EXCLI Journal最新文献

In recent years, the concept of self-efficacy has garnered attention in educational psychology research on motivation. Within an academic context, academic self-efficacy (ASE) reflects learners' belief in their ability to achieve educational goals. However, most research has focused on traditional face-to-face classroom settings, with little exploration in distance learning environments like online and e-learning. The current review aims to update a previous study (Yokoyama, 2019[40]) and examine differences in online learning types: asynchronous, synchronous, and blended learning. The study's findings reveal that in mixed environments combining synchronous and asynchronous elements, or in blended settings merging face-to-face classes with asynchronous learning, ASE positively impacts academic performance akin to traditional face-to-face classes. However, in asynchronous online learning environments, ASE's influence on academic performance might be slightly weaker compared to synchronous learning environments. The paper will subsequently discuss the pedagogical implications derived from these results.

Type 2 diabetes (T2D) significantly increases the risk of vascular complications (12-32 %), which are a major cause of death (over 50 %) in T2D patients. In T2D, both endothelial (ET) and vascular smooth muscle (VSM) cells are impaired, which act as independent risk factors for cardiovascular disease. Thus, the question of this systematic review and meta-analysis is: Do ET-dependent and -independent VSM relaxation impair in T2D? We systematically searched PubMed and Scopus databases until March 2024; 44 eligible clinical trial studies (68, 16, 30, and 50 study arms for acetylcholine (ACh), methacholine (MTH), sodium nitroprusside (SNP), and glyceryl trinitrate (GTN)) published were included. ET-dependent VSM relaxation in response to ACh (overall ES = -28.9 %, 95 % CI: -35.2, -22.7; p<0.001) and MTH (overall ES = -55.3 %, 95 % CI: -63.6, -47.1; p<0.001) decreased in T2D patients compared to controls. ET-independent VSM relaxation in response to SNP (overall ES = -17.2 %, 95 % CI: -35.2, -22.7; p<0.001) and GTN (overall ES = -63.2 %, 95 % CI: -81.0, -45.5; p<0.001) decreased in T2D patients compared to controls. Our meta-analysis showed reductions in both ET-dependent (~40 %) and ET-independent (~25 %) VSM relaxation. The decrease was more pronounced for MTH (~55 %) compared to ACh (~30 %) and for GTN (~63 %) compared to SNP (~17 %). These findings suggest that dysfunction of both ET and VSM contributes to impaired VSM relaxation in T2D patients. See also the graphical abstract(Fig. 1).

Clusterin is a ubiquitously expressed glycoprotein that is involved in a whole range of biological processes. This protein is known to promote tumor survival and resistance to therapy in cancer, which contrasts sharply with its neuroprotective functions in various neurological diseases. This duality has led to recent investigations into the potential therapeutic applications of clusterin inhibition, particularly in cancer treatment. Inhibition of clusterin has been shown to be able to induce cancer cell senescence, suppress their growth and increase their sensitivity to therapy. The involvement of clusterin in the aging process makes its biological effects even more complex and offers a broad perspective for research and therapeutic exploration of various pathological conditions. This review critically examines the multiple functions of clusterin in cancer and neurological disorders and addresses the controversies surrounding its role in these areas. The assessment includes an in-depth analysis of the existing literature and examining the relationship of clusterin to fundamental aspects of cancer progression, including cell proliferation, apoptosis, metastasis, and drug resistance. In addition, the review addresses the neurobiological implications of clusterin and examines its controversial role in neuroprotection, neurodegeneration, and synaptic plasticity. Attention is also paid to the epigenetic regulation of clusterin expression. By clarifying conflicting findings and discrepancies in the literature, this review aims to provide a nuanced understanding of the molecular mechanisms underlying clusterin functions and its potential clinical implications in both cancer and neurodisorders. See also the graphical abstract(Fig. 1).

The coexistence within a subcellular complex of inter-cellular proteins Ro60, responsible for preserving ncRNA quality, and Ro52, involved in intracellular proteolysis, has been a subject of ongoing debate. Employing molecular docking in tandem with experimental methods like Quartz Crystal Microbalance with Dissipation (QCM-D), Proximity Ligation Assay (PLA), and Indirect Immunofluorescence (IIF), we reveal the presence of Ro60 associating with Ro52 within the cytoplasm. This result unveils the formation of a weak transient complex with a K_a ≈ (3.7 ± 0.3) x 10⁶ M^-1, where the toroid-shaped Ro60 structure interacts with the Ro52's Fc receptor, aligning horizontally within the PRY-SPRY domains of the Ro52's homodimer. The stability of this complex relies on the interaction between Ro52 chain A and specific Ro60 residues, such as K133, W177, or L185, vital in the Ro60-YRNA bond. These findings bridge the role of Ro60 in YRNA management with Ro52's function in intracellular proteolysis, emphasizing the potential impact of transient complexes on cellular pathways. See also the graphical abstract(Fig. 1).

A major characteristic of cancer is dysregulated cell division, which results in aberrant growth of cells. Consequently, medicinal targets that prevent cell division would be useful in the fight against cancer. The primary regulator of proliferation is a complex consisting of cyclin and cyclin-dependent kinases (CDKs). The FDA has granted approval for CDK inhibitors (CDKIs) to treat metastatic hormone receptor-positive breast cancer. Specifically, CDK4/6 CDKIs block the enzyme activity of CDK4 and CDK6. Unfortunately, the majority of first-generation CDK inhibitors, also known as pan-CDK inhibitors because they target multiple CDKs, have not been authorized for clinical use owing to their serious side effects and lack of selection. In contrast to this, significant advancements have been created to permit the use of pan-CDK inhibitors in therapeutic settings. Notably, the toxicity and negative consequences of pan-CDK inhibitors have been lessened in recent years thanks to the emergence of combination therapy tactics. Therefore, pan-CDK inhibitors have renewed promise for clinical use when used in a combination regimen. The members of the CDK family have been reviewed and their primary roles in cell cycle regulation were covered in this review. Next, we provided an overview of the state of studies on CDK inhibitors.

Mushroom consumption is a worldwide custom that continues to grow in popularity. On the other hand, foraging for wild mushrooms can lead to serious disease and even death if deadly mushrooms are accidentally consumed. Mushroom poisoning is difficult to diagnose and treat since the symptoms are similar to those of other disorders. In terms of chemistry, mushroom poisoning is associated with extraordinarily strong toxins, meaning that isolating and identifying toxins has substantial scientific relevance, especially in understanding the lethal components of toxic mushrooms. Most of these toxins exhibit exceptional physiological features that might help enhance chemistry, biochemistry, physiology, and pharmacology research. Despite the discovery of more than 100 poisons, several dangerous mushrooms remain unexplored. This review covers the chemistry (including chemical structures, complete synthesis, and biosynthesis), as well as the toxicology, namely the toxicokinetics, mechanisms of toxicology, and clinical toxicology of these poisons, in addition to the discussion of the development of their most effective diagnostic and therapeutic strategies with the hopes of spurring additional studies, focusing on individual classes of toxins found in poisonous mushrooms such as amatoxins, gyromitrin, orellanine, and phallatoxins. See also the graphical abstract(Fig. 1).