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Background: Chat Generative Pre-Trained Transformer (ChatGPT) is a state-of-the-art large language model that has been evaluated across various medical fields, with mixed performance on licensing examinations. This study aimed to assess the performance of ChatGPT-3.5 and ChatGPT-4 in answering questions from the Taiwan Plastic Surgery Board Examination. Methods: The study evaluated the performance of ChatGPT-3.5 and ChatGPT-4 on 1375 questions from the past 8 years of the Taiwan Plastic Surgery Board Examination, including 985 single-choice and 390 multiple-choice questions. We obtained the responses between June and July 2023, launching a new chat session for each question to eliminate memory retention bias. Results: Overall, ChatGPT-4 outperformed ChatGPT-3.5, achieving a 59 % correct answer rate compared to 41 % for ChatGPT-3.5. ChatGPT-4 passed five out of eight yearly exams, whereas ChatGPT-3.5 failed all. On single-choice questions, ChatGPT-4 scored 66 % correct, compared to 48 % for ChatGPT-3.5. On multiple-choice, ChatGPT-4 achieved a 43 % correct rate, nearly double the 23 % of ChatGPT-3.5. Conclusion: As ChatGPT evolves, its performance on the Taiwan Plastic Surgery Board Examination is expected to improve further. The study suggests potential reforms, such as incorporating more problem-based scenarios, leveraging ChatGPT to refine exam questions, and integrating AI-assisted learning into candidate preparation. These advancements could enhance the assessment of candidates' critical thinking and problem-solving abilities in the field of plastic surgery.
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BACKGROUNDS: Post-thyroidectomy scarring is a common illness impacting patient quality of life. Fractional carbon dioxide (CO2) lasers and topical steroids delivered via laser-assisted drug delivery (LADD) have shown potential for scar treatment. However, ideal steroid formulations (cream vs. solution) when combined with laser therapy remain unclear. METHODS: This study included 12 patients receiving fractional CO2 laser on post-thyroidectomy scars. After laser treatment, one scar half received topically applied steroid cream, while the other half received steroid solution. The Patient and Observer Scar Assessment Scale (POSAS) was used to measure the scar conditions at the time prior to the first treatment and one year later by the patients themselves and by the surgeon who did the laser treatment. Scar appearance was photographically assessed at baseline and 6 months post-treatment by four blinded evaluators using scales. RESULTS: This study discovered a modest improvement in the appearance of post-thyroidectomy scars when combining fractional CO2 laser treatment with either topical steroid cream or solution. Patients and treating physicians examined the POSAS scores one year after treatment found significant improvements in all aspects of the scar conditions, with high efficacy and satisfaction levels reported by patients. CONCLUSIONS: Fractional CO2 laser combined with topical steroid delivery, either cream or solution form, significantly enhanced post-thyroidectomy scar appearance with modest effect and high patient satisfaction. This approach may represent a promising scar management strategy along with current scar treatment for the post-thyroidectomy scar.
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Circadian rhythms are essential regulators of a multitude of physiological and behavioral processes, such as the metabolism and function of the liver. Circadian rhythms are crucial to liver homeostasis, as the liver is a key metabolic organ accountable for the systemic equilibrium of the body. Circadian rhythm disruption alone is sufficient to cause liver cancer through the maintenance of hepatic metabolic disorder. Although there is evidence linking CRD to hepatocarcinogenesis, the precise cellular and molecular mechanisms that underlie the circadian crosstalk that leads to hepatocellular carcinoma remain unknown. The expression of CRD-related genes in HCC was investigated in this study via bulk RNA transcriptomic analysis and single-cell sequencing. Dysregulated CRD-related genes are predominantly found in hepatocytes and fibroblasts, according to the findings. By using a combination of single-cell RNA sequencing and bulk RNA sequencing analyses, the dysregulated CRD-related genes ADAMTS13, BIRC5, IGFBP3, MARCO, MT2A, NNMT, and PGLYRP2 were identified. The survival analysis using the Kaplan-Meier method revealed a significant correlation between the expression levels of BIRC5 and IGFBP3 and the survival of patients diagnosed with HCC.
