Custodial grandparents raising grandchildren: lack of legal relationship is a barrier for services.

In the United States, the majority of custodial grandparents are raising their grandchildren without a legal relationship. The lack of a legal relationship (i.e., foster care, custody, adoption) is a barrier for obtaining services and has resulted in limited access to information and public services, inadequate financial assistance, and difficulty providing medical and educational consent. This situation arises not only as a consequence of eligibility criteria, but also because children being raised by custodial grandparents remain outside the child welfare system. Federal and state policies were not designed for this population; subsequently, the majority of grandparent caregivers remain without access to services and support. In this article, perceptions of custodial grandparents concerning family obligations and the child welfare system as a barrier to pursuing a legal relationship are reviewed. Challenges with existing financial and health services, educational needs of grandparents and providers, and suggestions for policy changes are presented.

Debunking misconceptions about weight loss surgery.

The recent and steady rise in the U.S. obesity index has resulted in a consumer-driven market for more effective treatment interventions for the morbidly obese population. Given the relatively poor outcomes associated with traditional approaches for treating obesity, such as diet programs, behavioral modification, and pharmacotherapy, weight loss surgical procedures represent a safe and effective option for those who meet selection criteria. To provide optimal treatment and consumer education, psychiatric nurses need to be well informed about the psychological and physiological aspects of these surgical procedures. This article clarifies six common misconceptions related to weight loss surgery.

Psychosocial adjustments following weight loss surgery.

Recent interest in weight loss surgery has increased dramatically, largely due to the rising prevalence of severe obesity and the use of less invasive laparoscopic surgical procedures. Physiological postoperative outcomes are easily measured and have been well documented in the literature. The impact of weight loss surgery on psychosocial, behavioral, and psychological function is less clearly understood. Few long-term studies of postoperative weight loss surgery patients in the literature measure emotional health and quality of life. This article discusses some of the psychosocial, behavioral, and psychiatric issues and challenges patients commonly encounter following weight loss surgery.

Chondrogenesis mediated by PPi depletion promotes spontaneous aortic calcification in NPP1-/- mice.

OBJECTIVE: We recently linked human arterial media calcification of infancy to heritable PC-1/nucleotide pyrophosphatase phosphodiesterase 1 (NPP1) deficiency. NPP1 hydrolyzes ATP to generate PP(i), a physicochemical inhibitor of hydroxyapatite crystal growth. But pathologic calcification in NPP1 deficiency states is tissue-restricted and in perispinal ligaments is endochondral differentiation-mediated rather than simply a dystrophic process. Because ectopic chondro-osseous differentiation promotes artery calcification in atherosclerosis and other disorders, we tested the hypothesis that NPP1 and PP(i) deficiencies regulate cell phenotype plasticity to promote artery calcification. METHODS AND RESULTS: Using cultured multipotential NPP1-/- mouse bone marrow stromal cells, we demonstrated spontaneous chondrogenesis inhibitable by treatment with exogenous PP(i). We also demonstrated cartilage-specific gene expression, upregulated alkaline phosphatase, decreased expression of the physiological calcification inhibitor osteopontin, and increased calcification in NPP1-/- aortic smooth muscle cells (SMCs). Similar changes were demonstrated in aortic SMCs from ank/ank mice, which are extracellular PP(i)-depleted because of defective ANK transmembrane PP(i) transport activity. Moreover, NPP1-/- and ank/ank mice demonstrated aortic media calcification by von Kossa staining, and intra-aortic cartilage-specific collagen gene expression was demonstrated in situ in NPP1-/- mice. CONCLUSIONS: NPP1 and PP(i) deficiencies modulate phenotype plasticity in artery SMCs and chondrogenesis in mesenchymal precursors, thereby stimulating artery calcification by modulating cell differentiation.

Psychotherapy with older adults: benefits and barriers.

Psychotherapeutic treatments are known to be effective in older adults with mental illnesses. Depression, anxiety, and complicated bereavement must be considered psychiatric illnesses, rather than normal consequences of aging. To improve the rate of psychotherapy use among older adults, stigma surrounding psychiatric treatment, as well as misconceptions that older adults are incapable of change, must be unlearned and eliminated.

A Medicare Current Beneficiary Survey-Based Investigation of Alternative Primary Care Models in Nursing Homes: Cost and Utilization Differences.

The current study used the Medicare Current Beneficiary Survey-Based (MCBS) Cost and Use files for 2006-2008 to investigate whether health care costs and service utilization of nursing home residents varied with nurse practitioner (NP) and physician assistant (PA) involvement, compared to the use of medical doctors (MDs) only. The sample included Medicare beneficiaries 65 and older residing in a nursing home for the entire study year (433 annual observations). A generalized estimating equations procedure was used to assess whether health care cost and utilization measures varied by cohort. Point estimates indicated that the annual per-person cost of non-institutional services (total medical cost less the cost of the nursing home itself) was $3,847 and $3,170 more for individuals in the MD-only and MD-dominant cohorts, respectively, compared to those in the NP/PA-dominant cohort. [Res Gerontol Nurs. 2016; 9(3):115-122.].

