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1.
Nanoscale ; 2022 May 12.
Artigo em Inglês | MEDLINE | ID: mdl-35551370

RESUMO

The rational design, synthesis, and massive production of one-dimensional (1D) spinel composite oxides with multi-shelled nanostructures are critical for the realization of highly efficient energy conversion and storage. However, owing to the limitations of the synthetic methods, the 1D multi-shelled nanostructures, especially for multi-element oxides and binary-metal oxides, have been rarely fabricated. Herein, we design a facile and general method to fabricate 1D spinel composite oxides with complex architectures. It is found that the concentration of the precursor polymer PAN can control the structures of the products at optimal heating rate, including hollow nanofibers, wire-in-tube nanofibers, and tube-in-tube nanofibers. This technique could be extended to various inorganic multi-element oxides and binary-metal oxides. Moreover, numerous twin boundaries (TBs) are found to form in the Co0.5Ni0.5Fe2O4 tube-in-tube nanofibers. Benefiting from both large porosity and TBs structures, the tube-in-tube hollow nanostructures are measured to possess superior electrochemical performances with high energy and stability in lithium-ion storage.

2.
Diab Vasc Dis Res ; 19(1): 14791641221083396, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35345912

RESUMO

PURPOSE: Triglyceride-glucose (TyG) index is a reliable and inexpensive alternative indicator of insulin resistance. Previous studies have shown that elevated TyG index increases the risk of diabetes, coronary heart disease, and other diseases, but the relationship between TyG index and cardiac hemodynamics in patients with type 2 diabetes mellitus (T2DM) is not clear. This study was conducted in patients with T2DM to assess the relationship between TyG and cardiac hemodynamics and its predictive ability for T2DM. METHODS: A total of 647 individuals (348 males and 299 females) were enrolled in this study, including 446 T2DM patients and 201 healthy controls. The clinical data and related laboratory variables were assessed and recorded, and TyG index was calculated. Cardiac hemodynamics was measured by echocardiography. Pearson or Spearman correlation analysis and linear regression analysis were conducted to explore the association between TyG and cardiac hemodynamics. The receiver operating characteristics (ROC) curve was used to evaluate the efficacy of TyG index in the diagnosis of T2DM. RESULTS: Compared with healthy controls, the systolic blood pressure (SBP), body weight, body mass index (BMI), waist circumference (WC), hip circumference (HC), HOMA-IR, and TyG levels were higher in patients with T2DM. With the increase of TyG, the levels of left ventricular mass index (LVMI), left ventricular mass (LVM), left ventricular end diastolic diameter (LVDd), posterior wall thickness (PWT), and interventricular septum thickness (IVST) were also increased in T2DM individuals. Multivariate linear regression analysis showed that TyG was an independent determinant of LVEF, PWT, IVST, and ejection time (ET) after adjusting for confounding factors. In addition, individuals with visceral obesity had higher TyG and TyG can be used as a predictor of T2DM with an AUC of 0.903 (95% CI:0.879-0.927). CONCLUSIONS: The increase of TyG index is closely related to cardiac hemodynamics of T2DM patients, which is expected to be a simple and practical biological index to predict the changes of cardiac function in patients with T2DM.


Assuntos
Diabetes Mellitus Tipo 2 , Glicemia/análise , Diabetes Mellitus Tipo 2/complicações , Diabetes Mellitus Tipo 2/diagnóstico , Feminino , Glucose , Hemodinâmica , Humanos , Masculino , Fatores de Risco , Triglicerídeos
3.
Artigo em Inglês | MEDLINE | ID: mdl-35209814

RESUMO

BACKGROUND: Immune-related long noncoding RNAs (lncRNAs) play an important role in the development of cancer. This study aimed to identify immune-related lncRNAs in thyroid cancer (THCA) and to develop a prognostic model for THCA. METHOD: We downloaded immune-related gene sets from the Gene Set Enrichment Analysis (GSEA) website and obtained THCA gene expression and clinical data from The Cancer Genome Atlas (TCGA) database. Immune-related lncRNAs were then obtained by performing a correlation analysis on the expression of lncRNAs and immune-related genes. Prognostic model for THCA immune-related lncRNAs was developed though univariate Cox regression and multiple Cox regression analyses. We confirmed the results in clinical samples using quantitative real-time PCR Results: A totally of 26 immune-related lncRNAs in THCA were obtained. Then we constructed a prognosis model composed of seven lncRNAs (LINC01614, AC017074.1, LINC01184, LINC00667, ACVR2B-AS1, AC090673.1 and LINC00900). Our model can be used as an independent prognostic factor. Principal component analysis displayed that the lncRNAs in the model can distinguish between high and low-risk groups. Clinical correlation analysis showed that the expression levels of AC090673.1 (P<0.05), LINC01184 (P<0.001), and LINC01614 (P<0.001) were related to disease stage, and LINC00900 (P<0.001) and LINC01614 (P<0.001) were related to T stage. We validated this model in cancer and paracancerous tissues from 24 THCA patients. CONCLUSION: We identified and experimentally validated seven immune-related lncRNAs that can serve as potential biomarkers for THCA prognosis.

