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( Oday Al-dadah ),( Georgina Hawes ),( Philip J. Chapman-sheath ),( John William Tice ),( David S. Barrett ) 대한슬관절학회 2020 대한슬관절학회지 Vol.32 No.-
Purpose: Combined medial tibiofemoral and symptomatic patellofemoral osteoarthritis is not amenable to unicompartmental knee replacement (UKR). Total knee replacement (TKR) is an invasive option in younger adults with high functional demands. The aim of this study was to compare the clinical outcome of patients who have undergone UKR, bicompartmental knee replacement (BKR) and TKR up to 2 years post-operatively. Materials and methods: This prospective study comprised 133 subjects including 30 patients in the medial UKR group, 53 patients in the BKR group (combined medial UKR with patellofemoral joint replacement) and 50 patients in the TKR group. All subjects were evaluated using the Oxford Knee Score (OKS) and the Western Ontario and MacMaster Universities Osteoarthritis Index (WOMAC). Patients in each group were assessed using both scoring systems pre-operatively and 6 months, 1 year and 2 years post-operatively. Results: Significant improvement of OKS was found at 6 months compared to baseline for UKR (22.7 to 38.1, p = 0.046), BKR (22.6 to 36.8, p < 0.001) and TKR (16.6 to 34.5, p < 0.001). Significant improvement was also found for the WOMAC sub-scores for all three groups during this time period. After 6 months, there was no further statistically significant improvement in either outcome score in any of the groups up to the 2-year follow-up results. There was no significant difference in either outcome score post-operatively between the three groups. Conclusion: The magnitude of clinical improvement following knee replacement is greatest at 6 months; thereafter, only modest improvements continue to occur. This study also found no significant differences of outcomes at 2 years after surgery among UKR, BKR and TKR. BKR is a good alternative option for combined symptomatic medial and patellofemoral arthritis of the knee.
Nelson, Michael T,Joksovic, Pavle M,Su, Peihan,Kang, Ho-Won,Van Deusen, Amy,Baumgart, Joel P,David, Laurence S,Snutch, Terrance P,Barrett, Paula Q,Lee, Jung-Ha,Zorumski, Charles F,Perez-Reyes, Edward Society for Neuroscience 2007 The Journal of neuroscience Vol.27 No.46
<P>T-type Ca2+ channels (T-channels) are involved in the control of neuronal excitability and their gating can be modulated by a variety of redox agents. Ascorbate is an endogenous redox agent that can function as both an anti- and pro-oxidant. Here, we show that ascorbate selectively inhibits native Ca(v)3.2 T-channels in peripheral and central neurons, as well as recombinant Ca(v)3.2 channels heterologously expressed in human embryonic kidney 293 cells, by initiating the metal-catalyzed oxidation of a specific, metal-binding histidine residue in domain 1 of the channel. Our biophysical experiments indicate that ascorbate reduces the availability of Ca(v)3.2 channels over a wide range of membrane potentials, and inhibits Ca(v)3.2-dependent low-threshold-Ca2+ spikes as well as burst-firing in reticular thalamic neurons at physiologically relevant concentrations. This study represents the first mechanistic demonstration of ion channel modulation by ascorbate, and suggests that ascorbate may function as an endogenous modulator of neuronal excitability.</P>