Calcific aortic valve disease (CAVD) is a progressive fibrocalcific illness for which no effective pharmaceutical treatment exists. This study investigated whether carbamoylated high-density lipoprotein (C-HDL), a defective type of HDL that can develop during inflammation, contributes to CAVD progression and the involved molecular pathways. Male ApoE-/- mice were divided into three groups: CAVD model, cyanate-treated, and inhibitor, and analyzed after 12 weeks. C57BL/6 mice on a regular diet served as blank controls. Serum paraoxonase-1 (PON1), aortic valve calcification, cluster of differentiation 31 (CD31), phosphorylated nuclear factor kappa B p65 (p-p65), NOTCH receptor 1 (NOTCH1), and runt-related transcription factor 2 (RUNX2) were evaluated. In parallel, using RNA sequencing (RNA-seq), Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses, protein-protein interaction (PPI) network analysis, and quantitative real-time polymerase chain reaction. Cyanate treatment reduced serum PON1 levels, increased von Kossa-positive calcium deposition, and raised CD31, p-p65, NOTCH1, and RUNX2 levels compared with the model group, but Gly partially corrected these effects. Transcriptomic research identified 270 C-HDL-associated differentially expressed genes (DEGs) enriched in pathways associated with inflammatory signaling and NF-κB activity. Five potential hub genes (BIRC6, PIK3R1, ATM, IFIH1, and DDX58) were discovered and verified using qRT-PCR. These data show that C-HDL may accelerate CAVD by disrupting valve endothelial homeostasis and stimulating inflammatory signaling, and they identify potential molecular targets for future functional validation.
This randomized controlled trial evaluated dexmedetomidine combined with remifentanil versus remifentanil alone for monitored anesthesia care during radiofrequency catheter ablation for atrial fibrillation. Between January and December 2023, 100 patients were stratified by age, sex, BMI, and atrial fibrillation type, then randomly assigned (1:1, block size 4, sealed envelopes) to Group A (dexmedetomidine 1 μg/kg loading then 0.2-0.4 μg/kg/h plus remifentanil, n = 50) or Group B (saline control plus remifentanil, n = 50). Baseline characteristics were comparable (all P > 0.05). Hemodynamic parameters were recorded at baseline (T 0), 10 min after induction (T 1), maintenance (T 2), 10 min before surgery end (T 3), and at surgery end (T 4). Group A showed higher mean arterial pressure, cardiac index, and cardiac output at T 1-T 4 (P < 0.05), with lower heart rate and blood pressure (P < 0.05). Ramsay Sedation Score was higher at T 3-T 4 (P < 0.05). Adverse reactions and inflammatory markers (IL-6, TNF-α, CRP) were attenuated postoperatively (P < 0.05). Dexmedetomidine combined with remifentanil provides superior hemodynamic stability, enhanced sedation, reduced inflammation, and fewer adverse events during atrial fibrillation ablation.
Endometriosis is an estrogen-dependent disorder characterized by chronic inflammation, immune dysregulation, and altered hormone metabolism. Although gut microbiota-derived metabolites have been implicated in shaping immune microenvironments and lesion development, the underlying regulatory mechanisms remain incompletely understood. Here, we integrated multi-omics, protein-protein interaction (PPI), SHapley Additive exPlanations (SHAP), and single-cell transcriptomics to identify core targets and delineate their interactions with microbiota-derived metabolites, followed by molecular simulations to evaluate metabolite-target binding stability. In this study, we identified 61 differentially expressed genes (DEGs) associated with microbial metabolites. Among these, MET and SELL emerged as key hub genes, with MET showing a potentially protective association and SELL exhibiting a modest positive association with endometriosis risk. Specific gut microbes, including Bacteroides, Parabacteroides, and Bifidobacterium, along with metabolites such as palmitoylethanolamide and dihydroresveratrol, were implicated in modulating immune and inflammatory pathways relevant to lesion formation. Additionally, cell-cell communication analysis indicated that the 61 DEGs were enriched in the Macrophage migration inhibitory factor (MIF) and C-X-C motif chemokine ligand family (CXCL) signaling pathways, suggesting their potential importance in the endometriotic microenvironment. Computational simulations further indicated potential binding interactions between multiple metabolites and MET and SELL. These findings delineate a multi-layered regulatory framework linking gut microbiota, metabolites, molecular targets, and immune interactions, thereby providing a foundation for mechanistic studies and targeted therapeutic strategies.
