Collaborative Pharmacy Practice: An Update

Collaborative practice among health professionals is slowly coming of age, given the global focus on efficiency and effectiveness of care to achieve positive patient outcomes and to reduce the economic burden of fragmented care. Collaborative pharmacy practice (CPP) is accordingly evolving within different models including: disease management, medication therapy management, patient centered medical home, and accountable care organizations. Pharmacist roles in these models relate to drug therapy management and include therapy introduction, adjustment, or discontinuation, patient counseling and education, and identification, resolution, and prevention of problems leading to drug interactions and adverse reactions. Most forms of CPP occur with physicians in various settings. Collaborative practice agreements exist in many states in the US and are mentioned in the International Pharmaceutical Federation policy statement. Impetus for CPP comes from health system and economic concerns, as well as from a regulatory push. There are positive examples in community, ambulatory care, and inpatient settings that have well documented protocols, indicators of care, and measurement and reporting of clinical, economic, and patient reported outcomes; however, implementation of the practice is still not widespread. Conceptual and implementation challenges include health professional training, attitudes, confidence and comfort levels, power and communication issues, logistic barriers of time, workload, proximity, resistance to establish and adopt regulations, and importantly, payment models. Some of the attitudinal and perceptual challenges can be mitigated by incorporation of interprofessional concepts and practice in health profession education. Other challenges need to be addressed across health systems, given the inefficiencies and problems that arise from lack of communication and coordination of patient care including medication nonadherence, errors and patient safety, complexity of compounded health problems, and potential liability. The existing evidence needs to be examined to address some challenges and improve infrastructure for CPP

Do Binucleate Cardiomyocytes Have A Role in Myocardial Repair? Insights Using Isolated Rodent Myocytes and Cell Culture

Neonatal and adult cardiomyocytes were isolated from rat hearts. Some of the adult myocytes were cultured to allow for cell dedifferentiation, a phenomenon thought to mimic cell changes that occur in stressed myocardium, with myocytes regressing to a fetal pattern of metabolism and stellate neonatal shape

Persistent cAMP-Signals Triggered by Internalized G-Protein–Coupled Receptors

Real-time monitoring of G-protein-coupled receptor (GPCR) signaling in native cells suggests that the receptor for thyroid stimulating hormone remains active after internalization, challenging the current model for GPCR signaling

The Effect of Relaxin on Cell Proliferation in Mouse Cervix Requires Estrogen Receptor α Binding to Estrogen Response Elements in Stromal Cells

The study objective was to determine whether stromal and/or epithelial estrogen receptor-α (ERα) is required for relaxin to promote proliferation of stromal and epithelial cells in the mouse cervix. Four types of tissue recombinants were prepared with cervical stroma (St) and epithelium (Ep) from wild-type (wt) and ERα knockout (ko) mice: wt-St+wt-Ep, wt-St+ko-Ep, ko-St+wt-Ep and ko-St+ko-Ep. Tissue recombinants were grafted under the renal capsule of syngeneic female mice. After 3 wk of transplant growth, hosts were ovariectomized and fitted with silicon implants containing 17β-estradiol (treatment d 1). Animals were injected sc with relaxin or vehicle PBS at 6-h intervals from 0600 h on d 8 through 0600 h on d 10. To evaluate cell proliferation, 5-bromo-2′-deoxyuridine was injected sc 10 h before tissue recombinants were collected at 1000 h on d 10. Relaxin promoted marked proliferation of both epithelial and stromal cells in tissue recombinants containing wt St (P < 0.001) but far lower proliferation in recombinants prepared with ko St, regardless of whether Ep was derived from wt or ko mice. An additional experiment using mice expressing wt ERα, a mutant of ERα that selectively lacks classical signaling through estrogen response element binding, or no ERα demonstrated that ERα must bind to an estrogen response element to enable relaxin's proliferative effects. In conclusion, this study shows that ERα-expressing cells in St, using a classical signaling pathway, are necessary for relaxin to promote marked proliferation in both stromal and epithelial cells of the mouse cervix