11 results on '"Qian, Sun"'
Search Results
2. Long-Term Effect of Elevated CO2 on the Development and Nutrition Contents of the Pea Aphid (Acyrthosiphon pisum)
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Chunchun Li, Qian Sun, Yuping Gou, Kexin Zhang, Qiangyan Zhang, Jing-Jiang Zhou, and Changzhong Liu
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Acyrthosiphon pisum ,elevated CO2 ,generation ,development ,nutrition ,Physiology ,QP1-981 - Abstract
It is predicted that the current atmospheric CO2 level will be doubled by the end of this century. Here, we investigate the impacts of elevated CO2 (550 and 750 μL/L) on the development and nutrition status of the green pea aphid for six generations, which is longer than previous studies. All seven examined physiological parameters were not affected over six generations under the ambient CO2 level (380 μL/L). However, the elevated CO2 levels (550 and 750 μL/L) prolonged nymph duration, decreased adult longevity, female fecundity and protein content, and increased the contents of total lipid, soluble sugar and glycogen. There was a significant interaction between the effect of CO2 levels and the effect of generations on nymph duration, female fecundity and adult longevity. The elevated CO2 had immediate effects on the female fecundity and the contents of total protein, total lipid and soluble sugar, starting within F0 generation. The adult longevity decreased, and the glycogen content increased from the F1 generation. However, the significant effect on the nymph development was only observed after three generations. Our study indicates that the elevated CO2 levels first influence the reproduction, the nutrition and the energy supply, then initiate aphid emergency responses by shortening lifespan and increasing glucose metabolism, and finally result in the slow development under further persistent elevated CO2 conditions after three generations, possibly leading to population decline under elevated CO2 conditions. Our results will guide further field experiments under climate change conditions to evaluate the effects of elevated CO2 on the development of the pea aphids and other insects, and to predict the population dynamics of the green pea aphid.
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- 2021
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3. Chronic Unpredictable Mild Stress in Rats Induces Colonic Inflammation
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Lina Wei, Ye Li, Wenjun Tang, Qian Sun, Lixin Chen, Xia Wang, Qingyi Liu, Siqi Yu, Shuyan Yu, Chuanyong Liu, and Xuelian Ma
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chronic unpredictable mild stress ,microbiota ,depression ,intestinal barrier ,colonic inflammation ,Physiology ,QP1-981 - Abstract
Chronic psychological stress is associated with an increased risk for relapse of inflammatory bowel diseases (IBD) and impedes the treatment of this condition. However, the impact of stress on the risk of IBD onset remains unclear. The goal of the present study was to examine whether chronic unpredictable mild stress (CUMS) could initiate or aggravate the onset of colon inflammation in rats which, in turn, would be capable of triggering bowel disease. We found that CUMS exposure increased infiltration of CD-45 positive cells and MPO activity, as well as augmented the expression of the inflammatory cytokines, IFN-γ and IL-6 within the colon of these rats. In addition, CUMS treatment changed the composition and diversity of gut microbiota and enhanced intestinal epithelial permeability, indicating the presence of a defect in the intestinal barrier. This CUMS-induced disruption of mucosal barrier integrity was associated with a reduction in expression of the tight junction protein, occludin 1, and an inhibition in mucosal layer functioning via reductions in goblet cells. Results from bacterial cultures revealed an increased presence of bacterial invasion after CUMS treatment as compared with that observed in controls. Thus, our data indicate that CUMS treatment induces alterations of the fecal microbiome and intestinal barrier defects, which facilitates bacterial invasion into colonic mucosa and further exacerbates inflammatory reactions within the colon. Accordingly, chronic stress may predispose patients to gastrointestinal infection and increase the risk of inflammation-related gut diseases.
