In an attempt to fully delineate and quantify, these gait alterations, we analyzed joint kinematics, torques (rotational forces), and powers (rotational forces times angular velocity) in patients with PAD with unilateral claudication for both the affected and nonaffected legs.

Methods: Twelve patients with unilateral PAD (age, 61.69 +/- 10.53 years, ankle-brachial index [ABI]: affected limb 0.59 +/- 0.25; nonaffected limb 0.93 +/- 0.12) mid 10 healthy controls (age, 67.23 +/- 12.67 years, ABI >1.0 all subjects) walked over a force platform to acquire gait kinetics, while joint kinematics were recorded simultaneously.

Data were collected for the affected and nonaffected limbs during pain free (PAD-PF) and pain induced (PAD-P) trials. Kinetics and kinematics were combined to quantify torque and powers during the stance period from the hip, knee, and ankle joints.

Results:

The affected limb demonstrated significantly (P < .05) Selleck Dinaciclib reduced ankle plantar flexion torque compared to controls during late stance in both PAD-PF and PAD-P trials. There were significant reductions in ankle plantar flexion power generation during late stance for both the affected (P < .05) and nonaffected limbs (P < .05) compared to control during PAD-PF and PAD-P trials. No significant differences were noted in torque comparing the nonaffected limbs in PAD-PF and PAD-P conditions to control for knee and hip joints throughout selleck products the stance phase. Significant reductions were found in knee power absorption in early stance and knee power generation during mid stance for both limbs of the old patients with PAD as compared to control (P < .05).

Conclusion: Patients with PAD with unilateral claudication demonstrate significant gait impairments in both limbs that are present even before they experience any claudication symptoms. Overall, our data demonstrate significantly reduced ankle plantar flexion torque and power during late stance with reduced knee power during early and mid stance for the affected limb. Further studies are needed to determine if these findings are

dependent on the location and the severity of lower extremity ischemia and whether the changes in the nonaffected limb are the result of underlying PAD or compensatory changes from the affected limb dysfunction. (J Vase Surg 2010;51:80-8.)”
“Cerebral hypoxia is one of the main causes of cerebral injury. This study was conducted to investigate the potential protective effect of H(2)S in in vitro hypoxic models by subjecting SH-SY5Y cells to either oxygen glucose deprivation or Na(2)S(2)O(4) (an oxygen scavenger) treatment. We found that treatment with NaHS (an H(2)S donor, 10-100 mu M) 15 min prior to hypoxia increased cell viability in a concentration-dependent manner. Time-course study showed that NaHS was able to exert its protective effect even when added 8 h before or less than 4 h after hypoxia induction.