Adult day services: a potential antidote to social isolation and loneliness in marginalized older adults.

Loneliness and social isolation affect more than 1 in 4 community-dwelling older adults in the United States, who may also require long-term care support. Despite being seen as a solution to the long-term care crisis, most older adults prefer to age in place rather than using skilled nursing facilities. However, in-home care is unsustainable due to a shortage of direct care workers and may exacerbate social isolation by confining older adults to their homes.

A National Survey of Data Currently being Collected by Adult Day Service Centers Across the United States.

An understanding of adult day service centers' (ADC) impacts on clients' health and well-being has been hampered by a lack of large-scale data. Standardizing data collection is critical to strengthening ADC programs, demonstrating their effectiveness, and enabling them to leverage additional funding streams beyond Medicaid. We distributed an electronic survey on current data collection efforts to ADCs nationally to determine categories of data ADCs are collecting related to clients' health.

Identifying Research Priorities in Adult Day Centers to Support Evidence-Based Care of Vulnerable Older Adults.

Adult day centers (ADCs) are essential community resources that allow frail older adults to remain in their communities. Research demonstrates that ADC staff have the capacity to leverage their culturally and socially congruent relationships with clients and caregivers, to deliver evidence-based interventions that improve health outcomes. Yet, they remain a largely overlooked neighborhood resource for older adults with complex health care needs.

US28 is a potent activator of phospholipase C during HCMV infection of clinically relevant target cells.

Members of the cytomegalovirus family each encode two or more genes with significant homology to G-protein coupled receptors (GPCRs). In rodent models of pathogenesis, these viral encoded GPCRs play functionally significant roles, as their deletion results in crippled viruses that cannot traffic properly and/or replicate in virally important target cells. Of the four HCMV encoded GPCRs, US28 has garnered the most attention due to the fact that it exhibits both agonist-independent and agonist-dependent signaling activity and has been demonstrated to promote cellular migration and proliferation.

The carboxy-terminal tail of human cytomegalovirus (HCMV) US28 regulates both chemokine-independent and chemokine-dependent signaling in HCMV-infected cells.

The human cytomegalovirus (HCMV)-encoded G-protein-coupled receptor (GPCR) US28 is a potent activator of a number of signaling pathways in HCMV-infected cells. The intracellular carboxy-terminal domain of US28 contains residues critical for the regulation of US28 signaling in heterologous expression systems; however, the role that this domain plays during HCMV infection remains unknown. For this study, we constructed an HCMV recombinant virus encoding a carboxy-terminal domain truncation mutant of US28, FLAG-US28/1-314, to investigate the role that this domain plays in US28 signaling.

Retinoblastoma deficiency increases chemosensitivity in lung cancer.

The retinoblastoma (RB) tumor suppressor is mutated or functionally inactivated in the majority of human malignancies, and p16(INK4a)-cyclin D1-cyclin-dependent kinase 4-RB pathway aberrations are present in nearly all cases of non-small cell lung cancer (NSCLC). Here, the distinct role of RB loss in tumorigenic proliferation and sensitivity to chemotherapeutics was determined in NSCLC cells. Attenuation of RB led to a proliferative advantage in vitro and aggressive tumorigenic growth in xenograft models.

RB activity alters checkpoint response and chemosensitivity in lung cancer lines.

Background: The retinoblastoma tumor suppressor (RB) is a key regulator of cell cycle progression and is functionally inactivated in the majority of human non-small cell lung cancers (NSCLC). The specific influence of RB on therapeutic response in NSCLC remains elusive.

Materials And Methods: We investigated the consequence of reintroduction of RB on checkpoint response and chemosensitivity in NSCLC cell lines.

RB loss promotes aberrant ploidy by deregulating levels and activity of DNA replication factors.

The retinoblastoma tumor suppressor (RB) is functionally inactivated in many human cancers. Classically, RB functions to repress E2F-mediated transcription and inhibit cell cycle progression. Consequently, RB ablation leads to loss of cell cycle control and aberrant expression of E2F target genes.

Mitogenic action of the androgen receptor sensitizes prostate cancer cells to taxane-based cytotoxic insult.

Prostate cancer cells are dependent on androgen for growth and survival; as such, inhibition of androgen receptor (AR) activity is the first line of intervention for disseminated disease. Recently, specific cytotoxic agents have been shown to extend survival times in patients with advanced disease. Given the established ability of androgen to modify cell survival in prostate cancer cells, it is imperative to determine the effect of the hormonal environment on cytotoxic response.

Distinct action of the retinoblastoma pathway on the DNA replication machinery defines specific roles for cyclin-dependent kinase complexes in prereplication complex assembly and S-phase progression.

The retinoblastoma (RB) and p16ink4a tumor suppressors are believed to function in a linear pathway that is functionally inactivated in a large fraction of human cancers. Recent studies have shown that RB plays a critical role in regulating S phase as a means for suppressing aberrant proliferation and controlling genome stability. Here, we demonstrate a novel role for p16ink4a in replication control that is distinct from that of RB.

Inhibition of retinoblastoma tumor suppressor activity by RNA interference in lung cancer lines.

Background: Inactivation of retinoblastoma (RB) tumor suppressor function occurs frequently in lung cancer. Short-hairpin RNA can be constructed to target specific sequences and efficiently knock down protein expression. We developed a short-hairpin RNA approach to specifically target Rb in lung cancer cells to determine the influence of RB knockdown on proliferation.