Integrating mental health professionals in residencies to reduce health disparities.

Health disparities in primary care remain a continual challenge for both practitioners and patients alike. Integrating mental health services into routine patient care has been one approach to address such issues, including access to care, stigma of health-care providers, and facilitating underserved patients' needs. This article addresses examples of training programs that have included mental health learners and licensed providers into family medicine residency training clinics. Descriptions of these models at two Midwestern Family Medicine residency clinics in the United States are highlighted. Examples of cross-training both medical residents and mental health students are described, detailing specific areas where this integration improves mental health and medical outcomes in patients. Challenges to effective integration are discussed, including larger system buy-in, medical providers' knowledge of mental health treatment, and the skills for clinical providers to possess in order to present mental health options to patients. Patients who traditionally experience multiple barriers to mental health treatment now have increased access to comprehensive care. As a result of more primary care clinics ascribing to an integrated care model of practice, providers may benefit from not only increased coordination of patient services but also utilizing behavioral health professionals to address health barriers in patients' lives.

Ahrd Cyp1a2(-/-) mice show increased susceptibility to PCB-induced developmental neurotoxicity.

Polychlorinated biphenyls (PCBs) are developmental neurotoxicants that produce cognitive and behavioral changes in children exposed during gestation and lactation. Coplanar PCBs bind the aryl hydrocarbon receptor (AHR) and can be sequestered in liver by cytochrome P450 1A2 (CYP1A2). The AHR is a ligand-activated transcription factor which increases expression of the CYP1 family, including CYP1A2. Our previous work examining genetic susceptibility to developmental PCB neurotoxicity showed that Ahr(b)Cyp1a2(-/-) mice with the high-affinity Ahr(b) allele and lacking CYP1A2 were most susceptible while Ahr(b)Cyp1a2(+/+) and poor-affinity Ahr(d)Cyp1a2(+/+) mice were resistant. To follow up, a fourth line of mice was generated with the Ahr(d)Cyp1a2(-/-) genotype and compared with the background strain Ahr(b)Cyp1a2(+/+). Dams received a PCB mixture or the corn oil vehicle at gestational Day 10 (GD10) and postnatal Day 5 (PND5). Offspring were tested at PND60 in open field locomotor, acoustic startle with pre-pulse inhibition (PPI), novel object recognition and Morris water maze. Locomotor activity was increased in PCB-treated Ahr(b)Cyp1a2(+/+) mice, but no differences were seen in control vs. PCB-treated Ahr(d)Cyp1a2(-/-) mice. PCB-treated Ahr(d)Cyp1a2(-/-) mice had a higher baseline startle response and significantly reduced pre-pulse inhibition at the 74dB level compared with corn oil-treated controls (P<0.05). PCB-treated Ahr(d)Cyp1a2(-/-) mice had impairments in novel objective recognition (P<0.05) and during all three hidden platform phases of Morris water maze (P<0.01). Combined with our previous findings, these results indicate Cyp1a2 genotype is more important in susceptibility to PCB-induced deficits in learning and memory, but Ahr genotype appears more important when assessing acoustic startle-PPI and locomotor activity.