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OBJECTIVE: In the knee, synovial fibrosis after ligamentous injury is linked to progressive joint pain and stiffness. The objective of this study was to evaluate changes in synovial architecture, mechanical properties, and transcriptional profiles following naturally occurring cruciate ligament injury in canines and to test potential therapeutics that target drivers of synovial inflammation and fibrosis. DESIGN: Synovia from canines with spontaneous cruciate ligament tears and from healthy knees were assessed via histology (n = 10/group) and micromechanical testing (n = 5/group) to identify changes in tissue architecture and stiffness. Additional samples (n = 5/group) were subjected to RNA-sequencing to define the transcriptional response to injury. Finally, synovial tissue samples from injured animals (n = 6 (IL1) or n = 8 (IL6)/group) were assessed in vitro for response to therapeutic molecules directed against interleukin (IL) signaling (IL1 or IL6). RESULTS: Cruciate injury resulted in increased synovial fibrosis, vascularity, inflammatory cell infiltration, and intimal hyperplasia. Additionally, the stiffness of both the intima and subintima regions were higher in diseased compared to healthy tissue. Differential gene expression analysis showed that diseased synovium had an upregulation of immune response and cell adhesion pathways and a downregulation of Rho protein transduction pathways. In vitro application of small molecule therapeutics targeting IL1 (anakinra) or IL6 (tocilizumab) dampened expression of inflammatory and matrix deposition mediators. CONCLUSION: Spontaneous cruciate ligament injury in canines is associated with synovial inflammation and fibrosis in a relevant model for testing emerging intra-articular treatments. Small molecule therapeutics targeting IL pathways may be ideal interventions for delivery to the joint space after injury.
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OBJECTIVE: Synovial pathology has been linked to osteoarthritis (OA) pain in patients. Microscopic grading systems for synovial changes in human OA have been described, but a standardized approach for murine models of OA is needed. We sought to develop a reproducible approach and set of minimum recommendations for reporting of synovial histopathology in mouse models of OA. METHODS: Coronal and sagittal sections from male mouse knee joints subjected to destabilization of medial meniscus (DMM) or partial meniscectomy (PMX) were collected as part of other studies. Stains included Hematoxylin and Eosin (H&E), Toluidine Blue (T-Blue), and Safranin O/Fast Green (Saf-O). Four blinded readers graded pathological features (hyperplasia, cellularity, and fibrosis) at specific anatomic locations. Inter-reader agreement of each feature score was determined. RESULTS: There was acceptable to very good agreement when using 3-4 individual readers. After DMM and PMX, expected medial predominant changes in hyperplasia and cellularity were observed, with fibrosis noted at 12 weeks post-PMX. Synovial changes were consistent from section to section in the mid-joint area. When comparing stains, H&E and T-blue resulted in better agreement compared to Saf-O stain. CONCLUSIONS: To account for the pathologic and anatomic variability in synovial pathology and allow for a more standardized evaluation that can be compared across studies, we recommend evaluating a minimum set of 3 pathological features at standardized anatomic areas. Further, we suggest reporting individual feature scores separately before relying on a single summed "synovitis" score. H&E or T-blue are preferred, inter-reader agreement for each feature should be considered.