Diabetic nephropathy (DN) is a major complication of diabetes mellitus, and identifying effective therapeutic targets remains an urgent need. In this study, genes associated with DN were obtained from the gene expression omnibus (GEO) database, and Bioinformatics analysis revealed that mannosyl (alpha-1,6-)-glycoprotein beta-1,6-N-acetylglucosaminyltransferase (MGAT5) was downregulated in DN. Functional experiments demonstrated that MGAT5 overexpression activated the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway, enhanced DN-related cell viability, and reduced the levels of lactate dehydrogenase (LDH), cleaved caspase-3 (C-casp3), Bcl-2-associated X protein (Bax), interleukin-6 (IL-6), interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), malondialdehyde (MDA), acyl-CoA synthetase long-chain family member 4 (ACSL4), prostaglandin-endoperoxide synthase 2/cyclooxygenase-2 (PTGS2/COX-2), Fe2+ content, ROS production, and apoptosis. Meanwhile, MGAT5 overexpression increased the levels of B-cell lymphoma 2 (Bcl-2), glutathione (GSH), and glutathione peroxidase 4 (GPX4). Conversely, MGAT5 knockdown partially reversed these protective effects. These findings suggest that MGAT5 may alleviate DN-associated cellular injury by activating the Nrf2/HO-1 pathway and regulating oxidative stress, inflammatory responses, ferroptosis, and apoptosis. MGAT5 may represent a potential therapeutic candidate for further investigation in diabetic nephropathy.
Radioresistance remains a critical barrier to achieving durable locoregional control and improved survival outcomes in breast cancer. RAD18, an E3 ubiquitin ligase that regulates translesion synthesis and post-replication repair, has emerged as a candidate mediator of this phenotype by promoting proliferating cell nuclear antigen (PCNA) ubiquitination, facilitating replication stress tolerance, and enabling tumor cell survival following DNA damage. In parallel, the PI3K/AKT/mTOR (PAM) signaling pathway represents one of the most frequently dysregulated oncogenic networks in breast cancer and is increasingly recognized as a central determinant of therapeutic resistance. Notably, however, its biological and clinical relevance is highly context-dependent, with the strongest evidence observed in hormone receptor-positive (HR+)/HER2-negative disease and a more heterogeneous, less well-defined role in triple-negative breast cancer. In this narrative review, we integrate current evidence to examine the role of RAD18 in breast cancer radioresistance and to evaluate how RAD18-mediated DNA damage tolerance may be functionally embedded within broader PAM-driven survival programs. While existing data support a biologically plausible convergence between DNA damage tolerance mechanisms and oncogenic survival signaling, direct mechanistic evidence linking RAD18 to PAM pathway activity in breast cancer remains limited. We therefore propose a subtype-informed conceptual framework in which RAD18-dependent stress tolerance operates within a permissive survival signaling context. Such a framework may refine the interpretation of radioresistance and inform the development of predictive biomarkers as well as rational radiosensitization strategies.
Vocalizations provide an informative means of assessing the emotional states of animals, yet male vocal behaviour in domestic sheep remains unexplored. The study aimed to investigate whether rams' bleats vary across five distinct contexts associated with morning and night isolation, exposure to familiar ewe-bell sounds, feed anticipation, and feed denial. A total of 428 high-quality bleats were used to extract 20 acoustic parameters, which were then analyzed using a multivariate acoustic approach. Principal Component Analysis identified five independent acoustic components reflecting source-parameters, spectral energy, formant frequencies, voice stability, and temporal characteristics. Context significantly influenced the acoustic structure of bleats, with spectral, formant, vocal stability, and temporal characteristics showing context-dependent variation, whereas fundamental frequency-related parameters remained unaffected. Feed anticipation elicited higher formant-related scores; feed denial produced reduced spectral energy, and social isolation contexts were characterized by increased vocal instability. Discriminant analyses revealed moderate classification accuracy, indicating overlapping acoustic patterns and supporting graded rather than discrete vocal signals. Morphometric effects were minimal, with wither height affecting formant structure. The findings provide the first detailed evidence that rams modulate multiple acoustic features across contexts, demonstrating that male sheep encode emotional states through shifts in vocal parameter variation.
