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M Guftar Shaikh Department of Paediatric Endocrinology, Royal Hospital for Children, Glasgow, UK
Developmental Endocrinology Research Group, University of Glasgow, Glasgow, UK

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Timothy G Barrett Department of Endocrinology, Birmingham Womens and Children’s Hospital, Birmingham, UK
Institute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, UK

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Nicola Bridges Department of Paediatric Endocrinology, Chelsea and Westminster Hospital, London, UK

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Robin Chung Research Working Group, Prader-Willi Syndrome Association, Northampton, UK

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Evelien F Gevers Department of Paediatric Endocrinology, Barts Health NHS Trust, Royal London Hospital, London, UK
Centre for Endocrinology, William Harvey Research Institute, Barts and The London Medical School, Queen Mary University of London, London, UK

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Anthony P Goldstone PsychoNeuroEndocrinologyResearch Group, Division of Psychiatry, Department of Brain Sciences, Faculty of Medicine, Imperial College London, London, UK
Department of Endocrinology, Imperial College Healthcare NHS Trust, Hammersmith Hospital, London, UK

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Anthony Holland Department of Psychiatry, University of Cambridge, Cambridge, UK

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Shankar Kanumakala Royal Alexandra Children’s Hospital, Brighton, UK

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Ruth Krone Department of Endocrinology, Birmingham Womens and Children’s Hospital, Birmingham, UK

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Andreas Kyriakou Department of Paediatric Endocrinology, Royal Hospital for Children, Glasgow, UK
Department of Paediatric Endocrinology, Makarios Children's Hospital, Nicosia, Cyprus

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E Anne Livesey Royal Alexandra Children’s Hospital, Brighton, UK
Sussex Community NHS Trust, Brighton, UK

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Angela K Lucas-Herald Department of Paediatric Endocrinology, Royal Hospital for Children, Glasgow, UK
Developmental Endocrinology Research Group, University of Glasgow, Glasgow, UK

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Christina Meade CHI at Tallaght University Hospital, Dublin, Republic of Ireland

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Susan Passmore Prader-Willi Syndrome Association, Northampton, UK

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Edna Roche CHI at Tallaght University Hospital, Dublin, Republic of Ireland
The University of Dublin, Trinity College Dublin, Dublin, Republic of Ireland

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Chris Smith Royal Alexandra Children’s Hospital, Brighton, UK

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Sarita Soni Learning Disability Psychiatry, NHS Greater Glasgow and Clyde, Glasgow, UK

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Prader–Willi syndrome (PWS) is a rare orphan disease and complex genetic neurodevelopmental disorder, with a birth incidence of approximately 1 in 10,000–30,000. Management of people with PWS requires a multi-disciplinary approach, ideally through a multi-disciplinary team (MDT) clinic with community support. Hypotonia, poor feeding and faltering growth are characteristic features in the neonatal period, followed by hyperphagia and risk of rapid weight gain later in childhood. Children and adolescents (CA) with PWS usually display developmental delay and mild learning disability and can develop endocrinopathies, scoliosis, respiratory difficulties (both central and obstructive sleep apnoea), challenging behaviours, skin picking, and mental health issues, especially into adulthood. This consensus statement is intended to be a reference document for clinicians managing children and adolescents (up to 18 years of age) with PWS. It considers the bio-psycho-social domains of diagnosis, clinical assessment, and management in the paediatric setting as well as during and after transition to adult services. The guidance has been developed from information gathered from peer-reviewed scientific reports and from the expertise of a range of experienced clinicians in the United Kingdom and Ireland involved in the care of patients with PWS.

Open access
Camila Aparecida Moma Endocrinology Division, Department of Internal Medicine, Faculty of Medical Sciences, University of Campinas, Campinas, São Paulo, Brazil

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Icléia Siqueira Barreto Department of Pathology, Faculty of Medical Sciences, University of Campinas, Campinas, São Paulo, Brazil

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Ligia Vera Montali Assumpção Endocrinology Division, Department of Internal Medicine, Faculty of Medical Sciences, University of Campinas, Campinas, São Paulo, Brazil

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Denise Engelbrecht Zantut-Wittmann Endocrinology Division, Department of Internal Medicine, Faculty of Medical Sciences, University of Campinas, Campinas, São Paulo, Brazil

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Background

Papillary thyroid carcinoma has become increasingly prevalent over the years. Avoiding unnecessary treatments and the risk of complications is essential, as well as understanding the mechanisms of tumor progression and the conditions that indicate a worse prognosis. Assessment of the tumor microenvironment can allow us understand how the immune system organizes itself to contain neoplastic progression.

