The Experts below are selected from a list of 9219 Experts worldwide ranked by ideXlab platform

Therese A. Kosten - One of the best experts on this subject based on the ideXlab platform.

Dieter Cadosch - One of the best experts on this subject based on the ideXlab platform.

  • Pharmacological Blocking of the osteoclastic biocorrosion of surgical stainless steel in vitro.
    Journal of Biomedical Materials Research Part A, 2012
    Co-Authors: S. Lionetto, A. Little, Gatien Moriceau, Dominique Heymann, M. Decurtins, M. Plecko, Luis Filgueira, Dieter Cadosch
    Abstract:

    In vitro studies suggest that human osteoclasts (OC) are able to corrode surgical stainless steel 316L (SS). The aim of this study was to investigate whether osteoclastic biocorrosion can be blocked Pharmacologically. Human OCs were generated in vitro from peripheral blood monocytic cells (PBMCs) in the presence of OC differentiation cytokines. The osteoclastic viability, differentiation, and resorptive function (on both bone and SS) were assessed using standard colorimetric cell viability assay 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenil)-2H-tetrazolium, inner salt (MTS), fluorescence microscopy, tartrate-resistant acid phosphatase expression (flow cytometry), and scanning electron microscopy. OCs cultured on SS were exposed to nontoxic concentrations of bafilomycin A1, amiloride hydrochloride, or zoledronic acid. The extent of biocorrosion was quantified using atomic emission spectrometry (to measure the concentration of metal ions released into the supernatant) and scanning electron microscopy. PBMCs differentiated into mature and functional OC in the presence of all the drugs used. Osteoclastic resorption of SS was noted with differences in the resorption pattern for all drug treatments. Under the drug treatments, single areas of osteoclastic resorption were larger in size but less abundant when compared with positive controls. None of the drugs used were able to inhibit osteoclastic biocorrosion of SS.

  • Pharmacological Blocking of the osteoclastic biocorrosion of surgical stainless steelin vitro
    Journal of Biomedical Materials Research Part A, 2012
    Co-Authors: S. Lionetto, A. Little, Gatien Moriceau, Dominique Heymann, M. Decurtins, M. Plecko, Luis Filgueira, Dieter Cadosch
    Abstract:

    In vitro studies suggest that human osteoclasts (OC) are able to corrode surgical stainless steel 316L (SS). The aim of this study was to investigate whether osteoclastic biocorrosion can be blocked Pharmacologically. Human OCs were generated in vitro from peripheral blood monocytic cells (PBMCs) in the presence of OC differentiation cytokines. The osteoclastic viability, differentiation, and resorptive function (on both bone and SS) were assessed using standard colorimetric cell viability assay 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenil)-2H-tetrazolium, inner salt (MTS), fluorescence microscopy, tartrate-resistant acid phosphatase expression (flow cytometry), and scanning electron microscopy. OCs cultured on SS were exposed to nontoxic concentrations of bafilomycin A1, amiloride hydrochloride, or zoledronic acid. The extent of biocorrosion was quantified using atomic emission spectrometry (to measure the concentration of metal ions released into the supernatant) and scanning electron microscopy. PBMCs differentiated into mature and functional OC in the presence of all the drugs used. Osteoclastic resorption of SS was noted with differences in the resorption pattern for all drug treatments. Under the drug treatments, single areas of osteoclastic resorption were larger in size but less abundant when compared with positive controls. None of the drugs used were able to inhibit osteoclastic biocorrosion of SS

Yu-ke Tian - One of the best experts on this subject based on the ideXlab platform.