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Conventionally, for cartilage tissue engineering applications, transforming growth factor beta (TGF-ß) is administered at doses that are several orders of magnitude higher than those present during native cartilage development. While these doses accelerate extracellular matrix (ECM) biosynthesis, they may also contribute to features detrimental to hyaline cartilage function, including tissue swelling, type I collagen (COL-I) deposition, cellular hypertrophy, and cellular hyperplasia. In contrast, during native cartilage development, chondrocytes are exposed to moderate TGF-ß levels, which serve to promote strong biosynthetic enhancements while mitigating risks of pathology associated with TGF-ß excesses. Here, we examine the hypothesis that physiologic doses of TGF-ß can yield neocartilage with a more hyaline cartilage-like composition and structure relative to conventionally administered supraphysiologic doses. This hypothesis was examined on a model system of reduced-size constructs (∅2 × 2 mm or ∅3 × 2 mm) comprised of bovine chondrocytes encapsulated in agarose, which exhibit mitigated TGF-ß spatial gradients allowing for an evaluation of the intrinsic effect of TGF-ß doses on tissue development. Reduced-size (∅2 × 2 mm or ∅3 × 2 mm) and conventional-size constructs (∅4-∅6 mm × 2 mm) were subjected to a range of physiologic (0.1, 0.3, 1 ng/mL) and supraphysiologic (3, 10 ng/mL) TGF-ß doses. At day 56, the physiologic 0.3 ng/mL dose yielded reduced-size constructs with native cartilage-matched Young's modulus (EY) (630 ± 58 kPa) and sulfated glycosaminoglycan (sGAG) content (5.9 ± 0.6%) while significantly increasing the sGAG-to-collagen ratio, leading to significantly reduced tissue swelling relative to constructs exposed to the supraphysiologic 10 ng/mL TGF-ß dose. Furthermore, reduced-size constructs exposed to the 0.3 ng/mL dose exhibited a significant reduction in fibrocartilage-associated COL-I and a 77% reduction in the fraction of chondrocytes present in a clustered morphology, relative to the supraphysiologic 10 ng/mL dose (p < 0.001). EY was significantly lower for conventional-size constructs exposed to physiologic doses due to TGF-ß transport limitations in these larger tissues (p < 0.001). Overall, physiologic TGF-ß appears to achieve an important balance of promoting requisite ECM biosynthesis, while mitigating features detrimental to hyaline cartilage function. While reduced-size constructs are not suitable for the repair of clinical-size cartilage lesions, insights from this work can inform TGF-ß dosing requirements for emerging scaffold release or nutrient channel delivery platforms capable of achieving uniform delivery of physiologic TGF-ß doses to larger constructs required for clinical cartilage repair.
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BACKGROUND: The concept of "skin boosters" has evolved, marking a shift from traditional uses of hyaluronic acid (HA) fillers primarily for augmenting skin volume to a more diverse application aimed at improving dermal conditions. Restylane Vital and other HA fillers have been repurposed to combat skin aging and wrinkles by delivering HA directly to the dermis. OBJECTIVES: This review aims to define the term "skin booster" and to discuss the various components that constitute skin boosters. It seeks to provide a comprehensive overview of the different ingredients used in skin boosters, their roles, and their impact on enhancing dermal conditions. METHODS: A comprehensive review was conducted, focusing on representative skin booster ingredients. The approach involved analyzing the different elements used in skin boosters and their specific roles in enhancing dermal improvement. RESULTS: The findings indicate that skin boosters, encompassing a range of ingredients, are effective in improving the condition of the skin's dermis. The review identifies key ingredients in skin boosters and their specific benefits, including hydration, elasticity improvement, and wrinkle reduction. CONCLUSIONS: Skin boosters represent a significant development in dermatological treatments, offering diverse benefits beyond traditional HA fillers. This review provides valuable insights into the constituents of skin boosters and their effectiveness, aiding readers in making informed decisions about these treatments. The potential of skin boosters in dermatological practice is considerable, warranting further research and application.
Subject(s)
Cosmetic Techniques , Dermal Fillers , Skin Aging , Humans , Skin , Rejuvenation , Hyaluronic AcidABSTRACT
The investigation focused on the impact of Withania somnifera (ashwagandha) extract (WSE) on age-related mechanisms affecting skeletal muscle sarcopenia-related muscle atrophy in aged mice. Beyond evaluating muscular aspects, the study explored chronic low-grade inflammation, muscle regeneration, and mitochondrial biogenesis. WSE administration, in comparison to the control group, demonstrated no significant differences in body weight, diet, or water intake, affirming its safety profile. Notably, WSE exhibited a propensity to reduce epidermal and abdominal fat while significantly increasing muscle mass at a dosage of 200 mg/kg. The muscle-to-fat ratio, adjusted for body weight, increased across all treatment groups. WSE administration led to a reduction in the pro-inflammatory cytokines TNF-α and IL-1ß, mitigating inflammation-associated muscle atrophy. In a 12-month-old mouse model equivalent to a 50-year-old human, WSE effectively preserved muscle strength, stabilized grip strength, and increased muscle tissue weight. Positive effects were observed in running performance and endurance. Mechanistically, WSE balanced muscle protein synthesis/degradation, promoted fiber differentiation, and enhanced mitochondrial biogenesis through the IGF-1/Akt/mTOR pathway. This study provides compelling evidence for the anti-sarcopenic effects of WSE, positioning it as a promising candidate for preventing sarcopenia pending further clinical validation.