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- 2019
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4. Overexpression of Purinergic P2X4 Receptors in Hippocampus Rescues Memory Impairment in Rats with Type 2 Diabetes
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Yong-Chang Li, Rui-Xia Weng, Guang-Yin Xu, Qian Sun, Rui Wu, Hong-Hong Zhang, and Ping-An Zhang
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0301 basic medicine ,Male ,medicine.medical_specialty ,endocrine system diseases ,Physiology ,DNA damage ,Hippocampus ,Morris water navigation task ,Rats, Sprague-Dawley ,03 medical and health sciences ,0302 clinical medicine ,Downregulation and upregulation ,Internal medicine ,Type 2 diabetes mellitus ,medicine ,Memory impairment ,Animals ,Receptor ,P2X4 receptors ,Microglia ,business.industry ,General Neuroscience ,Purinergic receptor ,nutritional and metabolic diseases ,General Medicine ,Rats ,030104 developmental biology ,Endocrinology ,medicine.anatomical_structure ,nervous system ,Diabetes Mellitus, Type 2 ,Original Article ,business ,Cognition Disorders ,Receptors, Purinergic P2X4 ,030217 neurology & neurosurgery - Abstract
Purinergic receptors have been reported to be involved in brain disorders. In this study, we explored their roles and mechanisms underlying the memory impairment in rats with type 2 diabetes mellitus (T2DM). T2DM rats exhibited a worse performance in the T-maze and Morris water maze (MWM) than controls. Microglia positive for P2X purinoceptor 4 (P2X4R) in the hippocampus were reduced and activated microglia were increased in T2DM rats. Long Amplicon PCR (LA-PCR) showed that DNA amplification of the p2x4r gene in the hippocampus was lower in T2DM rats. Minocycline significantly reduced the number of activated microglia and the mean distance traveled by T2DM rats in the MWM. Most importantly, P2X4R overexpression suppressed the activated microglia and rescued the memory impairment of T2DM rats. Overall, T2DM led to excessive activation of microglia in the hippocampus, partly through the DNA damage-mediated downregulation of P2X4Rs, thus contributing to memory impairment. Electronic supplementary material The online version of this article (10.1007/s12264-020-00478-7) contains supplementary material, which is available to authorized users.
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- 2020
5. Urine metabolomics of rats with chronic atrophic gastritis
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Liang-Kun Zhang, Jian Chen, Xi-Jian Liu, Ling Li, Keyun Sun, Tao Han, Qian-Qian Sun, Hailiang Huang, and Guoxiu Zu
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Male ,Physiology ,Methylnitronitrosoguanidine ,Atrophic gastritis ,Nitrogen Metabolism ,Urine ,Biochemistry ,Mass Spectrometry ,Analytical Chemistry ,Pathogenesis ,chemistry.chemical_compound ,Spectrum Analysis Techniques ,Medicine and Health Sciences ,Metabolites ,Medicine ,Amino Acids ,Purine metabolism ,Liquid Chromatography ,Multidisciplinary ,Organic Compounds ,Chromatographic Techniques ,Body Fluids ,Chemistry ,Physical Sciences ,Purine Metabolism ,Metabolic Pathways ,Anatomy ,Basic Amino Acids ,Metabolic Networks and Pathways ,Research Article ,Gastritis, Atrophic ,medicine.medical_specialty ,Liquid Chromatography-Mass Spectrometry ,Science ,Research and Analysis Methods ,Metabolomics ,Internal medicine ,Animals ,Histidine ,Rats, Wistar ,business.industry ,Organic Chemistry ,Chemical Compounds ,Biology and Life Sciences ,Proteins ,Metabolism ,medicine.disease ,Rats ,Amino Acid Metabolism ,Disease Models, Animal ,Metabolic pathway ,Endocrinology ,chemistry ,business ,Biomarkers - Abstract
Background/aim To use liquid chromatography-mass spectrometry (LC-MS) to identify endogenous differential metabolites in the urine of rats with chronic atrophic gastritis (CAG). Materials and methods Methylnitronitrosoguanidine (MNNG) was used to produce a CAG model in Wistar rats, and HE staining was used to determine the pathological model. LC-MS was used to detect the differential metabolic profiles in rat urine. Diversified analysis was performed by the statistical method. Results Compared with the control group, the model group had 68 differential metabolites, 25 that were upregulated and 43 that were downregulated. The main metabolic pathways were D-glutamine and D-glutamic acid metabolism, histidine metabolism and purine metabolism. Conclusion By searching for differential metabolites and metabolic pathways in the urine of CAG rats, this study provides effective experimental data for the pathogenesis and clinical diagnosis of CAG.
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- 2020
6. Heterochromatin protects retinal pigment epithelium cells from oxidative damage by silencing p53 target genes.
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Lili Gong, Fangyuan Liu, Zhen Xiong, Ruili Qi, Zhongwen Luo, Xiaodong Gong, Qian Nie, Qian Sun, Yun-Fei Liu, Wenjie Qing, Ling Wang, Lan Zhang, Xiangcheng Tang, Shan Huang, Gen Li, Hong Ouyang, Mengqing Xiang, Quan Dong Nguyen, Yizhi Liu, and David Wan-Cheng Li
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HETEROCHROMATIN ,RHODOPSIN ,EPITHELIUM ,P53 antioncogene regulation ,GENE silencing ,OXIDATIVE stress ,PHYSIOLOGY - Abstract
Oxidative stress (OS)-induced retinal pigment epithelium (RPE) cell apoptosis is critically implicated in the pathogenesis of age-related macular degeneration (AMD), a leading cause of blindness in the elderly. Heterochromatin, a compact and transcriptional inert chromatin structure, has been recently shown to be dynamically regulated in response to stress stimuli. The functional mechanism of heterochromatin on OS exposure is unclear, however. Here we show that OS increases heterochromatin formation both in vivo and in vitro, which is essential for protecting RPE cells from oxidative damage. Mechanistically, OS-induced heterochromatin selectively accumulates at p53-regulated proapoptotic target promoters and inhibits their transcription. Furthermore, OS-induced desumoylation of p53 promotes p53-heterochromatin interaction and regulates p53 promoter selection, resulting in the locus-specific recruitment of heterochromatin and transcription repression. Together, our findings demonstrate a protective function of OS-induced heterochromatin formation in which p53 desumoylation-guided promoter selection and subsequent heterochromatin recruitment play a critical role. We propose that targeting heterochromatin provides a plausible therapeutic strategy for the treatment of AMD. [ABSTRACT FROM AUTHOR]
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- 2018
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7. Zinc deficiency mediates alcohol-induced apoptotic cell death in the liver of rats through activating ER and mitochondrial cell death pathways.
