Search Results
Search for other papers by Xi Wang in
Google Scholar
PubMed
Search for other papers by Qi Yu in
Google Scholar
PubMed
Objective
To evaluate the safety and efficacy of letrozole in girls with progressive precocious puberty (PP) associated with McCune–Albright syndrome (MAS).
Design
Monocentric retrospective cross-sectional and longitudinal study of consecutive patients.
Patients
Ten MAS patients treated at Peking Union Medical College Hospital between September 1999 and December 2017 were retrospectively reviewed; those with complications due to PP were followed.
Results
The mean age at letrozole initiation was 4.5 ± 2.6 years, while the mean duration of treatment was 3.3 ± 2.4 years. Letrozole was highly effective at decreasing the rate of skeletal maturation, with a significant decrease in the bone age-to-chronological age (BA/CA) ratio from 1.9 ± 1.1 pre-treatment to 1.5 ± 1.2 on letrozole treatment (P = 0.016). Moreover, growth velocity Z-scores declined from 0.41 ± 0.5 to −0.2 ± 0.31 with treatment (P < 0.001). Predicted adult height Z-scores increased significantly from −2.03 ± 2.33 at baseline to 1.13 ± 0.84 following treatment initiation (P = 0.029). Moreover, vaginal bleeding declined significantly on letrozole.
Conclusions
Our findings suggest that letrozole may be an effective therapy in some girls with MAS, as treatment results in improved BA/CA ratio, growth velocity and predicted adult height. Possible adverse effects include nettle rash.
Department of Clinical Medicine, Gansu University of Chinese Medicine, Lanzhou, Gansu, China
Search for other papers by Ningning Gong in
Google Scholar
PubMed
Search for other papers by Cuixia Gao in
Google Scholar
PubMed
Search for other papers by Xuedi Chen in
Google Scholar
PubMed
Search for other papers by Yu Wang in
Google Scholar
PubMed
Search for other papers by Limin Tian in
Google Scholar
PubMed
Department of Clinical Medicine, Gansu University of Chinese Medicine, Lanzhou, Gansu, China
Search for other papers by Ningning Gong in
Google Scholar
PubMed
Search for other papers by Cuixia Gao in
Google Scholar
PubMed
Search for other papers by Xuedi Chen in
Google Scholar
PubMed
Search for other papers by Yu Wang in
Google Scholar
PubMed
Search for other papers by Limin Tian in
Google Scholar
PubMed
The purpose of our study was to observe adipokine expression and endothelial function in subclinical hypothyroidism (sHT) rats and to determine whether levothyroxine (LT4) treatment affects these changes. Sixty-five male Wistar rats were randomly divided into five groups: the control group; sHT A, B and C groups and the sHT + T4 group. The sHT rats were induced by methimazole (MMI) and the sHT + T4 rats were administered LT4 treatment after 8 weeks of MMI administration. Thyroid function and lipid levels were measured using radioimmunoassays and enzymatic colorimetric methods, respectively. Serum adiponectin (APN), chemerin, TNF-α, endothelin (ET-1) and nitric oxide (NO) levels were measured using ELISA kits and a nitric-reductive assay. The expression of APN, chemerin and TNF-α in visceral adipose tissue (VAT) was measured in experimental rats using RT-PCR and Western blotting. Hematoxylin–eosin (HE) staining was used to observe changes in adipose tissue. The sHT rats had significantly higher levels of thyroid-stimulating hormone (TSH), TNF-α, chemerin, ET-1, total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) and lower levels of APN and NO than those in control and sHT + T4 rats. Based on Pearson correlation analysis, the levels of chemerin, TNF-α, ET-1, LDL-C, TC and triglyceride (TG) were positively correlated with TSH, but APN and NO levels were negatively correlated with TSH. These findings demonstrated that high TSH levels contribute to the changes of adipokines and endothelial dysfunction in sHT, but LT4 treatment ameliorates those changes.
