Search Results (2,297)

Scalp microbes are recognized as contributors to hair loss by influencing scalp homeostasis and hair growth. However, the in vitro anti-hair loss activity of microbial culture media derived from healthy scalps remains unclear. In this study, resident microbes from 20 Korean participants with healthy scalps and hair were isolated, and Staphylococcus capitis was used to produce S. capitis ferment filtrate (SCFF). SCFF anti-hair loss activity was evaluated in human follicle dermal papilla cells (HFDPCs) and human adult low-Calcium High-Temperature (HaCaT) keratinocytes via proliferation assays, qPCR, immunocytochemistry, and SA-β-gal staining at 250–1000 μg/mL. SCFF increased cell density after 48 h in a concentration-dependent manner. In HFDPCs, SCFF controlled growth (KGF, IGF-1, and HGF) and androgen (AR and TGF-β2) factors, regulating key mRNAs for hair growth. SCFF mitigated scalp and hair aging by promoting sirtuins 1 and 7 and collagen type 13, while suppressing p21 and X-Gal staining. In HaCaT cells, SCFF exhibited a scalp barrier-strengthening effect by significantly increasing filaggrin and involucrin levels. It suppressed reactive oxidative stress and exhibited DPPH and ABTS radical scavenging activity. These results suggest that SCFF may modulate key pathways associated with hair loss by promoting scalp and hair anti-aging, barrier strengthening, enhancing antioxidant activity, and supporting hair growth. Full article

Colorectal cancer (CRC) is the third most commonly diagnosed malignancy worldwide, with molecular heterogeneity complicating early detection and treatment stratification. The insulin-like growth factor (IGF) axis interacts bidirectionally with immune regulatory mechanisms in ways that shape tumor phenotype and therapeutic vulnerability. This review synthesizes evidence on how IGF signaling orchestrates immunosuppression through effects on tumor-associated macrophages, regulatory T cells, and myeloid-derived suppressor cells, while inflammatory cytokines reciprocally modulate IGF bioavailability. Three mechanistic principles emerge: IGF binding protein 2 (IGFBP-2) functions as a central coordinator linking growth factor signaling to immune evasion through STAT3-dependent pathways driving M2 macrophage polarization and regulatory T cell differentiation; IGF–immune crosstalk varies considerably across molecular subtypes, with microsatellite-stable tumors exhibiting high reliance on IGF-I receptor-mediated immune silencing; and local paracrine IGF production increasingly dominates over systemic regulation as disease progresses. These bidirectional connections establish self-reinforcing circuits that determine whether tumors remain immunologically responsive or develop immune exclusion. Multi-marker panels incorporating IGFBP-2 alongside complementary biomarkers have shown improved diagnostic performances for early CRC detection, underscoring the need for the large-scale prospective clinical evaluation of IGF network components as biomarkers for CRC in diverse populations. The convergence of IGF signaling with checkpoint regulation suggests that combined targeting warrants investigation for resistance in tumors lacking effective immunotherapy options. Full article

Background: The immunologically cold nature and immunosuppressive tumor microenvironment (TME) of intrahepatic cholangiocarcinoma (ICC) contribute to its poor prognosis. This study aims to identify novel biomarkers related to prognosis and TME in ICC. Methods: We first identified the high expression of m6A reader insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2) in ICC through bioinformatics screening. Subsequently, a retrospective study was conducted on 224 ICC patients who had undergone radical resection. The expression levels of IGF2BP2 and programmed death ligand 1 (PD-L1) were detected in a tissue microarray (TMA) using immunohistochemistry (IHC). The co-localization of IGF2BP2, PD-L1, programmed cell death protein 1 (PD-1), and CD8⁺T cells was evaluated by multiple immunofluorescence techniques. Results: IHC confirmed a significant upregulation of IGF2BP2 in tumor tissues compared with normal bile duct epithelia (p < 0.05). IGF2BP2 expression was positively correlated with PD-L1 expression (TPS R = 0.215, p = 0.016; CPS R = 0.295, p = 0.008). High IGF2BP2 expression was associated with increased PD-L1/PD-1 positivity and reduced CD8⁺T cell infiltration. Kaplan–Meier analysis revealed significantly worse 3-year overall survival (OS: 20.56% vs. 29.91%, p = 0.0291) and recurrence-free survival (RFS: 9.72% vs. 18.56%, p = 0.0372) in the IGF2BP2-high group. Multivariate analysis identified IGF2BP2 as an independent risk factor for both OS (HR = 1.683, p = 0.044) and RFS (HR = 1.946, p = 0.042). Conclusions: IGF2BP2, as a potential biomarker and independent prognostic factor for ICC, is associated with increased PD-L1 expression. Full article

