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1. Renovascular hypertension following by juxtaglomerular cell tumor: a challenging case with 12-year history of resistant hypertension and hypokalemia

Author

Guangshu Chen, Yang Zhang, Xiaoqing Xiong, Zhengming Li, Xing Hua, Zhenhui Li, Meizheng Lai, Ping Zhu, and Jianmin Ran

Subjects
Accessory renal artery, Fibromuscular dysplasia, Juxtaglomerular cell tumor, Secondary hyperaldosteronism, Renal artery stenosis, Diseases of the endocrine glands. Clinical endocrinology, RC648-665
Abstract

Abstract Background Adolescents with secondary hyperaldosteronism often present with severe and treatment-resistant hypertension, along with hypokalemia. Renovascular hypertension is frequently caused by renal artery stenosis, primarily due to atherosclerosis and fibromuscular dysplasia (FMD). The presence of an accessory renal artery (ARA) is a common anatomical variation that can contribute to secondary renal vascular hypertension. However, FMD occurring in the ARA is a rare cause of renal vascular hypertension. Juxtaglomerular cell tumor (JGCT) represents a rare etiology of renal hypertension. The co-occurrence of the pathogenic ARA with JGCT is infrequently reported in the existing literature. Case presentations This case study presents a young individual with a 12-year history of resistant hypertension, initially diagnosed with pathogenic ARA but later confirmed as JGCT 4 years later. Following surgery for JGCT, the patient experienced only temporary stabilization of blood pressure without anti-hypertensive medication. Stenosis of the ARA was definitively diagnosed one and a half years post-surgery, with FMD occurring on the ARA strongly suspected. The patient underwent balloon dilatation angioplasty 3 years later, leading to sustained blood pressure stability with the use of two medications. Conclusions The case study discussed herein involves a patient with resistant hypertension initially diagnosed with ARA but later determined to have late-onset JGCT and renal artery stenosis. It is imperative to consider atypical JGCT in young patients exhibiting resistant hypertension, hypokalemia, and hyperreninemia. Adequate management of renal artery stenosis is crucial in the management of hyperreninemic hypertension.

Published
2024
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2. Association between erectile dysfunction and the prevalence and prognosis of hyperglycemia in adults in the USA based on NHANES 2001–2004

Author

Guangshu Chen, Lehua Huang, Meizheng Lai, and Jianmin Ran

Subjects
Erectile dysfunction, Hyperglycemia, All-cause mortality, Cardiovascular mortality, Low physical activity, Medicine, Science
Abstract

Abstract Prior research has demonstrated that erectile dysfunction (ED) is a significant risk factor for cardiovascular disease (CVD) and premature mortality. Few studies have examined the link between ED and hyperglycemia, and the predictive power of ED for mortality in individuals with hyperglycemia. A cohort of 1584 adults diagnosed with hyperglycemia, consisting of 583 individuals with diabetes and 1001 individuals with prediabetes, was selected from the National Health and Nutrition Examination Survey (NHANES) conducted between 2001 and 2004. The study found a positive correlation between severe ED and hyperglycemia (OR, 2.03; 95% CI 1.53–2.68), while no significant relationship was observed between severe ED and CVD events (OR, 1.60; 95% CI 0.91–2.80). Additionally, no statistical association was found between diabetes or prediabetes status and ED. After multivariable adjustments, severe ED was found to be significantly associated with an increased risk of all-cause mortality (HR, 1.67; 95% CI 1.16–2.39), while no significant association was observed between severe ED and CVD mortality (HR, 1.92; 95% CI 0.92–3.98). Our study indicates a significant correlation between ED and hyperglycemia status. Hyperglycemia Individuals with ED generally exhibited an unfavorable prognosis for mortality due to all causes and CVD, particularly among those with low levels of physical activity.

