19 research outputs found

    When Traumatic Stressors are Not Past, But Now: Psychosocial Treatment to Develop Resilience with Children and Youth Enduring Concurrent, Complex Trauma

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    The article discusses a project called the Empowering Counseling Program (ECP) conducted in community schools using participatory action and consumer evaluation designs. It addressed the elements of treatment theories used by mental health providers such as values, assumptions and concepts. It cites findings that clients suffering from complex trauma in under-resourced communities, unavoidably traumatized concurrently with treatment do not benefit from treatment guidelines

    Hope Is the Ticket to Life: Insights From Disadvantaged African American Youth

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    It is important to look at strengths in populations, especially those termed at-risk or disadvantaged. Hope and compassion are positive qualities inner-city African American youth can possess, and further research on these constructs with this population is needed. This exploratory, mixed methods study included both quantitative measures of hope and compassion and qualitative interviews with inner-city African American youth who are participating in an after school program. The following research questions were addressed: (1) How do the youth describe hope?, (2) How do the youth\u27s relationships develop and maintain hope?, (3) How do the youth describe goal definition and pursuit as related to hope?, (4) How do the youth say the After School Matters program helps them develop hope and compassion?, and (5) What do the youth say is the relationship between experiences of compassion and the development of hope? Qualitative analysis yielded six overall themes: (1) Relationships with others, specifically caring, encouragement, and compassion from others, as these relate to developing and sustaining hope, (2) Religion and faith as these relate to hope, (3) Staying on track, staying focused, and perseverance as these relate to hope and goal achievement, (4) Hope as it relates to wanting something to happen or something that can happen, (5) Thinking positively (motivated, believing in yourself) as it related to sustaining hope, and (6) Hope as it relates to goals. Analysis of the quantitative scales found the youth to have above average levels of hope, average levels of compassion, and below average levels of empathy. A significant positive correlation was found between the Children\u27s Hope Scale and the Compassionate Love Scale Stranger-Humanity Version. Key findings were that disadvantaged youth do have hope and their hope comes from relationships. The strengths and weaknesses of the qualitative and quantitative methodology are discussed. Implications for social work practice (specifically after school programming and individual interventions), policy, and research are also addressed

    Clients’ Hope Arises from Social Workers’ Compassion: Young Clients’ Perspectives on Surmounting the Obstacles of Disadvantage

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    While social workers strive to build disadvantaged African American youths’ resilience by improving services, rarely are those youths’ perspectives included in research. In a previous evaluation of an after-school program, disadvantaged African American youths prioritized instructors’ compassion and said compassion engendered hope. This study explores their connection between compassion and hope more deeply. Focusing on Snyder’s hope theory, this study examines the connection between compassion and hope as individual traits (using standardized scales) and as relational, action-based experiences (using qualitative analysis of interview data). Instructor actions that youths identified as compassionate and as engendering hope were encouragement, problem solving, responsive empathy, and affirming that good choices could bring about good futures. Youths built their hope by internalizing their instructors’ compassion

    When Traumatic Stressors are Not Past, But Now: Psychosocial Treatment to Develop Resilience with Children and Youth Enduring Concurrent, Complex Trauma

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    While providing school-based treatment for 450 urban impoverished children and youth from 2006 to 2014, we found implementing specific elements of PTSD treatment models reduced engagement and aggravated clients’ symptoms. Clients’ traumas were neither past nor single-type, but were multiple (complex) and unavoidably occurring concurrently with treatment. We speculated that many trauma treatment elements needed revision to be effective. Using a participatory action research methodology, we developed a resilience-focused treatment model for concurrently-traumatized clients. Drawing from the strengths perspective, self-determination, and hope theories, key treatment elements revised here are triggers, re-enactment, avoidance, “silencing,” and dissociation. Treatment guidelines include creating a safe zone, entering clients’ worlds completely, frame flexibility, client self-determination of treatment agendas and duration, and pleasurable play

    IGFBP-3 blocks hyaluronan-CD44 signaling, leading to increased acetylcholinesterase levels in A549 cell media and apoptosis in a p53-dependent manner

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    Insulin-like growth factor binding protein-3 (IGFBP-3) belongs to a family of six IGF binding proteins. We previously found that IGFBP-3 exerts its cytotoxic effects on A549 (p53 wild-type) cell survival through a mechanism that depends on hyaluronan-CD44 interactions. To shed light on the mechanism employed, we used CD44-negative normal human lung cells (HFL1), A549, and H1299 (p53-null) lung cancer cells. A synthetic IGFBP-3 peptide (215-KKGFYKKKQCRPSKGRKR-232) but not the mutant (K228AR230A), was able to bind hyaluronan more efficiently than the analogous sequences from the other IGFBPs. In a manner comparable to that of the IGFBP-3 protein, the peptide blocked hyaluronan-CD44 signaling, and more effectively inhibited viability of A549 cells than viability of either H1299 or HFL1 cell lines. Treatment with the IGFBP-3 protein or its peptide resulted in increased acetylcholinesterase concentration and activity in the A549 cell media but not in the media of either HFL1 or H1299, an effect that correlated with increased apoptosis and decreased cell viability. These effects were diminished upon the same treatment of A549 cells transfected with either p53 siRNA or acetylcholinesterase siRNA. Taken together, our results show that IGFBP-3 or its peptide blocks hyaluronan-CD44 signaling via a mechanism that depends on both p53 and acetylcholinesterase