Methods

We compared characteristics related to the lymphocytic subpopulations in the thyroid tumor microenvironment and lymph nodes in two groups, with and without lymph node metastatic involvement.

Results

Of the 400 cases followed up at a thyroid cancer reference service, 32 were selected, of which, 13 cases did not present lymph node metastasis (N0 group) and 19 had lymph node involvement (N1 group). Clinical data were collected, and immunohistochemical reactions were performed for markers CD4, CD8, FoxP3, CD25, and CD20 in lymph nodes and peritumoral infiltrate. We found that the N1 group had larger tumor sizes, higher risk staging, higher frequency of extrathyroidal extension, shorter disease-free times, and higher expression of CD4+ T lymphocytes in lymph nodes; however, there was no difference in the expression of other markers or in the pattern of lymphocyte distribution in the lymph node.

Conclusion

In cervical lymph nodes, the higher frequency of CD4+ T lymphocytes is related to the presence of metastasis. However, there were no differences in lymphocytic subpopulations in the thyroid tumor microenvironment. The absence of changes in unaffected lymph nodes could not predict any tumor behavior.

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Gayana Amiyangoda G Amiyangoda, Department of Pharmacology, University of Peradeniya, Peradeniya, Sri Lanka

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C N Antonypillai C Antonypillai, Diabetes and Endocrinology Unit, National Hospital, Kandy, Sri Lanka

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S S C Gunatilake S Gunatilake, Diabetes and Endocrinology Unit, National Hospital, Kandy, Sri Lanka

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T T Weerathunge T Weerathunge, Department of Community Medicine, University of Colombo, Colombo, Sri Lanka

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D Ediriweera D Ediriweera, Health Data Science Unit, , University of Kelaniya Faculty of Medicine, Ragama, Sri Lanka

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S G P D Kosgallana S Kosgallana, Diabetes and Endocrinology Unit, National Hospital, Kandy, Sri Lanka

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R D P Jayawardana R Jayawardana, Department of Biochemistry, National Hospital, Kandy, Sri Lanka

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H A N D Thissera H Thissera, Department of Biochemistry, National Hospital, Kandy, Sri Lanka

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Wj Emalka W Emalka, Faculty of Medicine, University of Peradeniya, Peradeniya, Sri Lanka

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H U Daraniyagala H Daraniyagala, University of Peradeniya, Peradeniya, 20400, Sri Lanka

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Refractory hypothyroidism is associated with high morbidity and increased healthcare expenditure. In general, the use of the levothyroxine absorption test looks promising in evaluating refractory hypothyroidism but has shown significant variability in protocols in multiple settings. We intended to assess the usefulness of the levothyroxine absorption test in a low-resource setting and to assess the factors associated with refractory hypothyroidism. A cross-sectional study among age-matched 25 cases of refractory hypothyroidism and 24 treatment-responsive hypothyroid controls was conducted. A supervised levothyroxine absorption test was performed with levothyroxine 1000 μg tablets after a10 hours fast and serum-free tetraiodothyronine (FT4) levels were measured at 0,1,2,3,4,5 hours. Descriptive statistics, Chi-square test, student T-test, and logistic regression were used in the analysis. Results showed no significant difference in age, body weight, etiology of hypothyroidism, interfering medications, thyroxine storage, and ingestion technique in cases and controls. Cases had a longer duration of hypothyroidism and males had a higher peak FT4 concentration. During pooled analysis, serum FT4 peaked at 3 hours with an increment of 149.4% (128.4 - 170.5%) from baseline and plateaued thereafter. The absolute value of FT4 at 3 hours was 41.59 (SD 14.14) pmol/L (3.23 ng/dl). We concluded that there was no significant difference in the pattern of levothyroxine absorption in both groups. The commonest cause of refractory disease was pseudo malabsorption. Rapid supervised levothyroxine absorption test with two blood samples for FT4 at baseline and at the peak of absorption (3 hours) is simple, convenient, and cost-effective, particularly in low-resource settings.