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Carcinoma Hepatocelular , Ritmo Circadiano , Regulação Neoplásica da Expressão Gênica , Neoplasias Hepáticas , Análise de Sequência de RNA , Análise de Célula Única , Survivina , Carcinoma Hepatocelular/genética , Carcinoma Hepatocelular/patologia , Carcinoma Hepatocelular/metabolismo , Neoplasias Hepáticas/genética , Neoplasias Hepáticas/patologia , Neoplasias Hepáticas/metabolismo , Humanos , Ritmo Circadiano/genética , Survivina/genética , Survivina/metabolismo , Perfilação da Expressão Gênica , Transcriptoma , Proteína 3 de Ligação a Fator de Crescimento Semelhante à InsulinaRESUMO
Hepatocellular carcinoma (HCC) is associated with high rates of metastasis and recurrence, and is one of the most common causes of cancer-associated death worldwide. This study examined the protein changes within circulating exosomes in patients with HCC against those in healthy people using isobaric tags for a relative or absolute quantitation (iTRAQ)-based quantitative proteomics analysis. The protein levels of von Willebrand factor (VWF), cathelicidin antimicrobial peptide (CAMP), and proteasome subunit beta type-2 (PSMB2) were altered in HCC. The increased levels of VWF and PSMB2 but decreased CAMP levels in the serum of patients with HCC were validated by enzyme-linked immunosorbent assays. The level of CAMP (the only cathelicidin found in humans) also decreased in the circulating exosomes and buffy coat of the HCC patients. The serum with reduced levels of CAMP protein in the HCC patients increased the cell proliferation of Huh-7 cells; this effect was reduced following the addition of CAMP protein. The depletion of CAMP proteins in the serum of healthy people enhances the cell proliferation of Huh-7 cells. In addition, supplementation with synthetic CAMP reduces cell proliferation in a dose-dependent manner and significantly delays G1-S transition in Huh-7 cells. This implies that CAMP may act as a tumor suppressor in HCC.
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Carcinoma Hepatocelular , Catelicidinas , Neoplasias Hepáticas , Humanos , Carcinoma Hepatocelular/metabolismo , Catelicidinas/metabolismo , Linhagem Celular Tumoral , Proliferação de Células , Regulação Neoplásica da Expressão Gênica , Neoplasias Hepáticas/metabolismo , Fator de von Willebrand/metabolismoRESUMO
Background: Preeclampsia (PE) is the primary cause of perinatal maternal-fetal mortality and morbidity. The exact molecular mechanisms of PE pathogenesis are largely unknown. This study aims to identify the hub genes in PE and explore their potential molecular regulatory network. Methods: We downloaded the GSE148241, GSE190971, GSE74341, and GSE114691 datasets for the placenta and performed a differential expression analysis to identify hub genes. We performed Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), Disease Ontology (DO), Gene Set Enrichment Analysis (GSEA), and Protein-Protein Interaction (PPI) Analysis to determine functional roles and regulatory networks of differentially expressed genes (DEGs). We then verified the DEGs at transcriptional and translational levels by analyzing the GSE44711 and GSE177049 datasets and our clinical samples, respectively. Results: We identified 60 DEGs in the discovery phase, consisting of 7 downregulated genes and 53 upregulated genes. We then identified seven hub genes using Cytoscape software. In the verification phase, 4 and 3 of the seven genes exhibited the same variation patterns at the transcriptional level in the GSE44711 and GSE177049 datasets, respectively. Validation of our clinical samples showed that CADM3 has the best discriminative performance for predicting PE. Conclusion: These findings may enhance the understanding of PE and provide new insight into identifying potential therapeutic targets for PE.
