RESUMEN
Ceramics are high-strength and high-temperature resistant materials that are used in various functional parts. However, due to the high strength and brittleness properties, there are many difficulties in the fabrication of complex shapes. Therefore, there are many studies related to the fabrication of ceramic parts using 3D printing technology optimized for complex shapes. Among them, studies using photo-polymerization (PP) 3D printing technology with excellent dimensional accuracy and surface quality have received the most widespread attention. To secure the physical properties of sintered ceramic, the content and distribution of materials are important. This study suggests a novel 3D printing process based on a high-viscosity composite resin that maximizes the content of zirconia ceramics. For reliable printing, the developed 3D printers that can adjust the process environment were used. To minimize warpage and delamination, the divided micro square pattern images were irradiated in two separate intervals of 1.6 s each while maintaining the internal chamber temperature at 40 °C. This contributed to improved stability and density of the sintered structures. Ultimately, the ceramic parts with a Vickers hardness of 12.2 GPa and a relative density of over 95% were able to be fabricated based on a high-viscosity resin with 25,000 cps.
RESUMEN
BACKGROUND: Given higher component conformity, rotational availability of polyethylene insert, and more physiologic patellofemoral tracking, mobile-bearing (MB) total knee arthroplasty (TKA) is supposed to offer advantages in joint perception and crepitus. The purpose of this study was to investigate whether MB TKA offers superior outcomes over fixed-bearing (FB) TKA in terms of joint awareness and crepitus. METHODS: This prospective, randomized, controlled trial included 49 FB and 49 MB TKAs that shared the same posterior-stabilized femoral component. Primary outcomes included joint awareness assessed with the Forgotten Joint Score and crepitus graded according to severity and sound at 3 years postoperatively. Secondary outcomes were the range of motion, the Knee Society Score, Western Ontario and McMaster Universities Osteoarthritis Index, component position, and joint line level on radiographs. RESULTS: The Forgotten Joint Score showed no significant difference between the FB (67 points; range, 0-100) and MB groups (63 points; range, 13-100) (P = .440). For crepitus, no significant differences were found in the overall incidence rate (FB group, 18%; MB group, 12%; P = .386) and grade (grade 1, 6 versus 5; grade 2, 2 versus 1; grade 3, 1 versus 0, respectively). There were no significant differences in range of motion, Knee Society Score, and Western Ontario and McMaster Universities Osteoarthritis Index, as well as radiographic outcomes between the two groups (all, P > .05). CONCLUSION: MB TKA offers no benefits in terms of joint awareness and crepitus compared with FB TKA at mean 3 years postoperatively. The theoretical advantages of MB TKA have yet to be demonstrated in practice, leaving the selection of bearing type to the surgeon's judgment. LEVEL OF EVIDENCE: Level II.
Asunto(s)
Artroplastia de Reemplazo de Rodilla , Prótesis de la Rodilla , Osteoartritis de la Rodilla , Humanos , Osteoartritis de la Rodilla/cirugía , Estudios Prospectivos , Diseño de Prótesis , Articulación de la Rodilla/cirugía , Rango del Movimiento ArticularRESUMEN
Phytoestrogen (PE) has received considerable attention due to the physiological significance of its estrogenicity. Flemingia strobilifera (FS) has been used as a folk medicine in Asia for the treatment of inflammation, cancer, and infection; however, the estrogenic effects and chemical components of FS have not yet been reported. We aimed to uncover the estrogenic properties and PEs derived from FS using phytochemical and pharmacological evaluation. PEs from FS extract (FSE) were analyzed by NMR, HPLC, and MS. To evaluate estrogenic activity, FSE and its compounds were evaluated by in vitro and in vivo assays, including human estrogen receptor alpha (hERα) binding, estrogen response element (ERE)-luciferase reporter assays, and uterotrophic assays. FSE and its compounds 1-5 showed binding affinities for hERα and activated ERE transcription in MCF-7 cells. Additionally, FSE and compounds 1-5 induced MCF-7 cell proliferation and trefoil factor 1 (pS2) expression. In immature female rats, significant increases in uterine weight and pS2 gene were observed in FSE-treated groups. We identified estrogenic activities of FSE and its bioactive compounds, suggesting their possible roles as PEs via ERs. PEs derived from FSE are promising candidates for ER-targeted therapy for post-menopausal symptoms.