Open access
Peter Bond P Bond, Department of Internal Medicine, Elisabeth TweeSteden Hospital, Tilburg, Netherlands

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Tijs Verdegaal T Verdegaal, Department of Internal Medicine, Spaarne Gasthuis, Haarlem, Netherlands

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Diederik L Smit D Smit, Department of Internal Medicine, Elisabeth TweeSteden Hospital, Tilburg, Netherlands

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Erythrocytosis, or elevated hematocrit, is a common side effect of testosterone therapy (TTh) in male hypogonadism. Testosterone stimulates erythropoiesis through an initial rise in erythropoietin (EPO), establishment of a new EPO/hemoglobin ‘set point’, and a parallel decrease in the master iron regulator protein hepcidin, as well as several other potential mechanisms. Evidence shows an increased thrombotic risk associated with TTh–induced erythrocytosis. Several guidelines for the treatment of male hypogonadism by endocrine organizations recommend against starting TTh in patients presenting with elevated hematocrit at baseline or to stop TTh when its levels cannot be controlled by dose-adjustments. Importantly, therapeutic phlebotomy or venesection is mentioned as a means of reducing hematocrit in these patients. However, evidence supporting the efficacy or safety of therapeutic phlebotomy in lowering hematocrit in TTh–induced erythrocytosis is lacking. In light of this dearth of evidence, the recommendation to lower hematocrit using therapeutic phlebotomy is notable, as phlebotomy lowers tissue oxygen partial pressure (pO2) and, eventually, depletes iron stores, thereby triggering various biological pathways which might also increase thrombotic risk. The potential pros and cons should therefore be carefully weighed against each other and shared decision making is recommended for initiating therapeutic phlebotomy as a treatment in patients on TTh who present with increased hematocrit.

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Qing Zhou Department of Endocrinology, Fujian Maternity and Child Health Hospital, Fujian Children’s Hospital, Fuzhou, China

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Li Yong Zhang Department of Thyroid Surgery, Minimal Invasive Center, Fujian Medical University Union Hospital, Fuzhou, China

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Mei Feng Dai Department of Clinical Lab, Fujian Maternity and Child Health Hospital, Fuzhou, China

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Zhen Li Department of Endocrinology, Fujian Maternity and Child Health Hospital, Fujian Children’s Hospital, Fuzhou, China

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Chao Chun Zou Department of Endocrinology, The Children’s Hospital, Zhejiang University School of Medicine, Hangzhou, China

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Hui Liu Department of Endocrinology, Fujian Maternity and Child Health Hospital, Fujian Children’s Hospital, Fuzhou, China

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Graphical abstract

Abstract

Subclinical hypothyroidism (SCH) is closely related to insulin resistance, and thyroid-stimulating hormone (TSH) level is an independent factor for insulin resistance associated with subclinical hypothyroidism. This study aims to explore the effects of TSH levels on insulin signal transduction in adipocytes and to establish the role of endoplasmic reticulum (ER) stress in this process. In this study, the SCH mouse model was established, and 3T3-L1 adipocytes were treated with TSH or tunicamycin (TM), with or without 4-phenylbutyric acid (4-PBA), an inhibitor of ER stress. Subclinical hypothyroidism mice exhibited impaired glucose tolerance, inactivation of the IRS-1/AKT pathway, and activation of the IRE1/JNK pathway in adipose tissue, which can all be alleviated by 4-PBA. Supplementation with levothyroxine restored the TSH to normal, alongside alleviated ER stress and insulin resistance in SCH mice, which is characterized by improved glucose tolerance, decreased mRNA expression of IRE1, and decreased phosphorylation of JNK in adipose tissue. In 3T3-L1 adipocytes, TSH induces insulin resistance, leading to a decrease in glucose uptake. This effect is mediated by the downregulation of IRS-1 tyrosine phosphorylation, reduced AKT phosphorylation, and inhibited GLUT4 protein expression. Notably, all these effects can be effectively reversed by 4-PBA. Moreover, TSH induced TNF-α and IL-6 production and upregulated the expression of ER stress markers. Similarly, these changes can be recovered by 4-PBA. These findings indicate that TSH has the capability to induce insulin resistance in adipocytes. The mechanism through which TSH disrupts insulin signal transduction appears to involve the ER stress–JNK pathway.

