26 results on '"Qian, Sun"'
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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
- Full Text
- View/download PDF
4. Differential Responses of NHX1 and SOS1 Gene Expressions to Salinity in two Miscanthus sinensis Anderss. Accessions with Different Salt Tolerance
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Qian Sun, Toshihiko Yamada, Tetsuo Takano, and Yulai Han
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chemistry.chemical_classification ,biology ,Physiology ,Chemistry ,Salt (chemistry) ,Miscanthus sinensis ,Plant Science ,biology.organism_classification ,Biochemistry ,Salinity ,Botany ,SOS1 ,Gene ,Differential (mathematics) - Published
- 2021
5. Adult Stress Promotes Purinergic Signaling to Induce Visceral Pain in Rats with Neonatal Maternal Deprivation
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Guang-Yin Xu, Wan-Jie Du, Jian Song, Xin Li, Qian Sun, Ji-Tian Xu, Shufen Hu, and Ping-An Zhang
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Male ,0301 basic medicine ,medicine.medical_specialty ,Physiology ,Population ,Stress ,Irritable Bowel Syndrome ,Rats, Sprague-Dawley ,03 medical and health sciences ,0302 clinical medicine ,Downregulation and upregulation ,Dorsal root ganglion ,Stress, Physiological ,Ganglia, Spinal ,Internal medicine ,medicine ,Animals ,Receptor ,education ,Visceral hypersensitivity ,Maternal deprivation ,education.field_of_study ,business.industry ,Maternal Deprivation ,General Neuroscience ,Antagonist ,P2X3 receptor ,Visceral pain ,Visceral Pain ,General Medicine ,Purinergic signalling ,β2 adrenergic receptor ,Rats ,030104 developmental biology ,Endocrinology ,medicine.anatomical_structure ,Original Article ,medicine.symptom ,business ,Receptors, Purinergic P2X3 ,030217 neurology & neurosurgery ,Signal Transduction - Abstract
Chronic visceral pain is one of the primary symptoms of patients with irritable bowel syndrome (IBS), which affects up to 15% of the population world-wide. The detailed mechanisms of visceral pain remain largely unclear. Our previous studies have shown that neonatal maternal deprivation (NMD) followed by adult multiple stress (AMS) advances the occurrence of visceral pain, likely due to enhanced norepinephrine (NE)-β2 adrenergic signaling. This study was designed to explore the roles of P2X3 receptors (P2X3Rs) in the chronic visceral pain induced by combined stress. Here, we showed that P2X3Rs were co-expressed in β2 adrenergic receptor (β2-AR)-positive dorsal root ganglion neurons and that NE significantly enhanced ATP-induced Ca2+ signals. NMD and AMS not only significantly increased the protein expression of P2X3Rs, but also greatly enhanced the ATP-evoked current density, number of action potentials, and intracellular Ca2+ concentration of colon-related DRG neurons. Intrathecal injection of the P2X3R inhibitor A317491 greatly attenuated the visceral pain and the ATP-induced Ca2+ signals in NMD and AMS rats. Furthermore, the β2-AR antagonist butoxamine significantly reversed the expression of P2X3Rs, the ATP-induced current density, and the number of action potentials of DRG neurons. Overall, our data demonstrate that NMD followed by AMS leads to P2X3R activation, which is most likely mediated by upregulation of β2 adrenergic signaling in primary sensory neurons, thus contributing to visceral hypersensitivity.
