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Finally, we obtained a quantitative measure of tissue parasite burden to confirm if the observed benefits of PARP1 depletion are delivered through its effects on parasite persistence. Myocardial level of Tc18SrDNA were similarly increased in chagasic WT, PARP1+/-, and PARP1-/- mice (Fig 7I). Together, the results presented in Fig 6 and Fig 7 suggest that changes in the LV walls’ thickness (and thereby contractile capacity) contributed to compromised systolic and diastolic performance of the heart in chagasic WT mice. The benefits of PARP1 depletion in preserving LV hemodynamics and myocardial performance were delivered via control of collagenosis and stiffness of IVS and LVPW in the myocardium of chagasic mice.

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