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Stable precision grips using the fingertips are a cornerstone of human hand dexterity. However, our fingers become unstable sometimes and snap into a hyperextended posture. This is because multilink mechanisms like our fingers can buckle under tip forces. Suppressing this instability is crucial for hand dexterity, but how the neuromuscular system does so is unknown. Here we show that people rely on the stiffness from muscle contraction for finger stability. We measured buckling time constants of 50 ms or less during maximal force application with the index finger—quicker than feedback latencies—which suggests that muscle-induced stiffness may underlie stability. However, a biomechanical model of the finger predicts that muscle-induced stiffness cannot stabilize at maximal force unless we add springs to stiffen the joints or people reduce their force to enable cocontraction. We tested this prediction in 38 volunteers. Upon adding stiffness, maximal force increased by 34 ± 3%, and muscle electromyography readings were 21 ± 3% higher for the finger flexors (mean ± SE). Muscle recordings and mathematical modeling show that adding stiffness offloads the demand for muscle cocontraction, thus freeing up muscle capacity for fingertip force. Hence, people refrain from applying truly maximal force unless an external stabilizing stiffness allows their muscles to apply higher force without losing stability. But more stiffness is not always better. Stiff fingers would affect the ability to adapt passively to complex object geometries and precisely regulate force. Thus, our results show how hand function arises from neurally tuned muscle stiffness that balances finger stability with compliance. 

Introduction: The purpose of this study was to determine if pharmacological treatmentcould increase progenitor cell proliferation in the Sub-ventricular Zone of aged rats. Previous workhad shown that increasing progenitor cell proliferation in this region correlated well (R2=0.78; p=0.0007) with functional recovery in a damaged corpus callosum (white matter tract), suggesting thatprogenitor cell proliferation results in oligodendrocytes in this region. Methods: 10 month old male and female Sprague Dawley rats were fed the drugs for 30 days in cookiedough, then immunocytochemistry was performed on coronal brain sections, using Ki67 labeling todetermine progenitor cell proliferation. Results: Female rats showed low endogenous (control) progenitor cell proliferation, significantly differentfrom male rats (P<0.0001), at this age. Ascorbic Acid (20 mg/kg, daily for 30 days) increasedprogenitor cell proliferation overall, but maintained the innate gender difference in stem cell proliferation(P=0.001). Prozac (5 mg/kg, daily for 30 days) increased progenitor cell proliferation for femalesbut decreased stem cell proliferation for males, again showing a gender difference (P<0.0001).Simvastatin (1 mg/kg for 30 days) also increased progenitor cell proliferation in females and decreasedprogenitor cell proliferation in males, leading to a significant gender difference. Discussion: The three drug combinations (fluoxetine, simvastatin, and ascorbic acid, patent #9,254,281) led to ~ 4 fold increase in progenitor cell proliferation in females, while male progenitorcell proliferation was highest with 50 mg/kg ascorbic acid. However, the ascorbic acid increase in proliferationappears to be only on the sides of the ventricles, which is not the region that normally givesrise to oligodendrocytes. Conclusion: There are innate gender differences in progenitor cell proliferation at the Sub-VentricularZone at middle age in rats, possibly due to the loss of estrogen in females. We also see notable genderdifferences in progenitor cell proliferation in the Sub ventricular Zone in response to common drugs,such as fluoxetine, simvastatin and Vitamin C (ascorbic acid).