A Medicare current beneficiary survey-based investigation of alternative primary care models in nursing homes: functional ability and health status outcomes.

This study assessed how the health status and functioning of Medicare beneficiaries residing in nursing homes varies systematically with nurse practitioners (NPs) and physician assistants (PAs) providing primary care services. A secondary analysis was conducted using data from the 2006, 2007, and 2008 Medicare Current Beneficiary Surveys. The study sample included 433 participant-year observations within one of three cohorts: (a) medical doctor (MD)-only, those who received primary care services exclusively from a physician; (b) MD-dominant, those who received some primary care services from an NP or PA, but those visits accounted for less than one half of total primary care visits; and (c) NP/PA-dominant, those who received more than one half of their primary care visits from an NP or PA. Participants in the MD-only cohort had significantly less orientation and independence in activities of daily living compared to participants in the NP/PA-dominant cohort. Other study variables did not vary significantly by practice model. Although the study provides some evidence that NP/PA involvement is associated with improved functioning, it is premature to draw strong inferences.

Linked deficiencies in extracellular PP(i) and osteopontin mediate pathologic calcification associated with defective PC-1 and ANK expression.

Osteopontin and PP(i) both suppress hydroxyapatite deposition. Extracellular PP(i) deficiency causes spontaneous hypercalcification, yet unchallenged osteopontin knockout mice have only subtle mineralization abnormalities. We report that extracellular PP(i) deficiency promotes osteopontin deficiency and correction of osteopontin deficiency prevents hypercalcification, suggesting synergistic inhibition of hydroxyapatite deposition. Nucleotide pyrophosphatase phosphodiesterase (NPP) isozymes including PC-1 (NPP1) function partly to generate PP(i), a physiologic calcification inhibitor. PP(i) transport is modulated by the membrane channel protein ANK. Spontaneous articular cartilage calcification, increased vertebral cortical bone formation, and peripheral joint and intervertebral ossific ankylosis are associated with both PC-1 deficiency and expression of truncated ANK in ank/ank mice. To assess how PC-1, ANK, and PP(i) regulate both calcification and cell differentiation, we studied cultured PC-1 -/- and ank/ank mouse calvarial osteoblasts. PC-1 -/- osteoblasts demonstrated approximately 50% depressed NPP activity and markedly lowered extracellular PP(i) associated with hypercalcification. These abnormalities were rescued by transfection of PC-1 but not of the NPP isozyme B10/NPP3. PC-1 -/- and ank/ank cultured osteoblasts demonstrated not only comparable extracellular PP(i) depression and hypercalcification but also marked reduction in expression of osteopontin (OPN), another direct calcification inhibitor. Soluble PC-1 (which corrected extracellular PP(i) and OPN), and OPN itself (> or = 15 pg/ml), corrected hypercalcification by PC-1 -/- and ank/ank osteoblasts. Thus, linked regulatory effects on extracellular PP(i) and OPN expression mediate the ability of PC-1 and ANK to regulate calcification.

Distinct transglutaminase 2-independent and transglutaminase 2-dependent pathways mediate articular chondrocyte hypertrophy.

Altered chondrocyte differentiation, including development of chondrocyte hypertrophy, mediates osteoarthritis and pathologic articular cartilage matrix calcification. Similar changes in endochondral chondrocyte differentiation are essential for physiologic growth plate mineralization. In both articular and growth plate cartilages, chondrocyte hypertrophy is associated with up-regulated expression of certain protein-crosslinking enzymes (transglutaminases (TGs)) including the unique dual-functioning TG and GTPase TG2. Here, we tested if TG2 directly mediates the development of chondrocyte hypertrophic differentiation. To do so, we employed normal bovine chondrocytes and mouse knee chondrocytes from recently described TG2 knockout mice, which are phenotypically normal. We treated chondrocytes with the osteoarthritis mediator IL-1 beta, with the all-trans form of retinoic acid (ATRA), which promotes endochondral chondrocyte hypertrophy and pathologic calcification, and with C-type natriuretic peptide, an essential factor in endochondral development. IL-1 beta and ATRA induced TG transamidation activity and calcification in wild-type but not in TG2 (-/-) mouse knee chondrocytes. In addition, ATRA induced multiple features of hypertrophic differentiation (including type X collagen, alkaline phosphatase, and MMP-13), and these effects required TG2. Significantly, TG2 (-/-) chondrocytes lost the capacity for ATRA-induced expression of Cbfa1, a transcription factor necessary for ATRA-induced chondrocyte hypertrophy. Finally, C-type natriuretic peptide, which did not modulate TG activity, comparably promoted Cbfa1 expression and hypertrophy (without associated calcification) in TG2 (+/+) and TG2 (-/-) chondrocytes. Thus, distinct TG2-independent and TG2-dependent mechanisms promote Cbfa1 expression, articular chondrocyte hypertrophy, and calcification. TG2 is a potential site for intervention in pathologic calcification promoted by IL-1 beta and ATRA.