Intervention development to improve foster youth mental health by targeting coping self-efficacy and help-seeking.

This study articulates the iterative development of an intervention called Strengthening Youth Networks and Coping (SYNC), which is designed to target coping self-efficacy and help-seeking intentions and behaviors among youth in foster care. The overarching goal is to design an intervention that will be a feasible and acceptable enhancement to existing child welfare services, and that will address modifiable determinants among adolescents involved in child welfare system that are related to elevated risk for mental health challenges, limited support network capacity, and service disengagement after exiting foster care. In this paper, we describe our initial needs assessment, explain how we selected proximal intervention mechanisms (i.e., intermediate outcomes) to target, and outline the preliminary intervention development process, including ongoing insights we received from a research advisory group including members with lived experience. Next, we report and discuss the initial acceptability pre-testing data collected from youth (N = 30) as well as feasibility data collected from providers (N = 82), results from which were used to refine the SYNC intervention framework prior to robust efficacy testing. Findings highlight the need and importance of targeting youth coping and help-seeking, integrating programming within existing transition services, delivering this content in a group-based format that includes near-peer mentors and facilitators with lived experience, and developing options that work for the heterogeneous population of young people in foster care. The results also highlight the key objective of capturing youth's interests prior to enrolling in the program (e.g., language used in recruitment materials), holding their interest throughout the program (e.g., creating opportunities for youth to engage with other youth with similar experiences), and suggestions to encourage youth's engagement and participation. This paper articulates the value of this intervention development approach, and the sequential phases of this intervention development process as well as the results, which may be useful to applied researchers and practitioners working with youth in foster care and other priority populations.

Measuring the Impact of an Educational Intervention on Evidence-Based Practice.

Background With an increasingly complex health care system, there are greater demands for nurses to have a strong foundation in evidence-based practice (EBP) competencies because of their relationship to improved patient and organizational outcomes. Attributes such as knowledge, skills, and attitudes contribute to the development of EBP competencies. Method A quasi-experimental study with a pretest/posttest design was conducted to evaluate the outcomes for 30 RNs in an acute care setting who attended a 3-hour EBP educational intervention using the Healthcare EBP Assessment Tool questionnaire. Results The nurses demonstrated a significant improvement in their perceived understanding of EBP after the intervention (p = .005). Statistically significant improvements were also noted on the subscales of frequency, ability, desire, and barriers. Conclusion Advances in the perception of EBP competencies made by the participants of this intervention may enhance their feeling of contributing to the organization and result in improved patient outcomes and work environment. Further research is needed to investigate the effectiveness of other interventions, including opportunities to be involved in quality improvement projects and research studies. [J Contin Educ Nurs. 2022;53(3):109-114.].

Public servant, silent servant: A call to action for advocacy training in public service settings.

Views on what is important in training for psychologists are evolving, reflecting a broadening understanding of the role psychologists can and should play in societal change. Since the development of the scientist-practitioner model after World War II, arguments around training have focused on the appropriate balance between training in the practice of psychology versus training in research related to psychology. Recent calls reflect more radical change to include an advocacy emphasis within the formal coursework of psychology doctoral programs, well articulated by Mallinckrodt, Miles, and Levy (2014) as the tripartite model of Scientist-Practitioner-Advocate. In this paper, we present the argument for expanding a model that incorporates advocacy training into clinical psychology internships and postdoctoral programs and describe why we believe voices for advocacy have been largely silent in public-sector clinical psychology training and practices. We outline how this may be accomplished in public sector training settings, and we articulate a call to action for public servants to speak out so their voice can ignite a passion for advocacy within public sector psychology service and training. (PsycInfo Database Record (c) 2020 APA, all rights reserved).

Sucrose replacement in high ratio white layer cakes.