4.
Adipocyte ; 11(1): 56-68, 2022 12.
Artigo em Inglês | MEDLINE | ID: mdl-34974794

RESUMO

Adipose differentiation and excessive lipid accumulation are the important characteristics of obesity. Metformin, as a classic hypoglycaemic drug, has been proved to reduce body weight in type 2 diabetes, the specific mechanism has not been completely clear. A few studies have explored its effect on adipogenesis in vitro, but the existing experimental results are ambiguous. 3T3-L1 preadipocytes were used to explore the effects of metformin on the morphological and physiological changes of lipid droplets during adipogenesis. A high throughput sequencing was used to examine the effects of metformin on the transcriptome of adipogenesis. Considering the inevitable errors among independent experiments, we performed integrated bioinformatics analysis to identify important genes involved in adipogenesis and reveal potential molecular mechanisms. During the process of adipogenesis, metformin visibly relieved the morphological and functional changes. In addition, metformin reverses the expression pattern of genes related to adipogenesis at the transcriptome level. Combining with integrated bioinformatics analyses to further identify the potential targeted genes regulated by metformin during adipogenesis. The present study identified novel changes in the transcriptome of metformin in the process of adipogenesis that might shed light on the underlying mechanism by which metformin impedes the progression of obesity.


Assuntos
Diabetes Mellitus Tipo 2 , Metformina , Células 3T3-L1 , Adipócitos , Adipogenia , Animais , Diferenciação Celular , Sequenciamento de Nucleotídeos em Larga Escala , Metformina/farmacologia , Camundongos
5.
Int J Gynaecol Obstet ; 157(2): 375-382, 2022 May.
Artigo em Inglês | MEDLINE | ID: mdl-34368966

RESUMO

OBJECTIVE: To improve perinatal management for hypertensive disorders in pregnancy (HDP) using checklists. METHODS: A pre-post evaluation of the implementation of checklists was performed. The checklist for HDP was adapted for the local context through expert consultations and had been used within peripartum since September 2017. Data of 763 women with singleton pregnancies diagnosed with HDP were collected between April 2016 and March 2019 at the Obstetrics & Gynecology Hospital of Fudan University. The monitoring and control groups consisted of 394 and 369 cases, respectively. Analysis was carried out by intention-to-treat with respect to maternal and fetal complications and delivery outcomes. RESULTS: After the implementation of the checklists, patients had a significant reduction in anti-hypertensive treatment both orally (P = 0.028) and intravenously (P = 0.003), and increased utilization rate of MgSO4 management (P < 0.001). Gestation was prolonged in the expectant treatment (P = 0.012) and the rate of elective and intrapartum cesarean delivery decreased (P < 0.001 and P = 0.001, respectively). The neonates of these patients had a low rate of admission to the neonatal intensive care unit (P < 0.001). CONCLUSION: National clinical guidelines complied critically after the implementation of the checklists. These checklists could be used for improving the quality of the clinical strategy and treatment, which benefitted perinatal management.


Assuntos
Hipertensão , Resultado da Gravidez , Cesárea , Lista de Checagem , Feminino , Idade Gestacional , Humanos , Recém-Nascido , Gravidez , Melhoria de Qualidade
6.
Metabolism ; 126: 154921, 2022 01.
Artigo em Inglês | MEDLINE | ID: mdl-34715116