As a typical inflammatory arthritis, rheumatoid arthritis (RA) reduces the life quality of patients from all over the world. Magnolol has been reported to exert the anti-inflammation role in several diseases. Here, we aim to investigate the effect of magnolol on the inflammatory response in vivo and in vitro. Indicators like arthritic index and paw weight were measured after collagen-induced arthritis (CIA) induction and magnolol treatment. The tissues of the rats' left hind paws were subjected to hematoxylin & eosin staining to observe the morphological changes. The serum inflammatory cytokines and MH7A cells were evaluated by enzyme-linked immunosorbent and real time quantitative polymerase chain reaction. Cell viability assay and flow cytometry were prepared for evaluating the viability and apoptosis of MH7A cells, respectively. Magnolol alleviated the paw inflammation and joint swelling in CIA rat model. CIA-induced upregulation of the serum inflammatory markers was also significantly reduced by magnolol in polyarthritis rat model. For in vitro experiments, magnolol treatment enhanced the viability and decreased apoptosis of tumor necrosis factor-alpha (TNF-α)-stimulated MH7A cells. Inflammatory cytokines were also downregulated by magnolol in TNF-α-stimulated MH7A cells. Magnolol alleviated RA development by inhibiting inflammatory response in CIA-induced rat model or TNF-α-treated MH7A cells.
Phytoplankton are primary producers in marine ecosystems and play a central role in biogeochemical cycles, yet their physiological responses to altered seawater pH vary among taxa and over time. Here, we examined the effects of sustained pH manipulation on pigment composition, growth, and dark respiration in three ecologically important phytoplankton taxa - a diatom (Pseudo-nitzschia spp.), a dinoflagellate (Heterocapsa pygmaea), and a haptophyte (Emiliania huxleyi) - during a 15-day controlled laboratory experiment. Cultures were maintained at pH 8.1, 7.8, and 7.5, representing present-day and enhanced acidification conditions. Responses to pH were species-specific and strongly time-dependent. Growth and cell-specific respiration rates showed relatively small and often transient differences among pH treatments, suggesting short-term metabolic adjustment under altered pH. In contrast, pigment composition exhibited clearer and more consistent pH-related responses, primarily expressed as shifts in temporal patterns rather than uniform directional changes. In Pseudo-nitzschia spp. and H. pygmaea, several key pigments displayed pronounced pH-dependent trajectories, whereas E. huxleyi showed greater temporal variability and weaker separation among pH treatments. Overall, these results demonstrate that photophysiological traits respond sensitively to sustained pH changes even when population-level growth and respiration remain comparatively stable, highlighting pigment composition as a potentially sensitive indicator of short-term phytoplankton acclimation to ocean acidification.
This study investigated transrectal ultrasound parameters and total serum exosome levels in prostate cancer (PCa) patients with bone metastasis (BM), and evaluated their combined value in assessing metastatic status. 40 PCa patients were categorized into non-bone metastasis (NBM, 21 cases) and BM (19 cases) groups based on single photon emission computed tomography/computed tomography or bone scans. Serum exosomes were extracted and analyzed via nanoparticle tracking analysis, while transrectal ultrasound and ultrasound-guided biopsies were performed. The study compared exosome levels and ultrasound parameters between groups, and assessed their diagnostic value for BM using receiver operating characteristic (ROC) curves, and analyzed correlations between exosomes and ultrasound findings. PCa patients with BM showed significantly higher serum exosome concentrations and ultrasound parameters (peak intensity, area under the curve (AUC), and Grad) than NBM patients (p < 0.001). ROC analysis revealed optimal cutoff values for discriminating BM: 19.33 dB for PI, 1,156.63 dB s for AUC, 2.02 dB/s for Grad, and 3.34 × E10 particles/mL for exosomes. The combined test (AUC = 0.97) outperformed individual parameters (AUCs 0.83-0.89), demonstrating superior diagnostic performance in identifying PCa BM. In conclusion, this exploratory preliminary study indicates that exosomes may have potential application value in the assessment of PCa BM.
