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The stability and bifurcations of a double pendulum with a follower force are considered. The focus is placed on a doubly degenerate system that possesses a zero eigenvalue and a pair of pure imaginary eigenvalues; that is, coupled flutter and divergence bifurcation. The local qualitative behavior of the system is examined in the neighborhood of the degenerate system. The four-dimensional equations of motion are reduced to the two-dimensional ones by using some qualitative reduction theory for dynamic systems, and it is shown that two distinct bifurcations can occur in the system according to the ratio of two damping coefficients of the double pendulum.

The aim of this study was to clarify whether histological parameters reflected tumor aggressiveness in patients with hepatocellular carcinoma (HCC). The tumor volume doubling times (TVDTs) of 21 HCCs, less than 3 cm in diameter at the start of the observation period, were calculated in 21 patients in whom the natural progression of the lesion was observed by ultrasonography. Paraffin-embedded sections were prepared from samples obtained by ultrasound-guided fine-needle liver biopsy at the end of the observation period. The histological parameters examined were the MIB-1 labeling index (LI), for which we performed immunohistochemical staining with the MIB-1 monoclonal antibody, using an antigen retrieval method; the nucleo-cytoplasmic (N/C ratio), cellularity, and the nuclear form factor (NFF), were calculated with an imaging analyzer. We performed multiple regression analysis for estimating the growth of small HCCs. With the N/C ratio (0.154 +/- 0.068; mean +/- SD), cellularity (453 +/- 21.8 cells/10(4) microm2), NFF (1.150 +/- 0.096), and degree of HCC differentiation as independent variables, only the MIB-1 LI (11.8 +/- 6.1%) showed a significant correlation with TVDT (207.5 +/- 162.6 days) (r = -0.658; P < 0.05). Compared to the conventional indices of histological atypism tested, i.e., N/C ratio, cellularity NFF, and degree of HCC differentiation, only MIB-1 LI was significantly correlated with small HCC growth rate. The MIB-1 LI may therefore be a simple and useful index of tumor aggressiveness. [ABSTRACT FROM AUTHOR]

A rare case of severe acute hepatitis A complicated by pure red cell aplasia (PRCA) is reported. A 60-year-old man with jaundice and hepatomegaly was diagnosed as having acute hepatitis A by positive IgM anti-hepatitis A antibody (anti-HAV). Severe anemia rapidly developed 3 weeks after admission, and the patient was diagnosed with PRCA by both bone marrow smears and erythrocyte survival study. The anemia was transient and bone marrow recovered within 1 week. However, concomitant with bone marrow recovery, the hepatitis worsened. He became drowsy and disoriented and severe jaundice, ascites, prolonged prothrombin time, increased transaminase levels, and abnormal electroencephalogram (EEG) were exhibited. Plasma exchange transfusion and glucagon-insulin (GI) therapy improved the consciousness level, but bilirubin, transaminase levels, and IgM anti-HAV titer remained high. Intravenous administration of lipophilized prostaglandin E1 (lipo-PGE1) was added to the GI therapy. Bilirubin and transaminase levels were normalized in the 8th week after the initiation of this combination therapy (17 weeks after admission). The combined use of lipo-PGE1 with plasma exchange and GI therapy appeared to be useful for the prolonged severe hepatitis in this patient. [ABSTRACT FROM AUTHOR]

Patients with cholesterol gallstones have a reduced pool of bile acids. This study was undertaken to clarify the mechanism by which bile acid biosynthesis does not increase to supranormal levels to cause a reexpansion of the pool. We investigated the first two steps of the bile acid biosynthesis pathway by assaying the activities of cholesterol 7 alpha-hydroxylase, the rate-limiting enzyme in this pathway, and 3 beta-hydroxy-delta 5-C27-steroid dehydrogenase/isomerase, and by measuring the concentrations of 7 alpha-hydroxycholesterol and 7 alpha-hydroxy-4-cholesten-3-one in liver specimens from ten patients with cholesterol gallstones and ten gallstone-free controls. In the patients with gallstones, cholesterol 7 alpha-hydroxylase activity, 3 beta-hydroxy-delta 5-C27-steroid dehydrogenase/isomerase activity, and hepatic 7 alpha-hydroxy-4-cholesten-3-one concentration did not significantly different from levels in controls, but hepatic 7 alpha-hydroxycholesterol concentration was more than twofold that of controls (12.9 +/- 2.6 vs 5.3 +/- 1.2 nmol/g liver, P < 0.01). The concentration of 7 alpha-hydroxycholesterol positively correlated with the ratio of cholesterol 7 alpha-hydroxylase activity to 3 beta-hydroxy-delta 5-C27-steroid dehydrogenase/isomerase activity (r = 0.93; P < 0.005) in the gallstone-free controls. In contrast, this correlation disappeared in the patients with gallstones. These results suggest a derangement of the normal 7 alpha-hydroxycholesterol metabolism in the patients with gallstones. The reason for the accumulation of 7 alpha-hydroxycholesterol remains unclear; however, it is possible that, in patients with cholesterol gallstone, the accumulated 7 alpha-hydroxycholesterol causes inappropriate suppression of cholesterol 7 alpha-hydroxylase activity by product inhibition. [ABSTRACT FROM AUTHOR]

Trimethadione (TMO) was chosen as an indicator of quantitative hepatic microsomal function, and its pharmacokinetics were studied in 52 patients with chronic hepatitis. Findings in these patients were compared with those for 26 healthy subjects and 13 patients with renal failure. Patients with chronic hepatitis, but not those with renal failure, showed significant reduction in clearance (CL) and prolongation of half-life (t1/2), and the extent of abnormalities was found to reflect the severity of histologic changes in liver tissue. The serum dimethadione (DMO)/TMO ratio 4 h after the administration of TMO altered in parallel with the CL and t1/2 of TMO, and abnormalities in this simple ratio were also related to the histologic severity of changes in the liver tissue. A low DMO/TMO ratio (< 0.4) was associated with advanced histologic changes (chronic active hepatitis with bridging or chronic active hepatitis with cirrhosis), whereas a high DMO/TMO ratio (> 0.4) was associated with mild histologic changes (chronic persistent hepatitis or chronic active hepatitis) (sensitivity, 0.81; specificity, 0.86). These results indicate that the DMO/TMO ratio, which can be obtained from a single blood sampling, reflects the histologic severity of changes in tissue liver, and that the TMO tolerance test is a useful indicator of quantitative liver function. [ABSTRACT FROM AUTHOR]

