A Systematic Literature Review of Effective Interventions For African-American and Hispanic Alzheimer\u27s Caregivers

In this systematic review, an investigation of research on effective social work interventions for African-American and Hispanic caregivers of loved ones with Alzheimer\u27s disease (AD) was conducted. Through a comprehensive literature search, twelve articles met the set inclusion criteria. Peer-reviewed journal articles on quantitative or qualitative research studies on African-American and Hispanic AD caregivers served as the data source. The review found three categories of interventions: in-home programs, Cognitive Behavior Therapy (CBT) focused small groups, and support groups. The majority of the studies included a demonstrated effort to culturally tailor each intervention. The results of the review demonstrate an overall improvement in depression, diminished sense of burden, and other measures of healthy caregiver coping. The majority of the interventions demonstrated little difference between racial or ethnic groups, indicating that cultural tailoring is advantageous to creating effective AD caregiver interventions. Based on the findings, further research is needed to explore CBT\u27s efficacy for African-American caregivers and to assess interventions that address caregiver anxiety. Furthermore, this project indicates the ongoing need for social work practitioners to act with cultural sensitivity, curiosity, and responsiveness as a means for effective cross-cultural interventions

Formative influences of engineering extension on industrial education at Iowa State College

At Iowa State University, engineering educators promoted and established industrial education under the guidance of the College of Engineering. Until about 1890, several professors provided training for non-engineers. Such training became a major concern of several national organizations. Engineers in the American Association of Agricultural Colleges and Experiment Stations established the Mechanic Arts Section. Within the Society for the Promotion of Engineering Education, a Committee on Industrial Education sought ways for engineers to influence the growth of industrial education;John B. Johnson, Dean of the College of Engineering at the University of Wisconsin, began artisan training in 1901. It grew into an extensive engineering extension program, led after 1906 by Louis E. Reber. In Iowa, the Iowa State Manufacturers Association and Anson Marston, Dean of Engineering at Iowa State, won funding for an extension department. Two organizations also affected that development, the YMCA and the Land Grant College Engineering Association. Between 1913 and 1917, the extension engineers in Ames conducted programs which provided industrial education to thousands of Iowans. World War I and the Smith-Hughes Act altered the extension efforts, placing the vocational work under the Iowa State Board for Vocational Education. The Trades and Industries department, started in 1919, took over the teacher training work, and by about 1925, industrial teacher preparation stood as the sole function of the department. That also indicated that many direct ties to industry had been broken. The teaching mission characterized the Industrial Education department for several decades

A Systematic Literature Review of Effective Interventions For African-American and Hispanic Alzheimer’s Caregivers

In this systematic review, an investigation of research on effective social work interventions for African-American and Hispanic caregivers of loved ones with Alzheimer’s disease (AD) was conducted. Through a comprehensive literature search, twelve articles met the set inclusion criteria. Peer-reviewed journal articles on quantitative or qualitative research studies on African-American and Hispanic AD caregivers served as the data source. The review found three categories of interventions: in-home programs, Cognitive Behavior Therapy (CBT) focused small groups, and support groups. The majority of the studies included a demonstrated effort to culturally tailor each intervention. The results of the review demonstrate an overall improvement in depression, diminished sense of burden, and other measures of healthy caregiver coping. The majority of the interventions demonstrated little difference between racial or ethnic groups, indicating that cultural tailoring is advantageous to creating effective AD caregiver interventions. Based on the findings, further research is needed to explore CBT’s efficacy for African-American caregivers and to assess interventions that address caregiver anxiety. Furthermore, this project indicates the ongoing need for social work practitioners to act with cultural sensitivity, curiosity, and responsiveness as a means for effective cross-cultural interventions

Toll-like receptor 2 signaling is a mediator of apoptosis in herpes simplex virus-infected microglia