Department of Ultrasound, Shandong Provincial Hospital affiliated to Shandong First Medical University, Jinan, Shandong, China
Search for other papers by Yong Yu in
Google Scholar
PubMed
Search for other papers by Lin-Lin Shi in
Google Scholar
PubMed
Search for other papers by Hua-Wei Zhang in
Google Scholar
PubMed
Search for other papers by Qian Wang in
Google Scholar
PubMed
Background
Papillary thyroid carcinoma is the most common thyroid carcinoma worldwide. Papillary thyroid carcinoma metastasis to the cervical region increases the probability of local or regional recurrence and the requirement for further surgery. Contrast-enhanced ultrasound has been suggested as a possible adjunct diagnostic technique for evaluating papillary thyroid carcinoma metastatic lymph nodes in several studies. This meta-analysis aims to evaluate the diagnostic accuracy of contrast-enhanced ultrasound for cervical lymph nodes metastatic in papillary thyroid carcinoma patients.
Methods
A search for studies evaluating the role of contrast-enhanced ultrasound for assessing cervical lymph nodes metastatic in papillary thyroid carcinoma patients from January 2000 to May 2022 was performed in PubMed, Embase, OVID, and Web of Science databases. The Quality Assessment of Diagnostic Accuracy Studies 2 evaluated the quality of the studies. All analyses were performed using Review Manager 5.3 and Stata 17.0.
Results
A total of seven articles were finally included in this study. Perfusion type, enhancement homogeneous, hilum absent, and perfusion defect were involved in the meta-analysis as the standard of contrast-enhanced ultrasound, among which, perfusion type showed the best diagnostic performance. The pooled estimated sensitivity, specificity, positive likelihood, negative likelihood ratio, and diagnostic odds ratio of perfusion type in contrast-enhanced ultrasound for detecting lymph node metastasis were 0.95 (0.91, 0.97), 0.87 (0.69, 0.96), 7.51 (2.80, 20.14), 0.06 (0.03, 0.10), and 124.17 (42.78, 360.46), respectively. Heterogeneity was moderate.
Conclusion
The perfusion type in contrast-enhanced ultrasound has good diagnostic performance for cervical lymph nodes metastasis in papillary thyroid carcinoma patients.
Search for other papers by Yansu Wang in
Google Scholar
PubMed
Search for other papers by Yun Shen in
Google Scholar
PubMed
Search for other papers by Tingting Hu in
Google Scholar
PubMed
Search for other papers by Yufei Wang in
Google Scholar
PubMed
Search for other papers by Xiaojing Ma in
Google Scholar
PubMed
Search for other papers by Haoyong Yu in
Google Scholar
PubMed
Search for other papers by Yuqian Bao in
Google Scholar
PubMed
Objective
Clusterin is closely correlated with insulin resistance and its associated comorbidities. This study aimed to investigate the correlation between serum clusterin levels and non-alcoholic fatty liver disease (NAFLD) and further explore the mediating role of insulin resistance in this relationship.
Methods
This study enrolled 195 inpatients (41 males and 154 females) aged 18–61 years. Twenty-four patients were followed up for 12 months after bariatric surgery. Serum clusterin levels were measured using a sandwich enzyme-linked immunosorbent assay. Fatty liver disease was diagnosed on the basis of liver ultrasonography. The fatty liver index (FLI) was calculated to quantify the degree of hepatic steatosis. The mediating role of homeostasis model assessment-insulin resistance (HOMA-IR) was assessed using mediation analysis.
Results
Participants with NAFLD had significantly higher serum clusterin levels than those without NAFLD (444.61 (325.76–611.52) mg/L vs 294.10 (255.20–373.55) mg/L, P < 0.01). With increasing tertiles of serum clusterin levels, the prevalence of NAFLD displayed an upward trend (P < 0.01). Multivariate linear regression analysis showed that serum clusterin levels were a positive determinant of FLI (standardized β = 0.271, P < 0.001) after adjusting for multiple metabolic risk factors. Serum clusterin levels significantly decreased after bariatric surgery (298.77 (262.56–358.10) mg/L vs 520.55 (354.94–750.21) mg/L, P < 0.01). In the mediation analysis, HOMA-IR played a mediating role in the correlation between serum clusterin levels and FLI; the estimated percentage of the total effect was 17.3%.