Breast carcinoma is a major cause of cancer-related mortality among women worldwide. Identifying novel molecular targets remains essential, particularly for aggressive triple-negative breast cancer (TNBC). Leucine-rich alpha-2-glycoprotein 1 (LRG1) has been linked to tumor progression and angiogenesis, but its molecular mechanisms in breast cancer are poorly defined. We evaluated the effects of recombinant human LRG1 (rhLRG1) on cell viability and migration in MDA-MB-231 TNBC cells and performed transcriptomic profiling followed by functional enrichment analyses using GenArise, Cytoscape, and R-based tools. RhLRG1 treatment significantly increased cell viability and migration. Transcriptomic analysis revealed activation of key oncogenic cascades, including the PI3K/AKT, MAPK, and RAS signaling pathways. Hub-gene analysis identified upregulated genes involved in proliferation (NRAS, STAT5B, IGF2), angiogenesis (PGF, ANGPT2), and apoptosis (CASP8, BAD), whereas downregulated genes were associated with apoptotic resistance (BCL2, MCL1) and adhesion (LAMB1, ITGB4). Functional enrichment highlighted LRG1’s role in the bioinformatic analysis of differentially expressed genes that were obtained from microarray assays. LRG1 remodels the tumor microenvironment by promoting proliferation, angiogenesis, and apoptotic sensitivity while repressing resistance-related genes. These findings position LRG1 as a potential diagnostic biomarker and therapeutic target for advanced breast carcinoma. Full article

The reproductive caste of higher termites exhibits remarkable longevity, but the mechanisms by which they manage age-related oxidative stress during lifespan extension remain insufficiently understood. This study investigated the dynamic regulation of the insulin/IGF (IIS)–FOXO axis, a key anti-aging regulatory pathway that integrates insulin signaling with downstream processes, including antioxidant defense and DNA repair, as well as the superoxide dismutase (SOD) system in female Odontotermes formosanus reproductives at various life stages (Swarming Queen (SQ), 1-Year Queen (1YQ), 8-Year Queen (8YQ)) through transcriptomic, qRT-PCR, and enzyme activity analyses. Age-dependent upregulation of IIS pathway components (InR, chico, PDK1, Akt, Sirt1, FOXO) was observed, alongside the identification of six SOD transcripts, including two SOD1, two SOD2, and two SOD3 isoforms. Notably, mitochondrial SOD2 (particularly SOD2_b) showed a progressive increase with age, exhibiting the highest enzymatic activity and being associated with reduced mitochondrial oxidative stress and the disruption of reactive oxygen species (ROS) amplification cycles. These findings suggest that O. formosanus reproductives counteract the potential lifespan-reducing effects of chronic IIS activation by maintaining or enhancing FOXO activity, thereby supporting DNA repair, antioxidant defenses, and cellular homeostasis. The IIS–FOXO–SOD2 axis is identified as a key regulator of reproductive longevity in higher termites, offering new insights into the molecular mechanisms behind lifespan extension in social insects. Full article

