Immunosuppressive factor(s) specific for L-glutamic acid(50)-L- tyrosine(50) (GT). II. Presence of I-J determinants on the GT-suppressive factor

The responses to the synthetic antigens, L-glutamic acid(60)-L- alanine(30)-L-tyrosine(10) (GAT) and L-glutamic acid(50)-L-tyrosine(50) (GT) are controlled by genes in the I region of the mouse H-2 complex (1-3). Preimmunization of the mice bearing the H-2(p,q,s) nonresponder haplotypes with GAT stimulates the development of suppressor T cells that inhibit in vivo or in vitro antibody responses to GAT complexed to the immunogenic carrier, methylated bovine serum albumin (GAT-MBSA) (4). The copolymer GT is not immunogenic in any inbred mouse strain tested, and has a suppressive effect on the antibody responses to GT-MBSA in mouse strains bearing the H-2(d,f,k,s) haplotypes; suppressor T cells have been demonstrated to be responsible for specific GT suppression (3). We have obtained specific suppressive extracts from thymus and spleen cells of GAT-or GT-primed suppressor strains (5,6). The specific suppressive T-cell factors in the active extracts have been characterized (6,7) and appear similar to the carrier-specific suppressor factor described by Tada and Taniguchi (8). These products belong to a family of newly identified molecules coded for by the I region of the H-2 complex with affinity for antigen and helper (9,10) or suppressive (5-8) regulatory activity on the immune response. Recently, Tada et al. have reported that the keyhole limpet hemocyanin (KLH)-specific suppressor factor is coded for by the I-J subregion of the H-2 complex (11). We now demonstrate also that a GT-specific suppressor factor extracted from the spleens and thymuses of B10.BR (H-2(k)) mice bears determinants controlled by the I-J subregion of the H-2 complex

Alcoholism and Strongyloides stercoralis: Daily Ethanol Ingestion Has a Positive Correlation with the Frequency of Strongyloides Larvae in the Stools

It has been reported that Strongyloides stercoralis infection is more prevalent in chronic alcoholic patients than in non alcoholics living in the same country. In a retrospective study on the prevalence of S. stercoralis infection in a large sample of alcoholic patients, we demonstrate that this prevalence is significantly higher than in non-alcoholic patients admitted at the same hospital. Moreover, the frequency of the parasite was in close relationship with the daily amount of ingested ethanol, even in the absence of liver cirrhosis, reinforcing the idea that chronic alcoholism is associated with increased susceptibility to Strongyloides infection. Beside the bad hygiene profile of alcoholic patients, which explains high risk for acquisition of the parasite, the high prevalence of S. stercoralis in alcoholics may be in relationship with other effects of ethanol on the intestinal motility, steroid metabolism and immune system, which could enhance the chance of autoinfection and the survival and fecundity of females in duodenum. In this way, the number of larvae in the stools is higher in alcoholic patients, increasing the chance of a positive result in a stool examination by sedimentation method

An In Vitro and In Vivo Model Characterizing the Role of the Visfatin/PAK4/β-Catenin Axis in Obesity-Associated Liver Cancer

Introduction: Hepatocellular carcinoma is the most common type of primary liver cancer and ranks fifth in the U.S. as a major leading cause of cancer-related deaths. Obesity is a risk factor for liver cancer, and it may lead to the progression of nonalcoholic steatohepatitis (NASH) to liver cancer. This is concerning considering 49.1% of people in the U.S. are obese. Visceral adipose tissue releases adipocytokines such as visfatin, which is upregulated in liver cancer and obesity. The objective of this study was to determine whether visfatin binds to an unknown receptor activating PAK4, which then phosphorylates β-catenin and GSK-3β, allowing β-catenin to stabilize and move into the nucleus to begin transcription of pro-tumorigenic genes. We hypothesized that obesity-related increases in visfatin stimulate invasion, migration, and liver cancer growth through induction of the PAK4/β-catenin axis. Materials and Methods: The approach to this study was both in vitro and in vivo. Murine Hepa1-6 and human SNU-449 liver cancer cells were analyzed under the following conditions: serum free media (SFM), fetal bovine serum (FBS), SFM + visfatin (40 ng/mL), SFM + visfatin + PF-3758309 (PF, 1 nM; a PAK4 inhibitor), and SFM + PF. MTT and colony formation assays were used to determine cell viability and survival, respectively. Wound healing assay was used to determine migration. Invasion assay was used to determine invasive capacity. Western blot was used to detect proteins and activation. The mouse model included thirty-two 8-week-old mice randomized to either a high fat diet (DIO) or control diet (CON). At 21 weeks of age, mice were injected with Hepa1-6 cells. At 23 weeks of age, 6 mice from both the DIO and CON groups and 5 mice from the DIO and CON groups plus PF were injected with 12.5 mg/kg of PF every other day for 2 weeks. Results: PF-3758309 significantly decreased cell viability and invasion in both cell lines while visfatin promoted invasion. Cell survival was significantly suppressed in Hepa 1-6 cells. There were no statistical differences in migration among the treatment groups in either cell line. In both cell lines, visfatin increased phospho-PAK4, while PF-3758309 led to reduced phosphoPAK4. No differences were seen in phospho-β-cateninSer675 in either cell line. In Hepa1-6 cells, phospho-GSK-3βs9 was increased by FBS and visfatin and reduced by the inhibitor alone, but no differences were seen in visfatin-induced phosphorylation of GSK-3βs9 in the presence of PF375830. DIO mouse weights were significantly higher than the control mouse weights. Tumor weight and tumor volume in the DIO + PF group was significantly reduced compared to DIO without the inhibitor. Interestingly, liver and adipose tissue weights were significantly lower in the DIO + PF group compared to DIO alone despite being similar in weight. DIO mice had 15% increased serum visfatin levels compared to CON mice. Conclusion: In vitro, the PAK4 inhibitor resulted in varied outcomes among Hepa 1-6 and SNU-449 cell lines. Visfatin effects on cell growth and invasion are mediated through PAK4 signaling but not β-catenin. PAK4 may not be important for migration and colony formation. In vivo, PAK4 mediates obesity-induced tumor growth and tumor volume. PAK4 disrupts liver and adipose tissue homeostasis in DIO mice.Family and Consumer Science

Parent Satisfaction Rates in Relation to Child Life Program Size

The topic of this project is how parent satisfaction rates relate to Child Life Program Sizes. The problem is that child life programs are often understaffed. The purpose of this project is to explore the relationship between child life program size and parents' satisfaction with hospitals. In choosing articles for this literature review, an article was a good fit if it contained key words such as parent satisfaction, child life programs, or Certified Child Life Specialists (CCLS). The research needed to be related to parent satisfaction in hospitals or child life programs. I found my articles in Google Scholar or the Tech library database. The participants in these studies were either parents of children in hospitals or child life specialists. The authors sampled participants by inviting parents of children in hospitals to participate. Another study conducted research as they were implementing a child life program. The findings were 1. parents are typically satisfied with child life interventions, 2. parents experienced less concern regarding their child's emotional state, and 3. families expressed they valued the breaks given to them by the CCLSs. Thus, the more CCLSs are available, the more parents will experience these things. This in turn will raise parent satisfaction rates. The implications of this are that hospitals will benefit from hiring more CCLSs. In the future, researchers should explore the relationships between child life program size and CCLS satisfaction

Paralyzed By Our Paradigm - Finding Freedom From Patters That Paralyze Our Mission

As individuals, our understanding of church may be crippling our efforts to take part in the mission of God. Discover the needed paradigm shift to free you to serve Jesus and His Kingdom