Sentinel surveillance of influenza‐like illnesses revealed an increase in the cases of influenza C virus in children and adults in Austria, 2022, compared to previous years, following one season (2020/2021), wherein no influenza C virus was detected. Whole‐genome sequencing revealed no obvious genetic basis for the increase. We propose that the reemergence is explained by waning immunity from lack of community exposure due to restrictions intended to limit severe acute respiratory syndrome coronavirus 2 spread in prior seasons, pending further investigation. [ABSTRACT FROM AUTHOR]

Metyltetraprole is a novel quinone outside inhibitor (QoI) fungicide designed to avoid cross-resistance in cytochrome b G143A-harboring QoI-resistant phytopathogenic fungi. The resistance factors of G143A-harboring fungal isolates for metyltetraprole are around 1, but > 200 for the reference QoI fungicide azoxystrobin. In this study of metyltetraprole activities against azoxystrobin-resistant isolates carrying G137R, G137S, L299F, N256S + L299F, or L275F + L299F in cytochrome b, metyltetraprole had potent activity against all isolates with these cytochrome b haplotypes. The resistance factors ranged from 0.7 to 2.9 for metyltetraprole and from 3.0 to 175.1 for azoxystrobin. We revealed unique metyltetraprole inhibitory activities against QoI-resistant plant pathogens. [ABSTRACT FROM AUTHOR]

HLA-B*07:185 differs from B*07:02:01 by one nucleotide substitution in exon 2 at position 300G>C. [ABSTRACT FROM AUTHOR]

The article presents a case study of a 61-year-old Japanese woman presented with multiple small nodules on the fingers for two months and after two weeks of her surgery of pharyngeal tumour the lesion has appeared again. It states that the patient has no family history of xanthomatosis or premature coronary heart disease. She was diagnosed with normolipidaemic xanthomatosis and undergo a treatment of liquid nitrogen cryotherapy.

A letter to the editor is presented in response to the article "CD20+ Primary Cutaneous T-Cell Lymphoma Presenting As a Solitary Extensive Plaque" in the previous issue.

The article presents a case of a novel H1 domain mutation in the keratin 2 gene in a Japanese family with ichthyosis bullosa of siemens (IBS). IBS is a rare autosomal dominant skin disorder characterized by blister formation in the upper suprabasal layers of the epidermis. Information about the clinical features and treatment of the disease is also discussed.

We report numerical analysis and experimental observation of two dimensionally localized plasmonic modes guided by a nanogap in a thin metal film. Dispersion, dissipation, and field structure of these modes are analyzed using the finite-difference time-domain algorithm. The experimental observation is conducted by the end-fire excitation of the proposed gap plasmon waveguides and detection of the generated modes using their edge scattering and charge coupled device camera imaging. Physical interpretation of the obtained results is presented and origins of the described modes are discussed. [ABSTRACT FROM AUTHOR]

High-temperature superconducting (HTS) trapped field magnets can generate and maintain stable, high magnetic fields without requiring external power supplies. Recently, HTS-stacked ring magnets have garnered significant attention due to their flexible geometry, robust mechanical strength, and proven trapped field performance. In this study, we examine the magnetization characteristics of HTS-stacked ring magnets and observed a trapped field higher than the applied field during field cooling magnetization. We also observed that by inserting HTS stacks into the hollow cavity of the HTS-stacked rings, the center field ceased to exhibit an increased center field. Our analysis revealed that the unique induced current distribution and the penetration sequence are the underlying causes. Inspired by the investigation results, we explored deeper into the magnetization properties and identified that a final trapped field higher than the applied field can be achieved through proper design and magnetization of the HTS-stacked ring magnets. However, even though the trapped central field experiences an increase, this does not translate into an increment in the total trapped flux. Instead, a redistribution of the flux is observed. These findings hold significant implications for the design and application of superconducting magnets. [ABSTRACT FROM AUTHOR]

Cellular lipid membranes serve as the primary barrier preventing viral infection of the host cell and provide viruses with a critical initial point of contact. Occasionally, viruses can utilize lipids as viral receptors. Viruses depend significantly on lipid rafts for infection at virtually every stage of their life cycle. The pivotal role that proprotein convertase subtilisin/kexin Type 9 (PCSK9) plays in cholesterol homeostasis and atherosclerosis, primarily by post-transcriptionally regulating hepatic low-density lipoprotein receptor (LDLR) and promoting its lysosomal degradation, has garnered increasing interest. Conversely, using therapeutic, fully humanized antibodies to block PCSK9 leads to a significant reduction in high LDL cholesterol (LDL-C) levels. The Food and Drug Administration (FDA) has approved PCSK9 inhibitors, including inclisiran (Leqvio®), alirocumab (Praluent), and evolocumab (Repatha). At present, active immunization strategies targeting PCSK9 present a compelling substitute for passive immunization through the administration of antibodies. In addition to the current inquiry into the potential therapeutic application of PCSK9 inhibition in human immunodeficiency virus (HIV)-infected patients for hyperlipidemia associated with HIV and antiretroviral therapy (ART), preclinical research suggests that PCSK9 may also play a role in inhibiting hepatitis C virus (HCV) replication. Furthermore, PCSK9 inhibition has been suggested to protect against dengue virus (DENV) potentially and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) viruses. Recent evidence regarding the impact of PCSK9 on a variety of viral infections, including HCV, HIV, DENV, and SARS-CoV-2, is examined in this article. As a result, PCSK9 inhibitors and vaccines may serve as viable host therapies for viral infections, as our research indicates that PCSK9 is significantly involved in the pathogenesis of viral infections. [ABSTRACT FROM AUTHOR]

