AdipoRon Treatment Induces a Dose-Dependent Response in Adult Hippocampal Neurogenesis.

AdipoRon, an adiponectin receptor agonist, elicits similar antidiabetic, anti-atherogenic, and anti-inflammatory effects on mouse models as adiponectin does. Since AdipoRon can cross the blood-brain barrier, its chronic effects on regulating hippocampal function are yet to be examined. This study investigated whether AdipoRon treatment promotes hippocampal neurogenesis and spatial recognition memory in a dose-dependent manner. Adolescent male C57BL/6J mice received continuous treatment of either 20 mg/kg (low dose) or 50 mg/kg (high dose) AdipoRon or vehicle intraperitoneally for 14 days, followed by the open field test to examine anxiety and locomotor activity, and the Y maze test to examine hippocampal-dependent spatial recognition memory. Immunopositive cell markers of neural progenitor cells, immature neurons, and newborn cells in the hippocampal dentate gyrus were quantified. Immunosorbent assays were used to measure the serum levels of factors that can regulate hippocampal neurogenesis, including adiponectin, brain-derived neurotrophic factor (BDNF), and corticosterone. Our results showed that 20 mg/kg AdipoRon treatment significantly promoted hippocampal cell proliferation and increased serum levels of adiponectin and BDNF, though there were no effects on spatial recognition memory and locomotor activity. On the contrary, 50 mg/kg AdipoRon treatment impaired spatial recognition memory, suppressed cell proliferation, neuronal differentiation, and cell survival associated with reduced serum levels of BDNF and adiponectin. The results suggest that a low-dose AdipoRon treatment promotes hippocampal cell proliferation, while a high-dose AdipoRon treatment is detrimental to the hippocampus function.

Evidence and Implications Behind a National Decline in Primary Care Visits.

Primary care is the foundation of the health care system and the basis for new payment and delivery reforms in the USA. Yet since 2008, primary care visit rates dropped by 6-25% across a range of populations in five sources of national survey and administrative data. We hypothesize three likely mechanisms behind the decline: decreases in patients' ability, need, or desire to seek primary care; changes in primary care practice such as greater use of teams and non-face-to-face care; and replacement of in-person primary care visits with alternatives such as specialist, retail clinic, and commercial telemedicine visits. These mechanisms require further investigation. In the meantime, the trend prompts us to optimize the primary care visit and embrace the growth of alternatives while preserving the fundamental benefits of primary care.

Online Reputation Management and Patient Satisfaction.

Online reputation management is critical in orthopaedic practice. All orthopaedic surgeons have an online reputation. Some aspects of an orthopaedic surgeon's online reputation can be controlled and other aspects of an orthopaedic surgeon's online reputation cannot be controlled. Online reputation management involves enhancing patient-surgeon communication and, ultimately, patient satisfaction. Patient-reported outcome measures are increasingly drivers of physician behavior, and potential untoward consequences must be monitored. In the future, patient-experience data are very likely to be among the most prominent forms of quality data on the Internet.

Cutting edge: RIPK1 Kinase inactive mice are viable and protected from TNF-induced necroptosis in vivo.

The serine/threonine kinase RIPK1 is recruited to TNFR1 to mediate proinflammatory signaling and to regulate TNF-induced cell death. A RIPK1 deficiency results in perinatal lethality, impaired NFκB and MAPK signaling, and sensitivity to TNF-induced apoptosis. Chemical inhibitor and in vitro-reconstitution studies suggested that RIPK1 displays distinct kinase activity-dependent and -independent functions. To determine the contribution of RIPK1 kinase to inflammation in vivo, we generated knock-in mice endogenously expressing catalytically inactive RIPK1 D138N. Unlike Ripk1(-/-) mice, which die shortly after birth, Ripk1(D138N/D138N) mice are viable. Cells expressing RIPK1 D138N are resistant to TNF- and polyinosinic-polycytidylic acid-induced necroptosis in vitro, and Ripk1(D138N/D138N) mice are protected from TNF-induced shock in vivo. Moreover, Ripk1(D138N/D138N) mice fail to control vaccinia virus replication in vivo. This study provides genetic evidence that the kinase activity of RIPK1 is not required for survival but is essential for TNF-, TRIF-, and viral-initiated necroptosis.

DISCOVERING STRATEGY: A KEY CHALLENGE FOR ACADEMIC HEALTH CENTERS.

The health care marketplace is increasingly being driven by competition on value for patients - that is, meeting their needs as efficiently as possible. Academic medical centers must adapt to this shift through the development of true strategies aimed at creating value, as opposed to trying to deflect the pressures of competition through tactics such as merging with competitors. True strategies require clarity on what the organization is trying to do for whom, and how the organization is going to be different from its competitors. Six key questions are described and discussed: 1) What is our goal? 2) What businesses are we in? 3) What set of conditions shall we compete in? 4) How will we be different? 5) What synergies can be created across our sites? and 6) What is our appropriate density and scope? Academic medical centers have been the crown jewel of health care for the United States and, indeed, the rest of the world. Their research, teaching, and patient care missions all command respect, and their halls are filled with representatives of industry interested in scientific advances; trainees seeking expertise; and patients hoping for relief of their suffering - or at least peace of mind that all opportunities for improvement of health have been exhausted.

Teamwork: The competitive differentiator for the new marketplace.

Teamwork can help healthcare organizations compete more effectively in today's marketplace.