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BACKGROUND: Physiology is a subject that is considered difficult; it is associated with academic failure and causes high levels of stress and anxiety in students. METHODS: This study compared the effectiveness of a traditional lecture-based methodology with that of a flipped classroom scheme focusing on cooperative ludic learning among gastrointestinal and renal physiology students. Two groups were subjected to these two different methods to teach gastrointestinal and renal physiology content divided into 14 topics. Additionally, two subgroups were identified in each group: entrants and repeaters. There were no differences in age or gender between the subgroups. RESULTS: Levels of self-perceived stress (measured by the SISCO scale), biological stress (measured by awakening salivary cortisol levels), and anxiety (measured by the Zung scale) were high in all of the students; the cortisol levels increased in the entrants and some of the scores in SISCO scale increased in the repeaters, throughout the study. The self-reported study time was longer in the students subjected to the flipped classroom-based method. The final exam results were better only in the new students facing the flipped methodology, but not in the repeaters, who scored lower on the final evaluation. The quantitative and qualitative assessments completed by the participants regarding the different aspects of the flipped-classroom-based methodology were favorable; however, the participants believed that traditional lectures should be maintained for specific topics. CONCLUSIONS: A methodology based on flipped teaching was an effective strategy to improve academic performance ingastrointestinal and renal physiology, but only in new students.

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OBJECTIVE: To evaluate the effects of adipokines and insulin on intracellular calcium concentration ([Ca(2+)]i) and pH (pHi) in human articular chondrocytes from healthy (CHC) and osteoarthritic cartilage (COC). DESIGN: pHi and [Ca(2+)]i were measured using BCECF and Fura-2 fluorometric probes in CHC and COC under control conditions and following a hypotonic shock. The effects of interleukin-1ß (IL1ß), tumor necrosis factor-α (TNFα), insulin, leptin, resistin, and adiponectin were assessed. RESULTS: pHi was lower in COC than in CHC. Only IL1ß ß decreased pHi in both cell types; all the agents enhanced pHi recovery following an ammonium prepulse in CHC, effect that was attenuated by Na(+)-H(+) exchanger inhibitors, but they had no effect in COC. Hypotonic shock (HTS) caused a pHi increase, which was significantly smaller in COC. All the hormones attenuated this response and the effect of IL1ß was greater. The basal [Ca(2+)]i was similar in COC and CHC; IL1ß, TNFα, and insulin increased the [Ca(2+)]i, but leptin, resistin, and adiponectin did not. These effects were greater in COC. This [Ca(2+)]i increase was dependent on extracellular Ca(2+) and attenuated by Na(+)-Ca(2+) exchanger inhibitors. HTS caused a [Ca(2+)]i increase, which was inhibited by transient receptor potential vanilloid blockers and attenuated by all the hormones tested with the exception of adiponectin. CONCLUSIONS: These findings may help explain the association between obesity and osteoarthritis, in which these hormones are altered. The responses of CHC and COC are different, which suggests that a modification of pH and Ca(2+) homeostasis is part of the osteoarthritis pathophysiology.

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Chondrocytes, the only cell in cartilage, are subjected to hyperosmotic challenges continuously since extracellular osmolarity in articular cartilage increases in response to mechanical loads during joint movement. Hyperosmolarity can affect membrane transport, and it is possible that load modulates matrix synthesis through alterations in intracellular composition. In the present study, the effects of hyperosmotic challenges were evaluated using the whole-cell patch clamp technique, whole cell mode on freshly isolated human and bovine articular chondrocytes. In human chondrocytes, hypertonicity induced the activation of outward Ca(2+)-sensitive K(+) currents, which were inhibited by iberiotoxin and TEA-Cl. The current induced by hypertonic switching (osmolarity from 300 to 400 mOsm/l) caused cell hyperpolarization (from -39 mV to -70 mV) with a reversal potential of -96 ± 7 mV. These results suggest a role for Ca(2+)-activated K(+) channels in human articular chondrocytes, leading to hyperpolarization as a consequence of K(+) efflux through these channels. These channels could have a role in the articular chondrocyte's response to a hyperosmotic challenge and matrix metabolism regulation by load.

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The Na(+)/Ca(2+) exchanger (NCX) is an important bidirectional transporter of calcium in neurons and has been shown to be involved in neuroprotection. Calcium can activate a number of cascades that can result in apoptosis and cell death, and NCX is a key factor in regulating the cytoplasmic concentration of this ion. 17-ß-estradiol and insulin-like growth factor 1 (IGF-1) are known neuroprotective hormones with interacting mechanisms and effects on intracellular calcium; however, their relationship with the NCX has not been explored. In this article, the effects of these two hormones on neuronal NCX were tested using the whole-cell patch clamp technique on rat primary culture neurons. Both 17-ß-estradiol and IGF-1 produced an increase in the NCX-mediated inward current and a decrease in the NCX-mediated outward current. However, the IGF-1 effect was lower than that of 17-ß-estradiol, and the effect of both agents together was greater than the sum of each agent alone. Neither of the agents affected the pattern of regulation by extracellular or intrapipette calcium. Inhibitors of the IGF-1 and 17-ß-estradiol receptors and inhibitors of the main signaling pathways failed to change the observed effects, indicating that these actions were not mediated by the classical receptors of these hormones. These effects on the NCX could be a mechanism explaining the neuroprotective actions of 17-ß-estradiol and IGF-1, and these findings could help researchers to understand the role of the NCX in neuroprotection.

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Changes in external osmolarity arise from variations in mechanical loads on joints and may affect the homeostasis of chondrocytes, which are the only cell type responsible for matrix turnover. Accordingly, variations in membrane potential may affect cartilage production. The present study assessed the effects of variations in external osmolarity on membrane potential and the possible mechanisms responsible for this response. Membrane potential was measured by the patch clamp whole-cell technique using human articular chondrocytes freshly isolated from healthy and osteoarthritic cartilage. The membrane potential was -39±4 mV in articular human chondrocytes from healthy cartilage and -26±4 mV in those from osteoarthritic cartilage. Increasing the osmolarity produced a reversible hyperpolarization mediated by K+ efflux through BKCa channels in both groups of chondrocytes, but the response in osteoarthritic cells was significantly reduced; no other K+ pathways were involved in this effect. Alternatively, decreasing the osmolarity elicited depolarization in healthy chondrocytes but did not produce any response in chondrocytes from osteoarthritic cartilage. The depolarization was dependent on Na+ influx through Gd3+-sensitive stretch-activated cation channels and was independent of external Ca2+. The differential responses observed in chondrocytes from osteoarthritic cartilage suggest that disregulation on the responses to external osmolarity may be involved in the process that leads to the alterations in the cartilage structure observed in osteoarthritis.

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