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Biomedical subjects

Peter Yoo

Publications and source records attributed to Peter Yoo.

2 recordsLinked to original sources

Increase in scrotal temperature in laptop computer users.

BACKGROUND: Scrotal hyperthermia has been identified as a risk factor for male infertility. Laptop computers (LC) have become part of a contemporary lifestyle and have gained popularity among the younger population of reproductive age. LC are known to reach high internal operating temperatures. We evaluated the thermal effect of LC on the scrotum. METHODS: Right and left scrotal temperature (ScT) was measured in 29 healthy volunteers in two separate 60 min sessions. ScT was recorded from thermocouples on a digital datalogger every 3 min with the working LC in a laptop position and in the same sitting position with approximated thighs without LC. RESULTS: ScT increased significantly on the right and left side in the group with working LC (2.8 degrees C and 2.6 degrees C, respectively; P<0001) and without LC (2.1 degrees C, P<0.0001). However, ScT elevation with working LC was significantly higher (P<0.0001). CONCLUSIONS: Working LC in a laptop position causes significant ScT elevation as a result of heat exposure and posture-related effects. Long-term exposure to LC-related repetitive transient scrotal hyperthermia is a modern lifestyle feature that may have a negative impact upon spermatogenesis, specifically in teenage boys and young men. Further studies of such thermal effects on male reproductive health are warranted.

Adult↗

Neuropeptide Y induces ischemic angiogenesis and restores function of ischemic skeletal muscles.

Previously we showed that neuropeptide Y (NPY), a sympathetic vasoconstrictor neurotransmitter, stimulates endothelial cell migration, proliferation, and differentiation in vitro. Here, we report on NPY's actions, receptors, and mediators in ischemic angiogenesis. In rats, hindlimb ischemia stimulates sympathetic NPY release (attenuated by lumbar sympathectomy) and upregulates NPY-Y2 (Y2) receptor and a peptidase forming Y2/Y5-selective agonist. Exogenous NPY at physiological concentrations also induces Y5 receptor, stimulates neovascularization, and restores ischemic muscle blood flow and performance. NPY-mediated ischemic angiogenesis is not prevented by a selective Y1 receptor antagonist but is reduced in Y2(-/-) mice. Nonischemic muscle vascularity is also lower in Y2(-/-) mice, whereas it is increased in NPY-overexpressing rats compared with their WT controls. Ex vivo, NPY-induced aortic sprouting is markedly reduced in Y2(-/-) aortas and spontaneous sprouting is severely impaired in NPY(-/-) mice. NPY-mediated aortic sprouting, but not cell migration/proliferation, is blocked by an antifetal liver kinase 1 antibody and abolished in mice null for eNOS. Thus, NPY mediates neurogenic ischemic angiogenesis at physiological concentrations by activating Y2/Y5 receptors and eNOS, in part due to release of VEGF. NPY's effectiveness in revascularization and restoring function of ischemic tissue suggests its therapeutic potential in ischemic conditions.

Animals↗