Quantitative assessment of grasping strength in platyrrhine monkeys.

Objectives: Despite the longstanding importance of grasping adaptations in theories of primate evolution, quantitative data on primate grasping strength remain rare. We present the results of two studies testing the prediction that callitrichines-given their comparative retreat from a small-branch environment and specialization for movement and foraging on tree trunks and large boughs-should be characterized by weaker grasping forces and underdeveloped digital flexor muscles relative to other platyrrhines.

Methods: First, we directly measured manual grasping strength in marmosets (Callithrix jacchus) and squirrel monkeys (Saimiri boliviensis), using a custom-constructed force transducer.

Treatment with a corticotrophin releasing factor 2 receptor agonist modulates skeletal muscle mass and force production in aged and chronically ill animals.

Background: Muscle weakness is associated with a variety of chronic disorders such as emphysema (EMP) and congestive heart failure (CHF) as well as aging. Therapies to treat muscle weakness associated with chronic disease or aging are lacking. Corticotrophin releasing factor 2 receptor (CRF2R) agonists have been shown to maintain skeletal muscle mass and force production in a variety of acute conditions that lead to skeletal muscle wasting.

Selective targeting of matrix metalloproteinase inhibition in post-infarction myocardial remodeling.

Background: A cause-effect relationship has been established between MMP activation and left ventricular (LV) remodeling following myocardial infarction. The goal of the present study was to examine a selective MMP inhibitor (sMMPi) strategy that effectively spared MMP-1, -3, and -7 with effect to regional and global left ventricular remodeling in a pig model of myocardial infarction.

Methods And Results: Pigs instrumented with coronary snares and radiopaque markers within the area at risk were randomized to myocardial infarction-only (n = 10) or sMMPi (PGE-530742, 1 mg/kg TID) begun 3 days prior to myocardial infarction.

Selective matrix metalloproteinase inhibition attenuates progression of left ventricular dysfunction and remodeling in dogs with chronic heart failure.

Matrix metalloproteinases (MMPs) contribute to the progression of left ventricular (LV) dysfunction and remodeling associated with heart failure (HF). The present study examined the long-term effects of a selective MMP inhibitor PG-530742 (PG) on the progression of LV dysfunction and remodeling in dogs with HF. Chronic HF [LV ejection fraction (LVEF), View Article and Find Full Text PDF

Inhibition of p38 reduces myocardial infarction injury in the mouse but not pig after ischemia-reperfusion.

The MAPK family member p38 is activated in the heart after ischemia-reperfusion (I/R) injury. However, the cardioprotective vs. proapoptotic effects associated with p38 activation in the heart after I/R injury remain unresolved.

Selective targeting and timing of matrix metalloproteinase inhibition in post-myocardial infarction remodeling.

Background: A cause-and-effect relationship exists between matrix metalloproteinase (MMP) induction and left ventricular (LV) remodeling after myocardial infarction (MI). Whether broad-spectrum MMP inhibition is necessary and the timing at which MMP inhibition should be instituted after MI remain unclear. This study examined the effects of MMP-1 and MMP-7-sparing inhibition (sMMPi) on regional and global LV remodeling when instituted before or after MI.