BACKGROUND: Information regarding the response of brain cells to infection with herpes simplex virus (HSV)-1 is needed for a complete understanding of viral neuropathogenesis. We have recently demonstrated that microglial cells respond to HSV infection by producing a number of proinflammatory cytokines and chemokines through a mechanism involving Toll-like receptor 2 (TLR2). Following this cytokine burst, microglial cells rapidly undergo cell death by apoptosis. We hypothesized that TLR2 signaling might mediate the cell death process as well. METHODS: To test this hypothesis, we investigated HSV-induced cell death of microglia obtained from both wild-type and TLR2(-/- )mice. Cell death was studied by oligonucleosomal ELISA and TUNEL staining, and the mechanisms of apoptosis were further analyzed using murine apoptosis-specific microarrays. The data obtained from microarray analysis were then validated using quantitative real-time PCR assays. RESULTS: HSV infection induced apoptotic cell death in microglial cells from wild-type as well as TLR2 cells. However, the cell death at 24 h p.i. was markedly lower in knockout cells. Furthermore, microarray analyses clearly showed that the expression of pro-apoptotic genes was down-regulated at the time when wild-type cells were actively undergoing apoptosis, indicating a differential response to HSV in cells with or without TLR2. CONCLUSION: We demonstrate here that HSV induces an apoptotic response in microglial cells which is mediated through TLR2 signaling

Histoplasma capsulatum yeast phase-specific protein Yps3p induces Toll-like receptor 2 signaling

Histoplasma capsulatum is a common cause of fungal infection in certain geographic areas, and although most infections are asymptomatic, it is capable of causing histoplasmosis, a disseminated, life-threatening disease, especially in immunocompromised individuals. A deeper understanding of this host-pathogen interaction is needed to develop novel therapeutic strategies to counter lethal infection. Although several lines of evidence suggest that this fungus is neurotropic in HIV patients, little is known about the immunobiology of Histoplasma infection in the central nervous system [CNS]. The goal of the present study was to understand the innate neuroimmune mechanisms that recognize H. capsulatum during the initial stages of infection. Using a 293T stable cell line expressing murine Toll-like receptor 2 [TLR2], we show here that TLR2 recognizes H. capsulatum cell wall protein Yps3p and induces the activation of NF-κB. In further experiments, we tested the ability of Yps3p to induce signaling from TLR2 in primary microglial cells, the resident brain macrophages of the CNS. Our data show that H. capsulatum Yps3p induced TLR2 signaling in wild-type microglia, but not in microglia isolated from TLR2 KO mice, confirming that Yps3p is a ligand for TLR2. Furthermore, Yps3p-induced TLR2 signaling was suppressed by vaccinia virus-encoded TLR inhibitors. This is the first demonstration of a fungal protein serving as a TLR ligand and mediating signaling in primary brain cells

Persistent Humoral Immune Responses in the CNS Limit Recovery of Reactivated Murine Cytomegalovirus

Background: Experimental infection of the mouse brain with murine CMV (MCMV) elicits neuroimmune responses that terminate acute infection while simultaneously preventing extensive bystander damage. Previous studies have determined that CD8 + T lymphocytes are required to restrict acute, productive MCMV infection within the central nervous system (CNS). In this study, we investigated the contribution of humoral immune responses in control of MCMV brain infection. Methodology/Principal Findings: Utilizing our MCMV brain infection model, we investigated B-lymphocyte-lineage cells and assessed their role in controlling the recovery of reactivated virus from latently infected brain tissue. Brain infiltrating leukocytes were first phenotyped using markers indicative of B-lymphocytes and plasma cells. Results obtained during these studies showed a steady increase in the recruitment of B-lymphocyte-lineage cells into the brain throughout the timecourse of viral infection. Further, MCMV-specific antibody secreting cells (ASC) were detected within the infiltrating leukocyte population using an ELISPOT assay. Immunohistochemical studies of brain sections revealed co-localization of CD138 + cells with either IgG or IgM. Additional immunohistochemical staining for MCMV early antigen 1 (E1, m112–113), a reported marker of viral latency in neurons, confirmed its expression in the brain during latent infection. Finally, using B-cell deficient (Jh 2/2) mice we demonstrated that B-lymphocytes control recovery of reactivated virus from latently-infected brain tissue. A significantly higher rate of reactivated virus was recovered from the brains of Jh 2/2 mice when compared t