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Redes Reguladoras de Genes , Pré-Eclâmpsia , Gravidez , Feminino , Humanos , Perfilação da Expressão Gênica , Pré-Eclâmpsia/genética , Regulação Neoplásica da Expressão Gênica , Biologia ComputacionalRESUMO
Hepatocellular carcinoma (HCC) is one of the most common cancers and the main cause of cancer-related death globally. Immune dysregulation of CD4+ T cells has been identified to play a role in the development of HCC. Nevertheless, the underlying molecular pathways of CD4+ T cells in HCC are not completely known. Thus, a better understanding of the dysregulation of the lncRNA-miRNA/mRNA network may yield novel insights into the etiology or progression of HCC. In this study, circulating CD4+ T cells were isolated from the whole blood of 10 healthy controls and 10 HCC patients for the next-generation sequencing of the expression of lncRNAs, miRNAs, and mRNAs. Our data showed that there were different expressions of 34 transcripts (2 lncRNAs, XISTs, and MIR222HGs; 29 mRNAs; and 3 other types of RNA) and 13 miRNAs in the circulating CD4+ T cells of HCC patients. The expression of lncRNA-XIST-related miRNAs and their target mRNAs was confirmed using real-time quantitative polymerase chain reaction (qPCR) on samples from 100 healthy controls and 60 HCC patients. The lncRNA-miRNA/mRNA regulation network was created using interaction data generated from ENCORI and revealed there are positive correlations in the infiltration of total CD4+ T cells, particularly resting memory CD4+ T cells, and negative correlations in the infiltration of Th1 CD4+ T cells.
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Introduction: RNA modifications mediated by the m6A, m1A, and m5C regulatory genes are crucial for the progression of malignancy. This study aimed to explore the expression of regulator genes for m6A/m5C/m1A methylation at the single-cell level and to validate their expression in cancerous and adjacent para-cancerous liver tissues of adult patients with HCC who underwent tumor resection. Methods: The bulk sequencing from The Cancer Genome Atlas (TCGA) database and the single-cell RNA sequencing (scRNA-seq) data obtained from the Gene Expression Omnibus (GEO) database were used to identify the dysregulated m6A/m5C/m1A genes for hepatocellular carcinoma (HCC). A real-time polymerase chain reaction (real-time PCR) was used to measure the expression of dysregulated m6A/m5C/m1A genes in collected human HCC tissues and compared with adjacent para-cancerous liver tissues. Immune cell infiltration with these significantly expressed methylation-related genes was evaluated using Timer2.0. Results: A discrepancy in m6A/m5C/m1A gene expression was observed between bulk sequencing and scRNA-seq. The clustered heatmap of the scRNA-seq-identified dysregulated m6A/m5C/m1A genes in TCGA cohort revealed heterogeneous expression of these methylation regulators within the cancer, whereas their expression in the adjacent liver tissues was more homogeneous. The real-time PCR validated the significant overexpression of DNMT1, NSUN5, TRMT6, IGF2BP1, and IGFBP3, which were identified using scRNA-seq, and IGFBP2, which was identified using bulk sequencing. These dysregulated methylation genes are mainly correlated with the infiltration of natural killer cells. Discussion: This study suggests that cellular diversity inside tumors contributes to the discrepancy in the expression of methylation regulator genes between traditional bulk sequencing and scRNA-seq. This study identified five regulatory genes that will be the focus of further studies regarding the function of m6A/m5C/m1A in HCC.
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Purpose: Following major trauma, genes involved in adaptive immunity are downregulated, which accompanies the upregulation of genes involved in systemic inflammatory responses. This study investigated microRNA (miRNA)-mRNA interactome dysregulation in circulating T cells of patients with major trauma. Patients and Methods: This study included adult trauma patients who had an injury severity score ≥16 and required ventilator support for more than 48 h in the intensive care unit. Next-generation sequencing was used to profile the miRNAs and mRNAs expressed in CD3+ T cells isolated from patient blood samples collected during the injury and recovery stages. Results: In the 26 studied patients, 9 miRNAs (hsa-miR-16-2-3p, hsa-miR-16-5p, hsa-miR-185-5p, hsa-miR-192-5p, hsa-miR-197-3p, hsa-miR-23a-3p, hsa-miR-26b-5p, hsa-miR-223-3p, and hsa-miR-485-5p) were significantly upregulated, while 58 mRNAs were significantly downregulated in T cells following major trauma. A network consisting of 8 miRNAs and 22 mRNAs interactions was revealed by miRWalk, with three miRNAs (hsa-miR-185-5p, hsa-miR-197-3p, and hsa-miR-485-5p) acting as hub genes that regulate the network. Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis suggested that "chemokine signaling pathway" was the predominant pathway. Conclusion: The study revealed a miRNA-mRNA interactome consisting of 8 miRNAs and 22 mRNAs that are predominantly involved in chemokine signaling in circulating T cells of patients following major trauma.