RESUMO

BACKGROUND & AIMS: Angiopoietin-like protein 8 (ANGPTL8) is a 198 amino-acid long, novel secreted protein that is mainly expressed in the liver and brown adipose tissues. At present, evidence supporting the involvement of ANGPTL8 in the regulation of glucose metabolism is inconclusive, along with its function in the liver. Previous studies mainly focused on the effect of ANGPTL8 on glucose metabolism in non-diabetic mice, and few relevant studies in diabetic mice exist. Therefore, this study aimed to investigate the role of ANGPTL8 on glucose homeostasis and elucidate the underlying mechanisms in diabetic mice. METHODS: db/db diabetic and high-fat diet/streptozotocin-induced diabetic mice were injected with adenovirus expressing ANGPTL8 through the tail vein. Blood glucose levels were measured and glucose, insulin, and pyruvate tolerance tests were performed. To explore the molecular mechanism by which ANGPTL8 regulates hepatic glucose metabolism and manipulate mouse ANGPTL8 expression levels both in vivo and in vitro based on adenoviral transduction, gain- and loss-of-function strategies were adopted. RESULTS: Adenovirus-mediated overexpression of ANGPTL8 decreased fasting blood glucose levels and improved glucose tolerance and insulin sensitivity in db/db and high-fat diet/streptozotocin-induced diabetic mice. ANGPTL8 knockdown yielded the opposite effects. ANGPTL8 was upregulated in the cAMP/Dex-induced hepatocyte gluconeogenesis model. Moreover, ANGPTL8 overexpression in primary hepatocytes and diabetic mouse livers inhibited the expression of gluconeogenesis-related genes, including PEPCK and G6PC, by activating the AKT signaling pathway and, thereby, reducing glucose production. Therefore, the results demonstrated that ANGPTL8 improved glucose metabolism via inhibition of hepatic gluconeogenesis in diabetic mice. CONCLUSIONS: Current findings highlight a critical role of hepatic ANGPTL8 in glucose homeostasis, suggesting that increased ANGPTL8 expression could be an underlying factor for the inhibition of hepatic gluconeogenesis, which could be targeted for the prevention and treatment of type 2 diabetes.


Assuntos
/genética , Diabetes Mellitus Experimental/genética , Gluconeogênese/genética , Fígado/metabolismo , Transdução de Sinais/genética , /metabolismo , Animais , Diabetes Mellitus Experimental/metabolismo , Dieta Hiperlipídica , Hepatócitos/metabolismo , Resistência à Insulina/genética , Masculino , Camundongos , Fosfatidilinositol 3-Quinases/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo
7.
Front Endocrinol (Lausanne) ; 12: 737624, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34858327

RESUMO

Objective: Ectodysplasin A (EDA), a newly discovered hepatokine, has recently been considered to be closely related to glycolipid metabolism disorders, but the pathophysiological effects of EDA are still poorly understood. This study was the first time to determine the level of serum EDA in newly diagnosed type 2 diabetes mellitus (T2DM) patients, and to explore the relationships between serum EDA levels and various metabolic indexes. Methods: A total of 184 subjects were enrolled in the study, including 92 subjects with newly diagnosed T2DM and 92 subjects with age- and sex-matched normal glucose tolerance (NGT). Serum EDA levels were determined using enzyme-linked immunosorbent assay (ELISA). Oral glucose tolerance test, glycosylated hemoglobin c (HbA1c), and insulin were also measured. Results: Serum EDA levels were significantly increased in the T2DM group than in the NGT group (359.91 ± 117.99 vs. 265.82 ± 86.51 pg/ml, p < 0.001). Serum EDA levels were positively correlated with body mass index (BMI), waist-to-hip ratio (WHR), fasting plasma glucose (FPG), HbA1c, 2-hour postprandial plasma glucose (2hPG), fasting plasma insulin (FIns), fasting C peptide (FCP), triglyceride (TG), HOMA-IR, and negatively correlated with high-density lipoprotein cholesterol (HDL-c) and HOMA-ß (p < 0.05). Multiple stepwise regression analysis demonstrated that 2hPG and FIns were independent influencing factors of serum EDA level (p < 0.05). Logistic regression analysis showed that serum EDA level was significantly independently correlated with T2DM (p < 0.05). Conclusions: Serum EDA levels are significantly higher in T2DM patients, suggesting that EDA may play a role in the occurrence and development of T2DM.


Assuntos
Glicemia/metabolismo , Índice de Massa Corporal , Diabetes Mellitus Tipo 2/sangue , Ectodisplasinas/sangue , Adulto , Diabetes Mellitus Tipo 2/diagnóstico , Feminino , Teste de Tolerância a Glucose , Hemoglobina A Glicada/metabolismo , Humanos , Insulina/sangue , Resistência à Insulina , Masculino , Pessoa de Meia-Idade
8.
Front Physiol ; 12: 788411, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34938205

