3-D surgical planning for restorative osteotomy is costly and time-consuming because surgeons need to be helped from commercial companies to get 3-D printed bones. However, practitioners can save time and keep the cost to a minimum by utilizing free software and establishing their 3-D printers locally. Surgical planning for the corrective osteotomy of antebrachial growth deformities (AGD) is challenging for several reasons (the nature of the biapical or multiapical conformational abnormalities and lack of a reference value for the specific breed). Pre-operative planning challenges include: a definite description of the position of the center of rotation of angulation (CORA) and proper positioning of the osteotomies applicable to the CORA. In the present study, we demonstrated an accurate and reproducible bone-cutting technique using patient-specific instrumentations (PSI) 3-D technology. The results of the location precision showed that, by using PSIs, the surgeons were able to accurately replicate preoperative resection planning. PSI results also indicate that PSI technology provides a smaller standard deviation than the freehand method. PSI technology performed in the distal radial angular deformity may provide good cutting accuracy. In conclusion, the PSI technology may improve bone-cutting accuracy during corrective osteotomy by providing clinically acceptable margins.
Parkinson’s disease (PD) is characterized by progressive dopaminergic neuron loss or dysfunction and is the second most prevalent neurodegenerative disorder after Alzheimer’s disease. However, current therapeutic strategies for PD are limited to treating the outcomes of this disease rather than preventing it. Sinapic acid (SA) is a phenolic compound with potential antioxidant properties, which reportedly acts as a therapeutic agent against many diseases including cancer, as well as cardiac and liver diseases. However, little is known about the effects of SA against neurodegenerative disorders. Therefore, our study sought to evaluate the neuroprotective effects of non-cytotoxic concentrations of SA against 6-hydroxydopamine (6-OHDA)-induced neurotoxicity in SH-SY5Y human neuroblastoma cells, which we used as an in vitro PD model. SA increased cell viability and rescued the cells from 6-OHDA-induced apoptotic cell death. Additionally, oxidative stress responses were significantly blocked by SA, including reactive oxygen species (ROS) overproduction and decreased expression levels of antioxidant proteins. Notably, SA also attenuated mitochondrial dysfunction and endoplasmic reticulum (ER) stress. Moreover, SA dramatically inhibited the activation of mitogen-activated protein kinase (MAPK) proteins. Taken together, our findings highlight the potential PD prevention effects of SA, as well as its underlying mechanisms, making this compound a promising prevention and treatment agent for PD.
Oxidative stress, defined as an imbalance between reactive oxygen species (ROS) production and the antioxidant defense system, contributes to the pathogenesis of many heart diseases. Therefore, oxidative stress has been highlighted as a therapeutic target for heart disease treatment. Butein, a tetrahydroxychalcone, has potential biological activities, especially antioxidant properties. However, the effect of butein on oxidative-stressed heart cells has been poorly studied. Thus, we sought to identify the antioxidant effects of butein in H9c2 cardiomyoblasts. To elucidate these antioxidant effects, various concentrations of butein were used to pretreat H9c2 cells prior to H2O2 treatment. Thereafter, measures of oxidative damages, such as ROS production, antioxidant expression levels, and apoptosis, were evaluated. Butein effectively increased cell viability and rescued the cells from oxidative damage through the inhibition of ROS production, apoptosis, and increased antioxidant expression. Furthermore, butein dramatically inhibited mitochondrial dysfunction and endoplasmic reticulum (ER) stress, which are the main ROS inducers. Nrf2 protein translocated from the cytosol to the nucleus and consequently activated its target genes as oxidative stress suppressors. These findings demonstrate that butein has potential antioxidant effects in H9c2 cardiomyoblasts, suggesting that it could be used as a therapeutic substance for the treatment of cardiac diseases.
Return of spontaneous circulation (ROSC) through cardiopulmonary resuscitation (CPR) after cardiac arrest (CA) causes post-cardiac arrest syndrome (PCAS) due to dysfunction in various organs, which provokes acute kidney injury because of renal ischemia-reperfusion injury. Therapeutic hypothermia (TH) can reduce PCAS after CA and ROSC. However, it needs to be more sophisticated and effective. Hence, we aimed to elucidate the protective effects of olanzapine-induced TH against renal injury in asphyxial CA-induced rats. Every rat’s body temperature was maintained at 33 °C for 6 h after administering olanzapine post-CA and ROSC. Olanzapine-induced TH dramatically increased the survival rate of the rats and ameliorated renal tissue damage. Moreover, it suppressed oxidative stress responses through preservation of mitochondrial function and endoplasmic reticulum stress as the main contributor of oxidative stress. Notably, these actions of olanzapine-induced TH were mediated through the Sirt3-related signaling pathway, including the maintenance of Sirt3 and FOXO3a protein expression and the activation of AMPKα and superoxide dismutase 1 (SOD2, a mitochondrial antioxidant). This study is the first to disclose the protective effects of olanzapine-induced TH against renal injury after CA and ROSC, suggesting that olanzapine-induced TH could be utilized for treating CA followed by ROSC.
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