Subject(s)
Plant Extracts , Sarcopenia , Withania , Humans , Animals , Mice , Infant , Middle Aged , Sarcopenia/drug therapy , Sarcopenia/prevention & control , Muscular Atrophy/drug therapy , Muscular Atrophy/etiology , Muscular Atrophy/prevention & control , Ethanol , Inflammation , Body WeightABSTRACT
OBJECTIVES: Biological aspect and clinical research demonstrated that dual-frequency ultrasound (local dynamic micro-massage, LDM) waves of very high frequency can significantly modify cellular signaling providing anti-inflammatory and anti-fibrotic effects. During the recent past, these waves were successfully applied for the treatment of various inflammatory skin conditions, hypertrophic scars, and chronical wounds. Since the main complications after rhinoseptoplasty are caused by excessive inflammatory reactions and development of fibrosis along nasal implants which can lead to a revision rhinoseptoplasty, in this retrospective multicenter blinded study we have evaluated the efficacy of LDM ultrasound for the treatment of the postoperative perilesional ecchymosis and edema in patients after rhinoseptoplasty. METHODS: Twenty-four patients received daily LDM treatment (study group) for 5 days starting from the first day postoperative, whereas 24 patients (control group) were treated with conventional ice packs. Dynamic reduction of the postoperative perilesional ecchymosis and edema was followed up, and the total duration of these side effects was determined within specific paranasal anatomical areas. RESULTS: Post-rhinoseptoplasty ecchymosis and edema were observed in the areas of anterior cheek, lower eyelids, and upper eyelids. Duration of the postoperative perilesional edema was significantly reduced in the group treated with LDM (1.9 ± 0.9 days) compared with control group (4.5 ± 2.1 days). Duration of the ecchymosis was also significantly reduced in LDM group (2.8 ± 1.4 days) compared with controls (7.4 ± 2.8 days). Postoperative patient satisfaction in LDM-treated and control groups was 3.1 ± 1.3 and 1.5 ± 0.7, respectively, demonstrating significantly higher satisfaction in LDM-treated group. CONCLUSIONS: This study proved that the post-rhinoseptoplasty group treated with LDM ultrasound showed a significantly shorter duration of the postsurgical perilesional ecchymosis and edema, with no substantial adverse effects other than those observed in the control group. It can be suggested that ultrasound treatment can serve as an alternative option for the noninvasive management of postoperative perilesional ecchymosis and edema.
Subject(s)
Ecchymosis , Rhinoplasty , Humans , Ecchymosis/etiology , Ecchymosis/therapy , Edema/therapy , Edema/drug therapy , Nose/surgery , Postoperative Complications/etiology , Postoperative Complications/drug therapy , Rhinoplasty/methodsABSTRACT
For cartilage regeneration applications, transforming growth factor beta (TGF-ß) is conventionally administered at highly supraphysiologic doses (10-10,000 ng/mL) in an attempt to cue cells to fabricate neocartilage that matches the composition, structure, and functional properties of native hyaline cartilage. While supraphysiologic doses enhance ECM biosynthesis, they are also associated with inducing detrimental tissue features, such as fibrocartilage matrix deposition, pathologic-like chondrocyte clustering, and tissue swelling. Here we investigate the hypothesis that moderated TGF-ß doses (0.1-1 ng/mL), akin to those present during physiological cartilage development, can improve neocartilage composition. Variable doses of media-supplemented TGF-ß were administered to a model system of reduced-size cylindrical constructs (Ø2-Ø3 mm), which mitigate the TGF-ß spatial gradients observed in conventional-size constructs (Ø4-Ø6 mm), allowing for a novel assessment of the intrinsic effect of TGF-ß doses on macroscale neocartilage properties and composition. The administration of physiologic TGF-ß to reduced-size constructs yields neocartilage with native-matched sGAG content and mechanical properties while providing a more hyaline cartilage-like composition, marked by: 1) reduced fibrocartilage-associated type I collagen, 2) 77% reduction in the fraction of cells present in a clustered morphology, and 3) 45% reduction in the degree of tissue swelling. Physiologic TGF-ß appears to achieve an important balance of promoting requisite ECM biosynthesis, while mitigating hyaline cartilage compositional deficits. These results can guide the development of novel physiologic TGF-ß-delivering scaffolds to improve the regeneration clinical-sized neocartilage tissues.