RESUMO

Ectodysplasin A (EDA) is a member of the tumor necrosis factor (TNF) family of ligands that was initially reported to induce the formation of various ectodermal derivatives during normal prenatal development. EDA exerts its biological activity as two splice variants, namely, EDA-A1 and EDA-A2. The former binds to the EDA receptor (EDAR), resulting in the recruitment of the intracellular EDAR-associated death domain (EDARADD) adapter protein and the activation of the NF-κB signaling pathway, while the latter binds to a different receptor, EDA2R, also known as X-linked ectodermal dysplasia receptor (XEDAR). Inactivation mutation of the EDA gene or the genes coding for its receptors can result in hypohidrosis ectodermal dysplasia (HED), a condition that is characterized by oligotrichosis, edentulosis or oligodontia, and oligohidrosis or anhidrosis. Recently, as a new liver factor, EDA is gradually known and endowed with some new functions. EDA levels were observed to be upregulated in several metabolic diseases, such as non-alcoholic fatty liver disease (NAFLD), obesity, and insulin resistance. In addition, EDA and its receptors have been implicated in tumor pathogenesis through the regulation of tumor cell proliferation, apoptosis, differentiation, and migration. Here, we first review the role of EDA and its two-receptor system in various signaling pathways and then discuss the physiological and pathological roles of EDA and its receptors.

9.
Open Biol ; 11(9): 210106, 2021 09.
Artigo em Inglês | MEDLINE | ID: mdl-34582711

RESUMO

ANGPTL8 is an important cytokine, which is significantly increased in type 2 diabetes mellitus (T2DM), obesity and metabolic syndrome. Many studies have shown that ANGPTL8 can be used as a bio-marker of these metabolic disorders related diseases, and the baseline ANGPTL8 level has also been found to be positively correlated with retinopathy and all-cause mortality in patients with T2DM. This may be related to the inhibition of lipoprotein lipase activity and the reduction of circulating triglyceride (TG) clearance by ANGPTL8. Consistently, inhibition of ANGPTL8 seems to prevent or improve atherosclerosis. However, it is puzzling that ANGPTL8 seems to have a directing function for TG uptake in peripheral tissues; that is, ANGPTL8 specifically enhances the reserve and buffering function of white adipose tissue, which may alleviate the ectopic lipid accumulation to a certain extent. Furthermore, ANGPTL8 can improve insulin sensitivity and inhibit hepatic glucose production. These contradictory results lead to different opinions on the role of ANGPTL8 in metabolic disorders. In this paper, the correlation between ANGPTL8 and metabolic diseases, the regulation of ANGPTL8 and the physiological role of ANGPTL8 in the process of glucose and lipid metabolism were summarized, and the physiological/pathological significance of ANGPTL8 in the process of metabolic disorder was discussed.


Assuntos
/metabolismo , Homeostase , Doenças Metabólicas/patologia , Hormônios Peptídicos/metabolismo , Humanos , Doenças Metabólicas/metabolismo
10.
Int J Med Sci ; 18(14): 3280-3289, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34400897

RESUMO

Background/aim: Previous studies have suggested that the hepatic steatosis index (HSI) and fatty liver index (FLI) can be used as a predictor of non-alcoholic fatty liver disease (NAFLD). The aim of our study was to determine whether non-invasive indices of hepatic steatosis (HSI and FLI) are associated with carotid atherosclerosis in type 2 diabetes mellitus (T2DM). Methods: This was a cross-sectional study conducted in the T2DM patients (n=768). Carotid intima-media thickness (CIMT) was measured by the Color Doppler ultrasound. The HSI was calculated based on gender, body mass index (BMI), and transaminases level. The FLI was based on BMI, waist circumference (WC), triacylglycerols (TG) and g-glutamyl transferase (GGT). Results: Raised HSI and FLI levels was associated with increased CIMT levels in T2DM patients. Patients with greater CIMT had higher HSI (39.10 ± 5.70 vs 36.10 ± 4.18, P < 0.001) and FLI (46.35 (29.96, 65.54) vs 36.93 (18.7, 57.93), P < 0.001) than those with lower CIMT. Subjects with existing carotid plaque had higher HSI (38.28 ± 5.63 vs 35.69 ± 3.45 P < 0.001) and FLI (47.41 (27.77, 66.62) vs 37.19 (17.71, 51.78), P < 0.001) accordingly. HSI (r = 0.343, P < 0.001) and FLI (r = 0.184, P < 0.001) were positively related with the CIMT. In the linear regression, after full adjustment metabolic risk factors, smoking, and measures of insulin resistance, HSI and FLI were independently associated with CIMT (HSI: ß = 0.011, FLI: ß = 0.001, all P < 0.01). Further, logistic regression analyses showed that higher HSI and FLI had an impact on the risk for carotid atherosclerosis [HSI: OR (95%CI): 1.174 (1.123-1.228), FLI: OR (95%CI): 1.011(1.004-1.019), all P < 0.01]. Overall, increasing values of HSI and FLI were associated with CIMT (P < 0.05) significantly across different categories of age and hypertension. Conclusion: Current data suggest HSI and FLI are independently correlated with carotid atherosclerosis in T2DM. They may be a simple and useful marker for assessing the progression of diabetic macrovascular complications.