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Accumulation of lipid-laden foam cells in the arterial wall plays a central role in atherosclerotic lesion development, plaque progression, and late-stage complications of atherosclerosis. However, there are still fundamental gaps in our knowledge of the underlying mechanisms leading to foam cell formation in atherosclerotic arteries. Here, we investigated the role of receptor-independent macropinocytosis in arterial lipid accumulation and pathogenesis of atherosclerosis. Genetic inhibition of fluid-phase macropinocytosis in myeloid cells (LysMCre+ Nhe1fl/fl) and repurposing of a Food and Drug Administration (FDA)-approved drug that inhibits macrophage macropinocytosis substantially decreased atherosclerotic lesion development in low-density lipoprotein (LDL) receptor-deficient and Apoe-/- mice. Stimulation of macropinocytosis using genetic (H-RASG12V) and physiologically relevant approaches promoted internalization of unmodified native (nLDL) and modified [e.g., acetylated (ac) and oxidized (ox) LDL] lipoproteins in both wild-type and scavenger receptor (SR) knockout (Cd36-/-/Sra-/-) macrophages. Pharmacological inhibition of macropinocytosis in hypercholesterolemic wild-type and Cd36-/-/Sra-/- mice identified an important role of macropinocytosis in LDL uptake by lesional macrophages and development of atherosclerosis. Furthermore, serial section high-resolution imaging, LDL immunolabeling, and three-dimensional (3D) reconstruction of subendothelial foam cells provide visual evidence of lipid macropinocytosis in both human and murine atherosclerotic arteries. Our findings complement the SR paradigm of atherosclerosis and identify a therapeutic strategy to counter the development of atherosclerosis and cardiovascular disease.
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Aterosclerose , Células Espumosas , Animais , Apolipoproteínas E/genética , Artérias/patologia , Aterosclerose/patologia , Antígenos CD36 , Células Espumosas/metabolismo , Células Espumosas/patologia , Humanos , Lipoproteínas LDL/metabolismo , Camundongos , Camundongos KnockoutRESUMO
AIMS: Inhibitors of the anti-phagocytic CD47-SIRPα immune checkpoint are currently in clinical development for a variety of haematological and solid tumours. Application of immune checkpoint inhibitors to the cardiovascular field is limited by the lack of preclinical studies using genetic models of CD47 and SIRPα inhibition. In this study, we comprehensively analysed the effects of global and cell-specific SIRPα and CD47 deletion on atherosclerosis development. METHODS AND RESULTS: Here, we show that both SIRPα and CD47 expression are increased in human atherosclerotic arteries and primarily co-localize to CD68+ areas in the plaque region. Hypercholesterolaemic mice homozygous for a Sirpa mutant lacking the signalling cytoplasmic region (Sirpamut/mut) and myeloid cell-specific Sirpa-knockout mice are protected from atherosclerosis. Further, global Cd47-/- mice are protected from atherosclerosis but myeloid cell-specific deletion of Cd47 increased atherosclerosis development. Using a combination of techniques, we show that loss of SIRPα signalling in macrophages stimulates efferocytosis, reduces cholesterol accumulation, promotes lipid efflux, and attenuates oxidized LDL-induced inflammation in vitro and induces M2 macrophage phenotype and inhibits necrotic core formation in the arterial wall in vivo. Conversely, loss of myeloid cell CD47 inhibited efferocytosis, impaired cholesterol efflux, augmented cellular inflammation, stimulated M1 polarization, and failed to decrease necrotic core area in atherosclerotic vessels. Finally, comprehensive blood cell analysis demonstrated lower haemoglobin and erythrocyte levels in Cd47-/- mice compared with wild-type and Sirpamut/mut mice. CONCLUSION: Taken together, these findings identify SIRPα as a potential target in atherosclerosis and suggest the importance of cell-specific CD47 inhibition as a future therapeutic strategy.