Acute liver failure is often accompanied by neurological disturbances collectively referred to as hepatic encephalopathy (HE), characterized by neuroinflammation and subsequent cognitive decline. Insulin-like growth factor 1 (IGF1) is a neuroprotective peptide with anti-inflammatory properties in the brain. The role of IGF1 in cognitive deficits and neuroinflammation during HE remains largely unexplored. In C57Bl/6 mice, HE was established through an intraperitoneal injection of azoxymethane (AOM), and tissues were collected at defined time points during disease development. IGF1 expression in the cortex was downregulated following AOM administration. Central infusion of recombinant mouse IGF1 (rmIGF1) before AOM injection resulted in delayed neurological impairment, reduced microglial activation, and decreased proinflammatory cytokine and chemokine production in AOM mice. In vitro, rmIGF1 and conditioned media derived from rmIGF1-treated primary neurons attenuated phagocytic activity and C–C motif chemokine ligand 2 (CCL2) production in the microglial cell line EOC-20. Collectively, our results show that IGF1, whose levels decline during HE, alleviates neuroinflammation and improves the pathological state of AOM-treated mice through the suppression of microglial activation and the regulation of neuron–microglia paracrine communication. Full article

Background and Objectives: Fragmented anatomical, imaging, and surgical accounts of the gracilis muscle hinder reproducible reporting and operative planning. We aimed to integrate prior systems into an Integrated Gracilis Framework (IGF)—an integrative synthesis, not a new classification—that harmonizes terminology, defines imaging correlates/pitfalls, and links morphology to surgical decisions. Methods: Integrative narrative review (January 1900–October 2025) of PubMed/MEDLINE, Scopus, and Web of Science covering vascularization (pedicles, perforators), innervation (motor points/segments), imaging (ultrasound, MRI, MR neurography, CTA/MRA), and clinical applications (facial reanimation, elbow flexion, perineal and breast reconstruction). Two reviewers screened/extracted with consensus adjudication. Searches were restricted to English or records with reliable English-language summaries. Results: IGF consolidates morphological variants, motor-point/segmental innervation, and pedicle/perforator patterns with imaging correlates and common pitfalls. It provides a crosswalk mapping historical systems to IGF and a proposed preoperative workflow (anatomy → imaging → harvest → neurotization) for structured planning and reporting (proposed framework; not prospectively validated). We summarize considerations for free/functional gracilis in facial reanimation and elbow-flexion, and for pedicled/free myocutaneous or perforator flaps in perineal and breast reconstruction. Conclusions: IGF offers a standardized language and decision scaffold to improve study comparability and transparency in operative reporting; as a nonvalidated synthesis, it requires systematic validation through cadaver–imaging correlation and prospective surgical cohorts. Full article

Background: Growth hormone deficiency (GHD) in childhood impairs linear growth and may affect body composition, metabolism, and quality of life; recombinant human growth hormone (rhGH) therapy improves outcomes, but response is highly variable, especially in idiopathic GHD (IGHD). Objective: To summarize current evidence on predictors of growth response to rhGH therapy in children with IGHD, focusing on clinical, biochemical, and treatment-related determinants. Methods: This is a narrative review dealing with studies assessing clinical, auxological, biochemical and treatment-associated factors that may influence response to rhGH in IGHD. Results: Early treatment initiation, baseline short stature, prepubertal status, and higher early height growth velocity are strong clinical predictors; biochemical markers, including GH peak, IGF-1, and IGFBP-3, provide complementary information. Modifiable factors such as GH dose, adherence to therapy, and therapy duration also influence outcomes. Integrated predictive models improve accuracy but require further validation. Conclusions: Growth response to rhGH in IGHD is multifactorial and could be individualized: early identification of suboptimal responders and personalized treatment strategies that integrate clinical, biochemical, and treatment-related data may optimize the final outcome. Future research studies should focus on validated predictive models incorporating genetic and molecular markers. Full article