Asunto(s)
Fabaceae/química , Fitoestrógenos/farmacología , Animales , Peso al Nacer/efectos de los fármacos , Proliferación Celular/efectos de los fármacos , Femenino , Humanos , Células MCF-7 , Fitoestrógenos/química , Fitoestrógenos/aislamiento & purificación , Presenilina-2/genética , Ratas , Ratas Sprague-Dawley , Células Tumorales Cultivadas , Útero/efectos de los fármacosRESUMEN
Glucagon like peptide-1 (GLP-1) stimulates glucose-dependent insulin secretion. Dipeptidyl peptidase-4 (DPP-4) inhibitors, which block inactivation of GLP-1, are currently in clinical use for type 2 diabetes mellitus. Recently, GLP-1 has also been reported to have neuroprotective effects in cases of cerebral ischemia. We therefore investigated the neuroprotective effects of GLP-1 receptor (GLP-1R) agonist, exendin-4 (ex-4), after cerebral ischemia-reperfusion injury. Transient middle cerebral artery occlusion (tMCAO) was induced in rats by intracerebroventricular (i.c.v.) administration of ex-4 or ex9-39. Oxygen-glucose deprivation was also induced in primary neurons, bEnd.3 cells, and BV-2. Ischemia-reperfusion injury reduced expression of GLP-1R. Additionally, higher oxidative stress in SOD2 KO mice decreased expression of GLP-1R. Downregulation of GLP-1R by ischemic injury was 70% restored by GLP-1R agonist, ex-4, which resulted in significant reduction of infarct volume. Levels of intracellular cyclic AMP, a second messenger of GLP-1R, were also increased by 2.7-fold as a result of high GLP-1R expression. Moreover, our results showed that ex-4 attenuated pro-inflammatory cyclooxygenase-2 (COX-2) and prostaglandin E2 after MCAO. C-Jun NH2 terminal kinase (JNK) signaling, which stimulates activation of COX-2, was 36% inhibited by i.c.v. injection of ex-4 at 24 h. Islet-brain 1 (IB1), a scaffold regulator of JNK, was 1.7-fold increased by ex-4. GLP-1R activation by ex-4 resulted in reduction of COX-2 through increasing IB1 expression, resulting in anti-inflammatory neuroprotection during stroke. Our study suggests that the anti-inflammatory action of GLP-1 could be used as a new strategy for the treatment of neuroinflammation after stroke accompanied by hyperglycemia.
RESUMEN
Postconditioning has been shown to protect the mouse brain from ischemic injury. However, the neuroprotective mechanisms of postconditioning remain elusive. We have found that toll-like receptor 5 (TLR5) plays an integral role in postconditioning-induced neuroprotection through Akt/nuclear factor kappa B (NF-κB) activation in cerebral ischemia. Compared to animals that received 30 min of transient middle cerebral artery occlusion (tMCAO) group, animals that also underwent postconditioning showed a significant reduction of up to 60.51% in infarct volume. Postconditioning increased phospho-Akt (p-Akt) levels and NF-κB translocation to the nucleus as early as 1 h after tMCAO and oxygen-glucose deprivation. Furthermore, inhibition of Akt by Akt inhibitor IV decreased NF-κB promoter activity after postconditioning. Immunoprecipitation showed that interactions between TLR5, MyD88, and p-Akt were increased from postconditioning both in vivo and in vitro. Similar to postconditioning, flagellin, an agonist of TLR5, increased NF-κB nuclear translocation and Akt phosphorylation. Our results suggest that postconditioning has neuroprotective effects by activating NF-κB and Akt survival pathways via TLR5 after cerebral ischemia. Additionally, the TLR5 agonist flagellin can simulate the neuroprotective mechanism of postconditioning in cerebral ischemia.