Nursing education has undergone a significant transformation as a result of artificial intelligence (AI). Chatbots, specifically ChatGPT, have emerged as vital AI technologies within the nursing domain as it is a computer program designed to simulate human conversation through text or voice interactions. This study aims to conduct a bibliometric analysis to gain insights into the publication trends, citation impact, and thematic evolution in nursing education and practice concerning ChatGPT and chatbots. A comprehensive bibliometric analysis was performed using VOSViewer, concentrating on citation networks for data analysis and visualisation. A review of LENS.org identified 344 relevant research publications regarding chatbots and ChatGPT within the nursing discipline, all of which were utilised in the study. The study examined various aspects, including types of publications, prominent authors, leading journals, participating nations, institutions, and the impact of ChatGPT on nursing practice. The primary objectives included categorising the papers, identifying the most influential authors, delineating the prominent areas and institutions in the field, and examining the impact of ChatGPT on nursing education and practice. The findings indicate that ChatGPT positively impacts nursing education by enhancing learning experiences, improving communication, and aiding clinical decision-making. The findings indicate that journal articles accounted for 76% of publications, with the U.S. leading in research output. The findings indicate that ChatGPT positively impacts nursing education by enhancing learning experiences, improving communication, and aiding clinical decision-making. Future research should focus on establishing frameworks for integrating ChatGPT into nursing education, addressing ethical implications, and assessing the long-term impacts on patient care.

Metabolic dysfunction-associated steatotic liver disease (MASLD) has become the most prevalent chronic liver disease worldwide, affecting approximately 32%-38% of the adult population and posing a growing public health burden. MASLD represents a continuous disease spectrum ranging from simple steatosis to metabolic dysfunction-associated steatohepatitis (MASH), progressive hepatic fibrosis, cirrhosis, and ultimately hepatocellular carcinoma (HCC). The pathological core of MASLD lies in disruption of hepatic lipid metabolic homeostasis, characterized by an imbalance among de novo lipogenesis, fatty acid β-oxidation, and very-low-density lipoprotein (VLDL)-mediated lipid export. This metabolic disequilibrium subsequently drives inflammatory injury and fibrotic progression. Among the multiple regulatory pathways involved, thyroid hormone (TH) signaling has emerged as a central regulator of hepatic metabolic homeostasis. The liver is a major peripheral target organ of TH action, where TH predominantly exerts its metabolic effects through thyroid hormone receptor β (TRβ). Large-scale epidemiological studies and meta-analyses have demonstrated that hypothyroidism is significantly associated with increased MASLD prevalence, more severe histological injury, and advanced hepatic fibrosis, suggesting that dysregulation of TH signaling may participate throughout the entire MASLD disease spectrum. At the molecular level, TH regulates hepatic lipid metabolism by coordinating suppression of lipogenesis, enhancement of mitochondrial fatty acid oxidation, and promotion of VLDL assembly and secretion through integrated genomic actions of the T3-TRβ axis and non-genomic signaling pathways. Across different stages of MASLD, TH signaling exerts stage-dependent protective effects. In the steatosis stage, TH improves metabolic flexibility by modulating insulin sensitivity, glucose metabolism, and lipid droplet clearance, thereby alleviating early lipotoxic stress. During progression to MASH, TH attenuates inflammatory amplification by improving mitochondrial homeostasis, suppressing activation of the NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, and modulating the gut-liver axis microenvironment. In advanced stages, TH signaling influences hepatic stellate cell activation and extracellular matrix deposition, partly through interaction with the transforming growth factor-β (TGF-β)/SMAD pathway, while alterations in intrahepatic TH availability, mediated by dynamic changes in iodothyronine deiodinase 1 (DIO1), contribute to fibrosis progression and hepatocellular dedifferentiation. In hepatocellular carcinoma, coordinated downregulation of TRβ and DIO1 establishes a tumor-associated hypothyroid state that promotes metabolic reprogramming and tumor progression. The clinical relevance of TH signaling in MASLD has been underscored by the recent approval of Resmetirom, a liver-targeted TRβ‑selective agonist, for the treatment of non-cirrhotic MASH with moderate-to-severe fibrosis (F2-F3). This approval represents a landmark transition from mechanistic understanding to metabolism-centered precision therapy in MASLD. Clinical trials have demonstrated that Resmetirom not only improves key histological endpoints, including MASH resolution and fibrosis regression, but also favorably modulates atherogenic lipid profiles, highlighting the therapeutic potential of selectively targeting hepatic TH pathways. This review systematically summarizes the multidimensional regulatory roles of TH across the MASLD disease spectrum and discusses emerging diagnostic and therapeutic implications of TH-based interventions, aiming to inform future mechanistic research and optimize clinical management strategies.