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Qian Sun, Wei Zhong, Wenliang Zhang, Qiong Li, Xiuhua Sun, Xiaobing Tan, Xinguo Sun, Daoyin Dong, and Zhanxiang Zhou
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ALCOHOLIC liver diseases , *APOPTOSIS , *ZINC deficiency diseases , *MITOCHONDRIAL physiology , *ENDOPLASMIC reticulum , *PHYSIOLOGICAL effects of alcohol , *LIVER cells , *LABORATORY rats , *PHYSIOLOGY - Abstract
Hepatic zinc deficiency has been well documented in alcoholic patients, but the mechanisms by which zinc deficiency mediates cell death have not been well defined. The objectives of this study were to determine whether alcohol perturbs subcellular zinc homeostasis and how organelle zinc depletion may link with cell death pathways. Wistar rats were pair-fed with the Lieber-DeCarli control or ethanol diet for 5 mo. Chronic alcohol exposure significantly reduced zinc level in isolated hepatic endoplasmic reticulum (ER) and mitochondria. Among the detected zinc transporters, ER Zrt/Irt-like protein (ZIP)13 and mitochondrial ZIP8, which transport zinc from ER and mitochondria to cytosol, were significantly increased. Mitochondrial zinc transporter (ZnT) 4, which transports zinc from cytosol to mitochondria, was also increased. ER phosphorylated eukaryotic initiation factor 2α, activating transcription factor 4, and C/EBP homologous protein were significantly upregulated, and mitochondrial cytochrome c release and Bax insertion were detected in association with caspase-3 activation and apoptotic cell death. To define the role of zinc deficiency in ER and mitochondrial stress, H4IIEC3 cells were treated with 3 μM N,N,N'=,N'=-tetrakis (2-pyridylmethyl) ethylenediamine for 6 h with or without supplementation with zinc or N-acetylcysteine (NAC). The results demonstrated that zinc deprivation induced caspase-3 activation and apoptosis in association with ER and mitochondria dysfunction, which were inhibited by zinc as low as 10 μM but not by 2 mM NAC. These results suggest that chronic ethanol exposure induced in ER and mitochondrial zinc deficiency might activate intrinsic cell death signaling pathway, which could not be effectively rescued by antioxidant treatment. [ABSTRACT FROM AUTHOR]
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- 2015
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8. Vanadate restores glucose 6-phosphate in diabetic rats: a mechanism to enhance glucose metabolism.
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Qian Sun and Sekar, Natesampillai
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VANADIUM , *INSULIN resistance , *GLUCOSE-6-phosphatase , *GLUCOSE , *METABOLISM , *PHYSIOLOGY , *THERAPEUTICS - Abstract
Features a study which investigated the therapeutic effects of vanadium in diabetic rats. Overview of the mechanism of action of vanadium and vanadium theraphy; Methodology and results; Analysis of results.
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- 2000
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9. Effects of thyroid hormone on action potential and repolarizing currents in rat ventricular...
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Zhou-Qian Sun and Ojamaa, Kaie
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TRIIODOTHYRONINE , *HEART ventricles , *ELECTRIC properties of heart cells , *RAT physiology , *PHYSIOLOGY - Abstract
Studies the effects of triiodothyronine (T3) on the electrophysiological properties of ventricular myocytes isolated from euthyroid and hypothyroid rats using whole cell patch clamp techniques. Prolonged action potential duration shown by hypothyroid ventricular myocytes; Unaffected transient outward current with the acute application of T3.
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- 2000
10. Anesthesia with Dexmedetomidine and Low-dose Isoflurane Increases Solute Transport via the Glymphatic Pathway in Rat Brain When Compared with High-dose Isoflurane.