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This study aimed to identify and elucidate the mechanism underlying the protective effect of tricin-enriched Zizania latifolia (Z. latifolia) extract (ETZL) against free fatty acid (FFA)-induced lipid accumulation in vitro and non-alcoholic fatty liver disease (NAFLD) induced by a high-fat diet and fructose diet (HFD/F) in vivo. ETZL treatment significantly lowered body weight gain and decreased adipose tissue, lipid, aspartate aminotransferase (AST), and alanine aminotransferase (ALT) levels in HFD/F-fed mice. ETZL acted on phosphorylated acetyl-CoA carboxylase (ACC) and anti-peroxisome proliferator-activated receptor α (PPARα) by activating the adenosine monophosphate-activated protein kinase (AMPK) pathway and inhibiting sterol regulatory element-binding proteins-1 (SREBP)/fatty acid synthase (FAS) signaling to inhibit de novo adipogenesis and increase fatty acid oxidation. In addition, treatment with ETZL increased nuclear factor erythroid-2-related factor 2 (Nrf2) levels to activate the antioxidant pathway. FFA-induced oxidative stress and fatty acid accumulation in HepG2 cells confirmed the improvement in fat accumulation through the AMPK and Nrf2 pathway activities of ETZL. These results suggest that ETZL ameliorates NAFLD by regulating lipid metabolism and defending against oxidative stress via AMPK-dependent pathways.
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Background: Synovial pathology has been linked to osteoarthritis (OA) pain in patients. Microscopic grading systems for synovial changes in human OA have been described, but a standardized approach for murine models of OA is needed. We sought to develop a reproducible approach and set of minimum recommendations for synovial histopathology in mouse models of OA. Methods: Coronal and sagittal sections from male mouse knee joints subjected to destabilization of medial meniscus (DMM) or partial meniscectomy (PMX) were collected as part of other studies. Stains included Hematoxylin and Eosin (H&E), Toluidine Blue (T-Blue) and Safranin O/Fast Green (Saf-O). Four blinded readers graded pathological features (hyperplasia, cellularity, and fibrosis) at specific anatomic locations in the medial and lateral compartments. Inter-reader reliability of each feature was determined. Results: There was acceptable to very good agreement between raters. After DMM, increased hyperplasia and cellularity and a trend towards increased fibrosis were observed 6 weeks after DMM in the medial locations, and persisted up to 16 weeks. In the PMX model, cellularity and hyperplasia were evident in both medial and lateral compartments while fibrotic changes were largely seen on the medial side. Synovial changes were consistent from section to section in the mid-joint area mice. H&E, T-blue, and Saf-O stains resulted in comparable reliability. Conclusions: To allow for a standard evaluation that can be implemented and compared across labs and studies, we recommend using 3 readers to evaluate a minimum set of 3 pathological features at standardized anatomic areas. Pre-defining areas to be scored, and reliability for each pathologic feature should be considered.
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In cancer, solid stresses impede the delivery of therapeutics to tumours and the trafficking and tumour infiltration of immune cells. Understanding such consequences and the origin of solid stresses requires their probing in vivo at the cellular scale. Here we report a method for performing volumetric and longitudinal measurements of solid stresses in vivo, and findings from its applicability to tumours. We used multimodal intravital microscopy of fluorescently labelled polyacrylamide beads injected in breast tumours in mice as well as mathematical modelling to compare solid stresses at the single-cell and tissue scales, in primary and metastatic tumours, in vitro and in mice, and in live mice and post-mortem tissue. We found that solid-stress transmission is scale dependent, with tumour cells experiencing lower stresses than their embedding tissue, and that tumour cells in lung metastases experience substantially higher solid stresses than those in the primary tumours. The dependence of solid stresses on length scale and the microenvironment may inform the development of therapeutics that sensitize cancer cells to such mechanical forces.
Subject(s)
Lung Neoplasms , Mice , Animals , Tumor MicroenvironmentABSTRACT
BACKGROUND: Enlarged facial pores are a common dermatological and cosmetic concern, which are difficult to treat because their pathogenesis is multifactorial. Many technological treatments have been developed to treat enlarged pores. Despite these efforts, enlarged pores remain problematic for many patients. OBJECTIVES: Microcoring technology has recently been developed to treat pores and serve as a leading primary treatment option to address these concerns. METHODS: Three patients underwent a single treatment of rotational fractional resection. The 0.5 mm diameter rotating scalpels were used to resect the skin pores in the cheek region. The resected site was evaluated 30 days after treatment, and the patients underwent scanning in bilateral 45° views at 60 cm from the face with the same brightness setting. RESULTS: The three patients improved in terms of enlarged pores and had no severe skin-related adverse effects. Furthermore, the three patients showed satisfactory treatment outcomes after 30 days of follow-up. CONCLUSION: Rotational fractional resection is a new concept that produces measurable permanent results for enlarged pore removal. These cosmetic procedures produced promising outcomes in a single treatment. However, the current clinical procedures trend demands minimally invasive treatment for enlarged pores.
