The Affordable Care Act expands health insurance coverage to millions of Americans, but the availability of health care services for the newly insured population remains uncertain. We conducted a simulated patient (or "secret shopper") study to assess primary care appointment availability and wait times for new patients with Medicaid or private insurance before and after implementation of Michigan's Medicaid expansion in 2014. The expansion, which was made possible through a section 1115 waiver, has a unique requirement that new beneficiaries must be seen by a primary care provider within 60-90 days of enrollment. During a period of rapid coverage expansion in Michigan, we found that appointment availability increased 6 percentage points for new Medicaid patients and decreased 2 percentage points for new privately insured patients, compared to availability before the expansion. Wait times remained stable, at 1-2 weeks for both groups. Further research is needed to determine whether access to primary care for newly insured patients will endure over time.

Emphasizing the low risk of a man's LPC and enhancing physician trust may increase acceptability of AS. Standardizing terminology and presenting AS as a reasonable and recognized management option may also help increase its adoption.

Background Heterozygous mutations in the chromatin remodeling gene CHD7 cause CHARGE syndrome, a developmental disorder with variable craniofacial dysmorphisms and respiratory difficulties. The molecular etiologies of these malformations are not well understood. Homozygous Chd7 null mice die by E11, whereas Chd7Gt/+ heterozygous null mice are a viable and excellent model of CHARGE. We explored skeletal phenotypes in Chd7Gt/+ and Chd7 conditional knockout mice, using Foxg1-Cre to delete Chd7 (Foxg1-CKO) in the developing eye, ear, nose, pharyngeal pouch, forebrain, and gut and Wnt1-Cre (Wnt1-CKO) to delete Chd7 in migrating neural crest cells. Results Foxg1-CKO mice exhibited postnatal respiratory distress and death, dysplasia of the eye, concha, and frontal bone, hypoplastic maxillary shelves and nasal epithelia, and reduced tracheal rings. Wnt1-CKO mice exhibited frontal and occipital bone dysplasia, hypoplasia of the maxillary shelves and mandible, and cleft palate. In contrast, heterozygous Chd7Gt/+ mice had apparently normal skeletal development. Conclusions Conditional deletion of Chd7 in ectodermal and endodermal derivatives (Foxg1-Cre) or migrating neural crest cells (Wnt1-Cre) results in varied and more severe craniofacial defects than in Chd7Gt/+ mice. These studies indicate that CHD7 has an important, dosage-dependent role in development of several different craniofacial tissues.

Sixty-nine percent of cancer prevention and screening recommendation statements either did not quantify benefits and harms or presented them in an asymmetric manner. Improved presentation of benefits and harms in guidelines would better ensure that clinicians and patients have access to the information required for making informed decisions.

Targeting IL-18 or its signalling intermediates may prove to be a potentially novel therapeutic strategy for angiogenesis-dependent diseases, such as RA.