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Shams Ali Baig College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom

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Kashish Malhotra Department of Surgery, Rama Medical College Hospital and Research Centre, Hapur, Uttar Pradesh, India
Institute of Applied Health Research, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK

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Anagh Josh Banerjee College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom

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Mukunth Kowsik College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom

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Khushi Kumar College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom

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Fazna Rahman College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom

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Syeda Sabbah Batul College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom

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Mohammed Faraaz Saiyed College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom

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Vardhan Venkatesh College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom

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Pranav Viswanath Iyer College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom

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Punith Kempegowda Institute of Applied Health Research, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK
Queen Elizabeth Hospital, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK

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YouTube® is one of the leading platforms for health information. However, the lack of regulation of content and quality raises concerns about accuracy and reliability. CoMICs (Concise Medical Information Cines) are evidence-based short videos created by medical students and junior doctors and reviewed by experts to ensure clinical accuracy. We performed a systematic review to understand the impact of videos on knowledge and awareness about diabetes and PCOS. We then evaluated the quality of YouTube® videos about diabetes and PCOS using various validated quality assessment tools and compared these with CoMICs videos on the same topics. Quality assessment tools like DISCERN, JAMA benchmark criteria, and global quality scale (GQS) score were employed. Some of the authors of this study also co-authored the creation of some of the CoMICs evaluated. Our study revealed that while videos effectively improve understanding of diabetes and PCOS, there are notable differences in quality and reliability of the videos on YouTube®. For diabetes, CoMICs videos had higher DISCERN scores (CoMICs vs YouTube®: 2.4 vs 1.6), superior reliability (P < 0.01), and treatment quality (P < 0.01) and met JAMA criteria for authorship (100% vs 30.6%) and currency (100% vs 53.1%). For PCOS, CoMICs had higher DISCERN scores (2.9 vs 1.9), reliability (P < 0.01), and treatment quality (P < 0.01); met JAMA criteria for authorship (100% vs 34.0%) and currency (100% vs 54.0%); and had higher GQS scores (4.0 vs 3.0). In conclusion, CoMICs outperformed other similar sources on YouTube® in providing reliable evidence-based medical information which may be used for patient education.

Open access
Carlijn A Hoekx Division of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, The Netherlands
Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, The Netherlands

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Borja Martinez-Tellez Division of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, The Netherlands
Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, The Netherlands
Department of Nursing Physiotherapy and Medicine, SPORT Research Group (CTS-1024), CERNEP Research Center, University of Almería, Almería, Spain
Biomedical Research Unit, Torrecárdenas University Hospital, Almería, Spain
CIBER de Fisiopatología de la Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, Granada, Spain

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Maaike E Straat Division of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, The Netherlands
Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, The Netherlands

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Magdalena M A Verkleij Division of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, The Netherlands
Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, The Netherlands

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Mirjam Kemmeren Division of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, The Netherlands
Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, The Netherlands

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Sander Kooijman Division of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, The Netherlands
Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, The Netherlands

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Martin Uhrbom Bioscience Metabolism, Research and Early Development, Cardiovascular, Renal and Metabolism (CVRM), BioPharmaceuticals R&D, AstraZeneca Gothenburg, Sweden
Department of Medicine, Huddinge, Karolinska Institutet Campus Flemingsberg, Neo Building, Huddinge, Sweden

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Saskia C A de Jager Laboratory of Experimental Cardiology, University Medical Center Utrecht, Utrecht, The Netherlands

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Patrick C N Rensen Division of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, The Netherlands
Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, The Netherlands

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Mariëtte R Boon Division of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, The Netherlands
Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, The Netherlands

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Objectives

Cold exposure is linked to cardiometabolic benefits. Cold activates brown adipose tissue (BAT), increases energy expenditure, and induces secretion of the hormones fibroblast growth factor 21 (FGF21) and growth differentiation factor 15 (GDF15). The cold-induced increase in energy expenditure exhibits a diurnal rhythm in men. Therefore, we aimed to investigate the effect of cold exposure on serum FGF21 and GDF15 levels in humans and whether cold-induced changes in FGF21 and GDF15 levels differ between morning and evening in males and females.

Method

In this randomized cross-over study, serum FGF21 and GDF15 levels were measured in healthy lean males (n = 12) and females (n = 12) before, during, and after 90 min of stable cold exposure in the morning (07:45 h) and evening (19:45 h) with a 1-day washout period in between.