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- 2020
6. 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
7. Positive effects of selenium supplementation in women with newly diagnosed Hashimoto's thyroiditis in an area with low selenium status
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Jadwiga Kryczyk-Kozioł, Anna Błażewska-Gruszczyk, Marian Słowiaczek, Ewelina Prochownik, Mirosław Bartyzel, Lutz Schomburg, Qian Sun, Paweł Zagrodzki, and Ewa Ochab
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endocrine system ,endocrine system diseases ,chemistry.chemical_element ,Physiology ,Hashimoto Disease ,Thyroiditis ,Selenium ,Hypothyroidism ,medicine ,Humans ,Subclinical infection ,medicine.diagnostic_test ,business.industry ,Thyroid disease ,Thyroid ,General Medicine ,medicine.disease ,Anti-thyroid autoantibodies ,medicine.anatomical_structure ,chemistry ,Dietary Supplements ,Female ,Thyroid function ,business ,Lipid profile - Abstract
Objective Autoimmune thyroid diseases, including Hashimoto's thyroiditis, are the most common ones among autoimmune diseases. The reported effects of selenium supplementation on the course of Hashimoto's thyroiditis are not consistent. It is therefore important to continue this line of research. Design The participants received selenium in the form of sodium selenite(IV) at a dose of 100 µg/day for 6 months. Patients Newly diagnosed and previously untreated Hashimoto's thyroiditis with euthyroidism or subclinical hypothyroidism. A total of 36 patients (aged 20 to 52 years) qualified for this study, of whom 29 women were successfully enrolled and completed the intervention. Measurements Both before and after supplementation the following parameters in serum were tested: anti-thyroid peroxidase antibodies, thyroid function indicators, selenium as well as antioxidant status parameters and other biochemical parameters (lipid profile, glucose). Iodine supply and subjective assessment of physical and psychological health were also monitored. Results Selenium supplementation decreased significantly level of anti-thyroid peroxidase antibodies what might have had a stabilizing effect on thyroid function, as values of thyroid parameters were within normal range before and at the end of the study. Mean level of selenium among patients was not different to healthy people in Poland. Median of ioduria was within normal range. Conclusions The study shows a potential way of protective effect of selenium in limiting development of overt hypothyroidism. The increase in the concentrations of Se and SELENOP in the serum of patients verifies successful supplementation and good compliance, but did not affect the antioxidant status parameters measured.
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- 2021
8. Topographic heterogeneity of intrinsic excitability in mouse hippocampal CA3 pyramidal neurons
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Qian Sun, Yu-Qiu Jiang, and Melissa C Lu
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Male ,Physiology ,General Neuroscience ,Pyramidal Cells ,Hippocampus ,Action Potentials ,Hippocampal formation ,Biology ,Hippocampal region ,Spatial memory ,CA3 Region, Hippocampal ,Mice, Inbred C57BL ,Mice ,nervous system ,Homogeneous ,Marked heterogeneity ,Animals ,Female ,Neuroscience ,Episodic memory ,Input resistance ,Research Article - Abstract
Area CA3 in the hippocampus is traditionally thought to act as a homogeneous neural circuit that is vital for spatial navigation and episodic memories. However, recent studies have revealed that CA3 pyramidal neurons in dorsal hippocampus display marked anatomic and functional heterogeneity along the proximodistal (transverse) axis. The hippocampus is also known to be functionally segregated along the dorsoventral (longitudinal) axis, with dorsal hippocampus strongly involved in spatial navigation and ventral hippocampus associated with emotion and anxiety. Surprisingly, however, relatively little is known about CA3 functional heterogeneity along the dorsoventral axis. Here, we carried out mouse-brain-slice patch-clamp recordings and morphological analyses to examine the heterogeneity of CA3 cellular properties along both proximodistal and dorsoventral axes. We find that CA3 pyramidal neurons exhibit considerable heterogeneity of somatodendritic morphology and intrinsic membrane properties, with ventral CA3 (vCA3) displaying more elaborate somatodendritic morphology, lower intrinsic excitability, smaller input resistance, greater cell capacitance, and more prominent hyperpolarization‐activated current than dorsal CA3 (dCA3). Furthermore, although both dCA3 and vCA3 exhibit proximal-to-distal gradients in intrinsic properties and neuronal morphology, these proximal-to-distal gradients in vCA3 are more moderate than those in dCA3. Taken together, our results extend previous findings on the proximodistal heterogeneity of dCA3 function and uncover a complex, yet orderly, pattern of topographic organization of CA3 neuronal features that extends to multiple anatomic dimensions and may contribute to its in vivo functional diversity. NEW & NOTEWORTHY Area CA3 is a major hippocampal region that is classically thought to act as a homogeneous neural network vital for spatial navigation and episodic memories. Here, we report that CA3 pyramidal neurons exhibit marked heterogeneity of somatodendritic morphology and cellular electrical properties along both proximodistal and dorsoventral axes. These new results uncover a complex, yet orderly, pattern of topographic organization of CA3 neuronal features that may contribute to its in vivo functional diversity.