Background: and Purpose The pathogenesis of neurovascular diseases and various types of dementia is tightly connected to cerebral circulation. An area that requires further exploration is the system of deep cerebral perforating arteries—arteries branching directly from high-pressure intracranial arteries, supplying vital neural structures such as the internal capsule, and characterized by a diameter of well below 1 mm, which makes them difficult to visualize with standard radiological examinations. This study aimed to analyze the morphology of the perforator origins, which constitute connection points between high-pressure intracranial arteries and microcirculation. Methods: Twenty-three human basal ganglia specimens with the middle cerebral artery (MCA, including 172 perforating arteries) and ten brainstem specimens with the basilar artery (BA, including 162 perforating arteries) were prepared and scanned using microcomputed tomography. The geometry and structure of the perforating arteries were analyzed using radiological images and additional histological studies. Results: The ostia of the perforating arteries were ellipsoidal in shape with median stenosis severity of 23% and 20% for MCA and BA perforators, respectively. The local narrowing structure was typical of neointimal hyperplasia. Statistical analysis revealed that the severity of stenosis may be related to age and cardiovascular health. Conclusion Origins of the deep cerebral perforators are locally narrowed by neointimal hyperplasia, which may be a protective mechanism to adjust high blood pressure to the microcirculation. The narrowings may lead to chronic hypoperfusion and play a role in the pathophysiology of cerebral small vessel disease.

Background: The Microtubules-associated protein tau (MAPT), alpha-synuclein (SNCA), and leucine zipper tumor suppressor 3 (LZTS3) genes are implicated in neurodegeneration and tumor suppression, respectively. This study investigated the regulatory roles of eugenol on paraquat-altered genes. Results: Forty male Wistar rats divided into five groups of eight rats were used. The control group received normal saline; the Paraquat (PQ)-untreated group received only Paraquat. The low dose of eugenol was 200 mg/kg, the medium dose of eugenol was 400 mg/kg, and the high dose of eugenol was 600 mg/kg. All groups except the control group received 10 mg/kg of PQ orally for 14 days at one-day intervals, allowing PQ in the rats for 28 days.Eugenol treatment started on the 29th and lasted 14 days. Motor impairments were determined using wire string and beam-walk; biomarkers were estimated using cerebellar homogenates, while frozen cerebellum was used to study LZTS3, MAPT, and SNCA gene expression. LZTS3 was significantly suppressed in the PQ-untreated group and highly expressed in the eugenol-treated group. The MAPT and SNCA genes were overexpressed in the PQ-untreated group compared to the control group. Eugenol significantly decreased the expression of these genes compared to that in the PQ-untreated group. Antioxidants were reduced considerably, and oxidative stress markers were increased significantly, which could have caused increased protein fibrillation and reduced limb functionality. Histology revealed that eugenol mitigated the alterations caused by Paraquat. Conclusions PQ can enhance tumor expression in addition to causing neurotoxicity, which decreases limb functionality, while eugenol, an antioxidant, can mitigate the effects of PQ.

Microglial activation during aging is associated with neuroinflammation and cognitive impairment. Galectin-3 plays a crucial role in microglial activation and phagocytosis. However, the role of galectin-3 in the aged brain is not completely understood. In the present study, we investigated aging-related mechanisms and microglial galectin-3 expression in the mouse hippocampus using female 6-, 12-, and 24-month-old C57BL/6 mice. Western blot analysis revealed neurodegeneration, blood-brain barrier leakage, and increased levels of neuroinflammation-related proteins in 24-month-old mice compared to 6- and 12-month-old mice. Immunohistochemistry revealed an increase in activated microglia in the hippocampus of 24-month-old mice compared to 6- and 12-month-old mice. Furthermore, we found more galectin-3 and triggering receptor expressed on myeloid cells-2-positive microglia in 24-month-old mice compared to 6- and 12-month-old mice. Using primary mouse microglial cells, galectin -3 was also increased by lipopolysaccharide treatment. These findings suggest that galectin-3 may play an important role in microglial activation and neuroinflammation during brain aging.