Herpes simplex virus induces neural oxidative damage via microglial cell Toll-like receptor-2

<p>Abstract</p> <p>Background</p> <p>Using a murine model of herpes simplex virus (HSV)-1 encephalitis, our laboratory has determined that induction of proinflammatory mediators in response to viral infection is largely mediated through a Toll-like receptor-2 (TLR2)-dependent mechanism. Published studies have shown that, like other inflammatory mediators, reactive oxygen species (ROS) are generated during viral brain infection. It is increasingly clear that ROS are responsible for facilitating secondary tissue damage during central nervous system infection and may contribute to neurotoxicity associated with herpes encephalitis.</p> <p>Methods</p> <p>Purified microglial cell and mixed neural cell cultures were prepared from C57B/6 and TLR2^-/-mice. Intracellular ROS production in cultured murine microglia was measured via 2', 7'-Dichlorofluorescin diacetate (DCFH-DA) oxidation. An assay for 8-isoprostane, a marker of lipid peroxidation, was utilized to measure free radical-associated cellular damage. Mixed neural cultures obtained from β-actin promoter-luciferase transgenic mice were used to detect neurotoxicity induced by HSV-infected microglia.</p> <p>Results</p> <p>Stimulation with HSV-1 elevated intracellular ROS in wild-type microglial cell cultures, while TLR2^-/-microglia displayed delayed and attenuated ROS production following viral infection. HSV-infected TLR2^-/-microglia produced less neuronal oxidative damage to mixed neural cell cultures in comparison to HSV-infected wild-type microglia. Further, HSV-infected TLR2^-/-microglia were found to be less cytotoxic to cultured neurons compared to HSV-infected wild-type microglia. These effects were associated with decreased activation of p38 MAPK and p42/p44 ERK in TLR2^-/-mice.</p> <p>Conclusions</p> <p>These studies demonstrate the importance of microglial cell TLR2 in inducing oxidative stress and neuronal damage in response to viral infection.</p

Reactive oxygen species drive herpes simplex virus (HSV)-1-induced proinflammatory cytokine production by murine microglia

Abstract Background Production of reactive oxygen species (ROS) and proinflammatory cytokines by microglial cells in response to viral brain infection contributes to both pathogen clearance and neuronal damage. In the present study, we examined the effect of herpes simplex virus (HSV)-1-induced, NADPH oxidase-derived ROS in activating mitogen-activated protein kinases (MAPKs) as well as driving cytokine and chemokine expression in primary murine microglia. Methods Oxidation of 2', 7'-dichlorodihydrofluorescin diacetate (H2DCFDA) was used to measure production of intracellular ROS in microglial cell cultures following viral infection. Virus-induced cytokine and chemokine mRNA and protein levels were assessed using real-time RT-PCR and ELISA, respectively. Virus-induced phosphorylation of microglial p38 and p44/42 (ERK1/2) MAPKs was visualized using Western Blot, and levels of phospho-p38 were quantified using Fast Activated Cell-based ELISA (FACE assay). Diphenyleneiodonium (DPI) and apocynin (APO), inhibitors of NADPH oxidases, were used to investigate the role of virus-induced ROS in MAPK activation and cytokine, as well as chemokine, production. Results Levels of intracellular ROS were found to be highly elevated in primary murine microglial cells following infection with HSV and the majority of this virus-induced ROS was blocked following DPI and APO treatment. Correspondingly, inhibition of NADPH oxidase also decreased virus-induced proinflammatory cytokine and chemokine production. In addition, microglial p38 and p44/42 MAPKs were found to be phosphorylated in response to viral infection and this activation was also blocked by inhibitors of NADPH oxidase. Finally, inhibition of either of these ROS-induced signaling pathways suppressed cytokine (TNF-α and IL-1β) production, while chemokine (CCL2 and CXCL10) induction pathways were sensitive to inhibition of p38, but not ERK1/2 MAPK. Conclusions Data presented herein demonstrate that HSV infection induces proinflammatory responses in microglia through NADPH oxidase-dependent ROS and the activation of MAPKs.</p