Assuntos
Doenças das Artérias Carótidas/epidemiologia , Diabetes Mellitus Tipo 2/complicações , Hepatopatia Gordurosa não Alcoólica/epidemiologia , Idoso , Índice de Massa Corporal , Doenças das Artérias Carótidas/etiologia , Doenças das Artérias Carótidas/metabolismo , Espessura Intima-Media Carotídea , Estudos Transversais , Diabetes Mellitus Tipo 2/sangue , Diabetes Mellitus Tipo 2/metabolismo , Feminino , Humanos , Testes de Função Hepática , Masculino , Pessoa de Meia-Idade , Hepatopatia Gordurosa não Alcoólica/diagnóstico , Hepatopatia Gordurosa não Alcoólica/etiologia , Hepatopatia Gordurosa não Alcoólica/metabolismo , Medição de Risco/métodos , Fatores de Risco , Triglicerídeos/sangue , gama-Glutamiltransferase/sangue
11.
Microb Pathog ; 159: 105120, 2021 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-34358648

RESUMO

Diabetes and obesity have become the most popular metabolic diseases in the world. A large number of previous studies have shown that glucose and lipid metabolism disorder is an important risk factor and a main cause of diabetes and obesity. Schistosoma is a parasite transmitted by freshwater snails. It can induce a series of inflammatory and immune reactions after infecting the human body, causing schistosomiasis. However, in recent years, studies have found that Schistosoma infection or Schistosoma related products can improve or prevent some immune and inflammatory diseases, such as severe asthma, inflammatory bowel disease, diabetes and so on. Further experiments have also revealed that Schistosoma can promote the secretion of anti-inflammatory factors and regulate the glucose and lipid metabolism in the host body by polarizing immune cells such as T cells, B cells and dendritic cells (DCs). In this review, we summarize studies that investigated Schistosoma and Schistosoma-derived products and their relationship with glycolipid metabolism and related diseases, highlighting potential protective mechanisms.


Assuntos
Schistosoma , Esquistossomose , Animais , Glicolipídeos , Humanos , Metabolismo dos Lipídeos , Caramujos
12.
Diabetes Res Clin Pract ; 178: 108987, 2021 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-34329693

RESUMO

AIMS: Tsukushi, a newly identified hepatokine, has been recently characterized as a potent modifier in lipid metabolism and energy homeostasis, but the role of Tsukushi in diabetes remains almost unknown. We detected for the first time the serum Tsukushi levels in newly diagnosed type 2 diabetes, exploring the relationship between Tsukushi and various metabolic parameters. METHODS: A total of 172 participants were recruited, including 86 patients with newly diagnosed type 2 diabetes and 86 subjects with normal glucose tolerance according to oral glucose tolerance test. Serum Tsukushi was measured by ELISA. The insulin resistance, pancreas ß-cell function and insulin sensitivity were determined by homeostasis model assessment (HOMA-IR, HOMA-ß), Stumvoll insulin sensitivity index (ISIstumvoll) and Stumvoll metabolic clearance rate (MCRstumvoll). RESULTS: Serum Tsukushi was significantly higher in type 2 diabetes than in normal glucose tolerance [1.22(0.86,1.74) vs 0.8(0.5,1.38) ng/mL; P < 0.001]. Multiple regression analysis showed that BMI, 2-h post-OGTT glucose and TC were independently related factors influencing Tsukushi. Logistic regression analyses demonstrated that Tsukushi was associated with higher risk of type 2 diabetes independently. CONCLUSIONS: Circulating Tsukushi levels significantly increase in patients with type 2 diabetes, which suggest that Tsukushi may play a role in type 2 diabetes pathogenesis.


