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1.
Braz. J. Pharm. Sci. (Online) ; 59: e21129, 2023. tab
Article Dans Anglais | LILACS | ID: biblio-1439511

Résumé

Abstract We aimed to compare the effects of oxycodone hydrochloride and dezocine on hemodynamics and inflammatory factors in patients receiving gynecological laparoscopic surgery under general anesthesia. A total of 246 patients were divided into group A and B (n=123). Hemorheology indices were recorded 5 min after anesthesia (T0), 1 min after pneumoperitoneum (T1), when position was changed 5 min after pneumoperitoneum (T2), 15 min after pneumoperitoneum (T3), 1 min (T4) and 5 min (T5) after position was restored. Visual analogue scale scores 1, 2, 6, 12, 24 and 48 h after operation were recorded. Postoperative adverse reactions and visceral pain were observed. The expression levels of inflammatory factors were detected by enzyme-linked immunosorbent assay 12 h after operation. Compared with group A, group B had higher heart rate and mean arterial pressure at T2, lower central venous pressure and cardiac output at T1-T3, and higher systemic vascular resistance at T1-T5 (P<0.05). The incidence rate of pain syndrome in group A was lower (P<0.05). Group A had lower tumor necrosis factor-alpha and interleukin-6 expression levels and higher interleukin-10 level than those of group B (P<0.05). For gynecological laparoscopic surgery, oxycodone preemptive analgesia has superior outcomes to those of dezocine


Sujets)
Humains , Femelle , Adulte , Adulte d'âge moyen , Patients/classification , Laparoscopie/instrumentation , Anesthésie générale/instrumentation , Test ELISA/méthodes
2.
Braz. oral res. (Online) ; 34: e006, 2020. tab, graf
Article Dans Anglais | LILACS | ID: biblio-1055522

Résumé

Abstract Induced pluripotent stem (iPS) cells could be induced into ameloblast-like cells by ameloblasts serum-free conditioned medium (ASF-CM), and bone morphogenetic proteins (BMPs) might be essential during the regulation of this process. The present study investigates the signal transduction that regulates the ameloblastic differentiation of iPS cells induced by ASF-CM. Mouse iPS cells were characterized and then cultured for 14 days in epithelial cell medium (control) or ASF-CM. Bone morphogenetic protein receptor II (BMPR-II) siRNA, inhibitor of Smad1/5 phosphorylation activated by activin receptor-like kinase (ALK) receptors, and inhibitors of mitogen-activated protein kinases (MAPKs) phosphorylation were used to treat the iPS cells in combination with ASF-CM. Real-time PCR, western blotting, and immunofluorescent staining were used to evaluate the expressions of ameloblast markers ameloblastin, enamelin, and cytokeratin-14. BMPR-II gene and protein levels increased markedly in ASF-CM-treated iPS cells compared with the controls, while the mRNA levels of Bmpr-Ia and Bmpr-Ib were similar between the ASF-CM and control groups. ASF-CM stimulation significantly increased the gene and protein expression of ameloblastin, enamelin and cytokeratin-14, and phosphorylated SMAD1/5, p38 MAPK, and ERK1/2 MAPK compared with the controls. Knockdown of BMPR-II and inhibition of Smad1/5 phosphorylation both could significantly reverse the increased expression of ameloblastin, enamelin, and cytokeratin-14 induced by ASF-CM, while neither inhibition of p38 nor ERK1/2 phosphorylation had significant reversing effects. We conclude that smad1/5 signaling transduction, activated by ALK receptors, regulates the ameloblastic differentiation of iPS cells induced by ameloblast-conditioned medium.


Sujets)
Transduction du signal/physiologie , Protéine Smad-1/physiologie , Cellules souches pluripotentes induites/cytologie , Améloblastes/cytologie , Phosphorylation , Facteurs temps , Expression des gènes , Différenciation cellulaire/physiologie , Différenciation cellulaire/génétique , Cellules cultivées , Technique de Western , Technique d'immunofluorescence , Milieux de culture sans sérum , RT-PCR , Système de signalisation des MAP kinases/physiologie , Récepteur activine/analyse , Récepteur activine/physiologie , Interférence par ARN , p38 Mitogen-Activated Protein Kinases/analyse , p38 Mitogen-Activated Protein Kinases/physiologie , Récepteurs de la protéine morphogénique osseuse de type II/analyse , Récepteurs de la protéine morphogénique osseuse de type II/physiologie , Protéine Smad-1/analyse
3.
Braz. oral res. (Online) ; 34: e006, 2020. tab, graf
Article Dans Anglais | LILACS | ID: biblio-1089380