Allergic rhinitis (AR) is a common chronic inflammatory disorder characterized by nasal mucosal inflammation, sneezing, and rhinorrhea. Schisandrin A (Schis-A) has demonstrated significant anti-inflammatory effects in models of allergic asthma. This study aimed to evaluate the therapeutic efficacy of Schis-A in AR and to elucidate its underlying molecular mechanisms. An AR mouse model was established by sensitization and challenge with ovalbumin (OVA), followed by oral administration of Schis-A at doses of 40 and 80 mg/kg/day. Nasal symptoms were monitored and quantified. OVA-specific immunoglobulin E (IgE) levels and T helper (Th)1/Th2- and regulatory T cells (Treg)/Th17-associated cytokines were measured using enzyme-linked immunosorbent assay and quantitative real-time PCR. Treg and Th17 cell populations were analyzed by flow cytometry. The results showed that Schis-A treatment significantly reduced OVA-induced nasal rubbing and sneezing, indicating effective attenuation of allergic responses. Serum OVA-specific IgE levels were markedly reduced in Schis-A-treated AR mice. Moreover, Schis-A restored Th1/Th2 and Treg/Th17 cytokine balance, as indicated by upregulated expression of IFN-γ, IL-2, and Foxp3, alongside downregulation of IL-4, IL-5, IL-13, and IL-17. Flow cytometric analysis confirmed an increase in Treg cells and a reduction in Th17 cell populations. Mechanistically, Schis-A inhibited activation of the PI3K/AKT signaling pathway, suggesting that this pathway may contribute to its immunomodulatory effects. Schis-A alleviates AR by modulating Th1/Th2 and Treg/Th17 immune responses and inhibiting PI3K/AKT pathway activation, offering a promising therapeutic strategy for the treatment of AR.
BCR-ABL1 e6a2-positive chronic myeloid leukemia (CML) is a rare molecular subtype of CML, accounting for less than 1 % of CML cases. It was shown to be associated with aggressive clinical behavior and a tendency toward disease progression. Here, we report a 56-year-old man who presented with pancytopenia, cervical lymphadenopathy, and severe myelofibrosis, without the typical leukocytosis observed in classic CML. Concurrent active pulmonary tuberculosis further complicated the diagnostic process. Hyperuricemia and elevated levels of lactate dehydrogenase (LDH) suggested a high cell-turnover state, and cervical lymph node biopsy confirmed myeloid sarcoma. Cytogenetic analysis revealed t(9;22)(q34;q11.2) with trisomy 8. Real-time quantitative polymerase chain reaction (RT-qPCR) identified the rare BCR-ABL1 e6a2 transcript. The patient received second- and third-generation tyrosine kinase inhibitor (TKI)-based therapy combined with chemotherapy. An individualized rifamycin-sparing anti-tuberculosis regimen was also prescribed. The patient achieved complete remission with marked regression of myelofibrosis. This case suggests that e6a2-positive CML may present with atypical features, including pancytopenia, severe myelofibrosis, and extramedullary blast crisis. In patients with concurrent tuberculosis, timely tissue biopsy and molecular testing are essential to accelerate diagnosis.