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Aterosclerose , Células Mieloides , Animais , Humanos , Camundongos , InflamaçãoRESUMO
AIM: The aim of this study is to explore the effects of exercise interventions by type, duration and intensity of exercise for fatigue in breast cancer survivors who had completed their treatment. BACKGROUND: Most studies found that exercise has valuable outcomes for cancer survivors. This meta-analysis comprehensively summarizes the benefits of exercise intervention for fatigue in breast cancer patients who had completed their adjuvant treatments. METHODS: We conducted a meta-analysis on randomized control trials published during 1 January 2000 through 31 December 2019, from PubMed, Cochrane Library databases, EMBASE, Medline (ProQuest), CINAHL, PsycINFO, Chinese Electronic Periodical Service and Wan Fan Data with prespecified searching criteria. Breast cancer patients earlier than stage IIIc and completing adjuvant treatments were included, and the effects of exercise on fatigue were investigated. RESULTS: Nine randomized controlled trials (RCTs) were included (N = 581). Patients receiving exercise interventions showed reduced fatigue comparing with those without exercise. Exercise with low-moderate intensity, 20 min/day, three times per week and lasting up to 12 weeks had a significant effect on reducing fatigue for breast cancer survivors. CONCLUSION: Our study suggested that exercise interventions can reduce fatigue for this group of cancer survivors. The duration and intensity of exercise intervention could be prescribed for this specific group of cancer patients as a basic requirement to handle their reported fatigue.
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Neoplasias da Mama , Sobreviventes de Câncer , Neoplasias da Mama/complicações , Neoplasias da Mama/terapia , Exercício Físico , Fadiga/etiologia , Fadiga/terapia , Feminino , Humanos , Qualidade de Vida , SobreviventesRESUMO
AIM: This study aims to compare the early development of professional value between the students in the traditional programme (BSN) and those in the accelerated BSN (ABSN) programmes. DESIGN: A longitudinal design was conducted. METHODS: Data were collected from three schools of nursing during one academic year. A total of 117 BSN students and 101 ABSN students completed the survey of demographic information and the Nurses' Professional Values Scale-Revised questionnaires. All data were analysed by IBM SPSS-Statistics 22. RESULTS: Results showed that, in the beginning of the first professional nursing course, both students in the BSN and the ABSN programmes reported similar level of professional values. However, after one academic year, the changes in the professional value varied both between these two programmes and among the three different nursing schools. The increased professional value in school A represented the possibility for students to improve during their first-year professional nursing programme. As educators, we should redesign our teaching strategies according to the different conditions of students in each programme.
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Bacharelado em Enfermagem , Estudantes de Enfermagem , Bacharelado em Enfermagem/métodos , Humanos , Estudos Longitudinais , Escolas de Enfermagem , Inquéritos e QuestionáriosRESUMO
Background: Tranexamic acid has been reported to benefit the treatment of postinflammatory hyperpigmentation (PIH). Laser-assisted drug delivery (LADD) could facilitate the efficacy of topically applied drugs into the dermis. This split-area randomized prospective study aims to assess whether early utilization of the LADD procedure with tranexamic acid delivery followed by picosecond lasers can attenuate the PIH better than the utilization of picosecond lasers alone. Patients and methods: Ten post-traumatic cases of PIH in 10 patients (8 female and 2 male) with an average age of 34.2 ± 11.2 years were included in this clinical trial. Using block randomization to determine the treatment side, one side of each area of the PIH was separated from the midline into two halves belonging to the control and tranexamic acid groups. The half area of the tranexamic acid group was further topically applied with 10% tranexamic acid solution. This procedure was repeated every 6 weeks, four times in total. Results: The self-assessment of the hyperpigmentation and overall satisfaction of the treatment outcome were not significantly different between the treatment and control sides. Conclusions: This split-area study revealed that, compared with picosecond alone, there was no significant difference adopting tranexamic acid in LADD after nonablative fractional picosecond laser for PIH.