Résumé

Abstract Induced pluripotent stem (iPS) cells could be induced into ameloblast-like cells by ameloblasts serum-free conditioned medium (ASF-CM), and bone morphogenetic proteins (BMPs) might be essential during the regulation of this process. The present study investigates the signal transduction that regulates the ameloblastic differentiation of iPS cells induced by ASF-CM. Mouse iPS cells were characterized and then cultured for 14 days in epithelial cell medium (control) or ASF-CM. Bone morphogenetic protein receptor II (BMPR-II) siRNA, inhibitor of Smad1/5 phosphorylation activated by activin receptor-like kinase (ALK) receptors, and inhibitors of mitogen-activated protein kinases (MAPKs) phosphorylation were used to treat the iPS cells in combination with ASF-CM. Real-time PCR, western blotting, and immunofluorescent staining were used to evaluate the expressions of ameloblast markers ameloblastin, enamelin, and cytokeratin-14. BMPR-II gene and protein levels increased markedly in ASF-CM-treated iPS cells compared with the controls, while the mRNA levels of Bmpr-Ia and Bmpr-Ib were similar between the ASF-CM and control groups. ASF-CM stimulation significantly increased the gene and protein expression of ameloblastin, enamelin and cytokeratin-14, and phosphorylated SMAD1/5, p38 MAPK, and ERK1/2 MAPK compared with the controls. Knockdown of BMPR-II and inhibition of Smad1/5 phosphorylation both could significantly reverse the increased expression of ameloblastin, enamelin, and cytokeratin-14 induced by ASF-CM, while neither inhibition of p38 nor ERK1/2 phosphorylation had significant reversing effects. We conclude that smad1/5 signaling transduction, activated by ALK receptors, regulates the ameloblastic differentiation of iPS cells induced by ameloblast-conditioned medium.


Sujets)
Transduction du signal/physiologie , Protéine Smad-1/physiologie , Cellules souches pluripotentes induites/cytologie , Améloblastes/cytologie , Phosphorylation , Facteurs temps , Expression des gènes , Différenciation cellulaire/physiologie , Différenciation cellulaire/génétique , Cellules cultivées , Technique de Western , Technique d'immunofluorescence , Milieux de culture sans sérum , RT-PCR , Système de signalisation des MAP kinases/physiologie , Récepteur activine/analyse , Récepteur activine/physiologie , Interférence par ARN , p38 Mitogen-Activated Protein Kinases/analyse , p38 Mitogen-Activated Protein Kinases/physiologie , Récepteurs de la protéine morphogénique osseuse de type II/analyse , Récepteurs de la protéine morphogénique osseuse de type II/physiologie , Protéine Smad-1/analyse
4.
Acta cir. bras ; 34(7): e201900702, 2019. tab, graf
Article Dans Anglais | LILACS | ID: biblio-1038116

Résumé

Abstract Purpose: To investigate the effect of intermittent vibration at different intervals on bone fracture healing and optimize the vibration interval. Methods: Ninety sheep were randomized to receive no treatment (the control group), incision only (the sham control group), internal fixation with or without metatarsal fracture (the internal fixation group), and continuous vibration in addition to internal fixation of metatarsal fracture, or intermittent vibration at 1, 2, 3, 5, 7 and 17-day interval in addition to internal fixation of metatarsal fracture (the vibration group). Vibration was done at frequency F=35 Hz, acceleration a=0.25g, 15 min each time 2 weeks after bone fracture. Bone healing was evaluated by micro-CT scan, bone microstructure and mechanical compression of finite element simulation. Results: Intermittent vibration at 7-day interval significantly improved bone fracture healing grade. However, no significant changes on microstructure parameters and mechanical properties were observed among sheep receiving vibration at different intervals. Conclusions: Clinical healing effects should be the top concern. Quantitative analyses of bone microstructure and of finite element mechanics on the process of fracture healing need to be further investigated.


Sujets)
Animaux , Vibration/usage thérapeutique , Os du métatarse/traumatismes , Consolidation de fracture/physiologie , Fractures osseuses/imagerie diagnostique , Ovis , Os du métatarse/chirurgie , Os du métatarse/imagerie diagnostique , Répartition aléatoire , Analyse des éléments finis , Fractures osseuses/chirurgie , Fractures osseuses/thérapie , Microtomographie aux rayons X , Ostéosynthèse interne/instrumentation , Ostéosynthèse interne/normes
5.
Journal of Huazhong University of Science and Technology (Medical Sciences) ; (6): 779-783, 2011.
Article Dans Chinois | WPRIM | ID: wpr-248586

Résumé

This study examined the effects of clinically relevant concentrations of isoflurane on the amplitude of NMDA receptor current (INMDA) and the expression of cytochrome C in cultured developing rat hippocampal neurons.The hippocampi were dissected from newborn Sprague-Dawley rats.Hippocampal neurons were primarily cultured for 5 days and then treated with different concentrations of isoflurane [(0.25,0.5,0.75,1 minimum alveolar concentration (MAC))].The peak of INMDA was recorded by means of the whole cell patch clamp technique.The cytochrome C level was detected by Western blotting and quantitative real-time PCR.Our results showed that isoflurane (0.25,0.5,0.75 and 1 MAC) potentiated the amplitude of INMDA by (116±8.8)%,(122±11.7)%,(135±14.3)% and (132±14.6)%,respectively,and isoflurane increased the mRNA expression of cytochrome C in a concentration-dependent manner.The cytochrome C mRNA expression reached a maximum after 0.5 MAC isoflurane stimulation for 6 h (P<0.05).It was concluded that isoflurane enhances the expression of cytochrome C in cultured rat hippocampal neurons,which may be mediated by facilitation of NMDA receptor.

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