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- 2020
9. 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
10. Demonstration of reciprocal diurnal variation in human serum T3 and rT3 concentration demonstrated by mass spectrometric analysis and establishment of thyroid hormone reference intervals
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Likhona Masika, Livia Avallone, Yesim Ozarda, Brian Stolze, Toral Parikh, Kerry J. Welsh, Qian Sun, Steven J. Soldin, Katherine A Araque, and Jacqueline Jonklaas
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lcsh:RC648-665 ,business.industry ,Endocrinology, Diabetes and Metabolism ,Thyroid ,Diurnal temperature variation ,Physiology ,030209 endocrinology & metabolism ,reference interval ,diurnal variation ,Mass spectrometric ,lcsh:Diseases of the endocrine glands. Clinical endocrinology ,thyroid hormone ,Reference intervals ,03 medical and health sciences ,0302 clinical medicine ,medicine.anatomical_structure ,030220 oncology & carcinogenesis ,Thyroid hormones ,Medicine ,business ,Hormone ,Original Research ,mass spectrometry - Abstract
Background: There has been a wide range of reference intervals proposed in previous literature for thyroid hormones due to large between-assay variability of immunoassays, as well as lack of correction for collection time. We provided the diurnal reference intervals for five thyroid hormones, namely total thyroxine (TT4), total triiodothyronine (TT3), free thyroxine (FT4), free triiodothyronine (FT3), and reverse T3 (rT3), measured in serum samples of healthy participants using a liquid chromatography/tandem mass spectrometry (LC-MS/MS) method. Methods: Couplet serum samples (a.m. and p.m.) were collected from 110 healthy females and 49 healthy males. Healthy volunteers were recruited from four participating centers between 2016 and 2018. Measurements of thyroid hormones were obtained by LC-MS/MS analysis. Results: Our study revealed significant uptrend in AM to PM FT4 ( p Conclusion: When diagnosing thyroid disorders, it is important to have accurate measurement of thyroid hormones, and to acknowledge the diurnal fluctuation found, especially for FT3. Our study highlights the importance of standardization of collection times and implementation of LC-MS/MS in thyroid hormone measurement.
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- 2019
11. cGAS-mediated autophagy protects the liver from ischemia-reperfusion injury independently of STING
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Timothy R. Billiar, Melanie J. Scott, Zhao Lei, John E. Griepentrog, Patricia Loughran, Meihong Deng, Qian Sun, Feizhou Huang, Richard A. Shapiro, Hongbo Xu, Zhongjie Yi, Hai Huang, and Tunliang Li
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0301 basic medicine ,Interferon Inducers ,Physiology ,Ischemia ,Apoptosis ,Pharmacology ,Protective Agents ,Mice ,03 medical and health sciences ,Physiology (medical) ,Autophagy ,medicine ,Animals ,Hepatology ,business.industry ,Gastroenterology ,Membrane Proteins ,Hypoxia (medical) ,medicine.disease ,Nucleotidyltransferases ,eye diseases ,Mice, Inbred C57BL ,Sting ,030104 developmental biology ,Liver ,Reperfusion Injury ,DNA Nucleotidyltransferases ,Interferon Type I ,Nucleotides, Cyclic ,medicine.symptom ,business ,Reperfusion injury ,Research Article ,Signal Transduction - Abstract
Liver ischemia-reperfusion (I/R) injury occurs through induction of oxidative stress and release of damage-associated molecular patterns (DAMPs), including cytosolic DNA released from dysfunctional mitochondria or from the nucleus. Cyclic guanosine monophosphate–adenosine monophosphate (cGAMP) synthase (cGAS) is a cytosolic DNA sensor known to trigger stimulator of interferon genes (STING) and downstream type 1 interferon (IFN-I) pathways, which are pivotal innate immune system responses to pathogen. However, little is known about the role of cGAS/STING in liver I/R injury. We subjected C57BL/6 (WT), cGAS knockout (cGAS−/−), and STING-deficient (STINGgt/gt) mice to warm liver I/R injury and that found cGAS−/− mice had significantly increased liver injury compared with WT or STINGgt/gt mice, suggesting a protective effect of cGAS independent of STING. Liver I/R upregulated cGAS in vivo and also in vitro in hepatocytes subjected to anoxia/reoxygenation (A/R). We confirmed a previously published finding that hepatocytes do not express STING under normoxic conditions or after A/R. Hepatocytes and liver from cGAS−/− mice had increased cell death and reduced induction of autophagy under hypoxic conditions as well as increased apoptosis. Protection could be restored in cGAS−/− hepatocytes by overexpression of cGAS or by pretreatment of mice with autophagy inducer rapamycin. Our findings indicate a novel protective role for cGAS in the regulation of autophagy during liver I/R injury that occurs independently of STING. NEW & NOTEWORTHY Our studies are the first to document the important role of cGAS in the acute setting of sterile injury induced by I/R. Specifically, we provide evidence that cGAS protects liver from I/R injury in a STING-independent manner.