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Hiperpigmentação , Preparações Farmacêuticas , Ácido Tranexâmico , Adulto , Feminino , Humanos , Hiperpigmentação/tratamento farmacológico , Hiperpigmentação/etiologia , Lasers , Masculino , Pessoa de Meia-Idade , Estudos Prospectivos , Adulto JovemRESUMO
PURPOSE: Severe trauma may lead to the systemic release of inflammatory mediators into the circulation with profound acute-phase responses; however, the understanding of the expression of these mediators remains limited. This study aimed to characterize the alterations in the expression of circulating acute-phase proteins, cytokines, and checkpoint proteins in patients with severe trauma injuries. PATIENTS AND METHODS: The study population included trauma patients in the intensive care unit (ICU) with an injury severity score equal to or greater than 16 and who had used a ventilator for 48 hours. A total of 12 female and 28 male patients were recruited for the study; six patients died and 34 survived. Blood samples collected at acute stages were compared with those drawn at the subacute stage, the time when the patients were discharged from the ICU, or before the discharge of the patients from the hospital. RESULTS: The study identified that the expression of acute-phase proteins, such as alpha-1-acid glycoprotein and C-reactive protein, and cytokines, including granulocyte colony-stimulating factor, interleukin-6, and interleukin-1 receptor antagonist, was elevated in the circulation after severe trauma. In contrast, the levels of acute-phase proteins, such as alpha-2-macroglobulin, serum amyloid P, and von Willebrand factor, and cytokines, including interleukin-4 and interferon gamma-induced protein 10, were reduced. However, there were no significant differences in the expression of checkpoint proteins in the circulation. CONCLUSION: The dysregulated proteins identified in this study may serve as potential therapeutic targets or biomarkers for treating patients with severe trauma. However, the related biological functions of these dysregulated factors require further investigation to validate their functions.
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HYPOTHESIS: It has been verified that a surface of single micro-scale structures with certain roughness could exhibit petal effect. That is, water drops with a contact angle larger than 150° would pin on the petal effect surface. It is conjectured that the water drop could pin on the single micro-scale roughness petal effect surface by totally infiltrating into spaces (or grooves) between micro-pillars. EXPERIMENTS: An inverted optical microscopy system is synchronically applied in the process of advancing/receding contact angle (ACA/RCA) measurements to directly observe the wetting behavior of water droplets on hydrophobic patterned surfaces with regular arrays of square micro-pillars. FINDINGS: A sequence of wetting behavior evolution, Wenzel â petal â pseudo-lotus â lotus, is observed on the hydrophobic patterned surfaces along with increasing surface roughness. It is interesting to observe a Cassie-Wenzel transition for water drops on a petal substrate during the ACA measurement (embedded needle method), leading to two ACAs, one before (in Cassie state) and one after the transition (in Wenzel state). Thus, the petal substrates have large contact angle hysteresis (CAH) (with both ACA and RCA in Wenzel state) to pin the water drop in Wenzel state. A Cassie-Wenzel transition is consistently observed during the evaporation process of water drops on pseudo-lotus substrates, leading to two RCAs: one in Cassie state and one in Wenzel state. The pseudo-lotus substrates have CAH (with both ACA and RCA in Cassie state) small enough to make water drops easily slide off.
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Água , Molhabilidade , Fenômenos Biofísicos , Propriedades de SuperfícieRESUMO
Arterial accumulation of plasma-derived LDL and its subsequent oxidation contributes to atherosclerosis. Lymphatic vessel (LV)-mediated removal of arterial cholesterol has been shown to reduce atherosclerotic lesion formation. However, the precise mechanisms that regulate LV density and function in atherosclerotic vessels remain to be identified. The aim of this study was to investigate the role of native LDL (nLDL) and oxidized LDL (oxLDL) in modulating lymphangiogenesis and underlying molecular mechanisms. Western blotting and immunostaining experiments demonstrated increased oxLDL expression in human atherosclerotic arteries. Furthermore, elevated oxLDL levels were detected in the adventitial layer, where LV are primarily present. Treatment of human lymphatic endothelial cells (LEC) with oxLDL inhibited in vitro tube formation, while nLDL stimulated it. Similar results were observed with Matrigel plug assay in vivo. CD36 deletion in mice and its siRNA-mediated knockdown in LEC prevented oxLDL-induced inhibition of lymphangiogenesis. In addition, oxLDL via CD36 receptor suppressed cell cycle, downregulated AKT and eNOS expression, and increased levels of p27 in LEC. Collectively, these results indicate that oxLDL inhibits lymphangiogenesis via CD36-mediated regulation of AKT/eNOS pathway and cell cycle. These findings suggest that therapeutic blockade of LEC CD36 may promote arterial lymphangiogenesis, leading to increased cholesterol removal from the arterial wall and reduced atherosclerosis.