The 5-hydroxytryptamine type3 (5-HT3 ) receptor, a ligand-gated ion channel, plays a critical role in synaptic transmission. It has been implicated in various neuropsychiatric disorders. This study aimed to elucidate the mechanism by which quetiapine, an atypical antipsychotic, could inhibit 5-HT3 receptor-mediated currents in NCB20 neuroblastoma cells. Whole-cell patch-clamp recordings were used to study effects of quetiapine on receptor ion channel kinetics and its competitive antagonism. Co-application of quetiapine shifted 5-HT concentration-response curve rightward, significantly increasing the EC50 without altering the maximal response (Emax ), suggesting a competitive inhibition. Quetiapine's IC50 varied with 5-HT concentration and treatment condition. The IC50 value of quetiapine was 0.58 μM with 3μM 5-HT and 25.23 μM with 10 μM 5-HT, indicating an inverse relationship between quetiapine efficacy and agonist concentration. Pretreatment of quetiapine significantly enhanced its inhibitory potency, reducing its IC50 from 25.23 μM to 0.20 μM.Interaction kinetics experiments revealed an IC50 of 5.17 μM for an open state of the 5-HT3 receptor, suggesting weaker affinity during receptor activation. Quetiapine also accelerated receptor deactivation and desensitization, suggesting that it could stabilize the receptor in non-conducting states. Additionally, quetiapine significantly prolonged recovery from desensitization without affecting recovery from deactivation, demonstrating its selective impact on receptor kinetics. Inhibition of the 5-HT3 receptor by quetiapine was voltage-independent, and quetiapine exhibited no usedependency, further supporting its role as a competitive antagonist. These findings provide insights into inhibitory mechanism of quetiapine on 5-HT3 receptor and suggest its potential therapeutic implications for modulating serotonergic pathways in neuropsychiatric disorders.

Haloperidol is a typical antipsychotic drug effective in alleviating positive symptoms of schizophrenia by blocking dopamine receptor 2 (DR2). However, it is also known to produce neuropsychiatric effects by acting on various targets other than DR. In this study, we investigated effect of haloperidol on function of 5-hydroxytryptamine (5-HT) 3 receptor, a ligand-gated ion channel belonging to the serotonin receptor family using the whole-cell voltage clamp technique and NCB20 neuroblastoma cells. When co-applied with 5-HT, haloperidol inhibited 5-HT3 receptormediated currents in a concentration-dependent manner. A reduction in maximal effect (E max ) and an increase in EC 50 observed during co-application indicated that haloperidol could act as a non-competitive antagonist of 5-HT3 receptors. Haloperidol inhibited the activation of 5-HT3 receptor, while also accelerating their deactivation and desensitization. The inhibitory effect of haloperidol showed no significant difference between pre- and co-application. Haloperidol did not alter the reversal potential of 5-HT3 receptor currents. Furthermore, haloperidol did not affect recovery from deactivation or desensitization of 5-HT3 receptors. It did not show a use-dependent inhibition either. These findings suggest that haloperidol can exert its inhibitory effect on 5-HT3 receptors by allosterically preventing opening of ion channels. This mechanistic insight enhances our understanding of relationships between 5-HT3 receptors and pharmacological actions of antipsychotics.

Objective: Ciprofloxacin (CPFX) is frequently prescribed by fertility specialists and urologists to manage infections in male reproductive organs. However, it is toxic to the testicles and can lead to infertility. Dietary antioxidants are known to protect the testis from damage. This study aimed to investigate the effects of coenzyme Q10 (CoQ10) on the adverse side effects of CPFX using stereological methods. Methods: Sixty rats were divided into six groups: control (distilled water), CoQ10 (10 mg/kg/day), and low-dose (103 mg/kg/day) and high-dose (206 mg/kg/day) of CPFX (LD-CPFX, HD-CPFX) with or without CoQ10 consumption. The treatments lasted for 45 days. Sperm count, serum testosterone levels, and testicular parameters were evaluated. Results: Significant decreases in sperm count, motility, normal morphology, viability, and testosterone levels were observed in the LD-CPFX (p<0.003) and HD-CPFX- treated rats (p=0.0001) compared to the control groups. A 10% to 36% reduction in the volume of seminiferous tubules, tubular epithelium, and tubule length was noted in LD-CPFX (p<0.01) and HD-CPFX-treated rats (p<0.006), while the volume of the interstitium increased by 25% to 28% in LD-CPFX (p=0.03) and HD-CPFX (p=0.008) groups. The number of cells, including spermatogonia, spermatocytes, spermatids, Sertoli cells, and Leydig cells, decreased by 36% to 75% in the testes exposed to LD-CPFX (p<0.04) and HD-CPFX (p<0.01), compared to the control groups. However, these changes normalized in rats that received CoQ10. Conclusion CPFX exposure for 45 days, regardless of the dose, has detrimental effects on testicular parameters. CoQ10 can prevent CPFX-induced testicular structural impairments.