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- 2018
12. Chronic Unpredictable Mild Stress in Rats Induces Colonic Inflammation
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Qingyi Liu, Shuyan Yu, Chuanyong Liu, Xuelian Ma, Lixin Chen, Lina Wei, Xia Wang, Qian Sun, Ye Li, Wenjun Tang, and Siqi Yu
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0301 basic medicine ,Physiology ,Inflammation ,Gut flora ,Occludin ,lcsh:Physiology ,colonic inflammation ,Proinflammatory cytokine ,03 medical and health sciences ,0302 clinical medicine ,Physiology (medical) ,microbiota ,Medicine ,Chronic stress ,Microbiome ,Original Research ,lcsh:QP1-981 ,Tight junction ,biology ,business.industry ,medicine.disease ,biology.organism_classification ,intestinal barrier ,030104 developmental biology ,depression ,Immunology ,chronic unpredictable mild stress ,030211 gastroenterology & hepatology ,medicine.symptom ,business ,Infiltration (medical) - 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.
- Published
- 2019
13. Brassica yellows virus P0 protein impairs the antiviral activity of NbRAF2 in Nicotiana benthamiana
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Yuan-Yuan Li, Xian-Bing Wang, Zong-Ying Zhang, Yongliang Zhang, Jialin Yu, Qian Sun, Ying Wang, Hang-Hai Zhao, Chenggui Han, Dawei Li, and Tian-Yu Zhao
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0301 basic medicine ,food.ingredient ,NbRAF2 ,Physiology ,viruses ,Cell ,Nicotiana benthamiana ,Plant Science ,stromules ,Biology ,Antiviral Agents ,Virus ,Polerovirus ,Viral Proteins ,03 medical and health sciences ,food ,Ubiquitin ,Brassica yellows virus ,Tobacco ,medicine ,Gene silencing ,nuclear localization ,Plant Proteins ,Potato leafroll virus ,fungi ,food and beverages ,P0 ,biology.organism_classification ,Research Papers ,Cell biology ,Luteoviridae ,030104 developmental biology ,medicine.anatomical_structure ,Plant—Environment Interactions ,Tobacco rattle virus ,biology.protein - Abstract
The Brassica yellows virus genotype A P0 protein interacts with Rubisco assembly factor 2 in tobacco, affecting its nuclear accumulation and promoting viral infection., In interactions between poleroviruses and their hosts, few cellular proteins have been identified that directly interact with the multifunctional virus P0 protein. To help explore the functions of P0, we identified a Brassica yellows virus genotype A (BrYV-A) P0BrA-interacting protein from Nicotiana benthamiana, Rubisco assembly factor 2 (NbRAF2), which localizes in the nucleus, cell periphery, chloroplasts, and stromules. We found that its C-terminal domain (amino acids 183–211) is required for self-interaction. A split ubiquitin membrane-bound yeast two-hybrid system and co-immunoprecipitation assays showed that NbRAF2 interacted with P0BrA, and co-localized in the nucleus and at the cell periphery. Interestingly, the nuclear pool of NbRAF2 decreased in the presence of P0BrA and during BrYV-A infection, and the P0BrA-mediated reduction of nuclear NbRAF2 required dual localization of NbRAF2 in the chloroplasts and nucleus. Tobacco rattle virus-based virus-induced gene silencing of NbRAF2 promoted BrYV-A infection in N. benthamiana, and the overexpression of nuclear NbRAF2 inhibited BrYV-A accumulation. Potato leafroll virus P0PL also interacted with NbRAF2 and decreased its nuclear accumulation, indicating that NbRAF2 may be a common target of poleroviruses. These results suggest that nuclear NbRAF2 possesses antiviral activity against BrYV-A infection, and that BrYV-A P0BrA interacts with NbRAF2 and alters its localization pattern to facilitate virus infection.