Conclusion
Serum clusterin levels were associated with NAFLD. In addition, insulin resistance partially mediated the relationship between serum clusterin levels and FLI.
Search for other papers by Nannan Bian in
Google Scholar
PubMed
Search for other papers by Xiaomeng Sun in
Google Scholar
PubMed
Search for other papers by Biao Zhou in
Google Scholar
PubMed
Search for other papers by Lin Zhang in
Google Scholar
PubMed
Search for other papers by Qiu Wang in
Google Scholar
PubMed
Search for other papers by Yu An in
Google Scholar
PubMed
Search for other papers by Xiaohui Li in
Google Scholar
PubMed
Search for other papers by Yinhui Li in
Google Scholar
PubMed
Search for other papers by Jia Liu in
Google Scholar
PubMed
Search for other papers by Hua Meng in
Google Scholar
PubMed
Search for other papers by Guang Wang in
Google Scholar
PubMed
Objective
Bariatric surgery has become the most effective treatment for morbid obesity. Increasing evidence showed that bariatric surgery can alleviate insulin resistance and influence thyroid function. This study aimed to investigate the relationship between changes in thyroid function and adipose tissue insulin resistance (adipo-IR) after bariatric surgery.
Methods
A total of 287 non-diabetic participants with regular thyroid function were recruited and divided into the lean, overweight and obese groups. Among them, 50 morbidly obese patients submitted to bariatric surgery.
Results
The obese group had a higher level of adipo-IR, thyroid-stimulating hormone (TSH), free triiodothyronine (FT3), FT3/free thyroxine (FT4) and metabolism disorders than the lean and overweight groups. BMI was correlated with TSH, FT3, FT3/FT4 and adipo-IR (r = 0.309, 0.315, 0.322 and 0.651, respectively, all P < 0.001). Adipo-IR was significantly correlated with TSH (r = 0.402, P < 0.001), FT3 (r = 0.309, P < 0.001), and FT3/FT4 (r = 0.228, P < 0.05). Bariatric surgery resulted in a sharp decline in BMI, adipo-IR, TSH, FT3 and FT3/FT4 levels, meanwhile, metabolic disorders improved. The decrease in BMI after bariatric surgery was significantly correlated with reductions in adipo-IR (r = 0.577, P < 0.001) and TSH (r = 0.401, P = 0.005). Interestingly, the fasting blood glucose, fasting insulin, adipo-IR and TSH in the higher TSH group decreased more remarkably than in the lower TSH group.
Conclusion
Obese individuals with higher TSH levels had an obvious metabolic improvement after bariatric surgery.
Hunter Medical Research Institute, New Lambton, Newcastle, New South Wales, Australia
Search for other papers by Kirsty G Pringle in
Google Scholar
PubMed
Hunter Medical Research Institute, New Lambton, Newcastle, New South Wales, Australia
Search for other papers by Sarah J Delforce in
Google Scholar
PubMed
Hunter Medical Research Institute, New Lambton, Newcastle, New South Wales, Australia
Search for other papers by Yu Wang in
Google Scholar
PubMed
Hunter Medical Research Institute, New Lambton, Newcastle, New South Wales, Australia
Search for other papers by Katie A Ashton in
Google Scholar
PubMed
Search for other papers by Anthony Proietto in
Google Scholar
PubMed
Search for other papers by Geoffrey Otton in
Google Scholar
PubMed
Hunter Medical Research Institute, New Lambton, Newcastle, New South Wales, Australia
Search for other papers by C Caroline Blackwell in
Google Scholar
PubMed
Hunter Medical Research Institute, New Lambton, Newcastle, New South Wales, Australia
Division of Molecular Medicine, Pathology North, Newcastle, New South Wales, Australia
Search for other papers by Rodney J Scott in
Google Scholar
PubMed
Hunter Medical Research Institute, New Lambton, Newcastle, New South Wales, Australia
Search for other papers by Eugenie R Lumbers in
Google Scholar
PubMed