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Benveniste, Helene, Hedok Lee, Fengfei Ding, Qian Sun, Al-Bizri, Ehab, Makaryus, Rany, Probst, Stephen, Nedergaard, Maiken, Stein, Elliot A., Hanbing Lu, Lee, Hedok, Ding, Fengfei, Sun, Qian, and Lu, Hanbing
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ANIMAL experimentation , *BIOLOGICAL transport , *CELLULAR signal transduction , *CEREBRAL circulation , *COMBINATION drug therapy , *COMPARATIVE studies , *DOSE-effect relationship in pharmacology , *HIPPOCAMPUS (Brain) , *IMIDAZOLES , *ISOENZYMES , *ISOFLURANE , *LACTATE dehydrogenase , *MAGNETIC resonance imaging , *RESEARCH methodology , *MEDICAL cooperation , *PEPTIDES , *RATS , *RESEARCH , *RESEARCH funding , *EVALUATION research , *CONTRAST media , *INHALATION anesthetics , *PHYSIOLOGY - Abstract
Background: The glymphatic pathway transports cerebrospinal fluid through the brain, thereby facilitating waste removal. A unique aspect of this pathway is that its function depends on the state of consciousness of the brain and is associated with norepinephrine activity. A current view is that all anesthetics will increase glymphatic transport by inducing unconsciousness. This view implies that the effect of anesthetics on glymphatic transport should be independent of their mechanism of action, as long as they induce unconsciousness. We tested this hypothesis by comparing the supplementary effect of dexmedetomidine, which lowers norepinephrine, with isoflurane only, which does not.Methods: Female rats were anesthetized with either isoflurane (N = 8) or dexmedetomidine plus low-dose isoflurane (N = 8). Physiologic parameters were recorded continuously. Glymphatic transport was quantified by contrast-enhanced magnetic resonance imaging. Cerebrospinal fluid and gray and white matter volumes were quantified from T1 maps, and blood vessel diameters were extracted from time-of-flight magnetic resonance angiograms. Electroencephalograms were recorded in separate groups of rats.Results: Glymphatic transport was enhanced by 32% in rats anesthetized with dexmedetomidine plus low-dose isoflurane when compared with isoflurane. In the hippocampus, glymphatic clearance was sixfold more efficient during dexmedetomidine plus low-dose isoflurane anesthesia when compared with isoflurane. The respiratory and blood gas status was comparable in rats anesthetized with the two different anesthesia regimens. In the dexmedetomidine plus low-dose isoflurane rats, spindle oscillations (9 to 15 Hz) could be observed but not in isoflurane anesthetized rats.Conclusions: We propose that anesthetics affect the glymphatic pathway transport not simply by inducing unconsciousness but also by additional mechanisms, one of which is the repression of norepinephrine release. [ABSTRACT FROM AUTHOR]- Published
- 2017
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11. Synergistic Effect of Trehalose and Saccharose Pretreatment on Maintenance of Lyophilized Human Red Blood Cell Quality.
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Yan-Qiong Li, Rui Hu, Li-Hui Zhong, Qian Sun, and You-Ping Yan
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ERYTHROCYTES , *TREHALOSE , *SUCROSE , *FREEZE-drying , *SUPEROXIDE dismutase , *ADENOSINE triphosphatase , *GLUCOSE-6-phosphate dehydrogenase , *PHYSIOLOGY , *THERAPEUTICS - Abstract
Purpose: To investigate the synergistic effect of trehalose and saccharose pretreatment on maintenance of lyophilized human red blood cell (RBC) quality. Methods: RBCs were pre-treated with trehalose and saccharose, and then lyophilized and re-hydrated. Prior to lyophilization and after re-hydration, RBC parameters, RBC counts, total hemoglobin concentration, mean corpuscular hemoglobin (MCH), mean corpuscular volume (MCV), comprehensive deformation index, hemolysis ratio and phosphatidylserine (PS) expression, were determined using a hematology analyzer, an RBC deformation instrument, a spectrophotometer and a flow cytometer, respectively. Superoxide dismutase (SOD), glucose-6-phosphate dehydrogenase (G-6-PD), and adenosine triphosphatase (ATPase) activities were determined using kits for SOD, ATPase, and G-6- PD assay, respectively. Results: After lyophilization-rehydration, RBC counts and total hemoglobin recovery rates, deformability, and RBC SOD, ATPase, and G-6-PD activities were significantly decreased by 47.24 - 74.65% (p < 0.01), compared with the normal group. RBC osmotic fragility and PS expression on the outer surface of the RBC membrane were significantly increased by 168.53 and 629.30% (p < 0.01), respectively, compared with the normal group. RBC MCH and MCV values were not significantly affected by lyophilization-rehydration (p > 0.05). Trehalose and saccharose pretreatment significantly reversed the effects of lyophilization-rehydration on these RBC parameters by approximately 13.16 - 211.11% (p < 0.01), compared with the control group. The combined effects were synergistic. Conclusion: Trehalose and saccharose pretreatment synergistically enhances maintenance of lyophilized RBC quality. [ABSTRACT FROM AUTHOR]
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- 2016
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