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An international consensus seems to have developed in educational research--and among educational planners and policymakers--during the last 10-15 years proclaiming that learning is, and must be, a visible phenomenon. This paper questions this predominant view and serves an assemblage of points offering educational scientists at least four profound perspectives to reflect upon. First of all, learning is not immediately visible to the learning subject. It demands and deserves a qualitative lifelong perspective and--not to be underestimated--autonomous reflections to come to know and acknowledge what learning is and can be in an existential perspective. For the individual, it is always worth asking the question whether or not the things 'learned' in the first place were worth learning. Secondly, no one can examine the complex synaptic wiring process in the changeable and 'learning' brain (i.e., human neuroplasticity); the body-phenomenological depths and growth of a human being; or the manifold processes constituting the totality of historical social interactions surrounding the learning process and reduce them to something simple and already 'known' (a figure, a score, an effect, an answer in a test, an evaluation statement, etc). Thirdly, so-called visible learning for teachers has to be differentiated from both conscious and unconscious learning for pupils and students. The attempts to objectify and sometimes even instrumentalize learning risk running into obvious problems and fostering serious mistakes. Besides, the teacher and the 'learner' do not share the same perspectives and they often also have different interests. Fourthly, the concept of learning is not a value-neutral term and should only be used with an awareness of its historical development as a concept. I will argue that character formation--edification of character ("Bildung"), in light of the rich German "geisteswissenschaftliche" tradition--and the capability to think and become a vivid language user and creator demand much more than learning. Moreover, teaching is much more than a method to 'produce' learning, and to reproduce learning goals, and the purpose of education must transcend a teleological implementation of strategic national and international learning goals. In this paper, the revitalized concept of "Bildung" both serves as a critique of the visible learning paradigm and as a take-off of an alternative and more fertile way to conceptualize the task and possibilities of education. The line of the argument and ambition of the paper is to depict how blindness seems to be an inevitable part of educational seeing. The thesis is that powerful scientific and political adherents of learning cannot see what they cannot see--neither when they see what they (think they) see, nor when they do not see what they do not (want to) see.

Adipose tissues, particularly beige and brown adipose tissue, play crucial roles in energy metabolism. Brown adipose tissues' thermogenic capacity and the appearance of beige cells within white adipose tissue have spurred interest in their metabolic impact and therapeutic potential. Brown and beige fat cells, activated by environmental factors like cold exposure or by pharmacology, share metabolic mechanisms that drive non-shivering thermogenesis. Understanding these two cell types requires advanced, yet broadly applicable in vitro models that reflect the complex microenvironment and vasculature of adipose tissues. Here we present mouse vascularized adipose spheroids of the stromal vascular microenvironment from inguinal white adipose tissue, a tissue with 'beiging' capacity in mice and humans. We show that adding a scaffold improves vascular sprouting, enhances spheroid growth, and upregulates adipogenic markers, thus reflecting increased adipocyte maturity. Transcriptional profiling via RNA sequencing revealed distinct metabolic pathways upregulated in our vascularized adipose spheroids, with increased expression of genes involved in glucose metabolism, lipid metabolism, and thermogenesis. Functional assessment demonstrated increased oxygen consumption in vascularized adipose spheroids compared to classical 2D cultures, which was enhanced by β-adrenergic receptor stimulation correlating with elevated b-adrenergic receptor expression. Moreover, stimulation with the naturally occurring adipokine, FGF21, induced Ucp1 mRNA expression in the vascularized adipose spheroids. In conclusion, vascularized inguinal white adipose tissue spheroids provide a physiologically relevant platform to study how the stromal vascular microenvironment shapes adipocyte responses and influence activated thermogenesis in beige adipocytes. [ABSTRACT FROM AUTHOR]

Insulin deficiency in type 1 diabetes (T1D) leads to an impairment of glucose metabolism and mitochondrial function. Actovegin is a hemodialysate of calf blood, which has been shown to enhance glucose uptake and cell metabolism in healthy human skeletal muscle. The objectives of this study were to determine the effects of Actovegin on skeletal muscle mitochondrial respiration and functional aerobic capacity in a T1D mouse model. Effects on the expression of mitochondrial proteins, body mass, and food and water consumption were also investigated. Streptozotocin-induced T1D male C57B1/6 mice (aged 3–4 months) were randomized to an Actovegin group and a control group. Every third day, the Actovegin and control groups were injected intraperitoneally with (0.1 mL) Actovegin and (0.1 mL) physiological salt solution, respectively. Oxidative phosphorylation (OXPHOS) capacity of the vastus lateralis muscle was measured by high resolution respirometry in addition to the expression levels of the mitochondrial complexes as well as voltage-dependent anion channel. Functional aerobic capacity was measured using a rodent treadmill protocol. Body mass and food and water consumption were also measured. After 13 days, in comparison to the control group, the Actovegin group demonstrated a significantly higher skeletal muscle mitochondrial respiratory capacity in an ADP-restricted and ADP-stimulated environment. The Actovegin group displayed a significantly lesser decline in functional aerobic capacity and baseline body mass after 13 days. There were no significant differences in food or water consumption between groups. Actovegin could act as an effective agent for facilitating glucose metabolism and improving OXPHOS capacity and functional aerobic capacity in T1D. Further investigation is warranted to establish Actovegin's potential as an alternative therapeutic drug for T1D. [ABSTRACT FROM AUTHOR]

Background The aim of this study was to investigate the effect of prolonged endurance exercise on adipose tissue inflammation markers and mitochondrial respiration in younger and older men. Methods "Young" (aged 30 years, n = 7) and "old" (aged 65 years, n = 7) trained men were exposed to an exercise intervention of 15 consecutive days biking 7 to 9 hours/day at 63% and 65% of maximal heart rate (young and old, respectively), going from Copenhagen, Denmark to Palermo, Italy. Adipose tissue was sampled from both the gluteal and abdominal depot before and after the intervention. Mitochondrial respiration was measured by high-resolution respirometry, and adipose inflammation was assessed by immunohistochemical staining of paraffin embedded sections. Results An increased number of CD163+ macrophages was observed in both the gluteal and abdominal depot (P <.01). In addition, an increased mitochondrial respiration was observed in the abdominal adipose tissue from men in the young group with complex I (CI p) stimulated respiration, complex I + II (CI+II p) stimulated respiration and the capacity of the electron transport system (ETS) (P <.05), and in the older group an increase in CIp and CI+II p stimulated respiration (P <.05) was found. Conclusion Overall, we found a positive effect of prolonged endurance exercise on adipose tissue inflammation markers and mitochondrial respiration in both young and old trained men, and no sign of attenuated function in adipose tissue with age. [ABSTRACT FROM AUTHOR]