Harnessing quantum correlations can enable sensing beyond classical precision limits, with the realization of such sensors poised for transformative impacts across science and engineering. Real devices, however, face the accumulated impacts of noise and architecture constraints, making the design and success of practical quantum sensors challenging. Numerical and theoretical frameworks to optimize and analyze sensing protocols in their entirety are thus crucial for translating quantum advantage into widespread practice. Here, we present an end-to-end variational framework for quantum sensing protocols, where parameterized quantum circuits and neural networks form trainable, adaptive models for quantum sensor dynamics and estimation, respectively. The framework is general and can be adapted towards arbitrary qubit architectures, as we demonstrate with experimentally-relevant ansätze for trapped-ion and photonic systems, and enables to directly quantify the impacts that noise and finite data sampling. End-to-end variational approaches can thus underpin powerful design and analysis tools for practical quantum sensing advantage. [ABSTRACT FROM AUTHOR]

During mouse development, hematopoietic cells first form in the extraembryonic tissue yolk sac. Hematopoietic stem cells (HSCs), which retain their ability to differentiate into hematopoietic cells for a long time, form intra-aortic hematopoietic cell clusters (IAHCs) in the dorsal aorta at midgestation. These IAHCs emerge from the hemogenic endothelium, which is the common progenitor of hematopoietic cells and endothelial cells. HSCs expand in the fetal liver, and finally migrate to the bone marrow (BM) during the peripartum period. IAHCs are absent in the dorsal aorta in mice deficient in transcription factors such as Runx-1, GATA2, and c-Myb that are essential for definitive hematopoiesis. In this review, we focus on the transcription factor Sry-related high mobility group (HMG)-box (Sox) F family of proteins that is known to regulate hematopoiesis in the hemogenic endothelium and IAHCs. The SoxF family is composed of Sox7, Sox17, and Sox18, and they all have the HMG box, which has a DNA-binding ability, and a transcriptional activation domain. Here, we describe the functional and phenotypic properties of SoxF family members, with a particular emphasis on Sox17, which is the most involved in hematopoiesis in the fetal stages considering that enhanced expression of Sox17 in hemogenic endothelial cells and IAHCs leads to the production and maintenance of HSCs. We also discuss SoxF-inducing signaling pathways. [ABSTRACT FROM AUTHOR]

Autoimmune bullous diseases (AIBDs) are a group of conditions marked by the formation of blisters and erosions on the skin and mucous membranes. It occurs in all age groups, slightly more often affecting women. Several factors may be linked to the development of AIBDs, with nutrition being one of them. The literature mentions various food products and food ingredients acting as disease modifiers. Given the complex relationship between bullous diseases and nutrition, the current literature on AIBDs has been reviewed, with an emphasis on the influence of dietary modifications, various diets, and the nutritional consequences of these conditions. This review summarizes the role of nutrition in the pathogenesis and treatment of the following AIBDs: (i) pemphigus, (ii) bullous pemphigoid and mucous membrane pemphigoid, (iii) dermatitis herpetiformis, and (iv) epidermolysis bullosa acquisita. Several nutrients and dietary factors have been studied for their potential roles in triggering or exacerbating AIBDs. The key nutrients and their potential impacts include thiols and bulb vegetables (Allium), phenols, tannic acid, tannins, phycocyanin, isothiocyanates, all trans-retinoic acids, cinnamic acid, and walnut antigens. Many patients with ABIDs may require supplementation, particularly of vitamin D and B3, calcium, potassium, zinc, selenium, and cobalt. In addition, various diets play an important role. A soft diet is recommended for individuals with issues in the oral cavity and/or esophagus, particularly for those who experience difficulties with biting or swallowing. This approach is commonly used in managing pemphigus. A high-protein, high-calcium diet, DASH (Dietary Approaches to Stop Hypertension), and the Mediterranean diet are utilized during long-term glucocorticoid therapy. However, in dermatitis herpetiformis it is advisable to follow a gluten-free diet and eliminate iodine from the diet. When it comes to herbal supplements, Algae (Spirulina platensis), Echinacea, and St. John's wort (Hyperitum perforatum) enhance the ABIDs, while Cassia fistula may be recommended in the treatment of erosions in pemphigus vulgaris. Fast foods enhance the development of ABIDs. However, the pathomechanism is not yet fully understood. Future researchers should more precisely define the relationships between nutrients and nutrition and blistering diseases by also looking at, i.e., genetic predispositions, microbiome differences, or exposure to stress. [ABSTRACT FROM AUTHOR]

Fatty acid binding protein 7 (FABP7) is a multifunctional chaperone involved in lipid metabolism and signaling. It is primarily expressed in astrocytes and neural stem cells (NSCs), as well as their derived malignant glioma cells within the central nervous system. Despite growing evidence for FABP7's tumor-intrinsic onco-metabolic functions, its mechanistic role in regulating the brain tumor immune microenvironment (TIME) and its impact on prognosis at the molecular level remain incompletely understood. Utilizing combined transcriptome profiling and pan-cancer analysis approaches, we report that FABP7 mediates the expression of multiple onco-immune drivers, collectively impacting tumor immunity and clinical outcomes across brain cancer subtypes. An analysis of a single-cell expression atlas revealed that FABP7 is predominantly expressed in the glial lineage and malignant cell populations in gliomas, with nuclear localization in their parental NSCs. Pathway and gene enrichment analysis of RNA sequencing data from wild-type (WT) and Fabp7-knockout (KO) mouse brains, alongside control (CTL) and FABP7-overexpressing (FABP7 OV) human astrocytes, revealed a more pronounced effect of FABP7 levels on multiple cancer-associated pathways. Notably, genes linked to brain cancer progression and tumor immunity (ENO1, MUC1, COL5A1, and IL11) were significantly downregulated (>2-fold) in KO brain tissue but were upregulated in FABP7 OV astrocytes. Furthermore, an analysis of data from The Cancer Genome Atlas (TCGA) showed robust correlations between the expression of these factors, as well as FABP7, and established glioma oncogenes (EGFR, BRAF, NF1, PDGFRA, IDH1), with stronger associations seen in low-grade glioma (LGG) than in glioblastoma (GBM). TIME profiling also revealed that the expression of FABP7 and the genes that it modulates was significantly associated with prognosis and survival, particularly in LGG patients, by influencing the infiltration of immunosuppressive cell populations within tumors. Overall, our findings suggest that FABP7 acts as an intracellular regulator of pro-tumor immunomodulatory genes, exerting a synergistic effect on the TIME and clinical outcomes in brain cancer subtypes. [ABSTRACT FROM AUTHOR]

