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De-schooling Well-being: Toward a Learning-Oriented Definition

ECnU Review of Education 2020年第3期3卷 452-469页

作者： santiago rincòn-gallardo Michael Fullan’s Consulting Team

Purpose:(1)Critique conventional schooling as detrimental to student well-being and learning.(2)Articulate an alternative that is more conducive to learning and well-being in classrooms,schools,and educational systems.Design/Approach/Methods:I review the historical functions of compulsory schooling,the main critiques to conventional schooling developed over the past century,emerging knowledge on the neuroscience of learning and well-being,and cases of large-scale pedagogical transformation from the Global South.Findings:I argue that conventional schooling is detrimental to well-being,that deep learning is a precursor of well-being,and that compulsory schooling is not designed to cultivate it.Well-being has to be de-schooled so that students thrive in schools:The grammar of schooling has to be replaced with the language of learning.This requires deep and widespread cultural change,and some movements of pedagogical renewal from the Global South offer important lessons on how to accomplish this.Originality/Value:Expanding the scope of existing debates about student well-being by questioning the assumption that compulsory schooling is inherently good and pointing out that unless the default culture of schooling is replaced with cultures of robust learning,student well-being efforts will simply reproduce the very problems they seek to solve.

关键词： Cultural change educational change learning schooling student well-being

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Influence of Angiotensin II on α₁-Adrenergic Receptors Function in Rat Aorta and Expression in Vascular Smooth Muscle Cells

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Journal of Biosciences and Medicines 2024年第4期12卷 123-134页

作者： Itzell Alejandrina gallardo-Ortíz Juan Pablo de Jesús Benítez-Garrido santiago C. Sigrist-Flores Juan Javier López-Guerrero Enrique Hong Rafael Villalobos-Molina Unidad de Biomedicina Facultad de Estudios Superiores Iztacala Universidad Nacional Aut&#243noma de M&#233xico Tlalnepantla M&#233xico Carrera de Enfermerí a Facultad de Estudios Superiores Iztacala Universidad Nacional Aut&#243noma de M&#233xico Tlalnepantla M&#233xico Departamento de Farmacobiologí a Centro de Investigaci&#243n and de Estudios Avanzados-IPN Ciudad de M&#233xico M&#233xico Carrera de Mé dico Cirujano Facultad de Estudios Superiores Iztacala Universidad Nacional Aut&#243noma de M&#233xico Tlalnepantla M&#233xico

Angiotensin II (Ang II) is the main mediator of the Renin-Angiotensin-System acting on AT1 and other AT receptors. It is regarded as a pleiotropic agent that induces many actions, including functioning as a growth factor, and as a contractile hormone, among others. The aim of this work was to examine the impact of Ang II on the expression and function of α1-adrenergic receptors (α1-ARs) in cultured rat aorta, and aorta-derived smooth muscle cells. Isolated Wistar rat aorta was incubated for 24 h in DMEM at 37˚C, then subjected to isometric tension and to the action of added norepinephrine, in concentration-response curves. Ang II was added (1 × 10−5 M), and in some experiments, 5-Methylurapidil (α1A-AR antagonist), AH11110A (α1B-AR antagonist), or BMY-7378 (α1D-AR antagonist), were used to identify the α1-AR involved in the response. Desensitization of the contractile response to norepinephrine was observed due to incubation time, and by the Ang II action. α1D-AR was protected from desensitization by BMY-7378;while RS-100329 and prazosin partially mitigated desensitization. In another set of experiments, isolated aorta-derived smooth muscle cells were exposed to Ang II and α1-ARs proteins were evaluated. α1D-AR increased at 30 and 60 min post Ang II exposure, the α1A-AR diminished from 1 to 4 h, while α1B-AR remained unchanged over 24 h of Ang II exposure. Ang II induced an increase of α1D-AR at short times, and BMY-7378 protected α1D-AR from desensitization.