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BACKGROUND: During clinical practice we have noticed that some patients with hyperthyroidism have finer skin with less wrinkles, pores, and spots after thyroidectomy, and the improvement can be observed within a few weeks after the operation. However, there is no evidence or study in the literature to proof this finding. AIM AND OBJECTIVE: This study was designed to evaluate and quantify the skin characters of patients with hyperthyroidism before and after thyroidectomy. MATERIAL AND METHODS: This is a prospective study to include patients with hyperthyroidism who received total thyroidectomy between March 1st, 2018 and February 28th, 2019. The patients received blood test for T4 and TSH analysis and VISIA measurements for skin texture quantification, at the preoperative stage, three, and six months postoperatively. A total of 8 patients were included. Repeated measurement was used to determine the lab data and VISIA measurement changes before and after the operation. Mauchly's sphericity test was performed to determine whether the violation of sphericity occurs, and the Greenhouse-Geisser correction was used when the violation of sphericity occurs. RESULTS: All the patients were female and generally healthy without systemic medical disease except the hyperthyroidism. The T4 and TSH levels were not significantly different before and after the thyroidectomy. In terms of the skin character measurements, the wrinkles, texture, pores, UV spots, and brown spots were not improved after thyroidectomy. A trend of improvement in spots, red area, and porphyrin was noted, although not statistically significant. CONCLUSIONS: Surgical removal of the thyroid gland in patients with hyperthyroidism does not improve the skin quality and texture in examinations via the VISIA system.
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Face , Hipertireoidismo , Pele , Tireoidectomia , Técnicas Cosméticas/instrumentação , Feminino , Humanos , Hipertireoidismo/cirurgia , Estudos ProspectivosRESUMO
BACKGROUND: Metabolic syndrome has been shown to be a risk for new onset of cardiovascular disease (CVD) and type 2 diabetes. The subclasses of metabolic syndrome and any associated adverse health outcomes remain obscure. This study aimed to explore potential subtypes of metabolic syndrome, their associations with incidental diabetes, and any Major Adverse Cardiovascular Events (MACE). METHODS: Data for the retrospective cohort study were extracted from the New Taipei City Elderly Health Examination Database in the years 2014 and 2016. Demographic data, status of metabolic syndrome, its components, and latent class analysis (LCA) were analyzed. All participants were aged 65 years and older, with those having a prior history of CVD, cerebrovascular disease, diabetes mellitus (DM), and currently taking medications for hypertension, diabetes, and dyslipidemia were excluded. RESULTS: A total of 4,537 senior citizens were enrolled, with 2,207 (48.6%) of them identified as men. The prevalence of both metabolic syndrome and central obesity was increased with age. A 4-latent class model was fitted for participants diagnosed with metabolic syndrome. The central obesity (ABD)+ hyperglycemia (GLU)+ reduced HDL-C (HDL)+ high Blood Pressure (BP) group displayed the highest hazard ratio (HR) for predicting the new onset of diabetes, while the ABD+HDL+BP group showed a high risk for both CVD and MACE when compared after 2 years of follow-up. CONCLUSIONS: This epidemiological analysis demonstrated that the risks of developing new-onset diabetes, CVD, and MACE varied among the different subtypes of metabolic syndrome.