Maternal health during pregnancy is a leading factor influencing offspring risk. This study investigated whether postnatal dietary supplementation could reduce oxidative stress and gut leakiness in a rat model of autism spectrum disorder (ASD). Male rat pups were prenatally exposed to valproic acid (VPA) or lipopolysaccharide (LPS) to induce ASD-like conditions. A total of 54 offspring of Wistar albino rats were divided into nine groups to evaluate various postnatal treatments, including an artichoke-based prebiotic (AR), probiotics (Pro), and omega-3 fatty acids (ω3). The experimental design also included control groups (saline, VPA-only, and LPS-only), as well as a protective regimen in which AR was administered both prenatally and postnatally. Oxidative stress and gut permeability "leakiness" were assessed using Enzyme-Linked Immunosorbent Assay (ELISA). Prenatal exposure to VPA and LPS was associated with increased oxidative stress levels in brain homogenates, accompanied by a significant decrease in glutathione (GSH). Additionally, elevated plasma levels of gut permeability biomarkers were observed. In the VPA model, treatment with artichoke-derived prebiotics - administered either prenatally, postnatally, or in combination with probiotics - effectively improved oxidative stress markers, as evidenced by a significant increase in GSH levels. Conversely, similar interventions in the LPS-induced maternal immune activation model did not significantly ameliorate oxidative stress, although a modest increase in GSH levels was noted. Plasma levels of gut permeability biomarkers did not show significant improvement in either model following treatment with artichoke-derived probiotics alone or in combination with probiotics and omega-3 fatty acids. However, intestinal fatty acid-binding protein levels were significantly reduced in all treatment groups across both models. In contrast, lipopolysaccharide-binding protein (LBP) levels were not significantly reduced by artichoke extract monotherapy in either model, although combination therapy with probiotics and/or omega-3s led to significant reductions in LBP. These results support the use of both VPA and LPS as complementary models for studying ASD. The VPA model, characterized by direct and predictable neurotoxic effects, appears to be more suitable for evaluating preventive interventions. In contrast, the LPS model more accurately captures the complex immune-inflammatory mechanisms implicated in ASD, highlighting the need for broader and more individualized treatment strategies. The differing responses to artichoke-based interventions in these models underscore the importance of considering ASD etiology when designing dietary and microbiome-targeted therapies.
Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by memory loss and irreversible cognitive decline. Glycogen synthase kinase 3β (GSK-3β) is significant in tau hyperphosphorylation and neurodegeneration. The cholinergic hypothesis of AD links cognitive impairment to reduced synaptic acetylcholine (ACh). Increased acetylcholinesterase (AChE) activity exacerbates this issue. To search for a potential dual GSK-3β/AChE inhibitor, we focused on N-methylcytisine. This natural cytisine-derived alkaloid has not been studied for its various biological effects on the prevention of AD. The in vitro results indicated that N-methylcytisine displayed promising activity against GSK-3β and AChE with IC50 values of 11 and 22.7 µM, respectively. GSK-3β kinetic study according to the varying substrate or ATP concentrations at different N-methylcytisine levels revealed mixed-type inhibition. The results of the integrated in silico workflow indicate that N-methylcytisine exhibited favorable binding to AChE (docking score -9.6 kcal/mol; MM-GBSA -70.2 kcal/mol), comparable to the reference inhibitor galantamine (-10.8 kcal/mol; -70.6 kcal/mol). In contrast, its interaction with GSK-3β was more moderate (-5.3 kcal/mol; -50.3 kcal/mol) relative to staurosporine (-8.5 kcal/mol; -82.6 kcal/mol), consistent with its smaller scaffold. Overall, the results support a flexible, mixed-type interaction profile and highlight N-methylcytisine as a promising dual-acting candidate for Alzheimer's disease.
Darutoside (DA), a diterpenoid compound derived from Herba Siegesbeckiae, possesses notable anti-inflammatory properties. This study evaluated the effectiveness of DA in treating rheumatoid arthritis (RA) symptoms and elucidated the relevant mechanisms. The anti-RA efficacy of DA was investigated in a Complete Freund's Adjuvant (CFA)-induced arthritis mouse model, while RAW264.7 macrophages were used to examine DA's impact on macrophage polarization in vitro. Targets of DA for RA were predicted through protein-protein interaction networks and pathway enrichment analysis. Subsequently, mechanisms were verified through in vitro assays. The results showed that DA alleviated the symptoms in the CFA mouse model, as evidenced by reduced clinical scores, attenuated paw swelling, and decreased inflammatory response. Moreover, DA induced repolarization of M1/M2 macrophages in both the CFA model mice and RAW264.7 cells. Network pharmacology analysis suggested that DA may exert its anti-RA effects by modulating the JAK-STAT signaling pathway. Western blotting confirmed that DA inhibited the JAK2-STAT3-p65 pathway, thereby suppressing M1 macrophage polarization. Furthermore, the repolarization effect of DA on macrophages was counteracted in JAK2-silenced cells. These findings indicate that DA attenuates arthritis symptoms in CFA mice, and this effect may be attributed to its regulation of macrophage M1/M2 polarization through suppression of the JAK2-STAT3 pathway and downstream p65 activation.