Published
2024
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3. Association of neutrophil-lymphocyte ratio with all-cause and cardiovascular mortality in US adults with diabetes and prediabetes: a prospective cohort study

Author

Guangshu Chen, Li Che, Meizheng Lai, Ting Wei, Chuping Chen, Ping Zhu, and Jianmin Ran

Subjects
Diabetes, Prediabetes, Neutrophil-lymphocyte ratio, All-cause mortality, Cardiovascular mortality, Cohort study, Diseases of the endocrine glands. Clinical endocrinology, RC648-665
Abstract

Abstract Background The neutrophil-lymphocyte ratio (NLR) is a novel hematological parameter to assess systemic inflammation. Prior investigations have indicated that an increased NLR may serve as a potential marker for pathological states such as cancer and atherosclerosis. However, there exists a dearth of research investigating the correlation between NLR levels and mortality in individuals with diabetes and prediabetes. Consequently, this study aims to examine the connection between NLR and all-cause as well as cardiovascular mortality in the population of the United States (US) with hyperglycemia status. Methods Data were collected from a total of 20,270 eligible individuals enrolled for analysis, spanning ten cycles of the National Health and Nutrition Examination Survey (NHANES) from 1999 to 2018. The subjects were categorized into three groups based on tertiles of NLR levels. The association of NLR with both all-cause and cardiovascular mortality was evaluated using Kaplan-Meier curves and Cox proportional hazards regression models. Restricted cubic splines were used to visualize the nonlinear relationship between NLR levels and all-cause and cardiovascular mortality in subjects with diabetes after accounting for all relevant factors. Results Over a median follow-up period of 8.6 years, a total of 1909 subjects with diabetes died, with 671 deaths attributed to cardiovascular disease (CVD). And over a period of 8.46 years, 1974 subjects with prediabetes died, with 616 cases due to CVD. The multivariable-adjusted hazard ratios (HRs) comparing high to low tertile of NLR in diabetes subjects were found to be 1.37 (95% CI, 1.19–1.58) for all-cause mortality and 1.63 (95% CI, 1.29–2.05) for CVD mortality. And the correlation between high to low NLR tertile and heightened susceptibility to mortality from any cause (HR, 1.21; 95% CI, 1.03–1.43) and CVD mortality (HR, 1.49; 95% CI, 1.08–2.04) remained statistically significant (both p-values for trend

Published
2024
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4. A Building Heat Load Prediction Method Driven by a Multi-Component Fusion LSTM Ridge Regression Ensemble Model

Author

Yu Zhang and Guangshu Chen

Subjects
building heat load prediction, ensemble deep learning, seasonal and trend decomposition using LOESS, long short-term memory neural network, ridge regression, Technology, Engineering (General). Civil engineering (General), TA1-2040, Biology (General), QH301-705.5, Physics, QC1-999, Chemistry, QD1-999
Abstract

Under the background of “double carbon”, building carbon emission reduction is urgent, and improving energy efficiency through short-term building heat load forecasting is an efficient means of building carbon emission reduction. Aiming at the characteristics of the decomposed short-term building heat load data, such as complex trend changes, significant seasonal changes, and randomness, a single-step short-term building heat load prediction method driven by the multi-component fusion LSTM Ridge Regression Ensemble Model (ST-LSTM-RR) is designed and implemented. First, the trend and seasonal components of the heat load are decomposed by the STL seasonal decomposition algorithm, which are fused into the original data to construct three diversified datasets; second, three basic models, namely, the trend LSTM, the seasonal LSTM, and the original LSTM, are trained; and then, the ridge regression model is trained to fuse the predicted values of the three basic models to obtain the final predicted values. Finally, the method of this paper is applied to the heat load prediction of eight groups in a large mountain hotel park, and the root mean square error (RMSE) and mean absolute error (MAE) are used as the evaluation indexes. The experimental results show that the average RMSE and average MAE of the prediction results of the proposed method in this paper are minimized on the eight groups.

Published
2024
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5. D-P-Transformer: A Distilling and Probsparse Self-Attention Rockburst Prediction Method

Author

Yu Zhang, Jitao Li, Dongqiao Liu, Guangshu Chen, and Jiaming Dou

Subjects
rockburst prediction, acoustic emission, absolute energy, transformer, probsparse self-attention, distilling, Technology
Abstract