Subject(s)
Cosmetics , Face , Humans , Skin/pathology , Cheek/surgery , Treatment OutcomeABSTRACT
Chondrocyte phenotype is preserved when cells are round and the actin cytoskeleton is cortical. Conversely, these cells rapidly dedifferentiate in vitro with increased mechanoactive Rho signaling, which increases cell size and causes large actin stress fiber to form. While the effects of Rho on chondrocyte phenotype are well established, the molecular mechanism is not yet fully elucidated. Yap, a transcriptional coregulator, is regulated by Rho in a mechanotransductive manner and can suppress chondrogenesis in vivo. Here, we sought to elucidate the relationship between mechanoactive Rho and Yap on chondrogenic gene expression. We first show that decreasing mechanoactive state through Rho inhibition results in a broad increase in chondrogenic gene expression. Next, we show that Yap and its coregulator Taz are negative regulators of chondrogenic gene expression, and removal of these factors promotes chondrogenesis even in environments that promote cell spreading. Finally, we establish that Yap/Taz is essential for translating Rho-mediated signals to negatively regulate chondrogenic gene expression, and that its removal negates the effects of increased Rho signaling. Together, these data indicate that Rho is a mechanoregulator of chondrogenic differentiation, and that its impact on chondrogenic expression is exerted principally through mechanically induced translocation and activity of Yap and Taz.
Subject(s)
Adaptor Proteins, Signal Transducing , Transcription Factors , Adaptor Proteins, Signal Transducing/metabolism , Transcription Factors/metabolism , YAP-Signaling Proteins , Chondrogenesis , Gene ExpressionABSTRACT
BACKGROUND/OBJECTIVES: Benign prostatic hyperplasia (BPH) characterized by an enlarged prostate gland is common in elderly men. Corni Fructus (CF) and Schisandrae Fructus (SF) are known to have various pharmacological effects, including antioxidant and anti-inflammatory activities. In this study, we evaluated the inhibitory efficacy of CF, SF, and their mixture (MIX) on the development of BPH using an in vivo model of testosterone-induced BPH. MATERIALS/METHODS: Six-week-old male Sprague-Dawley rats were randomly divided into seven groups. To induce BPH, testosterone propionate (TP) was injected to rats except for those in the control group. Finasteride, saw palmetto (SP), CF, SF, and MIX were orally administered along with TP injection. At the end of treatment, histological changes in the prostate and the level of various biomarkers related to BPH were evaluated. RESULTS: Our results showed that BPH induced by TP led to prostate weight and histological changes. Treatment with MIX effectively improved TP-induced BPH by reducing prostate index, lumen area, epithelial thickness, and expression of BPH biomarkers such as 5α-reductase type 2, prostate-specific antigen, androgen receptor, and proliferating cell nuclear antigen compared to treatment with CF or SF alone. Moreover, MIX further reduced levels of elevated serum testosterone, dihydrotestosterone, and prostate-specific antigen in BPH compared to the SP, a positive control. BPH was also improved more by MIX than by CF or SF alone. CONCLUSIONS: Based on the results, MIX is a potential natural therapeutic candidate for BPH by regulating 5α-reductase and AR signaling pathway.