This single-center retrospective study evaluated the prognostic value of IGF-1R, VEGFR2, PDGFR, and c-MET expression in 94 patients with pathologically confirmed ESCC who underwent esophagectomy, and explored the potential relevance of combining immune checkpoint inhibitors (ICIs) with growth factor receptor tyrosine kinase inhibitors (TKIs). A prognostic nomogram was developed for clinically available factors and growth factor receptors with significant prognostic value, and the nomogram was validated with ROC curve analyses. Among the four growth factor receptors, VEGFR2 and IGF-1R expression differed significantly between death and survival groups. Worse prognosis was associated with advanced clinical stage, deeper tumor invasion, greater nodal involvement, high VEGFR2 expression, and high IGF-1R expression (clinical stage: HR = 2.15, 95 % CI: 1.45-3.20; T stage: HR = 1.78, 95 % CI: 1.12-2.83; N stage: HR = 2.42, 95 % CI: 1.61-3.64; VEGFR2: HR = 1.61, 95 % CI: 1.04-2.49; IGF-1R: HR = 1.74, 95 % CI: 1.12-2.70). PDGFR and c-MET expression were not significantly associated with cancer-specific survival. Although the nomogram showed prognostic performance (AUC = 0.512), the small sample size precluded formal histology-specific stratified analysis, limiting assessment of subtype-specific prognostic effects.
Clozapine, an atypical antipsychotic, is effective for treatment-resistant schizophrenia but frequently causes metabolic adverse effects, including hepatic lipid accumu-lation, inflammation and insulin resistance. Adiponectin, an adipocyte-derived cytokine with anti-inflammatory and insulin-sensitizing properties, may counteract these effects; however, its ability to mitigate clozapine-induced hepatic alterations remains unclear. This study examined whether adiponectin overexpression reduces clozapine-induced lipid accumulation, inflammatory signaling, and whether it restores insulin-related Akt signaling in human HepG2 liver cells. Cells were treated with 25 μM clozapine for 24 or 48 h, and adiponectin was overexpressed by plasmid transfection. Lipid accumulation was quantified by BODIPY staining. AdipoR1 and AdipoR2 expression was analyzed by qPCR, and protein levels of FASN, phosphorylated NF-κB, and phosphorylated Akt were assessed by Western blotting. Clozapine increased lipid accumulation, upregulated FASN, and reduced AdipoR1 and AdipoR2 expression. Adiponectin overexpression significantly decreased lipid levels, which was associated with reduced NF-κB phosphorylation, suggesting attenuation of inflammatory signaling. However, adiponectin did not restore insulin-stimulated Akt phosphorylation. In summary, adiponectin selectively reduced clozapine-induced lipid accumulation and inflammatory signaling in HepG2 cells, whereas impaired insulin-stimulated Akt phosphorylation remained unchanged under the present experimental conditions. These findings indicate a selective protective role of adiponectin and suggest its potential as a modulator of clozapine-induced metabolic side effects.
This study aimed to investigate the effects of hypoxia on mitochondrial function in C8-D1A astrocytes and to evaluate its association with apoptosis. Mouse C8-D1A astrocytes were allocated to a normoxia group (21 % O2, 5 % CO2, 37 °C) or a hypoxia group (1 % O2, 5 % CO2, 37 °C) and cultured for 24 h, 48 h, or 72 h. Compared with the normoxia group, the hypoxia group demonstrated a significant reduction in mean mitochondrial fluorescence intensity (p < 0.01) and a significant increase in mitochondrial ROS levels. Regarding mitochondrial dynamics-related proteins, Mfn1 expression was significantly decreased, and Mfn2 expression was significantly decreased at 72 h (p < 0.01). Drp1 expression was significantly increased at all time points (p < 0.01), and Fis1 expression was significantly upregulated (p < 0.01). The proportion of cells exhibiting reduced mitochondrial membrane potential was significantly higher in the hypoxia group. The percentage of apoptotic cells was significantly increased. TEM analysis revealed structural abnormalities of mitochondria in cells exposed to hypoxia. Hypoxia may promote apoptosis in C8-D1A astrocytes through disruption of mitochondrial morphology, function, and dynamics. These alterations are associated with decreased mitochondrial content and increased ROS production, which may contribute to mitochondrial dysfunction and apoptosis under hypoxic conditions.
