Mccartneyayala5423

007*), TNM stage (P = 0.016*) and lymph node metastasis (P = 0.011*), of patients with colon cancer. Our data further confirmed that SMYD2 affects cell proliferation, invasion, and apoptosis of colon cancer cells via the regulation of ERBB2/FUT4 signaling pathway. We also demonstrated SMYD2 contributed to tumor growth of colon cancer cells in vivo. We investigated the potential involvement of SMYD2 in the progression of colon, and therefore confirmed SMYD2 as a possible therapeutic target for colon cancer.INTRODUCTION Many environmental factors are related to the development of asthma. However, the key factors of childhood asthma onset have not been sufficiently elucidated. Further, low-weight births have increased in Japan. The aim of this study was to examine the risk factors for the incidence of childhood asthma and to evaluate whether these risk factors differ according to birth weight in Japan. METHODS We used the National Longitudinal Survey from 2001 to 2010. Multiple logistic regression analyses were conducted to determine the effects of gender, birth weight, single vs. multiple births, birth order, nutrition, keeping pets in the home, place of residence, annual household income, and parent ages, smoking behaviors, and educational backgrounds on asthma-related hospital visits. RESULTS Overall, 45,060 children were analyzed. The rate of cumulative hospital visits until age 10 was 18.9%. Birth weight  less then  2500 g (adjusted odds ratio [AOR] = 1.14, 95% confidence interval [CI] 1.03-1.26), being a boy (AOR = 1.27, 95% CI 1.21-1.33), having older siblings (AOR = 1.07, 95% CI 1.02-1.14), parental smoking behavior, mother`s age, and low household income (AOR = 1.17, 95% CI 1.10-1.24) were associated with asthma-related hospital visits. DISCUSSION Parental smoking behavior is a key risk factor for the development of asthma. Among low birth weight infants, being a boy, having older siblings, and father`s smoking behavior were predictive factors for the development of asthma. However, low birth weight was not associated with the development of asthma after 6 years of age.OBJECTIVES Very little research has explored the complex relation between ACEs, poverty, and obesity in young children with neurodevelopmental delays. The purpose of this study was to examine whether ACEs predicted overweight/obesity in young children with neurodevelopmental delays after income was taken into account, and to examine the extent to which poverty moderated the relation between ACEs and overweight/obesity. METHODS Participants were 180 children between the ages of 2 and 7 who were referred for a developmental and behavioral pediatrics evaluation (mean age 4.5 years old; 76% male) in the northeast United States. Parents completed a survey about their child's ACEs, and an electronic health record review was conducted. RESULTS ACEs did not directly predict obesity after income was taken into account. However, poverty moderated the relation between ACEs and obesity, such that when children experienced no ACEs, there was no difference in the rates of obesity between children above and below the poverty threshold. Among children who did experience ACEs, children who also lived in poverty had higher rates of obesity than children who did not live in poverty. CONCLUSIONS FOR PRACTICE Children with neurodevelopmental delays are at greater risk for overweight/obesity if they experience both risk factors of being in poverty and of experiencing ACEs. When conducting screenings, providers should understand that the impact of ACEs may vary by contextual factors such as poverty. More research is needed to identify factors that can mitigate the impact of poverty and ACEs on children's physical health.Neurodevelopmental imbalance models suggest that asynchrony in the maturation of interconnections between brain regions contributes to adolescents being more sensitive to emotionally salient events (e.g., negative feedback) than children. There may, however, be important individual differences to consider when investigating sensitivity to negative feedback. For example, worriers tend to have a greater sensitivity to negative feedback than low-worriers. Thus, it may be that adolescents' sensitivity to negative feedback is tied to worry. One way to test this question is to compare worriers to nonworriers separately for both children and adolescents. If only adolescent worriers are sensitive to negative feedback (i.e., low-worriers are not), then sensitivity to negative feedback may be linked to higher rates of worry. If however, adolescent nonworriers also have a sensitivity, then adolescents in general may be sensitive to negative feedback. The current study (N = 100, Mage = 11.26, standard deviation = 1.71) used event-related potentials (ERPs) to investigate neural differences in sensitivity to negative feedback among adolescents and children with high and low levels of worry. For both children and adolescents, worriers had a larger P3 amplitude to negative feedback than nonworriers. This difference, however, was smaller among the adolescents (i.e., adolescent nonworriers also had a large P3 amplitude to negative feedback). Our results support neurodevelopmental imbalance models that suggest adolescents in general are sensitive to emotionally salient events, such as receiving negative feedback.The aim of this study was to characterize neural activation during the processing of negative facial expressions in a non-clinical group of individuals characterized by two factors the levels of stress experienced in early life and in adulthood. Two models of stress consequences were investigated the match/mismatch and cumulative stress models. The match/mismatch model assumes that early adversities may promote optimal coping with similar events in the future through fostering