- Published
- 2018
14. Expression quantitative trait loci analysis of the Rubisco activase gene in maize
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Qian Sun, Z. L. Zhang, Zhitong Yin, B. Chen, Yu Zhang, Xin Kan, Min Cui, H. B. Shi, Dexiang Deng, and B. Jia
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0106 biological sciences ,0301 basic medicine ,Genetics ,medicine.medical_specialty ,education.field_of_study ,Physiology ,Population ,Plant Science ,Biology ,Quantitative trait locus ,01 natural sciences ,03 medical and health sciences ,030104 developmental biology ,Chromosome 4 ,Gene mapping ,Genetic marker ,Molecular genetics ,Expression quantitative trait loci ,medicine ,education ,Gene ,010606 plant biology & botany - Abstract
Expression quantitative trait loci (eQTL) analyses were applied in order to identify genetic factors that are relevant to the expression of a β-isoform Rubisco activase gene in maize, namely ZmRCAβ, in this study. During two years, a maize recombinant inbred line population was measured for ZmRCAβ expression levels at the grain filling stage. Based on a genetic map containing 916 molecular markers, we detected five eQTLs, namely qRCA2.1 on chromosome 2, and qRCA4.1, qRCA4.2, qRCA4.3, and qRCA4.4 on chromosome 4. These eQTLs explained the phenotypic variation ranging from 6.14% to 7.50% with the logarithm of the odd values ranging from 3.11 to 4.96. Based on the position of the eQTLs and ZmRCAβ on the chromosome, qRCA4.2 was inferred as a cis-eQTL and the remaining as a trans-eQTL, suggesting that a combination of both cis- and trans-acting elements might control ZmRCAβ expression. qRCA4.2, qRCA4.3, and qRCA4.4 were repeatedly detected during two years.
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- 2017
15. SYP22 and VAMP727 regulate BRI1 plasma membrane targeting to control plant growth in Arabidopsis
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Qian Sun, Yu Xi Duan, Yang Liu, Tian Ya Li, Lijie Chen, Yuan Hu Xuan, Jin Hee Jung, Liang Zhang, and Xiaofeng Zhu
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Plant growth ,biology ,Physiology ,Chemistry ,Arabidopsis Proteins ,Qa-SNARE Proteins ,Cell Membrane ,Arabidopsis ,Plant Development ,Plant Science ,biology.organism_classification ,Cell biology ,Membrane ,Brassinosteroids ,Mutation ,Protein Kinases ,Protein Binding - Published
- 2019
16. Defect of mitochondrial respiratory chain is a mechanism of ROS overproduction in a rat model of alcoholic liver disease: role of zinc deficiency
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Wei Zhong, Zhanxiang Zhou, Qian Sun, and Wenliang Zhang
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Male ,0301 basic medicine ,medicine.medical_specialty ,Mitochondrial DNA ,Physiology ,Liver and Biliary Tract Physiology/Pathophysiology ,Mitochondria, Liver ,Oxidative phosphorylation ,Biology ,Mitochondrion ,Oxidative Phosphorylation ,Electron Transport ,03 medical and health sciences ,Adenosine Triphosphate ,Cell Line, Tumor ,Physiology (medical) ,Internal medicine ,medicine ,Animals ,Humans ,NRF1 ,Rats, Wistar ,Liver Diseases, Alcoholic ,Membrane Potential, Mitochondrial ,Hepatology ,Gastroenterology ,TFAM ,Lipid Metabolism ,Immunohistochemistry ,Rats ,Oxidative Stress ,Zinc ,030104 developmental biology ,Endocrinology ,Mitochondrial respiratory chain ,Liver ,Mitochondrial biogenesis ,Reactive Oxygen Species ,Mitochondrial DNA replication - Abstract
Morphological and functional alterations of hepatic mitochondria have been documented in patients with alcoholic liver disease (ALD). Our recent study demonstrated that zinc level was decreased in whole liver and mitochondria by chronic alcohol feeding. The present study was undertaken to determine whether zinc deficiency mediates alcohol-induced mitochondrial electron transport chain (ETC) defect and whether defective ETC function may lead to generation of reactive oxygen species (ROS). Male Wistar rats were pair fed with the Lieber-DeCarli control or ethanol diet for 5 mo. Chronic alcohol exposure increased hepatic triglyceride, free fatty acid, and 4-hydroxynonenal (4HNE) levels; meanwhile hepatic mitochondrial 4HNE level was also increased. Moreover, hepatic mitochondrial respiratory complexes I, III, IV, and V and hepatic ATP production were decreased by chronic alcohol exposure. Chronic alcohol feeding decreased peroxisome proliferator-activated receptor gamma coactivator-1-alpha (PGC1α), nuclear respiratory factor 1 (NRF1), mitochondrial transcription factor A (TFAM), and mitochondrial DNA. HepG2 cells were treated with N, N, N′, N′-tetrakis (2-pyridylmethyl) ethylenediamine (TPEN) for 6 h. Zinc deficiency significantly decreased mitochondrial respiratory complexes I, III, and IV. In addition, PGC1α, NRF1, and TFAM levels as well as mitochondrial DNA were significantly decreased by TPEN treatment. Knockdown of mitochondrial respiratory complexes I, III, or IV by shRNA caused a decrease in mitochondrial membrane potential and an increase in ROS production. These results suggest that alcohol-induced hepatic zinc deficiency could inactivate mitochondrial biogenesis pathway and decrease mitochondrial DNA replication, which, in turn, decreases mitochondrial complex protein expression. The defect of mitochondrial respiratory complexes may worsen alcohol-induced ROS production.
