Tuberculosis contact-tracing among Syrian refugee populations: lessons from Jordan.

In response to the influx of displaced Syrians since 2011, the Jordanian National Tuberculosis Program (NTP) implemented a specific Tuberculosis (TB) reduction strategy, including contact-tracing (CT). Contacts of all refugees diagnosed with pulmonary TB (PTB) were registered by the International Organization for Migration and screened for active & latent TB infection (LTBI) in 6 NTP centres.The objectives of this study were to assess prevalence of active TB and LTBI, risk factors for LTBI as well as program performance. We performed a retrospective study among contacts ( = 481) of all PTB cases diagnosed between March 2011 and May 2014 ( = 76). CT was performed using verbal screening of TB-related symptoms, tuberculin skin test (TST) and chest X-ray. LTBI was diagnosed in 24.1% of contacts tested with TST while active TB was diagnosed in 2.1% of contacts. Main risk factors for positive TST included smear-positive index case (IC) (OR: 6.33) and previous TB infection in the family (OR: 4.94). Among children, the risk of LTBI was higher when their IC was a care-giving female (OR: 2.83). Prevalence of active TB was two times higher in children under five (U5 s) (5.3%) compared to adults (2.5%). We found a high prevalence of active TB and LTBI among contacts of PTB cases in the Syrian refugee population, emphasizing the urgent need for host countries to implement CT strategies for refugees. Our results underscore the vulnerability of U5s and contacts of smear-positive IC highlighting the need for specific actions focusing on those groups

Hypoxic Stress Decreases c-Myc Protein Stability in Cardiac Progenitor Cells Inducing Quiescence and Compromising Their Proliferative and Vasculogenic Potential

Abstract Cardiac progenitor cells (CPCs) have been shown to promote cardiac regeneration and improve heart function. However, evidence suggests that their regenerative capacity may be limited in conditions of severe hypoxia. Elucidating the mechanisms involved in CPC protection against hypoxic stress is essential to maximize their cardioprotective and therapeutic potential. We investigated the effects of hypoxic stress on CPCs and found significant reduction in proliferation and impairment of vasculogenesis, which were associated with induction of quiescence, as indicated by accumulation of cells in the G0-phase of the cell cycle and growth recovery when cells were returned to normoxia. Induction of quiescence was associated with a decrease in the expression of c-Myc through mechanisms involving protein degradation and upregulation of p21. Inhibition of c-Myc mimicked the effects of severe hypoxia on CPC proliferation, also triggering quiescence. Surprisingly, these effects did not involve changes in p21 expression, indicating that other hypoxia-activated factors may induce p21 in CPCs. Our results suggest that hypoxic stress compromises CPC function by inducing quiescence in part through downregulation of c-Myc. In addition, we found that c-Myc is required to preserve CPC growth, suggesting that modulation of pathways downstream of it may re-activate CPC regenerative potential under ischemic conditions