Matrikines (MKs), the products of enzymatic fragmentation of various extracellular matrix (ECM) proteins, regulate cellular activity by interacting with specific receptors. MKs affect cell growth, proliferation, and migration, can induce apoptosis and autophagy, and are also effectively used in biomedicine and functional nutrition. Recently, there has been great interest in the structural features and biological activity of MKs from various sources. This review summarized and analyzed the results of modern research on MKs from sea cucumbers, primarily from trepang (MKT). Particular attention is paid to the analysis of the existing knowledge on the antioxidant, anti-inflammatory and adaptogenic activities of these MKs and the possible mechanisms of their protective action. [ABSTRACT FROM AUTHOR]

Background: HTLV-1 is a worldwide distribution retrovirus with 10–20 million infected individuals. ATLL is an Adult T-cell leukaemia lymphoma caused by aggressive T-cell proliferation that is infected by HTLV-1 and is associated with an inferior prognosis. The exact molecular pathogenesis has yet to be fully understood. CREB, a transcription factor, acts as a molecular switch that controls the expression of numerous genes in response to various extracellular signals. Its activation is primarily mediated through phosphorylation by multiple kinases, including MAPKs. MAPKs, a family of serine/threonine kinases, serve as crucial mediators of intracellular signaling cascades. Method and material: This study investigated, 38 HTLV-I-infected individuals, including 18 HTLV-1 asymptomatic carriers (ACs) and 20 ATLL subjects. mRNA was extracted and converted to cDNA from Peripheral blood mononuclear cells (PBMCs), and then the expression of TAX, HBZ, CREB, and MAPK was analyzed by TaqMan qPCR. The genomic HTLV-1 Proviral loads were examined among the study group. Results: The data analysis showed a significant difference in the mean of CREB expression amongst study groups (ATLL and carriers, (p = 0.002). There is no statistical difference between the MAPK gene expression (p = 0.35). HBZ, TAX, and HTLV-1 proviral load weree significantly higher in ATLL subjects compared to ACs (p = 0.002, 0.000, and 0.000), respectively. Moreover, our results, demonstrated a direct positive correlation among HBZ, CREB, and TAX gene expression in ATLL patients (p = 0.001), whilst between the ACs, TAX gene expression had a positive significant correlation with HBZ and HTLV-1 proviral load (p = 0.007 and p = 0.004, respectively). Conclusion: The present study demonstrated that CREB gene expression was higher in the ATLL group than ACs, while there was no difference for MAPK. Therefore, this pathway may not strongly involve in the activation of CREB. The CREB may be a prognostic factor for the development of HTLV-I-associated diseases and can be used as a monitoring marker for the efficiency of the therapeutic regime and prognosis. [ABSTRACT FROM AUTHOR]

Peptide hormones regulate plant development, growth, and stress responses. Sulfated peptides represent a class of proteins that undergo posttranslational modification by tyrosylprotein sulfotransferase (TPST), followed by specific enzymatic cleavage to generate mature peptides. This process contributes to the formation of various bioactive peptides, including PSKs (PHYTOSULFOKINEs), PSYs (PLANT PEPTIDE CONTAINING SULFATED TYROSINE), CIFs (CASPARIAN STRIP INTEGRITY FACTOR), and RGFs (ROOT MERISTEM GROWTH FACTOR). In the past three decades, significant progress has been made in understanding the molecular mechanisms of sulfated peptides that regulate plant development, growth, and stress responses. In this review, we explore the sequence properties of precursors, posttranslational modifications, peptide receptors, and signal transduction pathways of the sulfated peptides, analyzing their functions in plants. The cross-talk between PSK/RGF peptides and other phytohormones, such as brassinosteroids, auxin, salicylic acid, abscisic acid, gibberellins, ethylene, and jasmonic acid, is also described. The significance of sulfated peptides in crops and their potential application for enhancing crop productivity are discussed, along with future research directions in the study of sulfated peptides. [ABSTRACT FROM AUTHOR]

Bioenergy sorghum's large and deep nodal root system and associated microbiome enables uptake of water and nutrients from and deposition of soil organic carbon into soil profiles, key contributors to the crop's resilience and sustainability. The goal of this study was to increase our understanding of bioenergy sorghum nodal root bud development. Sorghum nodal root bud initiation was first observed on the stem node of the 7th phytomer below the shoot apex. Buds were initiated near the upper end of the stem node pulvinus on the side of the stem opposite the tiller bud, then additional buds were added over the next 6-8 days forming a ring of 10-15 nascent nodal root buds around the stem. Later in plant development, a second ring of nodal root buds began forming on the 17th stem node immediately above the first ring of buds. Overall, nodal root bud development can take ~40 days from initiation to onset of nodal root outgrowth. Nodal root buds were initiated in close association with vascular bundles in the rind of the pulvinus. Stem tissue forming nascent nodal root buds expressed sorghum homologs of genes associated with root initiation (WOX4), auxin transport (LAX2, PIN4), meristem activation (NGAL2), and genes involved in cell proliferation. Expression of WOX11 and WOX5 , genes involved in root stem niche formation, increased early in nodal root bud development followed by genes encoding PLTs, LBDs (LBD29), LRP1, SMB, RGF1 and root cap LEAs later in development. A nodal root bud gene regulatory network module expressed during nodal root bud initiation predicted connections linking PFA5 , SPL9 and WOX4 to genes involved in hormone signaling, meristem activation, and cell proliferation. A network module expressed later in development predicted connections among SOMBRERO , a gene involved in root cap formation, and GATA19 , BBM , LBD29 and RITF1 /RGF1 signaling. Overall, this study provides a detailed description of bioenergy sorghum nodal root bud development and transcriptome information useful for understanding the regulation of sorghum nodal root bud formation and development. [ABSTRACT FROM AUTHOR]

