by the sequential actions of proteins encoded by autophagy-related genes (Atg). ATG9, the only transmembrane protein involved in this process, regulates phospholipid translocation to autophagosomes during the early phases of autophagy. In mammals, two Atg9 isoforms have been reported: Atg9a and Atg9b. In this study, we examined whether the molecular and cellular characteristics of these two isoforms differed in mice. Methods: Whole uteri were collected on days 1, 4, and 8 of pregnancy and from ovariectomized mice injected with vehicle, progesterone, or 17β-estradiol. Cells from reproductive tissues, such as granulosa cells, uterine epithelial cells (UECs), uterine stromal cells (USCs), and oocytes were collected. Two human uterine cell lines were also used in this analysis. Reverse transcription-polymerase chain reaction tests, Western blotting, and immunofluorescence staining were performed. Serum starvation conditions were used to induce autophagy in primary cells. Results: Atg9a and Atg9b were expressed in multiple mouse tissues and reproductive cells. Neither Atg9A nor Atg9B significantly changed in response to steroid hormones. Immunofluorescence staining of the UECs and USCs showed that ATG9A was distributed in a punctate-like pattern, whereas ATG9B exhibited a pattern of elongated tubular shapes in the cytoplasm. In human cancer cell lines, ATG9B was undetectable, whereas ATG9A was found in all cell types examined. Conclusion The Atg9 isoforms exhibited distinct subcellular localizations in UECs and may play different roles in autophagy. Notably, human uterine cells exhibited reduced ATG9B expression, suggesting that this suppression may be due to epigenetic regulation.

Objective: Autophagy is a major intracellular catabolic pathway governed by the sequential actions of proteins encoded by autophagy-related genes (Atg). ATG9, the only transmembrane protein involved in this process, regulates phospholipid translocation to autophagosomes during the early phases of autophagy. In mammals, two Atg9 isoforms have been reported: Atg9a and Atg9b. In this study, we examined whether the molecular and cellular characteristics of these two isoforms differed in mice. Methods: Whole uteri were collected on days 1, 4, and 8 of pregnancy and from ovariectomized mice injected with vehicle, progesterone, or 17β-estradiol. Cells from reproductive tissues, such as granulosa cells, uterine epithelial cells (UECs), uterine stromal cells (USCs), and oocytes were collected. Two human uterine cell lines were also used in this analysis. Reverse transcription-polymerase chain reaction tests, Western blotting, and immunofluorescence staining were performed. Serum starvation conditions were used to induce autophagy in primary cells. Results: Atg9a and Atg9b were expressed in multiple mouse tissues and reproductive cells. Neither Atg9A nor Atg9B significantly changed in response to steroid hormones. Immunofluorescence staining of the UECs and USCs showed that ATG9A was distributed in a punctate-like pattern, whereas ATG9B exhibited a pattern of elongated tubular shapes in the cytoplasm. In human cancer cell lines, ATG9B was undetectable, whereas ATG9A was found in all cell types examined. Conclusion The Atg9 isoforms exhibited distinct subcellular localizations in UECs and may play different roles in autophagy. Notably, human uterine cells exhibited reduced ATG9B expression, suggesting that this suppression may be due to epigenetic regulation.