Results

Cold exposure increased FGF21 levels in the evening compared to the morning both in males (+61% vs −13%; P < 0.001) and in females (+58% vs +8%; P < 0.001). In contrast, cold exposure did not significantly modify serum GDF15 levels, and no diurnal variation was found. Changes in FGF21 and GDF15 levels did not correlate with changes in cold-induced energy expenditure in the morning and evening.

Conclusion

Cold exposure increased serum FGF21 levels in the evening, but not in the morning, in both males and females. GDF15 levels were not affected by cold exposure. Thus, this study suggests that the timing of cold exposure may influence cold-induced changes in FGF21 levels but not GDF15 levels and seems to be independent of changes in energy expenditure.

Open access
Irfan Vardarli 5th Medical Department, Division of Endocrinology and Diabetes, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany

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Susanne Tan Department of Endocrinology, Diabetes and Metabolism, Clinical Chemistry – Division of Laboratory Research Endocrine Tumor Center at WTZ/Comprehensive Cancer Center, University Hospital Essen, University of Duisburg-Essen, Essen, Germany

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Rainer Görges Department of Nuclear Medicine, University Hospital Essen, University of Duisburg-Essen, Essen, Germany

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Bernhard K Krämer 5th Medical Department, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany

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Ken Herrmann Department of Nuclear Medicine, University Hospital Essen, University of Duisburg-Essen, Essen, Germany

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Christoph Brochhausen Institue of Pathology, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany

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Objective

The management of thyroid nodules with indeterminate cytology (ITN) is still a challenge. To evaluate the performance of commercial molecular tests for ITN, we performed this comprehensive meta-analysis.

Methods

We performed an electronic search using PubMed/Medline, Embase, and the Cochrane Library. Studies assessing the diagnostic accuracy of Afirma gene expression classifier (GEC), Afirma gene sequencing classifier (GSC), ThyroSeq v2 (TSv2), or ThyroSeq v3 (TSv3) in patients with ITN (only Bethesda category III or IV) were selected; Statistical analyses were performed by using Stata.

Results

Seventy-one samples (GEC, n = 38; GSC, n = 16; TSv2, n = 9; TSv3, n = 8) in 53 studies, involving 6490 fine needle aspirations (FNAs) with ITN cytology with molecular diagnostics (GEC, GSC, TSv2, or TSv3), were included in the study. The meta-analysis showed the following pooled estimates: sensitivity 0.95 (95% CI: 0.94–0.97), specificity 0.35 (0.28–0.43), positive likelihood ratio (LR+) 1.5 (1.3–1.6), and negative likelihood ratio (LR−) 0.13 (0.09–0.19), with the best performance for TSv3 (area under the ROC curve 0.95 (0.93–0.96), followed by TSv2 (0.90 (0.87–0.92)), GSC (0.86 (0.82–0.88)), and GEC (0.82 (0.78–0.85)); the best rule-out property was observed for GSC (LR−, 0.07 (0.02–0.19)), followed by TSv3 (0.11 (0.05–0.24)) and GEC (0.16 (0.10–0.28), and the best rule-in was observed for TSv2 (LR+, 2,9 (1.4–4.6)), followed by GSC (1.9 (1.6–2.4)). A meta-regression analysis revealed that study design, Bethesda category, and type of molecular test were independent factors.

Conclusion

We showed that in patients with ITN, TSv3 has the best molecular diagnostic performance, followed by TSv2, GSC, and GEC. As regards rule-out malignancy, GSC, and rule-in, TSV2 is superior to other tests.

Open access
Shikai Gui Department of Neurosurgery, the 2nd affiliated hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi Province, China
Nanchang University, Nanchang, Jiangxi Province, China
Institute of Neuroscience, Nanchang University, Nanchang, Jiangxi Province, China

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Wanli Yu Department of Neurosurgery, the 2nd affiliated hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi Province, China
Nanchang University, Nanchang, Jiangxi Province, China
Institute of Neuroscience, Nanchang University, Nanchang, Jiangxi Province, China

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Jiabao Xie Department of Neurosurgery, the 2nd affiliated hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi Province, China
Nanchang University, Nanchang, Jiangxi Province, China
Institute of Neuroscience, Nanchang University, Nanchang, Jiangxi Province, China

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Lunshan Peng Department of Neurosurgery, the 2nd affiliated hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi Province, China
Nanchang University, Nanchang, Jiangxi Province, China
Institute of Neuroscience, Nanchang University, Nanchang, Jiangxi Province, China

