Barriers and facilitators to collaborative care implementation within the New York State Collaborative Care Medicaid Program.

Background: Since 2015, the New York State Office of Mental Health has provided state primary care clinics with outreach, free training and technical assistance, and the opportunity to bill Medicaid for the Collaborative Care Model (CoCM) as part of its Collaborative Care Medicaid Program. This study aims to describe the characteristics of New York State primary care clinics at each step of CoCM implementation, and the barriers and facilitators to CoCM implementation for the New York State Collaborative Care Medicaid Program.

Methods: In this mixed-methods study, clinics were categorized into RE-AIM (Reach, Effectiveness, Adoption, Implementation, and Maintenance) steps.

Population-based implementation of behavioral health detection and treatment into primary care: early data from New York state.

Background: The Collaborative Care Model is a well-established, evidence-based approach to treating depression and other common behavioral health conditions in primary care settings. Despite a robust evidence base, real world implementation of Collaborative Care has been limited and very slow. The goal of this analysis is to better describe and understand the progression of implementation in the largest state-led Collaborative Care program in the nation-the New York State Collaborative Care Medicaid Program.

Extracellular matrix and radiation G1 cell cycle arrest in human fibroblasts.

It is thought that sublethal doses of radiation cause cells to pause in either G1 or G2 phase, but that then cells with repaired DNA damage reenter the cell cycle. However, it has been observed that gamma-irradiation causes normal human fibroblasts to arrest indefinitely in G1 phase unless the irradiated cells are subcultured. This indicates that cell adhesion plays a role in maintaining the arrest.

Cell cycle response to DNA damage differs in bronchial epithelial cells and lung fibroblasts.

Epithelial cells along the conducting airways can be more or less continuously exposed to DNA-damaging agents, which should limit their proliferation by inducing cell cycle checkpoints. Yet, paradoxically, airway epithelial cells frequently show a hyperplastic response when exposed to such agents. In this in vitro study, we assessed the hypothesis that normal human bronchial epithelial cells (BECs) are more resistant to the cell cycle-arresting effects of DNA damage than are human lung fibroblasts (HLFs), a cell type often investigated in the context of cell cycle checkpoints.

Temporal position of G1 arrest in normal human fibroblasts after exposure to gamma-rays.

G1 phase cell cycle arrest after exposure to ionizing radiation has been documented in cells with wild-type p53. The temporal location of this arrest within G1 phase, however, has not been determined. We have now used flow cytometric analysis of bromodeoxyuridine (BrdUrd)-labeled cells to obtain further information about the location of the G1 phase radiation checkpoint.