Mathematics plays a leading part in day-to-day life and has enhanced a necessary component for human accomplishments. Students from many countries do not reach the expected level in mathematics. Therefore, it is essential to pay close consideration to the causes related to ability in mathematics. Mathematics attitude is considered as one of the critical variables in the process of mathematics learning. This study aimed to determine students’ attitudes and achievements through problem-based learning in mathematics. The selected study group contained 600 students and 35 teachers from rural public secondary schools in District Rawalpindi, Pakistan. The data collection was done using questionnaires from students and teachers and collected data analyzed by SPSS 23 and Amos 23. This study’s result was carried out using Partial Least square structural equation Model (PLS-SEM), descriptive analysis, and hypotheses testing. The outcomes in this study indicated that the mean fluctuated between 1 to 4.5, 3.71 to 4.20, and Std. Deviation fluctuated between 0.6 to 2.0 and 0.75 to 1.55 in the students and teacher models, respectively. The results of the PLS-SEM students’ model show a negative attitude towards mathematics. The teachers’ PLS-SEM model showed the Effects of using problem-based learning (PBL) on students’ achievements. According to the hypotheses testing, the acceptance of hypotheses by stating that the Confidence in Learning Mathematics Scale (C), Value of Mathematics Scale (V), and Student Mathematics Motivation Scale (M) are significant effects for the Students’ Attitude Toward Problem-Based Learning (ATPBL). But the Attitude Toward Enjoyment in Mathematics Scale (AE) was rejected, and it did not significantly affect the ATPBL. As well as, the Problem-solving learning and students’ achievement (PLA), Advantages of problem-solving learning (APL) and Difficulties in using problem-solving learning (DPL) have a significant positive effect on the ATPBL. Finally, this study suggested that teachers also adopt new teaching methods corresponding to mathematics, and there is a need to explore particular mathematics skills to enhance students’ learning abilities.

Seizures induce the release of excitatory amino acids (EAAs) from the intracellular fluid to the extracellular fluid, and the released EAAs primarily comprise glutamic acid (Glu) and asparaginic acid (Asp). Glu neurotransmission functions via EAA transporters (EAATs) to maintain low concentrations of Glu in the extracellular space and avoid excitotoxicity. EAAT2, the most abundant Glu transporter subtype in the central nervous system (CNS), plays a key role in the regulation of glutamate transmission. Previous studies have shown that SB203580 promotes EAAT2 expression by inhibiting the p38 mitogen-activated protein kinase (MAPK) signaling pathway, but whether SB203580 upregulates EAAT2 expression in epileptic rats is unknown. This study demonstrated that EAAT2 expression was increased in the brain tissue of epileptic rats. Intraperitoneal injection of a specific inhibitor of p38 MAPK, SB203580, reduced the time to the first epileptic seizure and attenuated the seizure severity. In addition, SB203580 treatment increased the EAAT2 expression levels in the brain tissue of epileptic rats. These results suggest that SB203580 could regulate epileptic seizures via EAAT2.

Ischemic stroke is a common disease of the central nervous system, and ischemic brain injury (IBI) is its main manifestation. Recently, extracellular vesicles (EVs) have been strongly related to the diagnosis and treatment of IBI. However, the underlying mechanism of their effects remains enigmatic. In the present study, we aimed to study how miR‐155‐5p plays a role in choroid plexus epithelial (CPE) cell‐derived EVs in IBI pathology. We found that miR‐155‐5p expression was enriched in CPE cell‐derived EVs, which were subsequently internalized by neurons, enabling the delivery of miR‐155‐5p into neurons. An inducible oxygen and glucose deprivation and reoxygenation (OGD/R) cell model was developed to mimic ischemic neuronal injury in vitro. miR‐155‐5p overexpression led to reduced neuron viability, promoted apoptosis, elevated autophagic proteins’ expression, and activated NLR family pyrin domain‐containing 3‐ (NLRP3‐) related inflammasomes, thereby aggravating OGD‐induced neuronal injury. A dual‐luciferase reporter assay exhibited that miR‐155‐5p could inhibit the Ras homolog enriched in brain (Rheb) expression, a mechanism critical for miR‐155‐5p‐mediated neuronal injury. Furthermore, a mouse IBI model was developed using the transient middle cerebral artery occlusion (tMCAO) method. Animal experiments verified that miR‐155p delivery via CPE cell‐derived EVs aggravated IBI by suppressing Rheb expression. In conclusion, miR‐155‐5p in CPE‐derived EVs can aggravate IBI pathology by suppressing Rheb expression and promoting NLRP3‐mediated inflammasomes, suggesting its role as a potential therapeutic target in IBI.