Background: Executive functions can be viewed as a key indicator of how and when we perform routine behaviors. They help individuals set goals, regulate themselves, inhibit inappropriate responses, remain flexible, and focus on future-oriented actions. The aim of this study was to determine the effect of neurofeedback training on improving executive functions (working memory, cognitive flexibility, and sustained attention) in student athletes. Methods: This study used a quasi-experimental design, with the research being applied in nature and employing a pre-test/post-test control group desighn. The population consisted of 200 middle school students (aged 12 to 15 yr) in Shahroud. For sampling, 20 student athletes were first selected based on the results of a physical activity questionnaire and were then randomly assigned to either the experimental or control group. The experimental group underwent 13 neurofeedback training sessions (aimed at increasing beta waves, decreasing theta waves, and enhancing alpha waves), with three sessions per week, each lasting 30 minutes. The control group received no intervention. The research tools included the N-Back test, Wisconsin Card Sorting Test, and Continuous Performance Test to measure working memory, cognitive flexibility, and sustained attention, respectively. Results: The results of the two-way mixed ANOVA (2x2) indicated a significant difference between the experimental and control groups after controlling for the pre-test effect. According to the LSD post-hoc test, there was no significant difference between the experimental and control groups in the variables of working memory and sustained attention, while a significant difference was observed in cognitive flexibility. Further within-group comparisons, using repeated measures ANOVA, revealed no significant differences in any of the three variables between the groups. Conclusion: Neurofeedback seems capable of retraining brainwave activity to enhance athletic performance and improve certain mental and cognitive abilities, such as adaptability to changing conditions. However, neurofeedback training in healthy individuals requires further comprehensive research. [ABSTRACT FROM AUTHOR]

In vitro cell culture systems serve as instrumental platforms for probing biological phenomena and elucidating intricate cellular mechanisms. These systems afford researchers the opportunity to scrutinize cellular responses within a regulated environment, thereby circumventing the ethical and logistical challenges associated with in vivo experimentation. Three-dimensional (3D) cell cultures have emerged as a viable alternative to mimic in vivo environments. Within this context, spheroids are recognized as one of the most straightforward and efficacious models, presenting a promising substitute for conventional monolayer cultures. The application of 3D cultures of fish cells remains limited, focusing mainly on physiological and morphological characterization studies. However, given the capacity of spheroids to emulate in vivo conditions, researchers are exploring diverse applications of these 3D cultures. These include eco-toxicology, immunology, drug screening, endocrinology, and metabolism studies, employing a variety of cell types such as fibroblasts, hepatocytes, embryonic cells, gonadal cells, gastrointestinal cells, and pituitary cells. This review provides a succinct overview, concentrating on the most frequently employed methods for generating fish cell spheroids and their applications to date. The aim is to compile and highlight the significant contributions of these methods to the field and their potential for future research. [ABSTRACT FROM AUTHOR]

Spinocerebellar ataxia (SCA) is a heterogeneous disorder characterized by impaired balance and coordination caused by cerebellar dysfunction. The absence of treatments approved by the U.S. Food and Drug Administration for SCA has driven the investigation of alternative therapeutic strategies, including stem cell therapy. Mesenchymal stem cells (MSCs), known for their multipotent capabilities, have demonstrated significant potential in treating SCA. This review examines how MSCs may promote neuronal growth, enhance synaptic connectivity, and modulate brain inflammation. Recent findings from preclinical and clinical studies are also reviewed, emphasizing the promise of MSC therapy in addressing the unmet needs of SCA patients. Furthermore, ongoing clinical trials and future directions are proposed to address the limitations of the current approaches. [ABSTRACT FROM AUTHOR]

Mesenchymal stem cells (MSCs) are multilineage differentiating stromal cells with extensive immunomodulatory and anti-inflammatory properties. MSC-based therapy is widely used in the treatment of various pathologies, including bone and cartilage diseases, cardiac ischemia, diabetes, and neurological disorders. Along with MSCs, it is promising to study the therapeutic properties of exosomes derived from MSCs (MSC-Exo). A number of studies report that the therapeutic properties of MSC-Exo are superior to those of MSCs. In particular, MSC-Exo are used for tissue regeneration in various diseases, such as healing of skin wounds, cancer, coronary heart disease, lung injury, liver fibrosis, and neurological, autoimmune, and inflammatory diseases. In this regard, it is not surprising that the scientific community is interested in studying the therapeutic properties of MSCs and MSC-Exo in the treatment of psoriasis. This review summarizes the recent advancements from preclinical and clinical studies of MSCs and MSC-Exo in the treatment of psoriasis, and it also discusses their mechanisms of therapeutic action involved in the treatment of this disease. [ABSTRACT FROM AUTHOR]

Stem cells have shown great application potential in wound repair, tissue regeneration, and disease treatment. Therefore, a full understanding of stem cells and their related regulatory mechanisms in disease treatment is conducive to improving the therapeutic effect of stem cells. However, thus far, there are still many unsolved mysteries in the field of stem cells due to technical limitations, which hinder the in-depth exploration of stem cells and their wide clinical application. Single-cell sequencing (SCS) has provided very powerful and unbiased insights into cell gene expression profiles at the single-cell level, bringing exciting results to the stem cell field. At present, SCS has been widely applied in the field of stem cells, covering various aspects, including lineage tracing the development of stem cells, identifying new stem cell types, exploring cellular heterogeneity, and identifying internal functional subpopulations. In this paper, we focus on the latest research progress and discuss the application of SCS technology in stem cells. [ABSTRACT FROM AUTHOR]

Background/Aim: In spot-scanning proton therapy, intra-fractional anatomical changes by organ movement can lead to deterioration in dose distribution due to beam range variation. To explore a more robust treatment planning method, this study evaluated the dosimetric characteristics and robustness of two proton therapy planning methods for liver cancer. Patients and Methods: Two- or three-field treatment plans were created for 11 patients with hepatocellular carcinoma or metastatic liver cancer using a single-field uniform dose (SFUD) technique. The plans were optimized using either beam-specific planning target volume (BSPTV) or worst-case optimization (WCO). The target coverage for the gross tumor volume (GTV), planning target volume (PTV), and organs at risk (OAR) parameters related to toxicity were calculated from the perturbed dose distributions, considering setup and range uncertainties. Statistical analyses of the BSPTV and WCO plans were performed using the Wilcoxon signed-rank sum test (p<0.05). The calculation times for a single optimization process were also recorded and compared. Results: The robustness of the WCO plans in the worst-case scenario was significantly higher than that of the BSPTV plan in terms of GTV target coverage, prevention of maximum dose increase to the gastrointestinal tract, and the dose received by normal liver regions. However, there were no significant differences in PTV, and the calculation time required to create the WCO plan was considerably longer. Conclusion: In SFUD proton therapy for liver cancer, the WCO plans required a longer optimization time but exhibited superior robustness in GTV coverage and sparing of OARs. [ABSTRACT FROM AUTHOR]