- Published
- 2016
17. 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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Xinguo Sun, Xiuhua Sun, Wei Zhong, Zhanxiang Zhou, Wenliang Zhang, Qiong Li, Daoyin Dong, Xiaobing Tan, and Qian Sun
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Male ,Alcoholic liver disease ,Programmed cell death ,Time Factors ,Physiology ,Eukaryotic Initiation Factor-2 ,Caspase 3 ,Apoptosis ,Mitochondria, Liver ,Mitochondrion ,Activating Transcription Factor 4 ,Biology ,medicine.disease_cause ,Endoplasmic Reticulum ,Antioxidants ,Physiology (medical) ,Cell Line, Tumor ,medicine ,Animals ,Phosphorylation ,Rats, Wistar ,Cation Transport Proteins ,Liver Diseases, Alcoholic ,Chelating Agents ,Hepatology ,Ethanol ,Gastroenterology ,Membrane Transport Proteins ,medicine.disease ,Cell biology ,Disease Models, Animal ,Oxidative Stress ,Zinc ,Liver and Biliary Tract ,Liver ,Cancer research ,Zinc deficiency ,Carrier Proteins ,Deficiency Diseases ,Reactive Oxygen Species ,Oxidative stress ,Transcription Factor CHOP - 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.
- Published
- 2014
18. NFATc1 phosphorylation by DYRK1A increases its protein stability
- Author
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Long Chen, Ketao Wang, Heng Liu, Qian Sun, Xiulian Sun, Yuankai Zhang, and Shuai Chen
- Subjects
0301 basic medicine ,Cytoplasm ,DYRK1A ,Physiology ,Amino Acid Motifs ,lcsh:Medicine ,Biochemistry ,Ligases ,Database and Informatics Methods ,Ubiquitin ,Immune Physiology ,Serine ,Medicine and Health Sciences ,Post-Translational Modification ,Phosphorylation ,Amino Acids ,lcsh:Science ,Immune System Proteins ,Multidisciplinary ,integumentary system ,biology ,Organic Compounds ,Protein Stability ,Chemistry ,Kinase ,Protein-Tyrosine Kinases ,Precipitation Techniques ,Enzymes ,Cell biology ,Physical Sciences ,Cellular Structures and Organelles ,Sequence Analysis ,Research Article ,Proteasome Endopeptidase Complex ,NFATC2 ,Bioinformatics ,Immunoprecipitation ,Immunology ,Protein Serine-Threonine Kinases ,Research and Analysis Methods ,Antibodies ,03 medical and health sciences ,Sequence Motif Analysis ,Hydroxyl Amino Acids ,Humans ,Transcription factor ,NFATC Transcription Factors ,030102 biochemistry & molecular biology ,Organic Chemistry ,lcsh:R ,Ubiquitination ,Chemical Compounds ,Biology and Life Sciences ,Proteins ,Cell Biology ,Monoclonal Antibodies ,HEK293 Cells ,030104 developmental biology ,Tumor progression ,Proteolysis ,Enzymology ,biology.protein ,lcsh:Q - Abstract
NFATs are transcription factors involved in immune activation and tumor progression. Previous reports showed that DYRK1A suppressed NFATc2 transcriptional activity through phosphorylation. Nonetheless, our results showed that DYRK1A increased NFATc1/αA protein level and subsequent transcriptional activity. DYRK1A phosphorylation of NFATc1/αA at S261, S278, S403 and S409 interfered with NFATc1 ubiquitination and ubiquitin-proteasome degradation. Our results imply that DYRK1A is a positive kinase in regulation of NFATc1.
