Templetonalvarez1924

BACKGROUND The current study aims to evaluate the association between preterm birth and the quality of mother-child interaction of very preterm-, moderate preterm-, and full-term-born children at 18 and 36 months and to determine whether developmental and behavioral characteristics mediate the association between preterm birth and the quality of mother-child interaction. METHOD Participants included 110 preterm-born children and 39 full-term-born children assessed at ages 18 and 36 months. Mother-child free play interactions, the Mullen Scales of Early Learning, the Infant Behavior Questionnaire, and the Early Childhood Behavior Questionnaire were administered. RESULTS Significant associations between preterm birth and the quality of mother-child interaction were found at 18 and 36 months. The mother-child interaction quality was less optimal for the preterm-born children compared with the full-term-born children, mainly so for the very preterm-born children. Unlike behavioral characteristics, cognitive development was found to mediate the association between the gestational age-based group and the quality of mother-child interaction. CONCLUSIONS Intervention programs for preterm-born children and their families, should consider maternal and children's behaviors during mother-child interactions, in addition to cognitive, language, motor and emotional regulation abilities, and particularly so with very preterm-born children, who exhibit slower cognitive development. Autoimmunity and cancer affect millions worldwide and both, in principal, result from dysregulated immune responses. There are many well-known molecules involved in immunological process playing as a double-edged sword, by which associating autoimmune diseases and cancer. In this regard, Endoplasmic reticulum aminopeptidases (ERAP) 1, which belongs to the M1 family of aminopeptidases, plays a central role as a "molecular ruler", proteolyzing of N-terminal of the antigenic peptides before their loading onto HLA-I molecules for antigen presentation in the Endoplasmic Reticulum (ER). Several genome-wide association studies (GWAS) highlighted the significance of ERAP1 and ERAP2 in autoimmune diseases, including Ankylosing spondylitis, Psoriasis, Bechet's disease, and Birdshot chorioretinopathy, as well as in cancers. The expression of ERAP1/2 is mostly altered in different cancers compared to normal cells, but how this affects anti-cancer immune responses and cancer growth has been little explored. Recent studies on the immunological outcomes and the catalytic functions of ERAP1 and ERAP2 have provided a better understanding of their potential pathogenetic role in autoimmunity and cancer. In this review, we summarize the role of ERAP1 and ERAP2 in the autoimmune diseases and cancer immunity based on the recent advances in GWAS studies. The transglutaminase 2 (TG2) is one of the enigmatic enzymes with important functional diversity. It plays an important role in several pathologies such as celiac disease (CD). In patients with active CD, the abnormal retrotranscytosis of IgA/gliadin complexes is mediated by Transferrin Receptor 1 (TfR1). This triad association takes also place in IgA nephropathy (IgA-N). IgA-N is characterized by the formation of nephrotoxic complexes of IgA1 and soluble CD89 (sCD89). These complexes are abnormally deposited in the kidney. Using a humanized mouse model of IgA-N (α1KI-CD89Tg), we showed that IgA1-sCD89 complexes engender mesangial cell activation and proliferation with TfR1 and TG2 up-regulation, associated with IgA-N features. This TG2-TfR1 interaction enhances mesangial IgA1 deposition promoting inflammation. Humanized α1KI-CD89Tg mice deficient for TG2 show a decrease in TfR1 expression in kidney leading to reduced IgA1-sCD89 deposits and an improvement in IgA-N features. 17-AAG Moreover, TG2 is active and overexpressed in the intestine of IgA-N mice and gliadin participates to this renal pathology. In kidney as in intestine, the TG2 has a crucial role in the cooperation between TfR1-IgA and a central role in the pathogenic amplification. T cells able to control neoplasia or chronic infections display a signature gene expression profile similar or identical to that of central memory T cells. These cells have qualities of self-renewal and a plasticity that allow them to repeatedly undergo activation (growth, proliferation, and differentiation), followed by quiescence. It is these qualities that define the ability of T cells to establish an equilibrium with chronic infectious agents, and also preserve the ability of T cells to be re-activated (by checkpoint therapy) in response to malignant cancers. Here we describe distinctions between the forms of inhibition mediated by tumors and persistent viruses, we review the properties of T cells associated with long-term immunity, and we identify the transcription factor, FOXO1, as the control point for a program of gene expression that allows CD8+ T cells to undergo serial reactivation and self-renewal. BACKGROUND Hepatitis C virus (HCV) treatment uptake among people who inject drugs (PWID), a population with disproportionately high rates of HCV, remains low. Peers have been shown to positively impact a broad range of health outcomes for PWID. There is, however, limited data on the impact of PWID social network members on HCV treatment. METHODS HCV-infected PWID enrolled in an ongoing community-based cohort were recruited as "indexes" to complete an egocentric social network survey. The survey elicited from the index PWID a list of their network members and the index's perception of network member characteristics. Logistic regression analyses were conducted to compare individual and network factors associated with HCV treatment in the index PWID. RESULTS Among 540 HCV-infected PWID, the mean age was 55.7 years and the majority were black (87.2%) and male (69.8%). PWID reported a mean of 4.4 (standard deviation [SD] 3.2) network members, most of whom were relatives (mean 2.2 [SD 1.5]). In multivariable analysis, increasing index age and HIV infection were positively associated with HCV treatment, while drug use and homelessness in the preceding 6 months were negatively associated with HCV treatment. From a network perspective, having at least one network member who regularly talked with the index about seeing their doctor for HIV care was associated with HCV treatment (Adjusted Odds Ratio [AOR] 2.7; 95% Confidence Interval (CI) [1.3, 5.6]). Conversely, PWID who had at least one network member who helped them understand their HCV care were less likely to have been HCV treated (AOR 0.2; CI [0.1, 0.6). CONCLUSION HCV treatment uptake in this group of PWID appeared to be positively influenced by discussions with network members living with HIV who were in care and negatively influenced by HCV information sharing within PWID networks. These findings underscore the influence of peers on health seeking behaviors of their network members and emphasizes the importance of well-informed peers.