BACKGROUND: Several commercially available alternative sweeteners have potential in reducing the caloric content of baked products. Sugar alcohols and natural sweeteners have similar bulk as sucrose and can replace sucrose directly. High intensity sweeteners have high potency but light weight so bulking agents are often added. This study determined alternative sweeteners and combinations of alternative sweetener and a bulking agent that produced good quality white layer cakes. RESULTS: Cakes made with maltitol were acceptable but erythritol and fructose produced undesirable cakes. Maltodextrin and polydextrose were acceptable bulking agents, producing cakes that were similar to control cakes. The flavor of cakes sweetened with sucralose was acceptable but those with stevia had a disagreeable metallic aftertaste. Cakes made with sucralose plus maltodextrin were preferred over those containing sucralose plus polydextrose. Consumer acceptance of flavor, texture and overall liking of cakes containing maltitol was similar to sucrose and both were preferred over cakes containing maltodextrin plus sucralose. CONCLUSION: Replacing sucrose with maltitol in white layer cakes reduced the caloric content by 16% with no loss in quality. © 2016 Society of Chemical Industry.

Impact of Triticum mosaic virus infection on hard winter wheat milling and bread baking quality.

BACKGROUND: Triticum mosaic virus (TriMV) is a newly discovered wheat virus. Information regarding the effect of wheat viruses on milling and baking quality is limited. The objective of this study was to determine the impact of TriMV infection on the kernel characteristics, milling yield and bread baking quality of wheat. Commercial hard winter varieties evaluated included RonL, Danby and Jagalene. The TriMV resistance of RonL is low, while that of Danby and Jagalene is unknown. KS96HW10-3, a germplasm with high TriMV resistance, was included as a control. Plots of each variety were inoculated with TriMV at the two- to three-leaf stage. Trials were conducted at two locations in two crop years. RESULTS: TriMV infection had no effect on the kernel characteristics, flour yield or baking properties of KS96HW10-3. The effect of TriMV on the kernel characteristics of RonL, Danby and Jagalene was not consistent between crop years and presumably an environmental effect. The flour milling and bread baking properties of these three varieties were not significantly affected by TriMV infection. CONCLUSION: TriMV infection of wheat plants did not affect harvested wheat kernel characteristics, flour milling properties or white pan bread baking quality.

Induction of glucose metabolism in stimulated T lymphocytes is regulated by mitogen-activated protein kinase signaling.

T lymphocytes play a critical role in cell-mediated immune responses. During activation, extracellular and intracellular signals alter T cell metabolism in order to meet the energetic and biosynthetic needs of a proliferating, active cell, but control of these phenomena is not well defined. Previous studies have demonstrated that signaling from the costimulatory receptor CD28 enhances glucose utilization via the phosphatidylinositol-3-kinase (PI3K) pathway. However, since CD28 ligation alone does not induce glucose metabolism in resting T cells, contributions from T cell receptor-initiated signaling pathways must also be important. We therefore investigated the role of mitogen-activated protein kinase (MAPK) signaling in the regulation of mouse T cell glucose metabolism. T cell stimulation strongly induces glucose uptake and glycolysis, both of which are severely impaired by inhibition of extracellular signal-regulated kinase (ERK), whereas p38 inhibition had a much smaller effect. Activation also induced hexokinase activity and expression in T cells, and both were similarly dependent on ERK signaling. Thus, the ERK signaling pathway cooperates with PI3K to induce glucose utilization in activated T cells, with hexokinase serving as a potential point for coordinated regulation.

Extracellular collagenases and the endocytic receptor, urokinase plasminogen activator receptor-associated protein/Endo180, cooperate in fibroblast-mediated collagen degradation.

The collagens of the extracellular matrix are the most abundant structural proteins in the mammalian body. In tissue remodeling and in the invasive growth of malignant tumors, collagens constitute an important barrier, and consequently, the turnover of collagen is a rate-limiting process in these events. A recently discovered turnover route with importance for tumor growth involves intracellular collagen degradation and is governed by the collagen receptor, urokinase plasminogen activator receptor-associated protein (uPARAP or Endo180). The interplay between this mechanism and extracellular collagenolysis is not known. In this report, we demonstrate the existence of a new, composite collagen breakdown pathway. Thus, fibroblast-mediated collagen degradation proceeds preferentially as a sequential mechanism in which extracellular collagenolysis is followed by uPARAP/Endo180-mediated endocytosis of large collagen fragments. First, we show that collagen that has been pre-cleaved by a mammalian collagenase is taken up much more efficiently than intact, native collagen by uPARAP/Endo180-positive cells. Second, we demonstrate that this preference is governed by the acquisition of a gelatin-like structure by the collagen, occurring upon collagenase-mediated cleavage under native conditions. Third, we demonstrate that the growth of uPARAP/Endo180-deficient fibroblasts on a native collagen matrix leads to substantial extracellular accumulation of well defined collagen fragments, whereas, wild-type fibroblasts possess the ability to direct an organized and complete degradation sequence comprising both the initial cleavage, the endocytic uptake, and the intracellular breakdown of collagen.