- Published
- 2017
19. Dysregulation of hepatic zinc transporters in a mouse model of alcoholic liver disease
- Author
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Zhanxiang Zhou, Xiang Zhang, Jiayang Zhang, Xiuhua Sun, Xinmin Yin, Xinguo Sun, Qian Sun, Xiaobing Tan, Qiong Li, and Wei Zhong
- Subjects
Male ,medicine.medical_specialty ,Alcoholic liver disease ,Time Factors ,Physiology ,Peroxisome proliferator-activated receptor ,chemistry.chemical_element ,Zinc ,Biology ,medicine.disease_cause ,Cell Line ,Mice ,Physiology (medical) ,Internal medicine ,medicine ,Animals ,PPAR alpha ,Cation Transport Proteins ,Liver Diseases, Alcoholic ,chemistry.chemical_classification ,Zinc finger ,Aldehydes ,Hepatology ,Gastroenterology ,Cytochrome P-450 CYP2E1 ,Hydrogen Peroxide ,medicine.disease ,Mice, Inbred C57BL ,Hepatocyte nuclear factors ,Disease Models, Animal ,Oxidative Stress ,Liver and Biliary Tract ,Endocrinology ,Hepatocyte nuclear factor 4 ,chemistry ,Hepatocyte Nuclear Factor 4 ,Liver ,Zinc deficiency ,Deficiency Diseases ,Oxidative stress - Abstract
Zinc deficiency is a consistent phenomenon observed in patients with alcoholic liver disease, but the mechanisms have not been well defined. The objective of this study was to determine if alcohol alters hepatic zinc transporters in association with reduction of hepatic zinc levels and if oxidative stress mediates the alterations of zinc transporters. C57BL/6 mice were pair-fed with the Lieber-DeCarli control or ethanol diets for 2, 4, or 8 wk. Chronic alcohol exposure reduced hepatic zinc levels, but increased plasma and urine zinc levels, at all time points. Hepatic zinc finger proteins, peroxisome proliferator-activated receptor-α (PPAR-α) and hepatocyte nuclear factor 4α (HNF-4α), were downregulated in ethanol-fed mice. Four hepatic zinc transporter proteins showed significant alterations in ethanol-fed mice compared with the controls. ZIP5 and ZIP14 proteins were downregulated, while ZIP7 and ZnT7 proteins were upregulated, by ethanol exposure at all time points. Immunohistochemical staining demonstrated that chronic ethanol exposure upregulated cytochrome P-450 2E1 and caused 4-hydroxynonenal accumulation in the liver. For the in vitro study, murine FL-83B hepatocytes were treated with 5 μM 4-hydroxynonenal or 100 μM hydrogen peroxide for 72 h. The results from in vitro studies demonstrated that 4-hydroxynonenal treatment altered ZIP5 and ZIP7 protein abundance, and hydrogen peroxide treatment changed ZIP7, ZIP14, and ZnT7 protein abundance. These results suggest that chronic ethanol exposure alters hepatic zinc transporters via oxidative stress, which might account for ethanol-induced hepatic zinc deficiency.
- Published
- 2014
20. Heterochromatin protects retinal pigment epithelium cells from oxidative damage by silencing p53 target genes.
- Author
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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
- Subjects
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]
- Published
- 2018
- Full Text
- View/download PDF
21. Evidence for functional role of epsilonPKC isozyme in the regulation of cardiac Na(+) channels
- Author
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Guang-Qian Xiao, Yongxia Qu, Zhou-Qian Sun, Daria Mochly-Rosen, and Mohamed Boutjdir
- Subjects
Physiology ,Myocardium ,Xenopus ,Cell Biology ,Cell Separation ,In Vitro Techniques ,Sodium Channel Agonists ,Sodium Channels ,RNA, Complementary ,Rats ,Isoenzymes ,Oocytes ,Animals ,Tetradecanoylphorbol Acetate ,Cloning, Molecular ,Rats, Wistar ,Peptides ,Protein Kinase C ,Sodium Channel Blockers - Abstract
Investigation of the role of individual protein kinase C (PKC) isozymes in the regulation of Na+channels has been largely limited by the lack of isozyme-selective modulators. Here we used a novel peptide-specific activator (εV1–7) of εPKC and other peptide isozyme-specific inhibitors in addition to the general PKC activator phorbol 12-myristate 13-acetate (PMA) to dissect the role of individual PKCs in the regulation of the human cardiac Na+channel hH1, heterologously expressed in Xenopus oocytes. Peptides were injected individually or in combination into the oocyte. Whole cell Na+current ( INa) was recorded using two-electrode voltage clamp. εV1–7 (100 nM) and PMA (100 nM) inhibited INaby 31 ± 5% and 44 ± 8% (at −20 mV), respectively. These effects were not seen with the scrambled peptide for εV1–7 (100 nM) or the PMA analog 4α-phorbol 12,13-didecanoate (100 nM). However, εV1–7- and PMA-induced INainhibition was abolished by εV1–2, a peptide-specific antagonist of εPKC. Furthermore, PMA-induced INainhibition was not altered by 100 nM peptide-specific inhibitors for α-, β-, δ-, or ηPKC. PMA and εV1–7 induced translocation of εPKC from soluble to particulate fraction in Xenopus oocytes. This translocation was antagonized by εV1–2. In native rat ventricular myocytes, PMA and εV1–7 also inhibited INa; this inhibition was antagonized by εV1–2. In conclusion, the results provide evidence for selective regulation of cardiac Na+channels by εPKC isozyme.