Endometrial cancer (EC) is the most common gynaecological malignancy and its incidence is increasing. Dysregulation of the endometrial renin–angiotensin system (RAS) could predispose to EC; therefore, we studied the prevalence of RAS single nucleotide polymorphisms (SNPs) in Australian women with EC. SNPs assessed were AGT M235T (rs699); AGTR1 A1166C (rs5186); ACE A240T and T93C (rs4291, rs4292) and ATP6AP2 (rs2968915). They were identified using TaqMan SNP Genotyping Assays. The C allele of the AGTR1 SNP (rs5186) was more prevalent in women with EC (odds ratio (OR) 1.7, 95% confidence interval (CI) (1.2–2.3), P=0.002). The CC genotype of this SNP is associated with upregulation of the angiotensin II type 1 receptor (AGTR1). The G allele of AGT rs699, which is associated with higher angiotensinogen (AGT) levels, was less prevalent in women with EC (OR 0.54, 95% CI (0.39–0.74), P<0.001) compared with controls. AGT and AGT formed by removal of angiotensin I (des(Ang I)AGT) are both anti-angiogenic. In women with EC who had had hormone replacement therapy (HRT), the prevalence of the AGTR1 SNP (rs5186) and the ACE SNPs (rs4291 and rs4292) was greater than in women who had no record of HRT; SNP rs4291 is associated with increased plasma ACE activity. These data suggest there is an interaction between genotype, oestrogen replacement therapy and EC. In conclusion, the prevalence of two SNPs that enhance RAS activity was different in women with EC compared with healthy controls. These genetic factors may interact with obesity and hyperoestrogenism, predisposing ageing, obese women to EC.
Search for other papers by Ren-Lei Ji in
Google Scholar
PubMed
Search for other papers by Lu Huang in
Google Scholar
PubMed
Search for other papers by Yin Wang in
Google Scholar
PubMed
Search for other papers by Ting Liu in
Google Scholar
PubMed
Search for other papers by Si-Yu Fan in
Google Scholar
PubMed
State Key Laboratory of Developmental Biology of Freshwater Fish, College of Life Sciences, Hunan Normal University, Changsha, Hunan, People’s Republic of China
Search for other papers by Min Tao in
Google Scholar
PubMed
Search for other papers by Ya-Xiong Tao in
Google Scholar
PubMed
Melanocortin-3 receptor (MC3R) is a regulator of energy homeostasis, and interaction of MC3R and melanocortin-2 receptor accessory protein 2 (MRAP2) plays a critical role in MC3R signaling of mammals. However, the physiological roles of MC3R in teleosts are not well understood. In this study, qRT-PCR was used to measure gene expression. Radioligand binding assay was used to study the binding properties of topmouth culter MC3R (caMC3R). Intracellular cAMP generation was determined by RIA, and caMC3R expression was quantified with flow cytometry. We showed that culter mc3r had higher expression in the CNS. All agonists could bind and stimulate caMC3R to increase dose dependently intracellular cAMP accumulation. Compared to human MC3R, culter MC3R showed higher constitutive activity, higher efficacies, and R max to alpha-melanocyte-stimulating hormone (α-MSH), des-α-MSH, and adrenocorticotrophic hormone. Both caMRAP2a and caMRAP2b markedly decreased caMC3R basal cAMP production. However, only caMRAP2a significantly decreased cell surface expression, B max, and R max of caMC3R. Expression analysis suggested that MRAP2a and MRAP2b might be more important in regulating MC3R/MC4R signaling during larval period, and reduced mc3r, mc4r, and pomc expression might be primarily involved in modulation of MC3R/MC4R in adults. These data indicated that the cloned caMC3R was a functional receptor. MRAP2a and MRAP2b had different effects on expression and signaling of caMC3R. In addition, expression analysis suggested that MRAP2s, receptors, and hormones might play different roles in regulating culter development and growth.
