Search

Objective: With research progress on Rolandic epilepsy (RE), its "benign" nature has been phased out. Clinicians are exhibiting an increasing tendency toward a more assertive treatment approach for RE. Nonetheless, in clinical practice, delayed treatment remains common because of the "self‐limiting" nature of RE. Therefore, this study aimed to identify an imaging marker to aid treatment decisions and select a more appropriate time for initiating therapy for RE. Methods: We followed up with children newly diagnosed with RE, classified them into medicated and non‐medicated groups according to the follow‐up results, and compared them with matched healthy controls. Before beginning follow‐up visits, interictal magnetic data were collected using magnetoencephalography in treatment‐naïve recently diagnosed patients. The spectral power of the whole brain during initial diagnosis was determined using minimum normative estimation combined with the Welch technique. Results: A difference was observed in the magnetic source intensity within the left caudal anterior cingulate and precentral and postcentral gyri in the delta band between the medicated and non‐medicated groups. The results revealed good discriminatory ability within the receiver operator characteristic curve. In the medicated group, there was a specific change in the frontotemporal magnetic source intensity, which shifted from high to low frequencies, compared with the healthy control group. Significance: The intensity of the precentral gyrus magnetic source within the delta band showed good specificity. Considering the rigor of initial treatment, the intensity of the precentral gyrus magnetic source can provide some help as an imaging marker for initial RE treatment, particularly for the timing of treatment initiation. [ABSTRACT FROM AUTHOR]

Increasing evidence has solidified the involvement of [alpha]-synuclein ([alpha]-Syn) and neurotoxins in the pathogenesis of Parkinson's disease (PD), suggesting a combination of genetic and environmental influences. 2,3,5,4'-Tetrahydroxystilbene-2-O-[beta]-D-glucoside (TSG) is one of the main active components extracted from Polygonum multiflorum. The purpose of the present study was to investigate the effects of TSG on [alpha]-Syn aggregation, mitochondrial dysfunction, oxidative stress, and apoptosis in vitro. A53T mutant [alpha]-synuclein-transfected cells (A53T AS cells) plus [MPP.sup.+] exposure were used as a complex cell model of PD. The expression of proteins was determined by Western blot assay. Flow cytometry was utilized to measure mitochondrial membrane potential and apoptosis. The results showed that [MPP.sup.+] exposure for 24 h induced more severe damage in A53T AS cells than in vector control cells. Pretreatment of TSG for 24 h significantly increased the cell viability; decreased lactate dehydrogenase leakage; inhibited [alpha]-Syn over-expression and aggregation; elevated mitochondrial membrane potential; decreased reactive oxygen species, Bax/Bcl-2 ratio, and caspase-3 activity; and inhibited apoptosis in A53T AS cells exposed to [MPP.sup.+]. These results suggest that TSG may be an attractive candidate for PD therapy. Key words: tetrahydroxystilbene glucoside, [MPP.sup.+], [alpha]-synuclein, A53T [alpha]-synuclein-transfected cell, Parkinson's disease. De plus en plus en plus de donnees viennent confirmer la participation de l'[alpha]-synucleine ([alpha]-Syn) et de neurotoxines dans la pathogenese de la maladie de Parkinson (MP), ce qui laisse entrevoir la presence d'influences genetiques et environnementales. Le 2,3,5,4'-tetrahydroxystilbene-2-O-[beta]-D-glucoside (TSG) est l'un des principaux composants actifs que l'on peut extraire de la plante herbacee Polygonum multiflorum. Les presents travaux avaient pour but d'etudier in vitro les effets du TSG sur l'agregation de l'[alpha]-Syn, le dysfonctionnement mitochondrial, le stress oxydatif et l'apoptose. Comme modele cellulaire complexe de MP, nous avons utilise des cellules transfectees avec le gene de l'[alpha]-synucleine portant la mutation A53T (cellules A53T AS) et exposees au [MPP.sup.+]. Nous avons etabli l'expression des proteines par immunobuvardage de Western. Nous avons utilise la cytometrie en flux pour mesurer le potentiel membranaire mitochondrial et l'apoptose. Les resultats ont montre que 24 h d'exposition au [MPP.sup.+] entrainait des dommages plus graves dans les cellules A53T AS que dans les cellules vectrices temoins. L'exposition prealable (pendant 24 h) au TSG des cellules A53T AS mises en presence de [MPP.sup.+] a permis de faire les observations suivantes: augmentation notable de la viabilite des cellules; diminution de la fuite de deshydrogenase lactique; inhibition de la surexpression et de l'agregation de l'[alpha]-Syn; augmentation du potentiel membranaire mitochondrial; diminution des taux de derives reactifs de l'oxygene, du rapport Bax/Bcl-2 et de l'activite de la caspase-3; et inhibition de l'apoptose. Ces resultats laissent entendre que le TSG pourrait etre un candidat attrayant pour le traitement de la MP. [Traduit par la Redaction] Mots-cles : tetrahydroxystilbene glucoside, [MPP.sup.+], [alpha]-synucleine, cellules transfectees avec le gene de l'[alpha]-synucleine portant la mutation A53T, maladie de Parkinson., Introduction Parkinson's disease (PD) is pathologically characterized by the selective loss of dopaminergic neurons and the presence of Lewy bodies in the substantia nigra. Although the aetiology of PD has [...]