Rockburst may cause damage to engineering equipment, disrupt construction progress, and endanger human life. To this day, the occurrence of rockburst remains complex and difficult to predict. This study proposes the D-P-Transformer algorithm to address this issue by improving the embedding structure of the Transformer for specific applications to rockburst data. To reduce the computational requirement, sparse self-attention is adopted to replace self-attention. A distilling operation and multiple layer replicas are simultaneously used to enhance the robustness and speed up the algorithm’s process. Taking all relevant rockburst factors into consideration, multiple experiments are conducted on seven large-scale rockburst datasets with different training ratios to verify the reliability of the proposed D-P-Transformer rockburst prediction algorithm. As compared to the original algorithm, the proposed algorithm shows average reductions of 24.45%, 46.56%, 17.32%, and 48.11% in the mean absolute error (MAE), mean square error (MSE), root mean square error (RMSE), and mean absolute percentage error (MAPE), respectively. The results indicate that the novel D-P-Transformer rockburst prediction algorithm is superior to the Transformer prediction algorithm, and could be used for coal mine rockburst prediction analysis.

Published
2022
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6. A Chinese Family with Familial Dysalbuminemic Hyperthyroxinemia (FDH) due to R242H Mutation on Human Albumin Gene: Reevaluating the Role of FDH in Patients with Asymptomatic Hyperthyroxinemia

Author

Hongbing Liu, Jianmin Ran, Chuping Chen, Guangshu Chen, Ping Zhu, Rongshao Tan, and Yan Liu

Subjects
Diseases of the endocrine glands. Clinical endocrinology, RC648-665
Abstract

Objective. Familial dysalbuminemic hyperthyroxinemia (FDH) has now become an established cause for spurious asymptomatic hyperthyroxinemia. Several different codon mutations on albumin gene had been identified. We here provided an established but rarely reported heterozygous mutation based on gene sequencing results from a Chinese family. Methods. The proband is a 14-year-old girl with light goiter and asymptomatic clinical presentations, whose thyroid function test by a one-step immunoassay showed increased free thyroxine (FT4) and free triiodothyronine (FT3) but nonsuppressed thyrotropin (TSH). All thyroid auto-antibodies were in the normal range. Blood samples were collected from her and most of her immediate family members for target gene sequencing and verification. Results. Hyperthyroxinemia was also confirmed in the proband’s mother and one of her uncles and his son. In the proband and these three pedigrees, the high-throughput gene screening sequencing and the following Sanger sequencing disclosed a heterozygous mutation in the albumin gene, which located in its exon 7 (c.725G > A), and correspondingly leads to an arginine replacement with a histidine (R242H) in its protein. This is an established mutation named as R218H if present without signal peptide sequence. Conclusions. For patients with asymptomatic hyperthyroxinemia, FDH should be clinically excluded before embarking on further investigations for other specific causes.

Published
2019
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7. Rockburst Intensity Grade Prediction Model Based on Batch Gradient Descent and Multi-Scale Residual Deep Neural Network.

Author

Yu Zhang, Mingkui Zhang, Jitao Li, and Guangshu Chen

Subjects
ROCK bursts, ARTIFICIAL neural networks, DEEP learning, GEOTECHNICAL engineering, EXCAVATION
Abstract

Rockburst is a phenomenon inwhich free surfaces are formed during excavation, which subsequently causes the sudden release of energy in the construction of mines and tunnels. Light rockburst only peels off rock slices without ejection, while severe rockburst causes casualties and property loss. The frequency and degree of rockburst damage increases with the excavation depth. Moreover, rockburst is the leading engineering geological hazard in the excavation process, and thus the prediction of its intensity grade is of great significance to the development of geotechnical engineering. Therefore, the prediction of rockburst intensity grade is one problem that needs to be solved urgently. By comprehensively considering the occurrence mechanism of rockburst, this paper selects the stress index (σθ/σc), brittleness index (σc/σt), and rock elastic energy index (Wet) as the rockburst evaluation indexes through the Spearman coefficient method. This overcomes the low accuracy problem of a single evaluation index prediction method. Following this, the BGD-MSR-DNN rockburst intensity grade prediction model based on batch gradient descent and a multi-scale residual deep neural network is proposed. The batch gradient descent (BGD) module is used to replace the gradient descent algorithm, which effectively improves the efficiency of the network and reduces the model training time. Moreover, the multi-scale residual (MSR) module solves the problem of network degradation when there are too many hidden layers of the deep neural network (DNN), thus improving the model prediction accuracy. The experimental results reveal the BGDMSR-DNNmodel accuracy to reach 97.1%, outperforming other comparable models. Finally, actual projects such as Qinling Tunnel and Daxiangling Tunnel, reached an accuracy of 100%. The model can be applied in mines and tunnel engineering to realize the accurate and rapid prediction of rockburst intensity grade. [ABSTRACT FROM AUTHOR]