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AIMS: Impaired lymphatic drainage of the arterial wall results in intimal lipid accumulation and atherosclerosis. However, the mechanisms regulating lymphangiogenesis in atherosclerotic arteries are not well understood. Our studies identified elevated levels of matrix protein R-spondin 2 (RSPO2) in atherosclerotic arteries. In this study, we investigated the role of RSPO2 in lymphangiogenesis, arterial cholesterol efflux into lesion-draining lymph nodes (LNs) and development of atherosclerosis. METHODS AND RESULTS: The effect of RSPO2 on lymphangiogenesis was investigated using human lymphatic endothelial cells (LEC) in vitro and implanted Matrigel plugs in vivo. Cellular and molecular approaches, pharmacological agents, and siRNA silencing of RSPO2 receptor LGR4 were used to investigate RSPO2-mediated signalling in LEC. In vivo low-density lipoprotein (LDL) tracking and perivascular blockade of RSPO2-LGR4 signalling using LGR4-extracellular domain (ECD) pluronic gel in hypercholesterolemic mice were utilized to investigate the role of RSPO2 in arterial reverse cholesterol transport and atherosclerosis. Immunoblotting and imaging experiments demonstrated increased RSPO2 expression in human and mouse atherosclerotic arteries compared to non-atherosclerotic controls. RSPO2 treatment inhibited lymphangiogenesis both in vitro and in vivo. LGR4 silencing and inhibition of RSPO2-LGR4 signalling abrogated RSPO2-induced inhibition of lymphangiogenesis. Mechanistically, we found that RSPO2 suppresses PI3K-AKT-endothelial nitric oxide synthase (eNOS) signalling via LGR4 and inhibits activation of the canonical Wnt-ß-catenin pathway. ApoE-/- mice treated with LGR4-ECD developed significantly less atherosclerosis compared with control treatment. Finally, increased arterial lymphatic vessel density and improved lymphatic drainage of fluorescently labelled LDL to deep cervical LNs were observed in LGR4-ECD-treated mice. CONCLUSION: These findings demonstrate that RSPO2 inhibits lymphangiogenesis via LGR4 and downstream impairment of AKT-eNOS-nitric oxide signalling. These results may also inform new therapeutic strategies to promote lymphangiogenesis and improve cholesterol efflux from atherosclerotic arteries.
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Artérias/metabolismo , Aterosclerose/metabolismo , Peptídeos e Proteínas de Sinalização Intercelular/metabolismo , Linfangiogênese , Vasos Linfáticos/metabolismo , Trombospondinas/metabolismo , Idoso , Idoso de 80 Anos ou mais , Animais , Artérias/patologia , Aterosclerose/genética , Aterosclerose/patologia , Células Cultivadas , Modelos Animais de Doenças , Células Endoteliais/metabolismo , Células Endoteliais/patologia , Feminino , Humanos , Peptídeos e Proteínas de Sinalização Intercelular/genética , Vasos Linfáticos/patologia , Masculino , Camundongos Endogâmicos C57BL , Camundongos Knockout para ApoE , Pessoa de Meia-Idade , Óxido Nítrico Sintase Tipo III/genética , Óxido Nítrico Sintase Tipo III/metabolismo , Placa Aterosclerótica , Proteínas Proto-Oncogênicas c-akt/metabolismo , Receptores Acoplados a Proteínas G/genética , Receptores Acoplados a Proteínas G/metabolismo , Transdução de Sinais , Trombospondinas/genéticaRESUMO
Frailty is common among older people and results in adverse health outcomes. We investigated whether exposure to PM2.5 is associated with frailty. This cross-sectional study involved 20,606 community-dwelling participants aged ≥ 65 years, residing in New Taipei City, Taiwan. Analytic data included phenotypic frailty, disease burden by Charlson Comorbidity Index (CCI), urban or rural residence, and household income. PM2.5 exposure was calculated from air quality monitoring records, with low exposure defined as the lowest quartile of the study population. 1,080 frail participants (5.2%) were older, predominantly female, had more comorbidities, lived rurally, and had low PM2.5 exposure (all p < 0.001). In multinomial logistic regression analyses, the likelihood of high PM2.5 exposure was higher in prefrail (OR 1.4, 95% CI 1.3-1.5) and frail adults (OR 1.5, 95% CI 1.2-1.9) than in robust individuals, with stronger associations in those who were male (frail: OR 2.1, 95% CI 1.5-3.1; prefrail: OR 2.2, 95% CI 1.9-2.6), ≥ 75 years old (frail: OR 1.8, 95% CI 1.3-2.4; prefrail: OR 1.5, 95% CI 1.3-1.8), non-smokers (frail: OR 1.6, 95% CI 1.3-2.0; prefrail: OR 1.4, 95% CI 1.2-1.5), had CCI ≥ 2 (frail: OR 5.1, 95% CI 2.1-12.6; prefrail: OR 2.1, 95% CI 1.2-3.8), and with low household income (frail: OR 4.0, 95% CI 2.8-5.8; prefrail: OR 2.7, 95% CI 2.2-3.3). This study revealed a significant association between PM2.5 exposure and frailty, with a stronger effect in vulnerable groups.