Increasing evidence has solidified the involvement of α-synuclein (α-Syn) and neurotoxins in the pathogenesis of Parkinson's disease (PD), suggesting a combination of genetic and environmental influences. 2,3,5,4′-Tetrahydroxystilbene-2-O-β-D-glucoside (TSG) is one of the main active components extracted from Polygonum multiflorum. The purpose of the present study was to investigate the effects of TSG on α-Syn aggregation, mitochondrial dysfunction, oxidative stress, and apoptosis in vitro. A53T mutant α-synuclein-transfected cells (A53T AS cells) plus MPP+ exposure were used as a complex cell model of PD. The expression of proteins was determined by Western blot assay. Flow cytometry was utilized to measure mitochondrial membrane potential and apoptosis. The results showed that MPP+ exposure for 24 h induced more severe damage in A53T AS cells than in vector control cells. Pretreatment of TSG for 24 h significantly increased the cell viability; decreased lactate dehydrogenase leakage; inhibited α-Syn over-expression and aggregation; elevated mitochondrial membrane potential; decreased reactive oxygen species, Bax/Bcl-2 ratio, and caspase-3 activity; and inhibited apoptosis in A53T AS cells exposed to MPP+. These results suggest that TSG may be an attractive candidate for PD therapy. [ABSTRACT FROM AUTHOR]

Copyright of Canadian Journal of Physiology & Pharmacology is the property of Canadian Science Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: Most studies have indicated that peripheral insulin-like growth levels factor-1 (IGF-1) is valuable in diagnosing heart failure, although the results have been inconsistent. To help solve the debate, we performed a meta-analysis to explore the relationship between IGF-1 and heart failure (HF)., Methods: We conducted an extensive search across various databases such as Embase, Cochrane Library, Pubmed, Medline, and Web of Science on May 30, 2023. From the extensive pool of studies, we selected 16 relevant articles, encompassing a total of 1,380 cases and 1,153 controls, to conduct a rigorous meta-analysis., Results: The total results indicated that there is an association between lower IGF-1 level and HF. The random-effects model yielded a pooled standardized mean difference (SMD) of -0.598 (95% CI: -1.081 to -0.116, P  = 0.015). Further subgroup analysis also showed that IGF-1 levels were associated with HF in the age difference ≥5 years subgroup and body mass index difference >1 subgroup. Additionally, significant association between IGF-1 levels and HF were detected in the "serum" samples and "Europe" subgroups. Importantly, we observed IGF-1 showed significant lower levels in patients with reduced ejection fraction (HFrEF) compared to the controls, not in patients with preserved ejection fraction (HFpEF). The Begg's and Egger's tests revealed no indication of publication bias., Conclusions: Our meta-analysis has provided evidence suggesting a substantial correlation between reduced levels of IGF-1 and the occurrence of HF. Further prospective studies are necessary to ascertain the use of IGF-1 as a reliable biomarker for diagnosing HF, especially for HFrEF. But the diagnosis of HFpEF should be cautious., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (© 2024 Liu, Li, Fei, Sun, Chen, Tian, Zheng, Zhu and Wang.)

Introduction: Acute myocardial infarction (AMI) is characterized by the loss of cardiomyocytes, which impairs cardiac function and eventually leads to heart failure. The induction of cardiomyocyte cell cycle activity provides a new treatment strategy for the repair of heart damage. Our previous study demonstrated that morroniside exerts cardioprotective effects. This study investigated the effects and underlying mechanisms of action of morroniside on cardiomyocyte cell cycle activity and cardiac repair following AMI. Methods: Neonatal rat cardiomyocytes (NRCMs) were isolated and exposed to oxygen-glucose deprivation (OGD) in vitro . A rat model of AMI was established by ligation of the left anterior descending coronary artery (LAD) in vivo . Immunofluorescence staining was performed to detect newly generated cardiomyocytes. Western blotting was performed to assess the expression of cell cycle-related proteins. Electrocardiography (ECG) was used to examine pathological Q waves. Masson's trichrome and wheat germ agglutinin (WGA) staining assessed myocardial fibrosis and hypertrophy. Results: The results showed that morroniside induced cardiomyocyte cell cycle activity and increased the levels of cell cycle proteins, including cyclin D1, CDK4, cyclin A2, and cyclin B1, both in vitro and in vivo . Moreover, morroniside reduced myocardial fibrosis and remodeling. Discussion: In conclusion, our study demonstrated that morroniside stimulates cardiomyocyte cell cycle activity and cardiac repair in adult rats, and that these effects may be related to the upregulation of cell cycle proteins., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Zheng, Liu, Chen, Sun, Fei, Chen, Tian, Wu, Zhu, Zheng, Wang and Wang.)