Published
2023
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8. Bioinformatic Analysis Identifies Biomarkers and Treatment Targets in Primary Sjögren’s Syndrome Patients with Fatigue

Author

Guangshu Chen, Li Che, Xingdong Cai, Ping Zhu, and Jianmin Ran

Subjects
Sjogren's Syndrome, Article Subject, General Immunology and Microbiology, Gene Expression Profiling, Computational Biology, Humans, Medicine, General Medicine, Biomarkers, Fatigue, General Biochemistry, Genetics and Molecular Biology, Research Article
Abstract

We aim to identify the common genes, biological pathways, and treatment targets for primary Sjögren’s syndrome patients with varying degrees of fatigue features. We select datasets about transcriptomic analyses of primary Sjögren’s syndrome (pSS) patients with different degrees of fatigue features and normal controls in peripheral blood. We identify common differentially expressed genes (DEGs) to find shared pathways and treatment targets for pSS patients with fatigue and design a protein-protein interaction (PPI) network by some practical bioinformatic tools. And hub genes are detected based on the PPI network. We perform biological pathway analysis of common genes by Gene Ontology (GO) terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway. Lastly, potential treatment targets for pSS patients with fatigue are found by the Enrichr platform. We discovered that 27 DEGs are identified in pSS patients with fatigue features and the severe fatigued pSS-specific gene is RTP4. DEGs are mainly localized in the mitochondria, endosomes, endoplasmic reticulum, and cytoplasm and are involved in the biological process by which interferon acts on cells and cells defend themselves against viruses. Molecular functions mainly involve the process of RNA synthesis. The DEGs of pSS are involved in the signaling pathways of viruses such as hepatitis C, influenza A, measles, and EBV. Acetohexamide PC3 UP, suloctidil HL60 UP, prenylamine HL60 UP, and chlorophyllin CTD 00000324 are the four most polygenic drug molecules. PSS patients with fatigue features have specific gene regulation, and chlorophyllin may alleviate fatigue symptoms in pSS patients.

Published
2022

9. AGEs-induced MMP-9 activation mediated by Notch1 signaling is involved in impaired wound healing in diabetic rats

Author

Ping Zhu, Chuping Chen, Daoai Wu, Guangshu Chen, Rongshao Tan, and Jianmin Ran

Subjects
Glycation End Products, Advanced, Wound Healing, Endocrinology, Diabetes and Metabolism, NF-kappa B, General Medicine, Diabetes Mellitus, Experimental, Rats, Endocrinology, Matrix Metalloproteinase 9, Internal Medicine, Animals, Receptor, Notch1, Platelet Aggregation Inhibitors, Signal Transduction
Abstract

To elucidate the relationship between advanced glycation end products (AGEs), Notch1 signaling, nuclear factor-kappa B (NF-κB), and matrix metalloproteinase-9 (MMP-9) in diabetic wound healing in vitro and in vivo.We incubated primary keratinocytes with AGEs alone or AGEs along with γ-secretase inhibitor DAPT, and established diabetic rat wound model by intraperitoneal streptozotocin treatment. The Notch1 signaling components and MMP-9 expression were detected by qPCR, western blotting and gelatin zymography.The exposure of primary keratinocytes to AGEs led to a significant increase in Notch intracellular domain (NICD), Delta-like 4 (Dll4), and Hes1; however, Notch1 expression was inhibited by the RAGE siRNA. Furthermore, MMP-9 activation was up-regulated, secondary to AGEs treatment. In contrast, increased MMP-9 expression by AGEs-stimulation was eliminated after treatment with DAPT. NF-κB activation participated in the Notch1-modulated MMP-9 expression. Notably, in the diabetic animal model, inhibition of the Notch signaling pathway with DAPT attenuated NICD and MMP-9 overexpression, improved collagen accumulation, and ultimately accelerated diabetic wound healing.These findings identified that activation of the Notch1/NF-κB/MMP-9 pathway, in part, mediates the repressive effects of AGEs on diabetic wound healing and that targeting this pathway may be a potential strategy to improve impaired diabetic wound healing.

