Recidivism: Putting a Stop to the Revolving Door

Recidivism is a powerfully adverse factor in the lives of individuals who seek to reintegrate into society and the community at large. In this qualitative research, former inmates who were successfully released and had never been convicted within one year of their release were interviewed to discover the rationale. The research focused on understanding the skills and traits obtained through the Alternative Custody Program that can effectively reduce recidivism. Utilizing a phenomenological design, the purpose of this study was to understand the effects of program participation on the lives of former inmates concerning recidivism. Interviews lasting approximately an hour were subsequently transcribed by automated transcription software after they had been carefully proofread at the outset. The analysis revealed several key themes: inmates affirmed that reentry programs enhanced their mental health, and they found different forms of support helpful, such as therapy, counseling, and support groups, contributed a lot in dealing with the challenges of reintegration. They underscored the learning acquired from the schemes, such as effective communication skills, time management, and hands-on vocational training. These findings emphasize that community and support are of vital importance in successful reentry programs, creating feelings of attachment and doing the same thing. They also suggest that better outcomes arise through the betterment of reentry programs and social support establishment for released offenders. As such, the findings enrich the body of knowledge about effective reentry programs and help open the door for future studies that explore the fundamental components that can make a drastic difference in absolute reductions in recidivism

Myeloid-Derived Suppressor Cells in Murine Retrovirus-Induced AIDS Inhibit T- and B-Cell Responses In Vitro That Are Used To Define the Immunodeficiency

Myeloid-derived suppressor cells (MDSCs) have been characterized in several disease settings, especially in many tumor systems. Compared to their involvement in tumor microenvironments, however, MDSCs have been less well studied in their responses to infectious disease processes, in particular to retroviruses that induce immunodeficiency. Here, we demonstrate for the first time the development of a highly immunosuppressive MDSC population that is dependent on infection by the LP-BM5 retrovirus, which causes murine acquired immunodeficiency. These MDSCs express a cell surface marker signature (CD11b Gr-1 Ly6C ) characteristic of monocyte-type MDSCs. Such MDSCs profoundly inhibit immune responsiveness by a cell dose- and substan- tially inducible nitric oxide synthase (iNOS)-dependent mechanism that is independent of arginase activity, PD-1–PD-L1 ex- pression, and interleukin 10 (IL-10) production. These MDSCs display levels of immunosuppressive function in parallel with the extent of disease in LP-BM5-infected wild-type (w.t.) versus knockout mouse strains that are differentially susceptible to patho- genesis. These MDSCs suppressed not only T-cell but also B-cell responses, which are an understudied target for MDSC inhibi- tion. The MDSC immunosuppression of B-cell responses was confirmed by the use of purified B responder cells, multiple B-cell stimuli, and independent assays measuring B-cell expansion. Retroviral load measurements indicated that the suppressive Ly6Glow/ Ly6C CD11b -enriched MDSC subset was positive for LP-BM5, albeit at a significantly lower level than that of non- fractionated splenocytes from LP-BM5-infected mice. These results, including the strong direct MDSC inhibition of B-cell re- sponsiveness, are novel for murine retrovirus-induced immunosuppression and, as this broadly suppressive function mirrors that of the LP-BM5-induced disease syndrome, support a possible pathogenic effector role for these retrovirus-induced MDSCs

Adoptive Transfer of Polyclonal and Cloned Cytolytic T Lymphocytes (CTL) Specific for Mouse AIDS-associated Tumors is Effective in Preserving CTL Responses: A Measure of Protection Against LP-BM5 Retrovirus-induced Immunodeficiency.

Cytolytic T lymphocytes (CTL) can be raised against C57BL/6 B-cell lymphomas from mice with LP-BM5 murine leukemia virus-induced AIDS (MAIDS). Adoptive transfer of polyclonal anti-MAIDS tumor CTL or two CTL clones specific for the B6-1710 MAIDS lymphoma caused preservation of major histocompatibility complex-restricted and allogeneic CTL responses, which may be interpreted as indices of protection from LP-BM5 murine leukemia virus-induced immunodeficiency

Reviews

Teaching and Learning Materials and the Internet by Ian Forsyth, London: Kogan Page, 1996. ISBN: 0–7494‐ 20596. 181 pages, paperback. £18.99

Selective Involvement of the Checkpoint Regulator VISTA in Suppression of B-Cell, but Not T-Cell, Responsiveness by Monocytic Myeloid-Derived Suppressor Cells from Mice Infected with an Immunodeficiency-Causing Retrovirus