- Published
- 2001
22. Effects of thyroid hormone on action potential and repolarizing currents in rat ventricular myocytes
- Author
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Kaie Ojamaa, Michael Artman, William A. Coetzee, Zhuo-Qian Sun, and Irwin Klein
- Subjects
Male ,endocrine system ,medicine.medical_specialty ,Patch-Clamp Techniques ,endocrine system diseases ,Triiodothyronine, Reverse ,Physiology ,Endocrinology, Diabetes and Metabolism ,Heart Ventricles ,Action Potentials ,Rats, Sprague-Dawley ,chemistry.chemical_compound ,Cadmium Chloride ,Hypothyroidism ,Physiology (medical) ,Internal medicine ,medicine ,Myocyte ,Animals ,Euthyroid ,Patch clamp ,4-Aminopyridine ,Cardiac transient outward potassium current ,Triiodothyronine ,business.industry ,Electric Conductivity ,Heart ,Reverse triiodothyronine ,Rats ,Endocrinology ,chemistry ,Propylthiouracil ,cardiovascular system ,business ,hormones, hormone substitutes, and hormone antagonists ,medicine.drug - Abstract
Thyroid hormones play an important role in cardiac electrophysiology through both genomic and nongenomic mechanisms of action. The effects of triiodothyronine (T3) on the electrophysiological properties of ventricular myocytes isolated from euthyroid and hypothyroid rats were studied using whole cell patch clamp techniques. Hypothyroid ventricular myocytes showed significantly prolonged action potential duration (APD90) compared with euthyroid myocytes, APD90 of 151 ± 5 vs. 51 ± 8 ms, respectively. Treatment of hypothyroid ventricular myocytes with T3 (0.1 μM) for 5 min significantly shortened APD by 24% to 115 ± 10 ms. T3 similarly shortened APD in euthyroid ventricular myocytes, but only in the presence of 4-aminopyridine (4-AP), an inhibitor of the transient outward current ( I to), which prolonged the APD by threefold. Transient outward current ( I to) was not affected by the acute application of T3 to either euthyroid or hypothyroid myocytes; however, I to density was significantly reduced in hypothyroid compared with euthyroid ventricular myocytes.
- Published
- 2000
23. Zinc deficiency mediates alcohol-induced apoptotic cell death in the liver of rats through activating ER and mitochondrial cell death pathways.
- Author
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Qian Sun, Wei Zhong, Wenliang Zhang, Qiong Li, Xiuhua Sun, Xiaobing Tan, Xinguo Sun, Daoyin Dong, and Zhanxiang Zhou
- Subjects
- *
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]
- Published
- 2015
- Full Text
- View/download PDF
24. Vanadate restores glucose 6-phosphate in diabetic rats: a mechanism to enhance glucose metabolism.
- Author
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Qian Sun and Sekar, Natesampillai
- Subjects
- *
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.
- Published
- 2000
- Full Text
- View/download PDF
25. Anesthesia with Dexmedetomidine and Low-dose Isoflurane Increases Solute Transport via the Glymphatic Pathway in Rat Brain When Compared with High-dose Isoflurane.
- Author
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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
- Subjects
- *
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
- Full Text
- View/download PDF
26. Synergistic Effect of Trehalose and Saccharose Pretreatment on Maintenance of Lyophilized Human Red Blood Cell Quality.
- Author
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Yan-Qiong Li, Rui Hu, Li-Hui Zhong, Qian Sun, and You-Ping Yan
- Subjects
- *
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]
- Published
- 2016
- Full Text
- View/download PDF
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