Published
2022

10. Bioinformatics Approach Predicts Candidate Targets for SARS-CoV-2 Infections to COPD Patients

Author

Li Che, Guangshu Chen, Xingdong Cai, Zhefan Xie, Tingting Xia, Wei Zhang, and Shengming Liu

Subjects
Article Subject, General Immunology and Microbiology, SARS-CoV-2, Gene Expression Profiling, Artesunate, COVID-19, Computational Biology, General Medicine, Middle Aged, General Biochemistry, Genetics and Molecular Biology, Pulmonary Disease, Chronic Obstructive, Verapamil, Humans, Gene Regulatory Networks
Abstract

COVID-19 is still prevalent in more world regions and poses a severe threat to human health due to its high pathogenicity. The incidence of COPD patients is gradually increasing, especially in patients over 45 years old. COPD patients are susceptible to COVID-19 due to the specific lung receptor ACE2 of SARS-CoV-2. We attempt to reveal the genetic basis by analyzing the expression of common DEGs of the two diseases through bioinformatics approaches and find potential therapeutic agents based on the target genes. Thus, we search the GEO database for COVID-19 and COPD transcriptomic gene expression. We also study the enrichment of signaling regulatory pathways and hub genes for potential therapeutic treatments. There are 34 common DEGs in the two datasets. The signaling pathways are mainly enriched in intercellular junctions between virus and cytokine regulation. In the PPI network of common DEGs, we extract 5 hub genes. We find that artesunate CTD 00001840, dexverapamil MCF7 UP, and STOCK1N-35696 PC3 DOWN could be therapeutic agents for both diseases. We also analyze the regulatory network of differential genes with transcription factors and miRNAs. Therefore, we conclude that artesunate CTD 00001840, dexverapamil MCF7 UP, and STOCK1N-35696 PC3 DOWN can be therapeutic candidates in COPD combined with COVID-19.

Published
2021

11. Bioinformatic Analysis Identifies Biomarkers and Treatment Targets in Primary Sjögren's Syndrome Patients with Fatigue

Author

Guangshu Chen, Li Che, Xingdong Cai, Ping Zhu, Jianmin Ran, and Shengming Liu

Abstract

We aim to identify the common genes, biological pathways and treatment targets for primary Sjögren's syndrome patients with varying degrees of fatigue features. We select datasets about transcriptomic analyses of Primary Sjögren's syndrome(pSS) patients with different degrees of fatigue features and normal controls in peripheral blood. We identify common differentially expressed genes(DEGs) to find shared pathways and treatment targets for pSS patients with fatigue and design protein-protein interactions (PPIs) network by some practical bioinformatics tools. And hub genes are detected based on the PPIs network. We perform biological pathways analysis of common genes by gene ontology(GO) terms and Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway. Lastly, potential treatment targets for pSS patients with fatigue are found by the Enrichr platform. We discovered 27 DEGs are identified in pSS patients with fatigue features and the severe fatigued pSS-specific gene being RTP4. DEGs are mainly localized in the mitochondria, endosomes, endoplasmic reticulum, cytoplasm and are involved in the biological process by which interferon acts on cells and cells defend themselves against viruses. Molecular functions mainly involve the process of RNA synthesis. The DEGs of pSS are involved in the signaling pathways of viruses such as hepatitis C, influenza A, measles, and EBV. Acetohexamide PC3 UP, suloctidil HL60 UP, prenylamine HL60 UP, chlorophyllin CTD 00000324 are the four most polygenic drug molecules. PSS patients with fatigue features have specific gene regulation and chlorophyllin may alleviate fatigue symptoms in pSS patients.

Published
2021

12. A Chinese Family with Familial Dysalbuminemic Hyperthyroxinemia (FDH) due to R242H Mutation on Human Albumin Gene: Reevaluating the Role of FDH in Patients with Asymptomatic Hyperthyroxinemia

Author

Ping Zhu, Jianmin Ran, Yan Liu, Chuping Chen, Guangshu Chen, Rongshao Tan, and Hongbing Liu