The genes coding for the proteins of the ectodermal dysplasin pathway, EDA, EDAR and EDA2R are found in genomes of animals that long predate vertebrates. We show that EDA, EDAR and EDA2R are expressed in the sea anemone. A fourth gene in the pathway, EDARADD, only appears with the cyclostomes. With the appearance of EDARADD, the ectodermal dysplasin system was now complete, and the skin appendages emerged, first in the form of the cyclostome’s keratinized proto-teeth, until finally, feathers and then mammalian hair and eccrine glands evolved. We elaborate on the specific roles of the ectodermal dysplasin pathway proteins: EDA releases its extracellular circulating component, switching on the pathway at the appropriate stage in embryological development. EDA binds to EDAR, whose location in the embryo has been specified by a reaction-diffusion system. The EDA/EDAR complex now binds to intracellular EDARADD, directing the expression of downstream proteins that orchestrate the mechanics of the cell movements, building the placodes and the appropriate skin appendages.
Microbiome refers to the collection of microorganisms living in the human body. Skin, intestines and upper respiratory tract are particularly inhabited by microorganisms. The microbiota of the scalp and hair, though so far little understood, is particularly abundant in terms of microorganisms, which play an important role in maintaining the health of the scalp by inhibiting pathogens and promoting optimal skin condition. Dysbiosis of the scalp microbiota can be influenced by many factors, both exo and endogenous leading to the development of pathological conditions such as dandruff or seborrhoeic dermatitis. The aim of this preliminary study was the microbiological diagnosis of the scalp and hair in the group of individuals aged 20-40 years old. The samples for the research have been obtained from three different sites on the scalp of 6 individuals aged 20 to 40. The material for the study was collected using contact plates for total bacterial counts - Rodac Contact Test. The colonies grown on the microbiological media were characterised in terms of their size and shape. Subsequently, Gram staining was performed to assign the colonies of the bacteria to Gram-positive or Gram-negative bacteria, as well as fungi characterisation of the scalp and hair was conducted using a trichological camera. Finally, on the basis of the study following conclusions have been drawn. There were observed differences in the appearance of microbial colonies between younger and older people and in the group of 40-year-old, there was a significantly less colony diversity monitored. In terms of bacteria, Gram-positive cocci got isolated most frequently. In addition, yeast as well as filamentous fungi occurred abundant in the middle of the head of the research participants.
Halophytes such as Mesembryanthemum forsskalii Hochst. ex Boiss. are well-adapted to harsh environments characterized by high salinity and drought, offering both nutritional and medicinal benefits. However, the genetic and molecular basis of salinity tolerance in M. forsskalii remains largely unexplored. This study aimed to generate novel genomic resources and identify the genes, pathways, and transcriptional regulators associated with salt stress tolerance. Plant samples were treated with NaCl at 150 mM and 400 mM, resulting in transcriptomic sequencing yielding over 50 million reads for each concentration. Differential expression gene (DEG) analysis revealed 5,606 and 665 significantly upregulated and downregulated genes, respectively, in plants irrigated with 150 mM NaCl (C vs S1), while 10,730 DEGs were identified under 400 mM NaCl (C vs S2), of which 9,970 were upregulated and 760 downregulated. De novo assembly indicated that a substantial proportion of transcripts encoded novel or functionally unknown proteins. Approximately 29 % and 21 % of transcripts under 150 and 400 mM NaCl were functionally annotated in UniProt, GO, and KEGG databases. The most enriched molecular functions included manganese ion binding and oxidoreductase activity. Transcription factor families such as bHLH, NAC and MYB-related family proteins were highly represented. These findings will support salinity research.