the development of coping strategies. The cumulative stress model assumes that effects of stress are additive, regardless of the timing of the stressors. Previous studies suggested that stress can have both cumulative and match/mismatch effects on brain structure and functioning and, consequently, we hypothesized that effects on brain circuitry would be found for both models. We anticipated effects on the neural circuitry of structures engaged in face perception and emotional processing. Hence, the amygdala, fusiform face area, occipital face area, and posterior superior temporal sulcus were selected as seeds for seed-based functional connectivity analyses. The interaction between early and recent stress was related to alterations during the processing of emotional expressions mainly in to the cerebellum, middle temporal gyrus, and supramarginal gyrus. For cumulative stress levels, such alterations were observed in functional connectivity to the middle temporal gyrus, lateral occipital cortex, precuneus, precentral and postcentral gyri, anterior and posterior cingulate gyri, and Heschl's gyrus. This study adds to the growing body of literature suggesting that both the cumulative and the match/mismatch hypotheses are useful in explaining the effects of stress.PURPOSE We previously reported three cases of portal hypertension in patients with prolonged anorexia nervosa (AN) with laxative abuse and self-induced vomiting; we now report a fourth, similar case. METHODS A 34-year-old woman with anorexia nervosa, binge-eating/purging type (AN-BP), presented to the Kohnodai Hospital National Center for Global Health and Medicine Psychosomatic Medicine Department for treatment of low body weight. We conducted hepatic and renal biopsies and cardiac magnetic resonance imaging (CMR) to evaluate her complicated liver disease, renal failure, and cardiac insufficiency, respectively. RESULTS Enhanced computed tomography revealed ascites, splenomegaly, and gastroesophageal varices, indicating portal hypertension. The liver and kidney biopsies demonstrated chronic hepatitis without evidence of hepatic cirrhosis and tubulointerstitial nephritis, respectively. CMR demonstrated decreased myocardial mass. CONCLUSION We found tubulointerstitial nephritis and decreased myocardial mass in a patient with non-cirrhotic portal hypertension and prolonged AN with laxative abuse and habitual self-induced vomiting. We propose that reciprocal interactions between multiple factors related to AN, including laxative toxicity, dehydration, renal disorder, and cardiac insufficiency, result in portal hypertension. Level of Evidence Level V.Treatment for cancer has the potential to significantly diminish fertility and, further, to negatively impact the obstetrical outcomes of pregnancies that do occur. Cancer survivors have decreased rates of fertility and increased rates of pregnancy complications, such as preterm birth and low birth weight, after exposure to chemotherapy. To date, research on the impact of chemotherapy and radiotherapy on fertility and pregnancy outcomes has focused largely on the gonadotoxic effect of cancer treatments on ovaries, while the uterus and endometrium have not been extensively studied. It is intuitive, however, that decreased fertility and poorer obstetrical outcomes may be substantially mediated through injury to a highly mitotic tissue like the endometrium, which is also central to embryo implantation and utero-placental exchange. Pregnancy complications in cancer survivors might be due to compromised blood supply to the endometrium and myometrium affecting placentation or altered remodeling of the pregnant uterus secondary to radiation fibrosis. Alterations in endometrial receptivity at the molecular level could affect pregnancy implantation and early pregnancy loss, but later complications also can occur. click here This review focuses on understanding the unintended effects of chemotherapy and radiotherapy on uterine function in female cancer survivors and the impact on pregnancy, and summarizes mechanisms to protect and treat the uterus before and after cancer chemotherapy and radiotherapy.In pituitary adenoma (PA), invasiveness is the main cause of recurrence and poor prognosis. Thus, identifying specific biomarkers for diagnosis and effective treatment of invasive PAs is of great clinical significance. In this study, from the Gene Expression Omnibus database, we obtained and combined several microarrays of PA by the "sva" R package. Weighted gene co-expression network analysis was performed to construct a scale-free topology model and analyze the relationships between the modules and clinical traits. Our analysis results indicated that three key modules (dark turquoise, saddle brown, and steel blue) were associated with the invasiveness of PA. Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis and Gene Ontology analysis were performed for the functional annotation of the key modules. In addition, the hub genes in the three modules were identified and screened by differential expression analysis between normal samples and PA samples. Three upregulated differentially expressed genes (DGAT2, PIGZ, and DHRS2) were identified. The Fisher's exact test and receiver operating characteristic curve were used to validate the capability of these genes to distinguish invasive traits, and transcription factor interaction networks were used to further explore the underlying mechanisms of the three genes. Moreover, a lower expression level of DGAT2 in invasive PA tissue than in noninvasive PA tissue was validated by quantitative reverse transcription-polymerase chain reaction. In general, this study contributes to potential molecular biomarkers of invasive PAs and provides a broader perspective for diagnosis and new therapeutic targets for the invasive PAs.