Minority Older Adults' Access to and Use of Programs of All-Inclusive Care for the Elderly.

Programs of All-Inclusive Care for the Elderly (PACE) are an effective approach to improve care quality and delay institutional admissions especially for Black and Hispanic older adults who have seen a disproportionate rise in nursing home use. Guided by Andersen's Behavioral Model of Health Services Use and employing focus groups and one-on-one interviews, we qualitatively examined factors influencing access to and use of PACE by Black and Hispanic older adults. The study sample consisted of thirty-two PACE enrollees, six marketing-team members, and four family-caregivers from three PACE sites in a northeast urban city. Informed knowledge, cultural beliefs, and attitudes toward PACE were found to affect access. Community resources, available services, and care quality facilitated enrollment/participation. Barriers identified included poor dissemination of information and inadequate emphasis on staff's sensitivity to enrollees' cultural and disability differences. Findings will help healthcare leaders capitalize on facilitators and address barriers to enhance access and use of PACE by racial and ethnic minority older adults.

Structure of a Ty1 restriction factor reveals the molecular basis of transposition copy number control.

Excessive replication of Saccharomyces cerevisiae Ty1 retrotransposons is regulated by Copy Number Control, a process requiring the p22/p18 protein produced from a sub-genomic transcript initiated within Ty1 GAG. In retrotransposition, Gag performs the capsid functions required for replication and re-integration. To minimize genomic damage, p22/p18 interrupts virus-like particle function by interaction with Gag. Here, we present structural, biophysical and genetic analyses of p18m, a minimal fragment of Gag that restricts transposition. The 2.8 Å crystal structure of p18m reveals an all α-helical protein related to mammalian and insect ARC proteins. p18m retains the capacity to dimerise in solution and the crystal structures reveal two exclusive dimer interfaces. We probe our findings through biophysical analysis of interface mutants as well as Ty1 transposition and p18m restriction in vivo. Our data provide insight into Ty1 Gag structure and suggest how p22/p18 might function in restriction through a blocking-of-assembly mechanism.

Clinical and serological features of systemic sclerosis in a Chinese cohort.

Our goal was to study the prevalence of systemic sclerosis (SSc) subtypes, autoantibody profile, and pulmonary fibrosis in a large group of Han Chinese. Chinese SSc patients (n = 419) were recruited from a multicenter study including hospitals and outpatient clinics in China. All patients met the American College of Rheumatology classification criteria for SSc. Anti-topoisomerase (ATA), anti-centromere (ACA), anti-RNA polymerase III (anti-RNAP3), and anti-U1-ribonucleoprotein (anti-U1RNP) were detected utilizing commercially available kits. The clinical and autoantibody information in Chinese patients was compared to that in the US Caucasian patients (n = 834), recruited from the Genetics versus Environment in Scleroderma Outcome Study and Scleroderma Family Registry. Chi-square test was utilized for the abovementioned comparisons. Chinese patients showed 40.3 % limited (lcSSc) and 59.7 % diffuse (dcSSc) forms of SSc. ATA was found in 59.9 %, ACA in 13.4 %, anti-RNAP3 in 1.3 %, and anti-U1RNP in 18 % of Chinese SSc patients. Compared to US patients (65.1 % lcSSc, 34.9 % dcSSc, ATA in 18.7 %, ACA in 32.4 %, anti-RNAP3 in 17.4 %, and anti-U1RNP in 2.8 %), Chinese SSc patients are significantly higher in dcSSc and the frequencies of ATA and anti-U1RNP, but lower in ACA and anti-RNAP3. In addition, pulmonary fibrosis was observed in 78 % Chinese SSc patients and was strongly associated with the presence of ATA. The present study represents the first report of SSc features in a large group of Chinese patients. Clinical subtypes and the frequencies of SSc-related autoantibodies in Chinese SSc patients are significantly different from those in SSc patients of the US Caucasian descent.

Expanding the role of the dynein regulatory complex to non-axonemal functions: association of GAS11 with the Golgi apparatus.

The mammalian GAS11 gene is a candidate tumor suppressor of unknown function that was previously identified as one of several genes upregulated upon growth arrest. Interestingly, although GAS11 homologs in Trypanosoma brucei (trypanin) and Chlamydomonas reinhardtii (PF2) are integral components of the flagellar axoneme and are necessary for regulating flagellar beat, the GAS11 gene was discovered based on its expression in cells that do not assemble a motile cilium. This suggests that GAS11 function might not be restricted to the cilium. To investigate this possibility, we generated GAS11-specific antibodies and demonstrate here that GAS11 is expressed in a variety of mammalian cells that lack a motile cilium. In COS7 cells, GAS11 is associated with the detergent-insoluble cytoskeleton and exhibits a juxtanuclear localization that overlaps with the pericentrosomal Golgi apparatus. This localization is dependent upon intact microtubules and is cell-cycle regulated, such that GAS11 is dispersed throughout the cytoplasm as cells progress through mitosis. GAS11 remains associated with Golgi fragments following depolymerization of cytoplasmic microtubules but is dispersed upon disruption of the Golgi with brefeldin A. These data suggest that GAS11 is associated with the Golgi apparatus. In support of this, recombinant GAS11 binds Golgi membranes in vitro. In growth-arrested mIMCD3 cells, GAS11 co-localizes with gamma-tubulin at the base of the primary cilium. The pericentrosomal Golgi apparatus and base of the cilium both represent convergence points for microtubule minus ends and correspond to sites where dynein regulation is required. The algal GAS11 homolog functions as part of a dynein regulatory complex (DRC) in the axoneme (Rupp and Porter. J Cell Biol 2003;162:47-57) and our findings suggest that components of this axonemal dynein regulatory system have been adapted in mammalian cells to participate in non-axonemal functions.