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Emerging evidence suggest that long-term exposure to air pollution may induce adverse effects on the central nervous system. However, no study explored the associations in large industrial complex (IC) areas which are one of the major contributors to air pollution. Therefore, we aimed to investigate the pollution status and the association between residential proximity and incidence of neurological diseases near two major ICs characterized as multi-purposed ICs in Korea. A retrospective cohort of residents near the ICs was constructed using Korea's health insurance data and monitored from 2008 to 2019. Emission amounts of the ICs and the air pollution status in the nearby (exposed) and remote (control) area were evaluated using data from national regulatory networks, and hazard ratios (HRs) and 95% confidence intervals (CIs) for neurological diseases of the exposed group compared to the control group were calculated using Cox proportional regression models. Overall, the complexes emitted large amounts of VOCs, CO, NOx, and PM10, and annual levels of ambient PM (2.5, 10), gaseous substances (NO2, SO2), VOCs and PAHs were higher in the exposed area compared to the control and/or the national average. The risk of inflammatory disease of the CNS (G00-09) and extrapyramidal and movement disorders (G20-26) were higher in the exposed area with a HR (95% CI) of 1.36 (1.10-1.68) and 1.33 (1.27-1.39) respectively. Among the subclasses, other extrapyramidal and movement disorders (G25) and epilepsy (G40) were associated with higher risks in the exposed area (HR (95%CI): 1.11 (1.04-1.18), 1.08 (1.00-1.16)) after adjusting for potential confounders. These results suggest that people living near ICs are more likely to be exposed to higher air pollution levels and have higher risks of developing several neurological disorders. However, further epidemiological studies in these industrial areas supplemented with other indicators of environmental exposure and control of other diverse factors are warranted.
Subject(s)
Air Pollutants , Air Pollution , Movement Disorders , Nervous System Diseases , Humans , Air Pollutants/toxicity , Retrospective Studies , Cohort Studies , Particulate Matter/analysis , Air Pollution/adverse effects , Environmental Exposure/analysis , Nervous System Diseases/chemically induced , Nervous System Diseases/epidemiology , Republic of Korea/epidemiologyABSTRACT
We describe fluorescent probes to detect formaldehyde (FA) in aqueous solutions and cells. The probes rapidly respond to FA in aqueous solutions and have great selectivity toward FA over other biologically relevant analytes. The results of cell studies reveal that probe 1 can be utilized to monitor endogenous and exogenous FA in live cells.
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BACKGROUND: Glypican-3 (GPC3), a membrane-bound heparan sulfate proteoglycan, is a biomarker of hepatocellular carcinoma (HCC) progression. Aptamers specifically binding to target biomolecules have recently emerged as clinical disease diagnosis targets. Here, we describe 3D structure-based aptaprobe platforms for detecting GPC3, such as aptablotting, aptaprobe-based sandwich assay (ALISA), and aptaprobe-based imaging analysis. RESULTS: For preparing the aptaprobe-GPC3 platforms, we obtained 12 high affinity aptamer candidates (GPC3_1 to GPC3_12) that specifically bind to target GPC3 molecules. Structure-based molecular interactions identified distinct aptatopic residues responsible for binding to the paratopic nucleotide sequences (nt-paratope) of GPC3 aptaprobes. Sandwichable and overlapped aptaprobes were selected through structural analysis. The aptaprobe specificity for using in HCC diagnostics were verified through Aptablotting and ALISA. Moreover, aptaprobe-based imaging showed that the binding property of GPC3_3 and their GPC3 specificity were maintained in HCC xenograft models, which may indicate a new HCC imaging diagnosis. CONCLUSION: Aptaprobe has the potential to be used as an affinity reagent to detect the target in vivo and in vitro diagnosing system.
Subject(s)
Carcinoma, Hepatocellular , Liver Neoplasms , Carcinoma, Hepatocellular/pathology , Glypicans/metabolism , Humans , Liver Neoplasms/pathologyABSTRACT
BACKGROUND: Staphylococcus aureus (SA) nasal carriage (SA carriage) and IgE-sensitization to SA enterotoxin (SE IgE-sensitization) are known to be associated with chronic airway disease. OBJECTIVE: This study aimed to evaluate the differences in risk factors, type 2 inflammation and respiratory symptoms between SA carriage and SE IgE-sensitization. METHODS: We conducted a cross-sectional study of a community-based adult population to evaluate the environmental exposure and health impact of the Pohang Industrial Complex, Korea. Participants were examined based on self-reported questionnaires, nasal swab, and blood sampling. RESULTS: There were 307 participants, and the overall prevalence of SA carriage and SE IgE-sensitization was 26.1% (80/307) and 25.7% (79/307), respectively. An urban environment was significantly correlated with SA carriage, whereas age and obesity were significantly correlated with SE IgE-sensitization. SA carriage was not associated with an increase in total IgE and blood eosinophil count, whereas SE IgE-sensitization was associated with an increased total IgE and blood eosinophil count. SA carriage was significantly correlated with cough persisting for more than three weeks (OR, 3.044; 95% CI, 1.137-8.153) and sputum (OR, 2.429; 95% CI, 1.008-5.854). SE IgE-sensitization was a significant correlation with only sputum (OR, 2.452; 95% CI, 1.066-5.640). SA carriage and SE IgE-sensitization showed a synergistic effect on the prevalence of cough and sputum. CONCLUSION: SA carriage was associated with the urban environment, and SE IgE-sensitization was associated with the elderly and obesity. SA carriage and SE IgE-sensitization had different correlation with type 2 inflammation and airway symptoms.