Search for other papers by Lian Duan in
Google Scholar
PubMed
Search for other papers by Han-Yu Zhang in
Google Scholar
PubMed
Search for other papers by Min Lv in
Google Scholar
PubMed
Search for other papers by Han Zhang in
Google Scholar
PubMed
Search for other papers by Yao Chen in
Google Scholar
PubMed
Search for other papers by Ting Wang in
Google Scholar
PubMed
Search for other papers by Yan Li in
Google Scholar
PubMed
Search for other papers by Yan Wu in
Google Scholar
PubMed
Search for other papers by Junfeng Li in
Google Scholar
PubMed
Search for other papers by Kefeng Li in
Google Scholar
PubMed
Background and objective
Radioiodine therapy (RAI) is one of the most common treatment solutions for Graves’ disease (GD). However, many patients will develop hypothyroidism as early as 6 months after RAI. This study aimed to implement machine learning (ML) algorithms for the early prediction of post-RAI hypothyroidism.
Methods
Four hundred and seventy-one GD patients who underwent RAI between January 2016 and June 2019 were retrospectively recruited and randomly split into the training set (310 patients) and the validation set (161 patients). These patients were followed for 6 months after RAI. A set of 138 clinical and lab test features from the electronic medical record (EMR) were extracted, and multiple ML algorithms were conducted to identify the features associated with the occurrence of hypothyroidism 6 months after RAI.
Results
An integrated multivariate model containing patients’ age, thyroid mass, 24-h radioactive iodine uptake, serum concentrations of aspartate aminotransferase, thyrotropin-receptor antibodies, thyroid microsomal antibodies, and blood neutrophil count demonstrated an area under the receiver operating curve (AUROC) of 0.72 (95% CI: 0.61–0.85), an F1 score of 0.74, and an MCC score of 0.63 in the training set. The model also performed well in the validation set with an AUROC of 0.74 (95% CI: 0.65–0.83), an F1 score of 0.74, and a MCC of 0.63. A user-friendly nomogram was then established to facilitate the clinical utility.
Conclusion
The developed multivariate model based on EMR data could be a valuable tool for predicting post-RAI hypothyroidism, allowing them to be treated differently before the therapy. Further study is needed to validate the developed prognostic model at independent sites.
Search for other papers by Tsung-Hui Wu in
Google Scholar
PubMed
Search for other papers by Guan-Yu Su in
Google Scholar
PubMed
Search for other papers by Tsung-Yun Liu in
Google Scholar
PubMed
Institute of Pharmacology, College of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan
PhD Program in Toxicology, Kaohsiung Medical University, Kaohsiung, Taiwan
Search for other papers by Hsiang-Tsui Wang in
Google Scholar
PubMed
Faculty of Medicine, National Yang Ming Chiao Tung University School of Medicine, Taipei, Taiwan
Search for other papers by Chii-Min Hwu in
Google Scholar
PubMed
Acrolein, an unsaturated aldehyde, plays a pathological role in neurodegenerative diseases. However, less is known about its effects on peripheral neuropathy. The aim of this study was to investigate the association of acrolein and diabetic peripheral neuropathy in patients with type 2 diabetes. We recruited 148 ambulatory patients with type 2 diabetes. Each participant underwent an assessment of the Michigan Neuropathy Screening Instrument Physical Examination. Diabetic peripheral neuropathy was defined as Michigan Neuropathy Screening Instrument Physical Examination score ≥ 2.5. Serum levels and urinary levels of acrolein protein conjugates were measured. Urinary acrolein protein conjugates-to-creatinine ratios were determined. Patients with diabetic peripheral neuropathy had significantly higher urinary acrolein protein conjugates-to-creatinine ratios than those without diabetic peripheral neuropathy (7.91, 95% CI: 5.96–10.50 vs 5.31, 95% CI: 4.21–6.68, P = 0.029). Logarithmic transformation of urinary acrolein protein conjugates-to-creatinine ratios was positively associated with diabetic peripheral neuropathy in univariate logistic analysis, and the association remained significant in multivariate analysis (OR = 2.45, 95% CI: 1.12–5.34, P = 0.025). In conclusion, urinary acrolein protein conjugates-to-creatinine ratio may act as a new biomarker for diabetic peripheral neuropathy in type 2 diabetes. The involvement of acrolein in the pathogenesis of diabetic peripheral neuropathy warrants further investigation.