Background/Objectives: Aging is associated with declines in cognitive function and neurotrophic support. Brain-derived neurotrophic factor (BDNF) and insulin-like growth factor-1 (IGF-1) are peripheral biomarkers discussed in relation to brain health and aging. This study investigated changes in serum BDNF, IGF-1, and cognitive screening scores after a 16-week Hatha Yoga program performed twice or four times per week in older women. Methods: Fifty-one community-dwelling women aged 70–79 years were allocated to a twice-per-week yoga group (2YG; n = 17), a four-times-per-week yoga group (4YG; n = 17), or a non-exercise control group (CON; n = 17) based on availability and participant preference; forty-three participants completed the study. Serum BDNF and IGF-1 were analyzed using enzyme-linked immunosorbent assay and chemiluminescent immunoassay, and cognitive status was evaluated using the Cognitive Impairment Screening Test (CIST). Outcomes were analyzed using two-way repeated-measures ANOVA and additional ANCOVA models adjusting for corresponding baseline values. Exploratory correlations were examined between biomarker changes and CIST changes. Effect sizes and 95% confidence intervals were reported. Results: BDNF showed a significant main effect of time (p < 0.05) without a significant group × time interaction; ANCOVA adjusting for baseline BDNF showed no significant group effect (p = 0.270). IGF-1 showed a significant group × time interaction (p < 0.01) with increases in both yoga groups; ANCOVA adjusting for baseline IGF-1 showed a significant group effect (p = 0.001). CIST showed a significant main effect of time (p < 0.01), but changes were small and the group × time interaction was not significant; ANCOVA adjusting for baseline CIST showed no significant group effect (p = 0.114). Biomarker changes were not clearly correlated with CIST changes (ΔBDNF–ΔCIST: r = −0.244, p = 0.115; ΔIGF-1–ΔCIST: r = −0.050, p = 0.750). Conclusions: In this quasi-experimental study with non-random allocation and limited covariate information, changes in peripheral neurotrophic factors and only small changes in cognitive screening scores were observed after participation in a 16-week Hatha Yoga program. However, frequency-dependent conclusions are limited, and findings should be interpreted cautiously as screening-level, hypothesis-generating reference data. Nevertheless, the program is considered a feasible, low-risk health promotion activity for older women and may inform future randomized or well-controlled studies. Full article

The unique aroma of ginseng is linked to its recognized mood-enhancing properties. However, the specific aromatic compounds responsible for this effect, as well as the underlying mechanisms across different processed ginseng products, remain unclear. Here, the characteristic pleasant aroma compounds and their potential associations in five preparations—fresh ginseng, white ginseng, Dali ginseng, red ginseng, and black ginseng—were analyzed using flavoromics, bioinformatics, and computational modeling. The aroma evolved from “green” to “roasted-medicinal” notes, with pleasantness peaking in red ginseng, highlighting moderate processing as a key factor. Eight key pleasant aroma compounds were identified (including octanal and β-selinene), which were found to be potentially associated with olfactory- and emotion-related pathways involving IGF1 and OR6A2. Molecular interaction analysis revealed that these compounds may synergistically modulate pleasantness through hydrogen bonding and hydrophobic interactions. Furthermore, aroma harmony proved more decisive than aroma intensity in determining consumer preference, suggesting correlational evidence linking molecular interactions to sensory perception. Dynamic simulations further demonstrated stable interactions between β-selinene, octanal, and IGF1/OR6A2. This research offers new insights into the mood-modulating properties of ginseng aroma and may inform future studies exploring the development of specialized ginseng products for emotional well-being applications. Full article