  • Disruption of the GABAergic system contributes to the development of perioperative neurocognitive disorders after anesthesia and surgery in aged mice.
    CNS Neuroscience & Therapeutics, 2020
    Co-Authors: Wen Zhang, Bingrui Xiong, Long‐qing Zhang, Xian Huang, Wenchang Zhou, Qian Zou, Anne Manyande, Jie Wang, Xuebi Tian, Yu-ke Tian
    Abstract:

    Aims Perioperative neurocognitive disorders (PND) are associated with cognitive impairment in the preoperative or postoperative period, and neuroinflammation is thought to be the most important mechanisms especially during the postoperative period. The GABAergic system is easily disrupted by neuroinflammation. This study investigated the impact of the GABAergic system on PND after anesthesia and surgery. Methods An animal model of laparotomy with inhalation anesthesia in 16-month-old mice was addressed. Effects of the GABAergic system were assessed using biochemical analysis. Pharmacological Blocking of α5GABAA Rs or P38 mitogen-activated protein kinase (MAPK) were applied to investigate the effects of the GABAergic system. Results After laparotomy, the hippocampus-dependent memory and long-term potentiation were impaired, the levels of IL-6, IL-1β and TNF-α up-regulated in the hippocampus, the concentration of GABA decreased, and the protein levels of the surface α5GABAA Rs up-regulated. Pharmacological Blocking of α5GABAA Rs with L655,708 alleviated laparotomy induced cognitive deficits. Further studies found that the P38 MAPK signaling pathway was involved and Pharmacological Blocking with SB203,580 alleviated memory dysfunctions. Conclusions Anesthesia and surgery caused neuroinflammation in the hippocampus, which consequently disrupted the GABAergic system, increased the expressions of surface α5GABAA Rs especially through the P38 MAPK signaling pathway, and eventually led to hippocampus-dependent memory dysfunctions.

  • Disruption of the GABAergic system contributes to the development of perioperative neurocognitive disorders after anesthesia and surgery in aged mice
    'Wiley', 2020
    Co-Authors: Zhang Wen, Xiong Bing-rui, Zhang Long-qing, Huang Xian, Zhou Wen-chang, Zou Qian, Manyande Anne, Wang Jie, Tian Xue-bi, Yu-ke Tian
    Abstract:

    Aims: Perioperative neurocognitive disorders (PND) are associated with cognitive impairment in the preoperative or postoperative period, and neuroinflammation is thought to be the most important mechanisms especially during the postoperative period. The GABAergic system is easily disrupted by neuroinflammation. This study investigated the impact of the GABAergic system on PND after anesthesia and surgery. Methods: An animal model of laparotomy with inhalation anesthesia in 16-month old mice was addressed. Effects of the GABAergic system were assessed using biochemical analysis. Pharmacological Blocking of α5GABAARs or P38 mitogen-activated protein kinase (MAPK) was applied to investigate the effect of the GABAergic system. Results: After laparotomy, the hippocampus-dependent memory and long-term potentiation were impaired, the levels of IL-6, IL-1β and TNF-α upregulated in the hippocampus, the concentration of GABA decreased, and the protein levels of the surface α5GABAARs up-regulated. Pharmacological Blocking of α5GABAARs with L655,708 alleviated laparotomy induced cognitive deficits. A further study found that the P38 MAPK signaling pathway was involved and Pharmacological Blocking with SB203,580 alleviated memory dysfunction. Conclusions: Anesthesia and surgery caused neuroinflammation in the hippocampus, which consequently disrupted the GABAergic system, increased the expressions of surface α5GABAARs especially through the P38 MAPK signaling pathway, and eventually led to hippocampus-dependent memory dysfunctions

S. Lionetto - One of the best experts on this subject based on the ideXlab platform.

  • Pharmacological Blocking of the osteoclastic biocorrosion of surgical stainless steel in vitro.
    Journal of Biomedical Materials Research Part A, 2012
    Co-Authors: S. Lionetto, A. Little, Gatien Moriceau, Dominique Heymann, M. Decurtins, M. Plecko, Luis Filgueira, Dieter Cadosch
    Abstract:

    In vitro studies suggest that human osteoclasts (OC) are able to corrode surgical stainless steel 316L (SS). The aim of this study was to investigate whether osteoclastic biocorrosion can be blocked Pharmacologically. Human OCs were generated in vitro from peripheral blood monocytic cells (PBMCs) in the presence of OC differentiation cytokines. The osteoclastic viability, differentiation, and resorptive function (on both bone and SS) were assessed using standard colorimetric cell viability assay 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenil)-2H-tetrazolium, inner salt (MTS), fluorescence microscopy, tartrate-resistant acid phosphatase expression (flow cytometry), and scanning electron microscopy. OCs cultured on SS were exposed to nontoxic concentrations of bafilomycin A1, amiloride hydrochloride, or zoledronic acid. The extent of biocorrosion was quantified using atomic emission spectrometry (to measure the concentration of metal ions released into the supernatant) and scanning electron microscopy. PBMCs differentiated into mature and functional OC in the presence of all the drugs used. Osteoclastic resorption of SS was noted with differences in the resorption pattern for all drug treatments. Under the drug treatments, single areas of osteoclastic resorption were larger in size but less abundant when compared with positive controls. None of the drugs used were able to inhibit osteoclastic biocorrosion of SS.

  • Pharmacological Blocking of the osteoclastic biocorrosion of surgical stainless steelin vitro
    Journal of Biomedical Materials Research Part A, 2012
    Co-Authors: S. Lionetto, A. Little, Gatien Moriceau, Dominique Heymann, M. Decurtins, M. Plecko, Luis Filgueira, Dieter Cadosch
    Abstract:

    In vitro studies suggest that human osteoclasts (OC) are able to corrode surgical stainless steel 316L (SS). The aim of this study was to investigate whether osteoclastic biocorrosion can be blocked Pharmacologically. Human OCs were generated in vitro from peripheral blood monocytic cells (PBMCs) in the presence of OC differentiation cytokines. The osteoclastic viability, differentiation, and resorptive function (on both bone and SS) were assessed using standard colorimetric cell viability assay 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenil)-2H-tetrazolium, inner salt (MTS), fluorescence microscopy, tartrate-resistant acid phosphatase expression (flow cytometry), and scanning electron microscopy. OCs cultured on SS were exposed to nontoxic concentrations of bafilomycin A1, amiloride hydrochloride, or zoledronic acid. The extent of biocorrosion was quantified using atomic emission spectrometry (to measure the concentration of metal ions released into the supernatant) and scanning electron microscopy. PBMCs differentiated into mature and functional OC in the presence of all the drugs used. Osteoclastic resorption of SS was noted with differences in the resorption pattern for all drug treatments. Under the drug treatments, single areas of osteoclastic resorption were larger in size but less abundant when compared with positive controls. None of the drugs used were able to inhibit osteoclastic biocorrosion of SS

Sophie M Steculorum - One of the best experts on this subject based on the ideXlab platform.

  • inhibition of p2y6 signaling in agrp neurons reduces food intake and improves systemic insulin sensitivity in obesity
    Cell Reports, 2017
    Co-Authors: Sophie M Steculorum, Katharina Timper, Linda Engstrom Ruud, Nadine Evers, Lars Paeger, Stephan Bremser
    Abstract:

    Summary Uridine-diphosphate (UDP) and its receptor P2Y6 have recently been identified as regulators of AgRP neurons. UDP promotes feeding via activation of P2Y6 receptors on AgRP neurons, and hypothalamic UDP concentrations are increased in obesity. However, it remained unresolved whether inhibition of P2Y6 signaling Pharmacologically, globally, or restricted to AgRP neurons can improve obesity-associated metabolic dysfunctions. Here, we demonstrate that central injection of UDP acutely promotes feeding in diet-induced obese mice and that acute Pharmacological Blocking of CNS P2Y6 receptors reduces food intake. Importantly, mice with AgRP-neuron-restricted inactivation of P2Y6 exhibit reduced food intake and fat mass as well as improved systemic insulin sensitivity with improved insulin action in liver. Our results reveal that P2Y6 signaling in AgRP neurons is involved in the onset of obesity-associated hyperphagia and systemic insulin resistance. Collectively, these experiments define P2Y6 as a potential target to Pharmacologically restrict both feeding and systemic insulin resistance in obesity.