Subjects
Proband, medicine.medical_specialty, Article Subject, Endocrinology, Diabetes and Metabolism, 030209 endocrinology & metabolism, medicine.disease_cause, lcsh:Diseases of the endocrine glands. Clinical endocrinology, Asymptomatic, Thyroid function tests, 03 medical and health sciences, Exon, symbols.namesake, 0302 clinical medicine, Endocrinology, Hyperthyroxinemia, Internal medicine, medicine, Sanger sequencing, Mutation, lcsh:RC648-665, medicine.diagnostic_test, Endocrine and Autonomic Systems, business.industry, medicine.disease, Familial dysalbuminemic hyperthyroxinemia, 030220 oncology & carcinogenesis, symbols, medicine.symptom, business, Research Article
Abstract

Objective. Familial dysalbuminemic hyperthyroxinemia (FDH) has now become an established cause for spurious asymptomatic hyperthyroxinemia. Several different codon mutations on albumin gene had been identified. We here provided an established but rarely reported heterozygous mutation based on gene sequencing results from a Chinese family.Methods. The proband is a 14-year-old girl with light goiter and asymptomatic clinical presentations, whose thyroid function test by a one-step immunoassay showed increased free thyroxine (FT4) and free triiodothyronine (FT3) but nonsuppressed thyrotropin (TSH). All thyroid auto-antibodies were in the normal range. Blood samples were collected from her and most of her immediate family members for target gene sequencing and verification.Results. Hyperthyroxinemia was also confirmed in the proband’s mother and one of her uncles and his son. In the proband and these three pedigrees, the high-throughput gene screening sequencing and the following Sanger sequencing disclosed a heterozygous mutation in the albumin gene, which located in its exon 7 (c.725G > A), and correspondingly leads to an arginine replacement with a histidine (R242H) in its protein. This is an established mutation named as R218H if present without signal peptide sequence.Conclusions. For patients with asymptomatic hyperthyroxinemia, FDH should be clinically excluded before embarking on further investigations for other specific causes.

Published
2019

13. The Inflammatory Response Induced by RELMβ Upregulates IL-8 and IL-1β Expression in Bronchial Epithelial Cells in COPD

Author

Wenzhi Luo, Zhefan Xie, Guangshu Chen, Tingting Xia, Shengming Liu, Xingdong Cai, Jia-Xin Lin, Chao Yu, and Li Che

Subjects
resistin-like molecule beta/RELMβ, p38 mitogen-activated protein kinases, International Journal of Chronic Obstructive Pulmonary Disease, p38 MAPK, Proinflammatory cytokine, chronic obstructive pulmonary disease, Pulmonary Disease, Chronic Obstructive, Downregulation and upregulation, Gene expression, medicine, Humans, Interleukin 8, Gene, Original Research, COPD, IL-8, business.industry, Interleukin-8, Epithelial Cells, General Medicine, medicine.disease, respiratory tract diseases, IL-1β, Immunology, Cytokines, Signal transduction, business, Signal Transduction
Abstract

Li Che,1 Chao Yu,2 Guangshu Chen,3 Jiaxin Lin,1 Zhefan Xie,1 Tingting Xia,1 Wenzhi Luo,1 Xingdong Cai,1 Shengming Liu1 1Department of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Jinan University, Guangzhou, 510630, People’s Republic of China; 2Department of Pulmonary and Critical Care Medicine, Lu’an People’s Hospital of Anhui Province, Lu’an, 237016, People’s Republic of China; 3Department of Endocrinology, Guangzhou Red Cross Hospital, The Affiliated Hospital of Jinan University, Guangzhou, 510220, People’s Republic of ChinaCorrespondence: Shengming Liu; Xingdong CaiDepartment of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Jinan University, The West of Huangpu Road 613, Tianhe District, Guangzhou, Guangdong, People’s Republic of ChinaTel +86 20 38688628Email tlsm@jnu.edu.cn; cxd19790920@sina.comPurpose: Chronic obstructive pulmonary disease (COPD) is associated with a complex inflammatory regulatory network. Resistin-like molecule β (RELMβ) is highly expressed in the lungs of COPD patients. We aimed to investigate the proinflammatory effect of RELMβ on airway epithelial cells in COPD.Methods: First, a GEO dataset was used to analyze the expression of the RELMβ gene in the COPD and control groups as well as the protein levels of RELMβ in the sera of outpatients with COPD and normal control subjects in our hospital. We also stimulated 16HBE bronchial epithelial cells with recombinant RELMβ protein and analyzed the expression of IL-8 and IL-1β. We upregulated and downregulated the gene expression of RELMβ in 16HBE cells and analyzed the expression of the inflammatory cytokines IL-8 and IL-1β. In addition, we also examined the mechanism by which the p38 MAPK signaling pathway contributed to the regulation of IL-8 and IL-1β expression by RELMβ.Results: RELMβ expression was increased in COPD tissues in different data sets and in the serum of COPD patients in our hospital. IL-8 and IL-1β expression was also increased in COPD tissues with high RELMβ gene expression in different data sets. The RELMβ gene was mainly related to inflammatory factors and inflammatory signaling pathways in the PPI regulatory network. Experiments at the cellular level showed that RELMβ promoted the expression of the inflammatory cytokines IL-8 and IL-1β, and this regulation was mediated by the p38 MAPK signaling pathway.Conclusion: RELMβ can promote the expression of the inflammatory cytokines IL-8 and IL-1β in bronchial epithelial cells of patients with COPD and exert inflammatory effects. RELMβ may be a potential target for the treatment of COPD.Keywords: resistin-like molecule beta/RELMβ, chronic obstructive pulmonary disease, p38 MAPK, IL-8, IL-1&#x03B2

