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Ana Boquete-Castro,Juan-Manuel Cortés-Mejía,Raquel Alarcón-Sánchez,Pedro Mayoral-Sanz 대한수면학회 2021 sleep medicine research Vol.12 No.1
Sleep-related breathing disorders increase morbidity and mortality of those patients suffering from them. Snoring is a quite common disorder; however, there are no publications describing the knowledge of the patients that attend to the dental clinic on how snoring can be a severe health problem. To evaluate the knowledge of the severity of snoring and its impact on systemic health among the patients that attend to the dental clinic. Anonymous questionnaires were given to patients at dental clinics in 4 countries. The questionnaires were composed by nine questions related to snoring and how it affects general health in children and adults. A total of 200 subjects participated in this multicentric study. The mean age of the participants was 42.57 years. The results from the present study show that there is a great lack of knowledge on the severity of snoring. Forty-eight percent of the participants affirmed they snore; however, only 20% of the sample think it is important to consult a specialist due to this problem. This study reveals the great lack of knowledge regarding the negative impact of snoring on systemic health and the need of implementing educational programs.
Ana Sanchis,María Adelaida García-Gimeno,Antonio José Cañada-Martínez,María Dolores Sequedo,José María Millán,Pascual Sanz,Rafael P. Vázquez-Manrique 생화학분자생물학회 2019 Experimental and molecular medicine Vol.51 No.-
Huntington disease is a neurodegenerative condition for which there is no cure to date. Activation of AMP-activated protein kinase has previously been shown to be beneficial in in vitro and in vivo models of Huntington’s disease. Moreover, a recent cross-sectional study demonstrated that treatment with metformin, a well-known activator of this enzyme, is associated with better cognitive scores in patients with this disease. We performed a preclinical study using metformin to treat phenotypes of the zQ175 mouse model of Huntington disease. We evaluated behavior (motor and neuropsychiatric function) and molecular phenotypes (aggregation of mutant huntingtin, levels of brain-derived neurotrophic factor, neuronal inflammation, etc.). We also used two models of polyglutamine toxicity in Caenorhabditis elegans to further explore potential mechanisms of metformin action. Our results provide strong evidence that metformin alleviates motor and neuropsychiatric phenotypes in zQ175 mice. Moreover, metformin intake reduces the number of nuclear aggregates of mutant huntingtin in the striatum. The expression of brain-derived neurotrophic factor, which is reduced in mutant animals, is partially restored in metformin-treated mice, and glial activation in mutant mice is reduced in metformin-treated animals. In addition, using worm models of polyglutamine toxicity, we demonstrate that metformin reduces polyglutamine aggregates and restores neuronal function through mechanisms involving AMP-activated protein kinase and lysosomal function. Our data indicate that metformin alleviates the progression of the disease and further supports AMP-activated protein kinase as a druggable target against Huntington’s disease.
Jonay Poveda,Ana B Sanz,Susana Carrasco,Marta Ruiz-Ortega,Pablo Cannata-Ortiz,Maria D Sanchez-Niño,Alberto Ortiz 생화학분자생물학회 2017 Experimental and molecular medicine Vol.49 No.-
Acute kidney injury (AKI) is characterized by tubular cell death and interstitial inflammation. TWEAK promotes experimental kidney injury and activates the transcription factor NF-κB, a key regulator of genes involved in cell survival and inflammatory response. In search of potential therapeutic targets for AKI, we compared a transcriptomics database of NF-κB-related genes from murine AKI-kidneys with a transcriptomics database of TWEAK-stimulated cultured tubular cells. Four out of twenty-four (17%) genes were significantly upregulated (false discovery rate, FDRo0.05), while nine out of twenty-four (37%) genes were significantly upregulated at FDR o0.1 in both databases. Bcl3 was the top upregulated NF-κB-related gene in experimental AKI and one of the most upregulated genes in TWEAK-stimulated tubular cells. Quantitative reverse transcription PCR (qRT-PCR), western blot and immunohistochemistry confirmed Bcl3 upregulation in both experimental conditions and localized increased Bcl3 expression to tubular cells in AKI. Transcriptomics database analysis revealed increased Bcl3 expression in numerous experimental and human kidney conditions. Furthermore, systemic TWEAK administration increased kidney Bcl3 expression. In cultured tubular cells, targeting Bcl3 by siRNA resulted in the magnification of TWEAK-induced NF-κB transcriptional activity, chemokine upregulation and Klotho downregulation, and in the sensitization to cell death induced by TWEAK/TNFα/interferon-γ. In contrast, Bcl3 overexpression decreased NF-κB transcriptional activity, inflammatory response and cell death while dampening the decrease in Klotho expression. In conclusion, Bcl3 expressed in response to TWEAK stimulation decreases TWEAK-induced inflammatory and lethal responses. Therefore, therapeutic upregulation of Bcl3 activity should be explored in kidney disease because it has advantages over chemical inhibitors of NF-κB that are known to prevent inflammatory responses but can also sensitize the cells to apoptosis.
Pleural effusion secondary to minoxidil in a peritoneal dialysis patient
Palomar, Rosa,Morales, Pedro,Sanz de Castro, Saturnino,Tasis, Ana,Rodrigo, Emilio,Piñ,era, Celestino,Ruiz, Juan Carlos,Ferná,ndez-Fresnedo, Gema,Martin de Francisco, Angel Luis,Arias, Manu Oxford University Press 2004 Nephrology, dialysis, transplantation Vol.19 No.10
Reactivity of hydroxyl radicals with neonicotinoid insecticides: mechanism and changes in toxicity
Dell'Arciprete, Maria L.,Santos-Juanes, Lucas,Sanz, Antonio Arques,Vicente, Rafael,Amat, Ana M.,Furlong, Jorge P.,Martirea, Daniel O.,Gonzalez, Monica C. Korean Society of Photoscience 2009 Photochemical & photobiological sciences Vol.8 No.7
The reactivity of hydroxyl radicals ($HO^{\cdot}$) towards three neonicotonoid insecticides, namely imidacloprid, thiacloprid and acetamiprid was investigated. These radicals were generated by photolysis of $H_2O_2$ solutions. Flash photolysis experiments were used to determine the rate constants of $5.5{\times}10^{10}M^{-1}s{-1}$, $6{\times}10^{10}M^{-1}s^{-1}$, and $7.5{\times}10^{10}M^{-1}s^{-1}$, for the reactions of $HO^{\cdot}$ with acetamiprid, imidacloprid, and thiacloprid, respectively. Continuous irradiation experiments in the absence and presence of $H_2O_2$ allowed the identification and toxicity evaluation of the primary photo- and oxidation products of the insecticides. In all cases, the less toxic 6-chloronicotinic acid was found to be the major product at higher degrees of oxidation. The results reported here indicate that the half life of the insecticides due to their reaction with $HO^{\cdot}$ radicals in natural aquatic reservoirs may vary between 5 h and 19 days, and therefore the hydroxyl radical-mediated oxidation may be a significant abiotic elimination route. However, elimination of the insecticide under such conditions might not improve the quality of the contaminated water, as the primary products of degradation still show considerable toxicity to Vibrio fischeri assays.