Inhibition of T-cell responses in tumor microenvironments by myeloid-derived suppressor cells (MDSCs) is widely accepted. We demonstrated augmentation of monocytic MDSCs whose suppression of not only T-cell, but also B-cell, responsiveness paralleled the immunodeficiency during LP-BM5 retrovirus infection. MDSCs inhibited T cells by inducible nitric oxide synthase (iNOS)/nitric oxide (NO), but uniquely, inhibition of B cells was ~50% dependent each on iNOS/NO and the MDSC-expressed negative-checkpoint regulator VISTA. Blockade with a combination of iNOS/NO and VISTA caused additive or synergistic abrogation of MDSC-mediated suppression of B-cell responsiveness

The CD154/CD40 Interaction Required for Retrovirus-Induced Murine Immunodeficiency Syndrome Is Not Mediated by Upregulation of the CD80/CD86 Costimulatory Molecules

C57BL/6 (B6) mice infected with LP-BM5 retroviruses develop disease, including an immunodeficiency similar to AIDS. This disease, murine AIDS (MAIDS), is inhibited by in vivo anti-CD154 monoclonal antibody treatment. The similar levels of insusceptibility of CD40−/− and CD154−/− B6 mice indicate that CD154/CD40 molecular interactions are required for MAIDS. CD4+ T and B cells, respectively, provide the CD154 and CD40 expression needed for MAIDS induction. Here, the required CD154/CD40 interaction is shown to be independent of CD80 and CD86 expression: CD80/CD86−/− B6 mice develop MAIDS after LP-BM5 infection

SOCIAL SERVICES IN CAPE TOWN: AN ANALYSIS USING THE POLITICAL ETHICS OF CARE

At the time of South Africa’s transition to a constitutional democracy in 1994 the African National Congress (ANC) government inherited a deeply divided racially-based social welfare service system. Accordingly, the first priority of the newly elected government was to develop social policies to address the inequalities resulting from the apartheid period and to redirect resources to previously disadvantaged groups, especially black South Africans, since the white community had been the main beneficiaries of specialised professional services and institutional care (Bozalek, 1999; Follentine, 2004; Orner, 2003; Sevenhuijsen, Bozalek, Gouws & Minnaar-McDonald, 2003a; Republic of South Africa, 1997). The ANC’s election manifesto, its Reconstruction and Development (RDP) policy, had committed the government to a number of strategies to meet people’s basic needs and to alleviate poverty and inequality, among them were employment creation; a living wage for all citizens; the democratisation of state structures; housing provision; and land redistribution (Republic of South Africa, 1994). The Constitution reinforced these commitments in its recognition of socio-economic rights, including the rights to adequate housing, health care, food, water, education and social security. The Human Rights Commission and other independent bodies, such as the Gender Commission, were set up by the Constitution to monitor human rights violations. There were expectations that social services would deliver on the social and economic rights outlined in the South African Constitution (1996) within the available resource constraints (Republic of South Africa, 2006)

Voicing the Victims of Narcissistic Partners: A Qualitative Analysis of Responses to Narcissistic Injury and Self-esteem Regulation

Addressing an under-researched aspect of narcissism, this study investigated subclinical ‘grandiose’ and ‘vulnerable’ narcissism within the context of domestic violence. Common triggers evoking narcissistic rage, and differences in narcissistic injury response were explored. Qualitative semi-structured interviews with seven participants who reported being in a relationship with a narcissistic partner were thematically analysed. Three overarching themes emerged: (1) Overt and covert expressions of abuse, (2) Challenge to self-perceived authority, and (3) Fear of abandonment. Findings suggest both grandiose and vulnerable narcissists’ reactions to narcissistic injury are most likely covertly and overtly aggressive and violent; however, the underlying motives for the behaviour differed. For grandiose narcissists, violence was commonly triggered by threats to self-esteem, whereas vulnerable narcissists commonly experienced significant injury and rage from fear of abandonment. It is argued that attempts to regulate and restore self-esteem for the two subtypes of narcissistic presentation will differ, thus providing further support for theoretical distinctions between grandiose and vulnerable narcissists in intimate relationships. It is concluded that popular images of the narcissist are overly simplistic as the personality trait is more complex than the grandiose type typically presented. This study contributes new understanding to the nature of narcissism in domestic violence. Limitations and suggestions for future research are discussed

Cytolytic T Lymphocytes Specific for Tumors and Infected Cells from Mice with a Retrovirus-induced Immunodeficiency Syndrome.

LP-BM5 retrovirus complex-infected C57BL/6 mice develop immunodeficiency, somewhat analogous to AIDS, termed murine AIDS (MAIDS). After secondary stimulation with syngeneic B-cell lymphomas from LP-BM5-infected mice, C57BL/6 mice produced vigorous CD8+ cytotoxic T lymphocytes specific for MAIDS-associated tumors. An anti-LP-BM5 specificity was suggested because spleen and lymph node cells from LP-BM5-infected mice served as target cells in competition assays, and cells from LP-BM5, but not ecotropic, virus-infected mice functioned as secondary in vitro stimulators to generate cytotoxic T lymphocytes to MAIDS tumors