Simple Summary: This research aims to improve the precision of particle therapy for lung cancer treatment. The heterogeneous, microscopic structure of lung tissue leads to a broadening of the very sharp dose profiles of protons and other light ions. This can result in higher doses in healthy tissue as well as a reduced dose in the target volume and thereby reducing the potential benefit of particle therapy for lung cancer. This review summarizes existing models that account for these lung tissue effects and explore how they can be better integrated into treatment planning. By taking into account these so called lung modulation effects, it is possible to target tumors more precisely while minimizing harm to surrounding healthy tissues, ultimately benefiting cancer patients. Particle therapy presents a promising alternative to conventional photon therapy for treating non-small cell lung cancer (NSCLC). However, the heterogeneous structure of lung tissue leads to the degradation of the Bragg peak and thereby to the degradation of the dose distribution. This review offers a comprehensive overview of the models developed to account for these modulation effects. It summarizes studies focused on determining modulation power as a predictor of this so-called lung modulation. In addition, the review covers early investigations on dose uncertainties caused by lung modulation in CT-based lung phantoms and patient anatomies and discusses future challenges in integrating these solutions into clinical treatment planning routines. [ABSTRACT FROM AUTHOR]

The rapid geographic spread of the highly pathogenic avian influenza (HPAI) A(H5N1) virus in poultry, wild birds, and other mammalian hosts, including humans, raises significant health concerns globally. The recent emergence of HPAI A(H5N1) in agricultural animals such as cattle and goats indicates the ability of the virus to breach unconventional host interfaces, further expanding the host range. Among the four influenza types—A, B, C, and D, cattle are most susceptible to influenza D infection and serve as a reservoir for this seven-segmented influenza virus. It is generally thought that bovines are not hosts for other types of influenza viruses, including type A. However, this long-standing viewpoint has been challenged by the recent outbreaks of HPAI A(H5N1) in dairy cows in the United States. To date, HPAI A(H5N1) has spread into fourteen states, affecting 299 dairy herds and causing clinical symptoms such as reduced appetite, fever, and a sudden drop in milk production. Infected cows can also transmit the disease through raw milk. This review article describes the current epidemiological landscape of HPAI A(H5N1) in US dairy cows and its interspecies transmission events in other mammalian hosts reported across the globe. The review also discusses the viral determinants of tropism, host range, adaptative mutations of HPAI A(H5N1) in various mammalian hosts with natural and experimental infections, and vaccination strategies. Finally, it summarizes some immediate questions that need to be addressed for a better understanding of the infection biology, transmission, and immune response of HPAI A(H5N1) in bovines. [ABSTRACT FROM AUTHOR]

Voltage-gated potassium channels are a widely distributed subgroup of potassium channels responsible for the efflux of potassium in the repolarisation of the cell membrane, and hence contribute to the latency and propagation of action potentials. As they are causal to synaptic transmission, alterations to the structure of these channels can lead to a variety of neurological and psychiatric diseases. The Kv3 subfamily of voltage-gated potassium channels are found on many neurons in the brain, including inhibitory interneurons where they contribute to fast-frequency firing. Changes to the firing ability of these interneurons can lead to an imbalance of inhibitory and excitatory neurotransmission. To date, we have little understanding of the mechanism by which excitatory and inhibitory inputs become imbalanced. This imbalance is associated with cognitive deficits seen across neurological and neuropsychiatric disorders, which are currently difficult to treat. In this review, we collate evidence supporting the hypothesis that voltage-gated potassium channels, specifically the Kv3 subfamily, are central to many neurological and psychiatric disorders, and may thus be considered as an effective drug target. The collective evidence provided by the studies reviewed here demonstrates that Kv3 channels may be amenable to novel treatments that modulate the activity of these channels, with the prospect of improved patient outcome. [ABSTRACT FROM AUTHOR]

We propose a data-driven strategy for parameter selection in phase field nucleation models using machine learning and apply it to oxide nucleation in Fe-Cr alloys. A grand potential-based phase field model, incorporating Langevin noise, is employed to simulate oxide nucleation and benchmarked against the Johnson-Mehl-Avrami-Kolmogorov model. Three independent parameters in the phase field simulations (Langevin noise strength, numerical grid discretization and critical nucleation radius) are identified as essential for accurately modeling the nucleation behavior. These parameters serve as input features for machine learning classification and regression models. The classification model categorizes nucleation behavior into three nucleation density regimes, preventing invalid nucleation attempts in simulations, while the regression model estimates the appropriate Langevin noise strength, significantly reducing the need for time-consuming trial-and-error simulations. This data-driven approach improves the efficiency of parameter selection in phase field models and provides a generalizable method for simulating nucleation-driven microstructural evolution processes in various materials. [ABSTRACT FROM AUTHOR]

Voltage-gated potassium channels are a widely distributed subgroup of potassium channels responsible for the efflux of potassium in the repolarisation of the cell membrane, and hence contribute to the latency and propagation of action potentials. As they are causal to synaptic transmission, alterations to the structure of these channels can lead to a variety of neurological and psychiatric diseases. The Kv3 subfamily of voltage-gated potassium channels are found on many neurons in the brain, including inhibitory interneurons where they contribute to fast-frequency firing. Changes to the firing ability of these interneurons can lead to an imbalance of inhibitory and excitatory neurotransmission. To date, we have little understanding of the mechanism by which excitatory and inhibitory inputs become imbalanced. This imbalance is associated with cognitive deficits seen across neurological and neuropsychiatric disorders, which are currently difficult to treat. In this review, we collate evidence supporting the hypothesis that voltage-gated potassium channels, specifically the Kv3 subfamily, are central to many neurological and psychiatric disorders, and may thus be considered as an effective drug target. The collective evidence provided by the studies reviewed here demonstrates that Kv3 channels may be amenable to novel treatments that modulate the activity of these channels, with the prospect of improved patient outcome. [ABSTRACT FROM AUTHOR]

