Wen-Tzu Liao's research while affiliated with Chang Gung Memorial Hospital and other places

... This theory is supported by preclinical research that suggests low-intensity 10 kHz stimulation activates inhibitory interneurons in the dorsal horn without activating the dorsal column fibers that cause paresthesia [66]. High-frequency stimulation has also been observed to partially normalize spinal glutamate uptake activity, spinal glutamate levels, and miniature excitatory postsynaptic current frequency in rats with spared nerve injury-induced neuropathic pain [67]. A recent investigation of low-intensity 10 kHz SCS in diabetic rodent models demonstrated not only behavioral measures of reduced mechanical hypersensitivity (analog of clinical pain relief), but also a normalization of the receptive fields of dorsal horn neurons, thus reducing central sensitization [68]. ...

... In the von Frey test, temporal changes in PWT after SCS were repeatedly observed in several trials. It has been widely known that the duration of analgesic effect after SCS can continue for hours to days [29,30]. Similar to previous studies, the pain relief effect observed in this study was sustained for several hours. ...

... CFA and SNI models were chosen to induce inflammatory pain and neuropathic pain, respectively, in mammals in this study. CFA is a classic chronic inflammatory pain model inducer that is able to elicit mechanical allodynia and thermal hyperalgesia lasting more than 14 days (Liu et al. 2017). SNI is well established as an inducer of animal models of neuropathic pain that only minimally affects sympathetic nerves and can produce profound and reliable pain behaviors (Straube et al. 2013). ...

... Additionally, the first phase is induced by the ion channel TRPA 1, and the second phase After evaluating the effect of the CE extract through four pain tests, we confirmed that treatment with the extract, fractions, and compounds of the CE extract reduced the pain threshold, as evaluated by the von Frey filament test in STZ-induced diabetic mice. Diabetes induced by STZ causes glial activation, glutamate toxicity, and neuronal death, which could induce necrotic and apoptotic cell death (Chiu et al., 2016). STZ-induced diabetes is a commonly used experimental model of neuropathic pain (Huang et al., 2016) antinociceptive effect of ellagic acid, involving mediation by the opioidergic system and l-arginine-NO-cGMP-ATP sensitive K + channels pathway, and ellagic acid showed antinociceptive action in the acetic acid-induced mouse model of pain (Mansouri et al., 2015). ...

... Studies have established a link between F1Fo-ATPase dysfunction and the loss of dendritic spines, which have been reported in neurogenic muscle weakness, ataxia, and retinitis pigmentosa (NARP), Alzheimer's Disease (AD) and many other neurological diseases as well [51][52][53][54] . Alterations in oxidative phosphorylation mechanisms are associated with myelin and axonal degeneration [55] . ...

... Farklı bir çalışmada her ne kadar transplantasyon öncesi göğüs filmi tetkiki yapılsa da 2000cc kadar sıvının akut bir şekilde oluşup operasyon anında insidental olarak saptandığı da belirtilmiştir (15). Bu merkezin deneyiminde bu durumun saptandığı iki hastada postoperatif dönemde ek problem yaşanmamıştır. ...

... However, lesser evidence is present for the same in volatile anesthetic agents. A few studies on the subject have used end tidal Sevoflurane concentration [17] or difference in vaporizer weights [18] but neither have given accurate estimation of volatile anesthetic agent consumption. ...