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Other TitlesCenter to Advance Chronic Pain Research and Chronic Pain: Quick Facts
KeywordUniversity of Maryland, Baltimore. Center to Advance Chronic Pain Research
Center to Advance Chronic Pain Research
Identifier to cite or link to this itemhttp://hdl.handle.net/10713/11191
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Timing and chronicity of child neglect and substance use in early adulthoodDubowitz, H.; Roesch, S.; Arria, A.M.; Metzger, R.; Thompson, R.; Kotch, J.B.; Lewis, T. (Elsevier, 2019)Background: Neglect is the most common form of child maltreatment with consequences that appear to be as serious as for abuse. Despite this, the problem has received less than its due attention. Objective: To examine the relationship between the timing and chronicity of neglect during childhood and substance use in early adulthood. Participants and setting: The sample consisted of a subset of 475 participants from the prospective Longitudinal Studies of Child Abuse and Neglect (LONGSCAN) consortium from five geographic areas around the U.S. Method: Neglect was assessed using abstracted information from CPS reports (birth-18) and self-reports of neglect (12-18). Participants completed a follow-up online survey (mean age of 24 years) that probed their use of substances. Results: The prevalence of substance use during the past year was comparable in this high-risk sample to the general population. Latent class analysis supported the presence of three groups related to the presence and timing of neglect: Chronic Neglect, Late Neglect and Limited Neglect. Late Neglect was the pattern most strongly linked to substance use in early adulthood. Conclusions: High-risk youth experiencing neglect beginning in mid- adolescence are especially vulnerable to later substance use. Those working with such youth and their families can play a valuable role helping ensure their basic needs are adequately met, and recognizing early signs of substance use and abuse. Copyright 2019 Elsevier Ltd
Staphylococcus aureus Biofilm-Mediated Infections: Characterization of the Host Adaptive Immune Response and Its Role in Chronic InfectionPrabhakara, Ranjani; Shirtliff, Mark (2010)Staphylococcus aureus is one of the most common etiological agents of potentially life threatening prosthetic implant infections. Although it is well established that S. aureus infections can become chronic, due to the ability of S. aureus to grow as a biofilm, little is known about adaptive immune responses to these infections in vivo. We hypothesized that S. aureus elicits pro–inflammatory Th1 and Th17 responses, associated with biofilm formation and chronic implant infection, instead of protective Th2 and Treg responses. A previously developed murine model of prosthetic implant infection was modified to produce a long term, chronic biofilm infection. This model was utilized to determine chronic infection rates, local cytokine levels, Ab function, and T–cell populations at multiple time points throughout infection in both C57BL/6 and BALB/c mice. We also assessed chronic infection levels in STAT6 KO mice (BALB/c background), BALB/c mice receiving anti–CD25 treatment, and C57BL/6 mice receiving anti–IL–6 or anti–IL–12 p40 treatment. Similar to human hosts, S. aureus implant infection was chronic and remained localized in 100% of C57BL/6 mice, and was recalcitrant to the host immune response and antimicrobial therapy. In contrast, BALB/c mice were shown to more effectively clear the infection. Based on cytokine levels, we demonstrated that C57BL/6 mice mount ineffective Th1/Th17 responses, whereas BALB/c mice mount robust Th2/Treg responses compared to C57BL/6 mice. The ability of serum from these strains to enhance in vitro opsonization did not, however, differ. In addition, STAT6 KO mice lost the ability to effectively clear an S. aureus implant infection, as did BALB/c mice receiving anti–CD25. In contrast, C57BL/6 mice treated with anti–IL–12 p40 were able to more effectively clear the infection, although this protection was not observed after anti–IL–6 treatment. Together, these results indicate that Th2 and Treg responses are mechanisms of protection against chronic S. aureus implant infection, as opposed to Th1 and Th17 responses, which may play a role in development of chronic biofilm infection. Our results further suggest that anti–IL–12 p40 treatment may be used therapeutically to prevent chronic S. aureus implant infection in patients.