The human endometrium is a highly regenerative tissue capable of undergoing scarless repair during the menstruation and postpartum phases. This process is mediated by endometrial adult stem/progenitor cells. During the healing of endometrial injuries, swift reepithelization results in the rapid covering of the wound surface and facilitates subsequent endometrial restoration. The involvement of endogenous endometrial epithelial stem cells, stromal cells, and bone marrow-derived cells in the regeneration of the endometrial epithelium has been a subject of prolonged debate. Increasing evidence suggests that the regeneration of the endometrial epithelium mainly relies on epithelial stem cells rather than stromal cells and bone marrow-derived cells. Currently, no consensus has been established on the identity of epithelial stem cells in the epithelial compartment. Several markers, including stage-specific embryonic antigen-1 (SSEA-1), sex-determining region Y-box 9 (SOX9), neural-cadherin (N-cadherin), leucine-rich-repeat-containing G-protein-coupled receptor 5 (LGR5), CD44, axis inhibition protein 2 (Axin2), and aldehyde dehydrogenase 1A1 (ALDH1A1), have been suggested as potential candidate markers for endometrial epithelial stem cells. The identification of endometrial epithelial stem cells contributes to our understanding of endometrial regeneration and offers new therapeutic insights into diseases characterized by regenerative defects in the endometrium, such as intrauterine adhesion. This review explores different perspectives on the origins of human and mouse endometrial epithelial cells. It summarizes the potential markers, locations, and hierarchies of epithelial stem cells in both human and mouse endometrium. It also discusses epithelial cell-based treatments for intrauterine adhesion, hoping to inspire further research and clinical application of endometrial epithelial stem cells. [ABSTRACT FROM AUTHOR]

Nasal respiratory disorders are linked to craniofacial anomalies and systemic dysfunctions. However, the implications of nasal respiratory disorders on brain development and their subsequent impact on brain functionalization remain largely unknown. Here, we describe that nasal obstruction from postnatal developmental stages in mice precipitates deficits in cerebellum-associated behaviors and compromised refinement and maturation of neural circuits in the cerebellum. We show that mice with nasal obstruction during developmental phases exhibit marked impairments in motor function and exhibit increased immobility time in forced swimming test. Additionally, we identified critical periods during which nasal respiration is essential for optimizing motor function and preserving mental health. Our study also reveals that nasal obstruction in mice disrupts the typical developmental process of synapse elimination in the cerebellum and hinders the normal transition of activity patterns in cerebellar Purkinje cell populations during development. Through comparing activity patterns in mouse models subjected to nasal obstruction at various stages, we suggest that the maturation of specific activity pattern among Purkinje cell populations is fundamental to the functional integrity of the cerebellum. Our findings highlight the indispensable role of adequate nasal respiration during development for the establishment and functional integrity of neural circuits, thereby significantly affecting brain function. Nasal obstruction during specific critical periods leads to motor deficits and depressive-like behaviors in mice, mediated by impaired synapse elimination and disrupted cerebellar activity patterns. [ABSTRACT FROM AUTHOR]

Arboviruses, transmitted by medical arthropods, pose a serious health threat worldwide. During viral infection, Post Translational Modifications (PTMs) are present on both host and viral proteins, regulating multiple processes of the viral lifecycle. In this study, a mammalian E3 ubiquitin ligase WWP2 (WW domain containing E3 ubiquitin ligase 2) is identified, which interacts with the NS1 protein of Zika virus (ZIKV) and mediates K63 and K48 ubiquitination of Lys 265 and Lys 284, respectively. WWP2‐mediated NS1 ubiquitination leads to NS1 degradation via the ubiquitin‐proteasome pathway, thereby inhibiting ZIKV infection in mammalian hosts. Simultaneously, it is found Su(dx), a protein highly homologous to host WWP2 in mosquitoes, is capable of ubiquitinating NS1 in mosquito cells. Unexpectedly, ubiquitination of NS1 in mosquitoes does not lead to NS1 degradation; instead, it promotes viral infection in mosquitoes. Correspondingly, the NS1 K265R mutant virus is less infectious to mosquitoes than the wild‐type (WT) virus. The above results suggest that the ubiquitination of the NS1 protein confers different adaptations of ZIKV to hosts and vectors, and more importantly, this explains why NS1 K265‐type strains have become predominantly endemic in nature. This study highlights the potential application in antiviral drug and vaccine development by targeting viral proteins' PTMs. [ABSTRACT FROM AUTHOR]

Background: Cognitive function plays a crucial role in human life, and its maintenance and improvement are essential in both young and older adults. Since cognitive decline can be associated with oral function decline, preventing the decline in both cognitive and oral functions is an urgent social issue. Several training methods to improve each function have been proposed. Previous studies have indicated that greater brain activity during training is associated with increased benefits for cognitive function. Although adding cognitive function elements to oral function training may promote the activation of brain activity during oral function training, the effects have not been validated. The main purpose of this study is to develop a novel training program that combines oral function training with cognitive training, which is expected to activate key brain regions involved in oral and cognitive functions, such as the left dorsolateral prefrontal cortex (DLPFC) and right medial prefrontal cortex (mPFC). Methods: Four types of training programs combining oral and cognitive training: PaTaKaRa × calculation, lip exercise × N-back, tongue exercise × inhibition, and tongue exercise × memory, were developed. Each program had seven levels of difficulty [level 0 (no cognitive load) and level 6 (maximum difficulty)]. Twelve healthy young adults participated in the study and were instructed to perform all four programs. Brain activity in the left DLPFC and right mPFC were measured during each training session using two-channel near-infrared spectroscopy (NIRS). Results: No significant brain activity was observed during training at level 0. Brain activity in the left DLPFC was significantly increased at levels 1 and 2 and in the left DLPFC and right mPFC at level 6 during PaTaKaRa × calculation training. Brain activity in the left DLPFC was significantly increased at level 6 during tongue exercise × inhibition training. Brain activity in the left DLPFC and right mPFC was significantly increased at level 6 during lip exercise × N-back training. Conclusion: Oral function training did not significantly increase brain activity; nevertheless, oral function with cognitive training stimulated brain activity in the prefrontal cortex. Trial registration: : UMIN-CTR. ID: UMIN000039678. date: 06/03/2020. [ABSTRACT FROM AUTHOR]