关键词： Angiotensin II α1D-AR α1-AR Expression Rat aorta Smooth Muscle Cells

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A decrease of docosahexaenoic acid in testes of mice fed a high-fat diet is associated with impaired sperm acrosome reaction and fertility

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Asian Journal of Andrology 2021年第3期23卷 306-313页

作者： Julio Bunay Luz-Maria gallardo Jorge Luis Torres-Fuentes M Veronica Aguirre-Arias Renan Orellana nestor Sepulveda Ricardo D Moreno Physiology Department Faculty of Biological SciencesPontificia Universidad Cat6lica de Chile(PUC)Santiago 8331150Chile Department of Chemistry and Biological Sciences Health Sciences FacultyUniversidad Bernardo 0 HigginsSantiago 8370854Chile Center of Excellence in Biotechnology of Reproduction Universidad de la FronteraTemuco 4780000Chile.

Obesity is a major worldwide health problem that is related to most chronic diseases,including male infertility.Owing to its wide impact on health,mechanisms underlying obesity-related infertility remain unknown.In this study,we report that mice fed a high-fat diet(HFD)for over 2 months showed reduced fertility rates and increased germ cell apoptosis,seminiferous tubule degeneration,and decreased intratesticular estradiol(E2)and E2-to-testosterone ratio.Interestingly,we also detected a decrease in testicular fatty acid levels,behenic acid(C22:0),and docosahexaenoic acid(DHA,22:6n-3),which may be related to the production of dysfunctional spermatozoa.Overall,we did not detect any changes in the frequency of seminiferous tubule stages,sperm count,or rate of in vitro capacitation.However,there was an increase in spontaneous and progesterone-induced acrosomal exocytosis(acrosome reaction)in spermatozoa from HFD-fed mice.These data suggest that a decrease in E2 and fatty acid levels influences spermatogenesis and some steps of acrosome biogenesis that will have consequences for fertilization.Thus,our results add new evidence about the adverse effect of obesity in male reproduction and suggest that the acrosomal reaction can also be affected under this condition.

关键词： cholesterol estradiol fat acid testis testosterone

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Endogenous norepinephrine Desensitizes α_1D-Adrenoceptors in Cultured Rat Aorta

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生物科学与医学(英文) 2023年第10期11卷 168-180页

作者： Itzell Alejandrina gallardo-Ortíz Jesús David Gómez-Rodríguez Juan Javier López-Guerrero santiago C. Sigrist-Flores Rafael Villalobos-Molina Unidad de Biomedicina Facultad de Estudios Superiores Iztacala Universidad Nacional Autónoma de México Tlalnepantla México Carrera de Enfermería Facultad de Estudios Superiores Iztacala Universidad Nacional Autónoma de México Tlalnepantla México Ciencias de la Salud Unidad Xochimilco Universidad Autónoma Metropolitana Ciudad de México México Carrera de Médico Cirujano Facultad de Estudios Superiores Iztacala Universidad Nacional Autónoma de México Tlalnepantla México

Desensitization is a process characterized by the loss of cellular response to an agonist when this is present for a long time. α1D-adrenergic receptor (α1D-AR) desensitization is important since this receptor is involved in the contraction of large caliber arteries, such as the aorta. The aim of this research was to evaluate the desensitization of α1D-AR due to the endogenous release of norepinephrine in cultured rat aorta. Wistar rat aorta was incubated for 2 h or 24 h in DMEM at 37°C, and then subjected to isometric tension and the action of added norepinephrine, in concentration-response curve (CRC). In some experiments, BMY-7378 (α1D-AR antagonist) or 5-methylurapidil (α1A-AR antagonist) was used to identify the α1-AR involved in the response, or BMY-7378 to protect the α1D-AR from desensitization. Results showed that α1D-AR was desensitized when the aorta was incubated for 24 h, since the CRC to exogenous norepinephrine showed lower maximal contraction and the curve was displaced to the right, indicating that the receptor involved in contraction was not the α1D-AR, as compared to the aorta incubated 2 h. The receptor stimulated by norepinephrine at 24 h was neither the α1A-AR, as shown by the lack of displacement of the curve by 5-methylurapidil, but rather it seems that α1B-AR is inducing contraction. When the aorta was incubated with BMY-7378 for 24 h, the α1D-AR antagonist protected the receptor from desensitization. Endogenous norepinephrine desensitizes α1D-AR in the cultured aorta, and the α1D-AR is protected by BMY-7378.

关键词： Desensitization norepinephrine α1D-Adrenergic Receptor BMY-7378 Rat Aorta

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