Published
2021

14. 503-P: Inhibition of Glucose Transporter 9 Increases Serum Uric Acid Level but Attenuates Renal Albumin Excretion in Streptozotocin-Induced Diabetic Rats: A Role of Hepatic Uric Acid Metabolism

Author

Ping Zhu, Qiu Jingxian, Yan Liu, Jianmin Ran, Guangshu Chen, Ruyi Zhang, Chuping Chen, and Rongshao Tan

Subjects
Creatinine, medicine.medical_specialty, Kidney, Endocrinology, Diabetes and Metabolism, medicine.disease, Streptozotocin, Excretion, chemistry.chemical_compound, Endocrinology, medicine.anatomical_structure, chemistry, Internal medicine, Diabetes mellitus, Internal Medicine, medicine, Uric acid, Xanthine oxidase, Blood urea nitrogen, medicine.drug
Abstract

Background: In previous studies, we confirmed that endogenous uric acid (UA) formation increases in the streptozotocin (STZ)-induced diabetic rats with renal injury. Yet changes of renal UA reabsorption and hepatic UA metabolism remain unclear in this model. Methods: STZ-induced diabetic rats and control rats were treated with benzbromarone (BZ), a glucose transporter 9 (GLUT9) inhibitor for 8 weeks. At baseline, 4 and 8 weeks after BZ treatment, blood samples were collected for fasting blood glucose (FBG), serum uric acid (SUA), serum creatinine (SCr), and blood urea nitrogen (BUN). Simultaneous urinary samples were tested and daily urinary amount of albumin (UAE), uric acid (UUA), creatinine (UCR), urea nitrogen (UUN) were calculated. Gene expressions of GLUT9, xanthine oxidase (XO), urate transporter 1 (URAT1) in the kidney and GLUT9, XO as well as uricase in the liver were detected by RT-PCR. Results: 1) Compared with normal rats, FBG, BUN, UUN, UAE and UUA were significantly increased, while SUA was significantly decreased in diabetic rats, while SCr and UCR levels were compared. Treatment with BZ did not change FBG in both rats. BZ significantly decreased SCr, BUN and UAE levels but increased SUA in diabetic rats. 2) In the kidney, expression of GLUT9 and XO was increased, while URAT1 was not altered in diabetic rats if compared with control rats. BZ treatment exerted no any effects on gene expression of GLUT9 and XO. 3) In the liver, gene expression of XO and uricase was compared between diabetic and normal rats, while GLUT9 was significantly upregulated in diabetic rats. BZ treatment remarkably inhibited GLUT9 expression but left XO and uricase unchanged in diabetic rats. Conclusions: 1) Inhibition of hepatic GLUT9 in STZ-induced diabetic rats increased SUA indicates that GLUT9 pathway for UA metabolism is critical in this model. 2) BZ treatment attenuates urinary albumin excretion in diabetes. Disclosure C. Chen: None. J. Ran: None. R. Zhang: None. G. Chen: None. P. Zhu: None. J. Qiu: None. R. Tan: None. Y. Liu: None.

Published
2019

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