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Yuanyuan Xiong Department of Neurosurgery, the 2nd affiliated hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi Province, China
Nanchang University, Nanchang, Jiangxi Province, China

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Zhen Song Nanchang University, Nanchang, Jiangxi Province, China
Department of Urology, the 2nd affiliated hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi Province, China

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Haitao Luo Department of Neurosurgery, the 2nd affiliated hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi Province, China

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Juexian Xiao Department of Neurosurgery, the 2nd affiliated hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi Province, China

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Shengtao Yuan Jiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, Nanjing, Jiangsu Province, China

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Zujue Cheng Department of Neurosurgery, the 2nd affiliated hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi Province, China
Nanchang University, Nanchang, Jiangxi Province, China
Institute of Neuroscience, Nanchang University, Nanchang, Jiangxi Province, China

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Invasive pituitary neuroendocrine tumors (PitNETs) are the most prevalent types of intracranial and neuroendocrine tumors. Their aggressive growth and difficulty in complete resection result in a high recurrence rate. Cystine transporter solute carrier family 7 member 11 (SLC7A11) is overexpressed in various cancers, which contributes to tumor growth, progression, and metastasis by promoting cystine uptake and glutathione biosynthesis. We identified SLC7A11 as an invasive biomarker based on three Gene Expression Omnibus cohorts. This study aimed to investigate the role of SLC7A11 in invasive PitNETs. Cell proliferation was assessed using CCK-8 and colony formation assays, while cell apoptosis was estimated with flow cytometry. Wound healing assays and transwell assays were utilized to evaluate migration and invasion ability. Our findings demonstrated that SLC7A11 was markedly upregulated in invasive PitNETs, and was associated with the invasiveness of PitNETs. Knockdown of SLC7A11 could largely suppress tumor cell proliferation, migration, and invasion, while inducing apoptosis. Furthermore, SLC7A11 depletion was implicated in regulating epithelial–mesenchymal transition and inactivating the PI3K/AKT signaling pathway. These insights suggest SLC7A11 as a potential therapeutic target for invasive PitNETs.

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Niels B Dalsgaard Center for Clinical Metabolic Research, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark

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Lærke S Gasbjerg Center for Clinical Metabolic Research, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark
Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

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Laura S Hansen Center for Clinical Metabolic Research, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark

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Dennis S Nielsen Department of Food Science, Faculty of Science, University of Copenhagen, Copenhagen, Denmark

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Torben S Rasmussen Department of Food Science, Faculty of Science, University of Copenhagen, Copenhagen, Denmark

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Filip K Knop Center for Clinical Metabolic Research, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Steno Diabetes Center Copenhagen, Gentofte, Denmark

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Aim

The alpha-glucosidase inhibitor acarbose is approved for the treatment of type 2 diabetes (T2D). It acts in the lumen of the gut by reducing intestinal hydrolysis and absorption of ingested carbohydrates. This reduces postprandial blood glucose concentration and increases the content of carbohydrates in the distal parts of the intestine potentially influencing gut microbiome (GM) composition and possibly impacting the gut microbiome (GM) dysbiosis associated with T2D. Here, we investigated the effect of acarbose on GM composition in patients with T2D.

Methods

Faecal samples were collected in a previously conducted randomised, placebo-controlled, double-blind, crossover study in which 15 individuals with metformin-treated T2D (age 57–85 years, HbA1c 40–74 mmol/mol, BMI 23.6–34.6 kg/m2) were subjected to two 14-day treatment periods with acarbose and placebo, respectively, separated by a 6-week wash-out period. Faecal samples were collected before and by the end of each treatment period. The GM profiles were evaluated by 16S rRNA gene amplicon sequencing.

Results

The GM profiles after the treatment periods with acarbose or placebo remained unaffected (P > 0.7) when compared with the GM profiles before treatment. This applied to the analysis of within-sample diversity (α-diversity) and between-sample bacterial composition diversity (β-diversity). Additionally, no dominant bacterial species differentiated the treatment groups, and only minor increases in the relative abundances of Klebsiella spp. and Escherichia coli (P < 0.05) were observed after acarbose treatment.

Conclusion

In patients with metformin-treated T2D, 14 days of treatment with acarbose showed only minor effects on GM as seen in increased relative abundances of Klebsiella spp. and Escherichia coli.

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