Assuntos
Diabetes Mellitus Tipo 2 , Resistência à Insulina , Células Secretoras de Insulina , Glicemia , Diabetes Mellitus Tipo 2/diagnóstico , Glucose , Teste de Tolerância a Glucose , Humanos , Insulina
13.
Adv Sci (Weinh) ; 8(18): e2100950, 2021 09.
Artigo em Inglês | MEDLINE | ID: mdl-34279055

RESUMO

Effective delivery of anticancer drugs into the nucleus for pharmacological action is impeded by a series of intratumoral transport barriers. Despite the significant potential of magnetic nanovehicles in electromagnetic field (EF)-activated drug delivery, modularizing a tandem magnetoresponsive activity in a one-nanoparticle system to meet different requirements at both tissue and cellular levels remain highly challenging. Herein, a strategy is described by employing sequential EF frequencies in inducing a succession of magnetoresponses in the magnetic nanovehicles that aims to realize cascaded tissue penetration and nuclear accumulation. This nanovehicle features ferrimagnetic vortex-domain iron oxide nanorings coated with a thermo-responsive polyethylenimine copolymer (PI/FVIOs). It is shown that the programmed cascading of low frequency (Lf)-EF-induced magnetophoresis and medium frequency (Mf)-EF-stimulated magneto-thermia can steer the Doxorubicin (DOX)-PI/FVIOs to the deep tissue and subsequently trigger intracellular burst release of DOX for successful nuclear entry. By programming the order of different EF frequencies, it is demonstrated that first-stage Lf-EF and subsequent Mf-EF operation enables DOX-PI/FVIOs to effectively deliver 86.2% drug into the nucleus in vivo. This nanodelivery system empowers potent antitumoral activity in various models of intractable tumors, including DOX-resistant MCF-7 breast cancer cells, triple-negative MDA-MB-231 breast cancer cells, and BxPC-3 pancreatic cancer cells with poor permeability.


Assuntos
Antineoplásicos/administração & dosagem , Neoplasias da Mama/tratamento farmacológico , Campos Eletromagnéticos , Neoplasias Pancreáticas/tratamento farmacológico , Animais , Linhagem Celular Tumoral , Modelos Animais de Doenças , Feminino , Humanos , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Nanopartículas
14.
Bioengineered ; 12(1): 3711-3725, 2021 12.
Artigo em Inglês | MEDLINE | ID: mdl-34269159

RESUMO

Rectal cancer is a life­threatening disease worldwide. Chemotherapy resistance is common in rectal adenocarcinoma patients and has unfavorable survival outcomes; however, its related molecular mechanisms remain unknown. To identify genes related to the initiation and progression of rectal adenocarcinoma, three datasets were obtained from the Gene Expression Omnibus database. In total, differentially expressed genes were analyzed from 294 tumor and 277 para-carcinoma samples from patients with rectal cancer. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes functions were investigated. Cytoscape software and MicroRNA Enrichment Turned Network were applied to construct a protein-protein interaction network of the dependent hub genes and related microRNAs. The Oncomine database was used to identify hub genes. Additionally, Gene Expression Profiling Interactive Analysis was applied to determine the RNA expression level. Tumor immune infiltration was assessed using the Tumor Immune Estimation Resource database. The expression profiles of hub genes between stages, and their prognostic value, were also evaluated. During this study, data from The Cancer Genome Atlas were utilized. In rectal adenocarcinoma, four hub genes including CXCL1, CXCL2, CXCL3, and GNG4 were highly expressed at the gene and RNA levels. The expression of CXCL1, CXCL2, and CXCL3 was regulated by has-miR-1-3p and had a strong positive correlation with macrophage and neutrophil. CXCL2 and CXCL3 were differentially expressed at different tumor stages. High expression levels of CXCL1 and CXCL3 predicted poor survival. In conclusion, the CXCL1 and CXCL3 genes may have potential for prognosis and molecular targeted therapy of rectal adenocarcinoma.


Assuntos
Adenocarcinoma , Quimiocina CXCL1/genética , Quimiocinas CXC/genética , Neoplasias Retais , Adenocarcinoma/diagnóstico , Adenocarcinoma/genética , Adenocarcinoma/mortalidade , Biomarcadores Tumorais , Bases de Dados Genéticas , Humanos , Prognóstico , Neoplasias Retais/diagnóstico , Neoplasias Retais/genética , Neoplasias Retais/mortalidade , Transcriptoma/genética
15.
Front Aging Neurosci ; 13: 650371, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34135748