Endometrial cancer (EC) is a common malignant tumor in the female reproductive system. Circular RNAs (circRNAs) and N6-methyladenosine (m6A) modification are widely involved in cancer progression. Nevertheless, the cross-talk between circ-NAB1 and m6A as well as the biological functions of circ-NAB1 in EC remain unclear. Circ-NAB1 was observed to be upregulated in EC tissues and cells by RT-qPCR. MeRIP and RNA pull-down assays were utilized for detecting the m6A modification of circ-NAB1. The interaction between circ-NAB1 and RNAs was also detected. Colony formation, transwell, flow cytometry, and western blot were utilized for measuring EC cell behaviors. Mechanically, we proved the m6A demethylase alkylation repair homolog protein 5 (ALKBH5) can mediate circ-NAB1 expression through an m6A-YTHDF2-dependent manner. Circ-NAB1 overexpression can promote cell proliferation, migration, invasion, epithelial-mesenchymal transition (EMT) process, and cell cycle through functional assays. Circ-NAB1 knockdown exerts the opposite function on EC cells. Furthermore, we proved that circ-NAB1 can sponge miR-876-3p to upregulate the target gene cyclin-dependent kinase inhibitor 3 (CDKN3) in EC cells. CDKN3 overexpression can reverse the impacts of circ-NAB1 depletion on EC cell behaviors. Collectively, we proved that ALKBH5-mediated m6A modification of circ-NAB1 promoted EMT process and cell cycle in EC via targeting the miR-876-3p/CDKN3 axis.

Background: Hemorrhagic transformation (HT) after endovascular treatment (EVT) for acute ischemic stroke (AIS) remains a major clinical challenge, particularly in populations vulnerable to vascular and endothelial injury. Beyond conventional clinical predictors, microcirculatory dysfunction and blood–brain barrier (BBB) vulnerability may critically influence the risk of hemorrhagic complications following reperfusion. However, existing prediction models often rely on isolated imaging markers or basic clinical variables, failing to capture the integrated pathophysiological processes linking collateral circulation, microvascular perfusion, and BBB integrity. Methods: This retrospective study analyzed 202 consecutive AIS patients undergoing EVT (2021–2024). Collateral circulation was assessed via ASITN/SIR scale; CT perfusion (CTP)-derived parameters (rCBF, rCBV, rMTT, rTTP, rPS) quantified microcirculation and BBB integrity. Clinical/laboratory variables (including serum globulin) were collected. Multivariate logistic regression identified HT/parenchymal hematoma (PH) predictors; a nomogram was validated via ROC, calibration, bootstrap, DCA, and CIC. HT subtypes were correlated with functional outcomes. Results: HT occurred in 82 patients (40.6%, 37 PH cases). Higher ASITN/SIR grade (OR = 0.616), rCBF (OR = 0.053), and rCBV (OR = 0.204) were protective; rPS (OR = 2.624) and serum globulin (OR = 1.138) were risk factors for HT. The multimodal model (integrating three mechanistic pathways) showed excellent discrimination (AUC = 0.867) and superior net clinical benefit. For PH, ASITN/SIR was protective (AUC = 0.745). HT patients had poorer outcomes ( p < 0.001), with PH worse than HI ( p = 0.046). Conclusion: This study demonstrates that BBB vulnerability, microcirculatory dysfunction, and collateral status are key determinants of hemorrhagic transformation after endovascular treatment in acute ischemic stroke. By integrating these interrelated vascular and endothelial mechanisms, the proposed model provides insight into susceptibility to reperfusion-related hemorrhagic injury and offers a practical framework for individualized risk stratification in the peri-procedural setting.

Background: Olfactory dysfunction is frequently observed in patients with multiple sclerosis (MS); however, its underlying mechanisms remain poorly understood. To date, no studies have directly examined the nasal mucosal microbiota in MS. This study aimed to explore potential relationships among olfactory function, nasal microbiota composition, and superior turbinate volume in MS.Methods: This single‐center observational study included 42 patients with MS and 37 healthy controls (HC) in China. Olfactory function was evaluated using the University of Pennsylvania Smell Identification Test (UPSIT). Deep nasal microbiota profiles and MRI‐based measurements of superior turbinate volume were analyzed.Results: A reduced relative abundance of Prevotella buccalis (P. buccalis) was observed in MS with lower UPSIT scores (p = 0.030). In HC, a positive correlation was found between UPSIT scores and the superior turbinate volume (R_p = 0.329, p = 0.041), whereas no such correlation was observed in MS (R_s = −0.022, p = 0.625), suggesting a dissociation between olfactory performance and turbinate morphology in MS. Additionally, in MS, superior turbinate volume showed negative correlations with several genera, including Cupriavidus, Methylobacterium‐Methylorubrum, Ideonella, and Acinetobacter (all p < 0.05), indicating potential associations between mucosal structure and microbial composition.Discussion: These preliminary findings suggest that alterations in nasal microbiota may be linked to olfactory impairment and mucosal structural changes in MS. While P. buccalis emerged as a potential microbial correlate of olfactory dysfunction, its role remains unclear and may reflect secondary ecological shifts. Further mechanistic studies and larger cohorts are needed to determine causality and assess the diagnostic or therapeutic value of nasal microbiome features in MS.