    Biochemical determinants of the IGFBP‐3–hyaluronan interaction

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    IGFBP-3, the most abundant IGFBP and the main carrier of insulin-like growth factor I (IGF-I) in the circulation, can bind IGF-1 with high affinity, which attenuates IGF/IGF-IR interactions, thereby resulting in antiproliferative effects. The C-terminal domain of insulin-like growth factor-binding protein-3 (IGFBP-3) is known to contain an 18-basic amino acid motif capable of interacting with either humanin (HN) or hyaluronan (HA). We previously showed that the 18-amino acid IGFBP-3 peptide is capable of binding either HA or HN with comparable affinities to the full-length IGFBP-3 protein and that IGFBP-3 can compete with the HA receptor, CD44, for binding HA. Blocking the interaction between HA and CD44 reduced viability of A549 human lung cancer cells. In this study, we set out to better characterize IGFBP-3-HA interactions. We show that both stereochemistry and amino acid identity are important determinants of the interaction between the IGFBP-3 peptide and HA and for the peptide\u27s ability to exert its cytotoxic effects. Binding of IGFBP-3 to either HA or HN was unaffected by glycosylation or reduction of IGFBP-3, suggesting that the basic 18-amino acid residue sequence of IGFBP-3 remains accessible for interaction with either HN or HA upon glycosylation or reduction of the full-length protein. Removing N-linked oligosaccharides from CD44 increased its ability to compete with IGFBP-3 for binding HA, while reduction of CD44 rendered the protein relatively ineffective at blocking IGFBP-3-HA interactions. We conclude that both deglycosylation and disulfide bond formation are important for CD44 to compete with IGFBP-3 for binding HA

    Interaction of amyloid beta with humanin and acetylcholinesterase is modulated by ATP

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    Humanin (HN) is known to bind amyloid beta (Aβ)-inducing cytoprotective effects, while binding of acetylcholinesterase (AChE) to Aβ increases its aggregation and cytotoxicity. Previously, we showed that binding of HN to Aβ blocks aggregation induced by AChE and that HN decreases but does not abolish Aβ-AChE interactions in A549 cell media. Here, we set out to shed light on factors that modulate the interactions of Aβ with HN and AChE. We found that binding of either HN or AChE to Aβ is not affected by heparan sulfate, while ATP, thought to reduce misfolding of Aβ, weakened interactions between AChE and Aβ but strengthened those between Aβ and HN. Using media from either A549 or H1299 lung cancer cells, we observed that more HN was bound to Aβ upon addition of ATP, while levels of AChE in a complex with Aβ were decreased by ATP addition to A549 cell media. Exogenous addition of ATP to either A549 or H1299 cell media increased interactions of endogenous HN with Aβ to a comparable extent despite differences in AChE expression in the two cell lines, and this was correlated with decreased binding of exogenously added HN to Aβ. Treatment with exogenous ATP had no effect on cell viability under all conditions examined. Exogenously added ATP did not affect viability of cells treated with AChE-immunodepleted media, and there was no apparent protection against the cytotoxicity resulting from immunodepletion of HN. Moreover, exogenously added ATP had no effect on the relative abundance of oligomer versus total Aβ in either cell line

    Humanin blocks the aggregation of Amyloid-β induced by acetylcholinesterase, an effect abolished in the presence of IGFBP-3

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    It is known that the humanin (HN) peptide binding to amyloid-β (Aβ) protects against its cytotoxic effects, while acetylcholinesterase (AChE) binding to Aβ increases its aggregation and cytotoxicity. HN is also known to bind the insulin-like growth factor binding protein-3 (IGFBP-3). Here, we examined the regulation of Aβ conformations by HN, AChE, and IGFBP-3 both in vitro and in the conditioned media from A549 and H1299 lung cancer cells. Our in vitro results showed the following: IGFBP-3 binds HN and blocks it from binding Aβ in the absence or presence of AChE; HN and AChE can simultaneously bind Aβ but not when in the presence of IGFBP-3; HN is unable to reduce the aggregation of Aβ in the presence of IGFBP-3; and HN abolishes the aggregation of Aβ induced by the addition of AChE in the absence of IGFBP-3. In the media, AChE and HN can simultaneously bind Aβ. While both AChE and HN are detected when using 6E10 Aβ antibodies, only AChE is detected when using the Aβ 17–24 antibody 4G8, the anti-oligomer A11, and the anti-amyloid fibril LOC antibodies. No signal was observed for IGFBP-3 with any of the anti-amyloid antibodies used. Exogenously added IGFBP-3 reduced the amount of HN found in a complex when using 6E10 antibodies and correlated with a concomitant increase in the amyloid oligomers. Immunodepletion of HN from the media of the A549 and H1299 cells increased the relative abundance of the oligomer vs the total amount of Aβ, the A11-positive prefibrillar oligomers, and to a lesser extent the LOC-positive fibrillar oligomers, and was also correlated with diminished cell viability and increased apoptosis
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