RESUMO

Many clinical symptoms of sporadic Parkinson's disease (sPD) cannot be completely explained by a lesion of the simple typical extrapyramidal circuit between the striatum and substantia nigra. Therefore, this study aimed to explore the new potential damaged pathogenesis of other brain regions associated with the multiple and complex clinical symptoms of sPD through magnetic resonance imaging (MRI). A total of 65 patients with mid-stage sPD and 35 healthy controls were recruited in this study. Cortical structural connectivity was assessed by seed-based analysis using the vertex-based morphology of MRI. Seven different clusters in the brain regions of cortical thickness thinning derived from the regression analysis using brain size as covariates between sPD and control were selected as seeds. Results showed that the significant alteration of cortical structural connectivity mainly occurred in the bilateral frontal orbital, opercular, triangular, precentral, rectus, supplementary-motor, temporal pole, angular, Heschl, parietal, supramarginal, postcentral, precuneus, occipital, lingual, cuneus, Rolandic-opercular, cingulum, parahippocampal, calcarine, olfactory, insula, paracentral-lobule, and fusiform regions at the mid-stage of sPD. These findings suggested that the extensive alteration of cortical structural connectivity is one of possible pathogenesis resulting in the multiple and complex clinical symptoms in sPD.

16.
Arch Physiol Biochem ; : 1-12, 2021 May 28.
Artigo em Inglês | MEDLINE | ID: mdl-34048666

RESUMO

Diabetic nephropathy (DN) is a common complication of diabetes, and it is also the main cause of chronic renal failure. Physiological/pathological changes mediated by high glucose are the main factors causing injury of DN, including the enhancement of polyol pathway, the accumulation of advanced glycation products (AGEs), and the activation of protein kinase C (PKC) and transforming growth factor-ß (TGF-ß) signals. In addition, the abnormal activation of renin-angiotensin system (RAS) and oxidative stress are also involved. Melatonin is a physiological hormone mainly secreted by the pineal gland which has been proved to be related to diabetes. Studies have shown that exogenous melatonin intervention can reduce blood glucose and alleviate high glucose mediated pathological damage. At the same time, melatonin also has a strong antioxidant effect, and can inhibit the activation of RAS. Therefore, it is of great significance to explore the therapeutic effect and value of melatonin on DN.

17.
Biofactors ; 47(4): 512-521, 2021 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-33759220

RESUMO

Tsukushi (TSK), a newly identified hepatokine, is a member of the small leucine-rich proteoglycans (SLRPs) family. TSK was originally isolated and identified in the lens of the chicken. Preliminary research on TSK has focused on its role in various physiological processes such as growth and development, wound healing, and cartilage formation. In recent years, the role of TSK in regulating cell signaling pathways, cell proliferation, and differentiation has been studied. In addition, the research has gradually expanded to the fields of glycolipid metabolism and energy balance. This article briefly reviews the role of TSK in the physiological and pathological process.


Assuntos
Neoplasias da Mama/genética , Carcinogênese/genética , Matriz Extracelular/metabolismo , Peptídeos e Proteínas de Sinalização Intercelular/genética , Hepatopatia Gordurosa não Alcoólica/genética , Proteoglicanas/genética , Transdução de Sinais/genética , Animais , Neoplasias da Mama/metabolismo , Neoplasias da Mama/patologia , Carcinogênese/metabolismo , Carcinogênese/patologia , Cartilagem/citologia , Cartilagem/metabolismo , Diferenciação Celular , Linhagem Celular Tumoral , Proliferação de Células , Metabolismo Energético/genética , Matriz Extracelular/patologia , Regulação da Expressão Gênica no Desenvolvimento , Humanos , Peptídeos e Proteínas de Sinalização Intercelular/metabolismo , Hepatopatia Gordurosa não Alcoólica/metabolismo , Hepatopatia Gordurosa não Alcoólica/patologia , Proteoglicanas/metabolismo , Proteínas Smad/genética , Proteínas Smad/metabolismo , Cicatrização/genética , beta Catenina/genética , beta Catenina/metabolismo
18.
J Cell Physiol ; 236(1): 55-67, 2021 01.
Artigo em Inglês | MEDLINE | ID: mdl-32583417

RESUMO

Sedentary and high-calorie diets are associated with increased risk of obesity and type 2 diabetes mellitus, while exercise and diet control are also important nondrug treatments for diabetes. Fibroblast growth factor 21 (FGF21) is an important cytokine, which is mainly expressed in liver, fat and muscle tissue responding to nutrition and exercise, and plays an important role in the improvement of glucose and lipid metabolism. Due to the increasing serum FGF21 level in obesity and diabetes, FGF21 can be used as a predictor or biomarker of diabetes. A variety of clinical antidiabetic drugs can reduce the content of FGF21, possibly for the improvement of FGF21 sensitivity. In this paper, we reviewed the interactions between FGF21 and nondrug therapy (diet and exercise) for diabetes and explored the potential value of the combined application of clinical antidiabetic drugs and FGF21.