Background: Prostate cancer (PCa) arises from complex interactions among host genetics, androgen signaling, and microbial communities. Emerging genomic evidence supports the presence of microbial consortia within prostate tissue, suggesting that microbial genes, metabolites, and host–microbe interactions may contribute to chronic inflammation, oncogenic signaling, and therapeutic resistance. Methods: We conducted a narrative review using targeted searches of PubMed and Google Scholar for studies published between 2020 and 2025, complemented by selected mechanistic reports published in March 2026. Human studies and experimental research providing mechanistic insights into prostate models were prioritized. Due to the heterogeneous methodologies, evidence was synthesized qualitatively, with an emphasis on genomic and signaling perspectives. Results: Low-biomass microbial DNA is consistently detected in prostate tissue. Proteomic analyses of Corpora amylacea suggest a “fossil record” of past infections through sequestered microbial DNA and antimicrobial proteins, potentially priming tissue for long-term carcinogenic processes, although contamination remains a key limitation. Recurrent bacterial and viral signals, including Cutibacterium acnes, Escherichia coli, Pseudomonas, Acinetobacter, human papillomavirus, Epstein–Barr virus, and cytomegalovirus, appear to converge on a restricted set of tumor-relevant pathways, including TLR–NF-κB, MAPK, PI3K/AKT/mTOR, cGAS–STING, and p53/pRb disruption. These interactions may promote cytokine production, oxidative stress, DNA damage, epithelial–mesenchymal transition, extracellular matrix remodeling, immune evasion, and resistance to therapy. The gut–prostate axis further links intestinal dysbiosis and microbial metabolites with systemic IGF-1 signaling and castration resistance. Conclusions: Microbial genomic consortia in the prostate and gut may shape inflammatory, metabolic, and immune networks that influence PCa initiation and progression. However, most available data remain correlative and are limited by low-biomass sampling, contamination risk, and heterogeneous study designs. Future research should prioritize rigorous contamination control, longitudinal and prostate-specific mechanistic studies, and integrated multi-omic approaches to clarify causality and identify actionable microbial targets for prevention, diagnosis, and therapy. Full article

Insulin-like growth factor 2 (IGF2) plays a pivotal role in regulating growth and development; however, its functional involvement in skeletal muscle satellite cells (SMSCs) remains incompletely understood. To elucidate the regulatory role of IGF2, goose SMSCs were engineered to overexpress IGF2 via lentiviral transduction, followed by comprehensive transcriptomic profiling. Comparative analysis revealed 2802 differentially expressed genes (DEGs) in IGF2-overexpressing cells relative to controls, comprising 1202 upregulated and 1600 downregulated genes. IGF2 overexpression markedly activated fibrogenic programs, as evidenced by the upregulation of AP-1 complex components (FOS, JUN), extracellular matrix-related genes (COL1A1, COL5A3), and Wnt signaling receptors (FZD1, FZD7). In contrast, genes involved in myogenic differentiation and contractile function were broadly suppressed, including key myogenic transcription factors (MEF2C, MEF2D), sarcomeric structural proteins (MYBPC1, ACTN2, MYOM3), and metabolic enzymes. Through the construction of protein–protein interaction networks coupled with functional enrichment analysis, we observed a concerted suppression of myogenic regulatory networks critical for myofiber formation. Quantitative real-time PCR validation further confirmed the reliability of the transcriptomic data. Collectively, these findings suggest that overexpression of IGF2 induces a phenotypic shift from myoblasts toward a fibroblast-like state, uncoupling proliferation from differentiation while enhancing fibrogenic identity. This study provides novel insights into IGF2-mediated regulatory mechanisms underlying skeletal muscle development and fibrotic processes. Full article