Complementary roles of intracellular and pericellular collagen degradation pathways in vivo.

Collagen degradation is essential for cell migration, proliferation, and differentiation. Two key turnover pathways have been described for collagen: intracellular cathepsin-mediated degradation and pericellular collagenase-mediated degradation. However, the functional relationship between these two pathways is unclear and even controversial. Here we show that intracellular and pericellular collagen turnover pathways have complementary roles in vivo. Individual deficits in intracellular collagen degradation (urokinase plasminogen activator receptor-associated protein/Endo180 ablation) or pericellular collagen degradation (membrane type 1-matrix metalloproteinase ablation) were compatible with development and survival. Their combined deficits, however, synergized to cause postnatal death by severely impairing bone formation. Interestingly, this was mechanistically linked to the proliferative failure and poor survival of cartilage- and bone-forming cells within their collagen-rich microenvironment. These findings have important implications for the use of pharmacological inhibitors of collagenase activity to prevent connective tissue destruction in a variety of diseases.

Increased expression of the collagen internalization receptor uPARAP/Endo180 in the stroma of head and neck cancer.

Local growth, invasion, and metastasis of malignancies of the head and neck involve extensive degradation and remodeling of the underlying, collagen-rich connective tissue. Urokinase plasminogen activator receptor-associated protein (uPARAP)/Endo180 is an endocytic receptor recently shown to play a critical role in the uptake and intracellular degradation of collagen by mesenchymal cells. As a step toward determining the putative function of uPARAP/Endo180 in head and neck cancer progression, we used immunohistochemistry to determine the expression of this collagen internalization receptor in 112 human squamous cell carcinomas and 19 normal or tumor-adjacent head and neck tissue samples from the tongue, gingiva, cheek, tonsils, palate, floor of mouth, larynx, maxillary sinus, upper jaw, nasopharynx/nasal cavity, and lymph nodes. Specificity of detection was verified by staining of serial sections with two different monoclonal antibodies against two non-overlapping epitopes on uPARAP/Endo180 and by the use of isotype-matched non-immune antibodies. uPARAP/Endo180 expression was observed in stromal fibroblast-like, vimentin-positive cells. Furthermore, expression of the collagen internalization receptor was increased in tumor stroma compared with tumor-adjacent connective tissue or normal submucosal connective tissue and was most prominent in poorly differentiated tumors. These data suggest that uPARAP/Endo180 participates in the connective tissue destruction during head and neck squamous cell carcinoma progression by mediating cellular uptake and lysosomal degradation of collagen.

Matrix metalloproteinases in colorectal cancer: is it worth talking about?

Matrix metalloproteinases (MMPs), a family of extracellular matrix degrading enzymes, are expressed in various stages of colorectal cancer (CRC) and correlate with survival and prognosis. There is considerable evidence in preclinical models that MMP inhibitors (MMPIs) are effective at multiple stages of CRC tumor progression, including reducing the number of intestinal adenomas, inhibiting the growth and establishment of primary CRC tumors, and reducing metastasis to the lung and liver. However, clinical trials with MMPIs in other tumor types have been largely unsuccessful, raising the question as to whether MMPs represent therapeutic targets in CRC. This review focuses on the expression, role, and contribution of MMP family members to various stages of CRC tumor progression. The conclusion is that there is considerable evidence to suggest that MMP inhibition may be an effective strategy if applied at either end of the tumor progression spectrum; the prevention of adenomas, or the treatment of micrometastatic disease.