Background: Cognitive function plays a crucial role in human life, and its maintenance and improvement are essential in both young and older adults. Since cognitive decline can be associated with oral function decline, preventing the decline in both cognitive and oral functions is an urgent social issue. Several training methods to improve each function have been proposed. Previous studies have indicated that greater brain activity during training is associated with increased benefits for cognitive function. Although adding cognitive function elements to oral function training may promote the activation of brain activity during oral function training, the effects have not been validated. The main purpose of this study is to develop a novel training program that combines oral function training with cognitive training, which is expected to activate key brain regions involved in oral and cognitive functions, such as the left dorsolateral prefrontal cortex (DLPFC) and right medial prefrontal cortex (mPFC). Methods: Four types of training programs combining oral and cognitive training: PaTaKaRa × calculation, lip exercise × N-back, tongue exercise × inhibition, and tongue exercise × memory, were developed. Each program had seven levels of difficulty [level 0 (no cognitive load) and level 6 (maximum difficulty)]. Twelve healthy young adults participated in the study and were instructed to perform all four programs. Brain activity in the left DLPFC and right mPFC were measured during each training session using two-channel near-infrared spectroscopy (NIRS). Results: No significant brain activity was observed during training at level 0. Brain activity in the left DLPFC was significantly increased at levels 1 and 2 and in the left DLPFC and right mPFC at level 6 during PaTaKaRa × calculation training. Brain activity in the left DLPFC was significantly increased at level 6 during tongue exercise × inhibition training. Brain activity in the left DLPFC and right mPFC was significantly increased at level 6 during lip exercise × N-back training. Conclusion: Oral function training did not significantly increase brain activity; nevertheless, oral function with cognitive training stimulated brain activity in the prefrontal cortex. Trial registration: : UMIN-CTR. ID: UMIN000039678. date: 06/03/2020. [ABSTRACT FROM AUTHOR]

Knowledge of Mexican immigrant sleep health is limited. We investigated the association between acculturation, depression, and having trouble sleeping among a nationally representative sample of Mexican immigrant adults. We used a logistic regression model on cross-sectional data from the 2005–2018 National Health and Nutrition Examination Survey on 2,670 non-U.S.-born Mexican adults aged ≥18 years old. Living in the U.S. for ≥10 years (Adjusted Odds Ratio (AOR) = 2.18; 95% Confidence Interval (CI) = 1.39–3.41), speaking majority English (AOR = 1.62; 95% CI = 1.00–2.64), and mild (AOR = 2.70; 95% CI = 1.82–4.02), moderate (AOR = 3.96; 95% CI = 2.53–6.19), and moderately severe/severe (AOR = 5.75; 95% CI = 3.08–10.75) depression levels were associated with having trouble sleeping. Non-U.S. citizenship status was associated with lower odds of having trouble sleeping (AOR = 0.62; 95% CI = 0.43–0.88). Greater acculturation and depression are associated with higher odds of having trouble sleeping. We provide new knowledge on how citizenship status may be linked to the sleep health of Mexican immigrant communities. [ABSTRACT FROM AUTHOR]

Voltage-gated potassium channels are a widely distributed subgroup of potassium channels responsible for the efflux of potassium in the repolarisation of the cell membrane, and hence contribute to the latency and propagation of action potentials. As they are causal to synaptic transmission, alterations to the structure of these channels can lead to a variety of neurological and psychiatric diseases. The Kv3 subfamily of voltage-gated potassium channels are found on many neurons in the brain, including inhibitory interneurons where they contribute to fast-frequency firing. Changes to the firing ability of these interneurons can lead to an imbalance of inhibitory and excitatory neurotransmission. To date, we have little understanding of the mechanism by which excitatory and inhibitory inputs become imbalanced. This imbalance is associated with cognitive deficits seen across neurological and neuropsychiatric disorders, which are currently difficult to treat. In this review, we collate evidence supporting the hypothesis that voltage-gated potassium channels, specifically the Kv3 subfamily, are central to many neurological and psychiatric disorders, and may thus be considered as an effective drug target. The collective evidence provided by the studies reviewed here demonstrates that Kv3 channels may be amenable to novel treatments that modulate the activity of these channels, with the prospect of improved patient outcome. [ABSTRACT FROM AUTHOR]

The prevalence of age-related degenerative joint diseases, particularly intervertebral disc degeneration and osteoarthritis, is increasing, thereby posing significant challenges for the elderly population. Mitochondrial dysfunction is a critical factor in the etiology and progression of these disorders. Therapeutic interventions that incorporate mitochondrial transplantation exhibit considerable promise by increasing mitochondrial numbers and improving their functionality. Existing evidence suggests that exogenous mitochondrial therapy improves clinical outcomes for patients with degenerative joint diseases. This review elucidates the mitochondrial abnormalities associated with degenerative joint diseases and examines the mechanisms of mitochondrial intercellular transfer and artificial mitochondrial transplantation. Furthermore, therapeutic strategies for mitochondrial transplantation in degenerative joint diseases are synthesized, and the concept of engineered mitochondrial transplantation is proposed. [ABSTRACT FROM AUTHOR]

Background: Exercise can be used as a model to understand immunometabolism. Biological data on elite athletes are limited, especially for female athletes, including relevant data on acute-phase proteins and amino acid metabolism. Methods: We analyzed acute-phase proteins and amino acids collected at South American, Pan-American, and Olympic Games for 16 Olympic sports. We compared female and male elite athletes (447 vs. 990 samples) across four states (fasting, pre-exercise, post-exercise, and resting) to understand sex-specific immunometabolic responses in elite athletes. Results: Considering all states and sports, we found that elite female athletes exhibited higher concentrations of C-reactive protein, lipopolysaccharide-binding protein, myeloperoxidase, haptoglobin, and IGF1, with ratios ranging from 1.2 to 2.0 (p < 0.001). Women exhibited lower concentrations of most amino acids, except for glutamate and alanine. Although almost 30% lower in women, branched-chain amino acids (BCAAs) showed a similar pattern in all states (ρ ≥ 0.9; p < 0.001), while aromatic amino acids (AAAs) showed higher consumption during exercise in women. Conclusion: We established sex dimorphism in elite athletes' metabolic and inflammatory responses during training and competition. Our data suggest that female athletes present a lower amino acid response towards central fatigue development than male athletes. Understanding these differences can lead to insights into sex-related immuno-metabolic responses in sports or other inflammatory conditions. [ABSTRACT FROM AUTHOR]