Background/Objectives: Neuritogenesis and synaptogenesis support learning and cognitive function, and hippocampal neurons play central roles in these processes. Cleistocalyx nervosum var. paniala (CNP), a Southeast Asian berry, has reported neuroprotective activities, but its direct effects on hippocampal neurons remain unclear. We investigated whether CNP extract modulates hippocampal neuronal transcriptomes, neuritogenesis, and synaptogenesis. Methods: Primary hippocampal neurons isolated from male and female Wistar rat pups were treated with CNP extract in vitro. Cytotoxicity was assessed to define non-cytotoxic concentrations. Transcriptomic responses were profiled by RNA sequencing and validated by RT-qPCR. Neuritogenesis was quantified by neurite morphology and Sholl analysis. Synaptogenesis was evaluated by synaptic immunocytochemistry. Molecular docking of cyanidin-3-glucoside (C3G) and resveratrol was used to generate mechanistic hypotheses. Results: At 0.1–10 µg/mL, CNP was non-cytotoxic, whereas a 100 µg/mL dose reduced viability; therefore, 10 µg/mL was used in subsequent experiments. Exploratory RNA-seq profiling identified thousands of differentially expressed genes enriched in synapse- and neurite-related pathways, including synaptogenesis signaling, axon guidance, and neuritogenesis. RT-qPCR showed upregulation of Igf1 in males and Glul in females, with sex-dependent modulation of Bdnf and Cask. CNP increased neurite length, branching, and Sholl complexity in both sexes, with a more pronounced effect in males. A male-biased effect was also observed in synapse-related marker colocalization, with increased Syn1–Psd95 colocalization detected in males. Docking suggested plausible interactions of C3G and resveratrol with regulators such as MYC, TP53, and CREB1. Conclusions: CNP extract alters transcriptional networks and enhances neurite outgrowth in primary hippocampal neurons in a sex-dependent manner, with male-biased effects on Syn1–Psd95 colocalization. These findings support further dose–response, mechanistic, and sex-stratified in vivo studies to evaluate its neurobiological potential. Full article

Sorghum is known for its anti-cancer, anti-inflammatory, and antioxidant properties, but its effect on cell growth is not well understood. First, the cytotoxicity of various sorghum extract (SE) concentrations was evaluated in C2C12 (murine myoblasts) and C3H10T1/2 (murine embryonic fibroblasts). The extent of DNA damage was then assessed, and the activation of the JAK2/STAT5b and IGF-1 pathways was observed. Studies on the transcriptional regulatory function of STAT5b revealed that SE increased STAT5b/DNA binding and transcriptional promoter activity. Consequently, STAT5b upregulation led to the increased expression of IGF-1. Moreover, other factors, such as growth hormone receptor and bone morphogenetic protein 7, were also upregulated. The results of these experiments suggest that sorghum may enhance muscle recovery or promote growth factors by stimulating the JAK2/STAT5b and IGF-1 pathways. Therefore, sorghum is expected to be an effective functional food for bone growth and muscle recovery, without inducing adverse side effects. Full article

Modern genetic selection for high productivity has created a physiological conflict in ruminants, where the metabolic demands of lactation compete directly with the energy requirements of reproduction. This review provides a mechanistic synthesis of how key nutritional factors modulate the endocrine and cellular pathways governing reproductive success in cattle and sheep. Negative energy balance (NEB), characteristic of the early postpartum period, suppresses the hypothalamic–pituitary–gonadal (HPG) axis by impairing the pulsatile secretion of gonadotropin-releasing hormone (GnRH) and luteinizing hormone (LH), mediated through reduced kisspeptin signaling, growth hormone (GH) resistance, and decreased circulating insulin, insulin-like growth factor-1 (IGF-1), and leptin. At the macronutrient level, excess rumen-degradable protein elevates blood urea nitrogen and impairs the uterine environment, while omega-3 polyunsaturated fatty acids inhibit prostaglandin F2α synthesis to support corpus luteum maintenance. At the micronutrient level, selenium, copper, and zinc are essential antioxidant cofactors protecting gametes and embryos from oxidative stress, while vitamins A, D, and E regulate gene expression in reproductive tissues. Furthermore, maternal nutrition during critical gestational windows programs the reproductive capacity of offspring through epigenetic modifications, with profound implications for long-term herd fertility. Understanding these nutritional–reproductive interactions is crucial for developing precision feeding strategies that optimize herd fertility, improve animal welfare, and ensure the economic sustainability of livestock management. A thorough understanding of these nutritional–reproductive interactions is essential for developing precision feeding strategies that optimize fertility in high-producing ruminants. Full article