13 research outputs found

    Hospitalization-Associated Disability in Adults Admitted to a Safety-Net Hospital.

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    BackgroundLittle is known about hospitalization-associated disability (HAD) in older adults who receive care in safety-net hospitals.ObjectivesTo describe HAD and to examine its association with age in adults aged 55 and older hospitalized in a safety-net hospital.DesignSecondary post hoc analysis of a prospective cohort from a discharge intervention trial, the Support from Hospital to Home for Elders.SettingMedicine, cardiology, and neurology inpatient services of San Francisco General Hospital, a safety-net hospital.ParticipantsA total of 583 participants 55 and older who spoke English, Spanish, or Chinese. We determined the incidence of HAD 30 days post-hospitalization and ORs for HAD by age group.MeasurementsThe outcome measure was death or HAD at 30 days after hospital discharge. HAD is defined as a new or additional disability in one or more activities of daily living (ADL) that is present at hospital discharge compared to baseline. Participants' functional status at baseline (2 weeks prior to admission) and 30 days post-discharge was ascertained by self-report of ADL function.ResultsMany participants (75.3 %) were functionally independent at baseline. By age group, HAD occurred as follows: 27.4 % in ages 55-59, 22.2 % in ages 60-64, 17.4 % in ages 65-69, 30.3 % in ages 70-79, and 61.7 % in ages 80 or older. Compared to the youngest group, only the adjusted OR for HAD in adults over 80 was significant, at 2.45 (95 % CI 1.17, 5.15).ConclusionsIn adults at a safety-net hospital, HAD occurred in similar proportions among adults aged 55-59 and those aged 70-79, and was highest in the oldest adults, aged ≥ 80. In safety-net hospitals, interventions to reduce HAD among patients 70 years and older should consider expanding age criteria to adults as young as 55

    Mucosal immune responses to HIV-1 in elite controllers: a potential correlate of immune control

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    There exists a unique group of persons who are able to durably control HIV in the absence of therapy. The mechanisms of control in these persons remain poorly defined. In this study, we examined CD8+ T-cell responses in blood and rectal mucosa from 17 “elite controllers” (viral load < 75 copies/mL), 11 “viremic controllers” (75-2000 copies/mL), 14 noncontrollers (> 10 000 copies/mL), and 10 antiretroviral-treated persons (< 75 copies/mL). Production of interferon-γ, interleukin-2, tumor necrosis factor-α, macrophage inflammatory protein-1β, and CD107a by CD8+ T cells in response to HIV-1 Gag stimulation was measured using flow cytometry. Our hypothesis was that “polyfunctional” T cells producing multiple antiviral factors would be most abundant in mucosal tissues of HIV controllers. Mucosal CD8+ T-cell responses were significantly stronger and more complex in controllers than in antiretroviral-suppressed persons (P = .0004). The frequency of 4-function responses in rectal mucosa was higher in controllers than in noncontrollers and patients on therapy (P < .0001). Mucosal responses in controllers were frequently stronger and more complex than blood responses. These findings demonstrate that many controllers mount strong, complex HIV-specific T-cell responses in rectal mucosa. These responses may play an important role in mucosal immune surveillance, as suggested by their relative enrichment among persons who control HIV in the absence of therapy

    Correlating cellular and molecular signatures of mucosal immunity that distinguish HIV controllers from noncontrollers

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    HIV “controllers” are persons infected with human immunodeficiency virus, type I (HIV) who maintain long-term control of viremia without antiviral therapy and who usually do not develop the acquired immune deficiency syndrome (AIDS). In this study, we have correlated results from polychromatic flow cytometry and oligonucleotide expression arrays to characterize the mucosal immune responses of these subjects in relation to untreated HIV+ persons with high viral loads and progressive disease (“noncontrollers”). Paired peripheral blood and rectosigmoid biopsies were analyzed from 9 controllers and 11 noncontrollers. Several cellular immune parameters were found to be concordant between the 2 compartments. Compared with noncontrollers, the mucosal tissues of controllers had similar levels of effector T cells and fewer regulatory T cells (Tregs). Using principal component analysis to correlate immunologic parameters with gene expression profiles, transcripts were identified that accurately distinguished between controllers and noncontrollers. Direct 2-way comparison also revealed genes that are significantly different in their expression between controllers and noncontrollers, all of which had reduced expression in controllers. In addition to providing an approach that integrates flow cytometry datasets with transcriptional profiling analysis, these results underscore the importance of the sustained inflammatory response that attends progressive HIV disease
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