Assuntos
Diabetes Mellitus Tipo 2/metabolismo , Fatores de Crescimento de Fibroblastos/metabolismo , Animais , Biomarcadores/metabolismo , Diabetes Mellitus Tipo 2/tratamento farmacológico , Dieta , Glucose/metabolismo , Humanos , Hipoglicemiantes/farmacologia , Hipoglicemiantes/uso terapêutico , Metabolismo dos Lipídeos/fisiologia
19.
Diabetes Metab Syndr Obes ; 13: 4413-4422, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33235479

RESUMO

BACKGROUND: This study was conducted in patients with type 2 diabetes mellitus (T2DM) to assess the association between visceral fat area (VFA) and cardiac hemodynamics. METHODS: A total of 568 patients with type 2 diabetes (mean age 54±12 years; 40.8% of women) were enrolled. Visceral fat area (VFA, m2) and subcutaneous fat area (SFA, m2) were evaluated by a bioelectrical impedance analyzer. Cardiac hemodynamics were measured by echocardiography, and other clinical and laboratory variables were also assessed and recorded. Patients were divided into those with VFA ≤ 100 (n=369) and those with VFA > 100 (n=199). RESULTS: VFA, SFA, LVMI (left ventricular mass index), left atrial diameter, left ventricular diastolic diameter (LvDd), interventricular septal thickness (IVST), left ventricular systolic diameter (LvSd), and posterior wall thickness (PWT) levels in high-V groups were significantly higher than those in low-V groups. Correlation analysis showed that VFA was positively correlated with LVMI (r=0.120, p=0.004), LVM (r=0.249, p<0.0001), left atrial diameter (r=0.375, p<0.0001), aortic root diameter (r=0.243, p<0.0001), left ventricular systolic diameter (LvSd) (r=0.211, p<0.0001) and negatively correlated with LVEF (r=-0.107, p=0.011). In multivariate linear regression analysis, VFA was the strongest independent determinant of LVMI (ß=0.04, p=0.016), LVEF (ß=-0.01, p=0.023), and left atrial diameter (ß=0.035, p<0.0001), Internal diameter of the aortic root (ß=0.014, p<0.0001) and LvSd (ß=0.017, p<0.0001). In addition, the VFA also better predicted cardiovascular disease risk with AUC of 0.609 (95% CI:0.563-0.656), compared with SFA, waist-hip ratio (WHR), in a statistically significant manner. CONCLUSION: We found a significant correlation between VFA (but not SFA) and cardiac hemodynamic parameters. The VFA has advantages as a predictor of visceral obesity and is significantly associated with the development of cardiovascular risk factors (CVD) in T2DM patients.

20.
Diabetes Metab Syndr Obes ; 13: 4341-4351, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33223841

RESUMO

AIM: We detected whether serum asprosin levels play a role in the occurrence and development of albuminuria in patients with type 2 diabetes mellitus (T2DM), which has not been previously discussed. METHODS: Based on urinary albumin/creatinine ratio (UACR), 207 T2DM patients were divided into T2DM patients with normoalbuminuria (UACR<30 mg/g), microalbuminuria (30≤UACR<300 mg/g), and macroalbuminuria (UACR≥300 mg/g). Serum asprosin levels were determined by enzyme-linked immunosorbent assay. RESULTS: Comparatively, the serum asprosin levels in T2DM patient groups with macroalbuminuria [2.37 (1.63-3.57)] and microalbuminuria [2.10 (1.60-2.90)] were significantly increased than the normoalbuminuria group [1.59 (1.18-2.09)] (P<0.001). Importantly, the serum level of asprosin was positively correlated with UACR (r=0.304, P<0.001), creatinine (r=0.157, P=0.024), blood urea nitrogen (BUN) (r=0.244, P<0.001), and negatively with glomerular filtration rate (eGFR) (r=-0.159, P=0.022). Furthermore, multiple stepwise regression analyses showed that asprosin was significantly and independently related to UACR, BUN, DBP, and LDL-C (P<0.05). Besides, after adjustment for the confounders, the serum asprosin level was constantly and independently associated with the development of albuminuria in T2DM patients [OR (95% CI): 2.003 (1.37~2.928), P <0.001]. CONCLUSION: Obviously, the serum asprosin level was independently correlated with UACR in T2DM patients, which implies circulating asprosin may play an essential role in the pathogenesis of diabetic nephropathy.

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