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The Korean National Environmental Health Survey (KoNEHS) program provides useful information on chemical exposure, serves as the basis for environmental health policies, and suggests appropriate measures to protect public health. Initiated on a three-year cycle in 2009, it reports the concentrations of major environmental chemicals among the representative Korean population. KoNEHS Cycle 3 introduced children and adolescents into the analysis, where the blood and urine samples of 6167 participants were measured for major metals, phthalates, phenolics, and other organic compounds. Lead, mercury, cadmium, metabolites of DEHP and DnBP, and 3-phenoxybenzoic acid levels of the Korean adult population tended to decrease compared to previous survey cycles but remained higher than those observed in the US or Canada. Both bisphenol A (BPA) and trans,trans-muconic acid concentrations have increased over time. Heavy metal concentrations (blood lead, and cadmium) in children and adolescents were approximately half that of adults, while some organic substances (e.g., phthalates and BPA) were high. BPA showed higher levels than in the US or Canada, whereas BPF and BPS showed lower detection rates in this cycle; however, as these are increasingly used as a substitute for BPA, further research is necessary. As environmental chemicals may affect childhood health and development, additional analyses should assess exposure sources and routes through continuous observations.
Subject(s)
Environmental Pollutants , Metals, Heavy , Adolescent , Adult , Asian People , Benzhydryl Compounds/urine , Child , Environmental Exposure/analysis , Environmental Health , Environmental Pollutants/analysis , Humans , Metals, Heavy/analysis , Republic of KoreaABSTRACT
Depending on the extraction method, numerous compounds that have specific pharmacological effects can be obtained from M. alba L. There is a growing scientific interest in health problems related to aging. Efforts to develop safe immune-enhancing pharmaceuticals are increasing. This review aims to summarize and critically discuss the immunity enhancement effects and pharmaceutical efficacy of M. alba L. extracts. The scientific database search was conducted using Google Scholar, Web of Science, and PubMed until May 2021. Additional articles were identified and obtained from references in the retrieved articles. Ethanol or methanol extraction of various parts of M. alba L. identified a large amount of phenols and flavonoids, which are effective for immunosuppression, antioxidants, and cardiovascular diseases, and are antibacterial, and anticancer. Water extraction of M. alba L. enhanced the innate immune response based on immune cell activation. A polysaccharide and an alkaloid related to increased macrophage activity were isolated from M. alba L. fruit extracts. M. alba L. fruit water extracts primarily induced the production of pro-inflammatory substances, in model organisms, via TLR4 in immune cells. Water extracts have been shown to be effective in pathogen defense and tumor suppression by enhancing macrophage activity. Based on our literature review on the bioactivity of M. alba L. fruit extracts, particularly in relation to their immunity enhancement activity, we anticipate that M. alba-derived pharmaceuticals will have excellent potential in future medical research.
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Binge drinking patterns easily produce a state of oxidative stress that disturbs liver function. Eventually, this leads to alcoholic liver disease. A safe and effective therapy for alcoholic liver disease remains elusive. Enzyme-treated Z. latifolia extract (ETZL) was studied as a potential agent for treating alcohol-induced liver disease. In addition, its underlying mechanisms were elucidated. In the binge model, ETZL was pretreated with alcohol (5 g/kg) three times at 12-h intervals. Our results showed that ETZL pretreatment decreased the serum levels of ALT, AST, ALP, and TG. ETZL treatment appeared to prevent an increase in hepatic TG and MDA levels, and there was a decrease in total GSH following alcohol treatment. Histopathological examination showed that lipid droplets were significantly reduced in the ETZL group compared to the control group. ETZL also exhibited radical scavenging activity. It significantly reduced t-BHP-induced cytotoxicity and the production of reactive oxygen species (ROS) in HepG2 cells. ETZL also enhanced NRF2 nuclear translocation and increased expression of the downstream target genes HO-1, NQO1, and GCLC as an antioxidant defense. Finally, ETZL treatment significantly reduced cell death. Our study suggests that ETZL ameliorates binge ethanol-induced liver injury by upregulating the antioxidant defense mechanism.