Does Maternal Buprenorphine Dose Affect Severity or Incidence of Neonatal Abstinence Syndrome?

Objectives: To measure the incidence, onset, duration, and severity of neonatal abstinence syndrome (NAS) in infants born to mothers receiving buprenorphine and to assess the association between buprenorphine dose and NAS outcomes.

Methods: We reviewed charts of all mother-infant pairs maintained on buprenorphine who delivered in our hospital from January 1, 2000 to April 1, 2016.

Results: In 89 infants, NAS incidence requiring morphine was 43.

A novel non-opioid protocol for medically supervised opioid withdrawal and transition to antagonist treatment.

Background: The clinical feasibility of a novel non-opioid and benzodiazepine-free protocol was assessed for the treatment of medically supervised opioid withdrawal and transition to subsequent relapse prevention strategies.

Methods: A retrospective chart review of DSM-IV diagnosed opioid-dependent patients admitted for inpatient medically supervised withdrawal examined 84 subjects (52 males, 32 females) treated with a 4-day protocol of scheduled tizanidine, hydroxyzine, and gabapentin. Subjects also received ancillary medications as needed, and routine counseling.

Urokinase plasminogen activator induces pro-fibrotic/m2 phenotype in murine cardiac macrophages.

Objective: Inflammation and fibrosis are intertwined in multiple disease processes. We have previously found that over-expression of urokinase plasminogen activator in macrophages induces spontaneous macrophage accumulation and fibrosis specific to the heart in mice. Understanding the relationship between inflammation and fibrosis in the heart is critical to developing therapies for diverse myocardial diseases.

Plasminogen mediates the atherogenic effects of macrophage-expressed urokinase and accelerates atherosclerosis in apoE-knockout mice.

Urokinase-type plasminogen activator (uPA) is expressed at elevated levels in atherosclerotic human arteries, primarily in macrophages. Plasminogen (Plg), the primary physiologic substrate of uPA, is present at significant levels in blood and interstitial fluid. Both uPA and Plg have activities that could affect atherosclerosis progression.

Mechanisms of cardiac fibrosis induced by urokinase plasminogen activator.

Human hearts with end-stage failure and fibrosis have macrophage accumulation and elevated plasminogen activator activity. However, the mechanisms that link macrophage accumulation and plasminogen activator activity with cardiac fibrosis are unclear. We previously reported that mice with macrophage-targeted overexpression of urokinase plasminogen activator (SR-uPA+/o mice) develop cardiac macrophage accumulation by 5 weeks of age and cardiac fibrosis by 15 weeks.