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1. The Influence of Autophagy in Advanced Atherosclerosis | |||
Zhu Yuning,Fan Wenjing,Zhang Chi,Guo Fang,Li Wei,Wang Yufei,Jiang Zhisheng,Qu Shunlin | |||
Basic Medicine 02 December 2015 | |||
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Abstract:Atherosclerosis (AS) is still the leading cause for cardiovascular disease global morbidity and mortality, such as it is a key cause of cardiopathy, myocardial infarction and peripheral vascular diseases. It does great harm to human health. Macrophages play a crucial role in atherosclerotic plaque stabilization and rupture. In this case, the selectivity of macrophage removal may be beneficial to the stability of the plaques. Autophagy is a catabolic recycling pathway that is triggered by various intracellular or extracellular stimuli and then during autophagy, diverse cytosolic constituents are enveloped by double-membrane vesicles, autophagosomes, which later fuse with lysosomes or the vacuole to degrade their cargo. Because autophagy has the function of maintaining cell homeostasis and promoting cell survival,and therefore imbalance in autophagy is related closely to a diverse range of pathologies including cardiovascular diseases, the leading cause of death in the world. | |||
TO cite this article:Zhu Yuning,Fan Wenjing,Zhang Chi, et al. The Influence of Autophagy in Advanced Atherosclerosis[OL].[ 2 December 2015] http://en.paper.edu.cn/en_releasepaper/content/4665970 |
2. 3D rotary culture system augment megakaryopoiesis and thrombopoiesis | |||
YANG Yiqing,Liu Cuicui,Lei Xiaohua,Zhou Jiaxi | |||
Basic Medicine 25 November 2015 | |||
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Abstract:Platelets transfusion has been widely used by patients undergoing chemotherapy or radiotherapy, but the shortage of platelet supply limits the care of patients. While derivation of clinical-scale platelets in vitro would provide new source for transfusion, devices and procedures for deriving scalable platelets for clinical applications have not been established. In this study, we found that a rotary cell culture system (RCCS) can potentiate megakaryopoiesis and significantly improve the efficiency of platelet generation. Shear force, simulated microgravity and better diffusion of nutrients and oxygen from RSCCS altogether may account for the improved efficient platelet generation. The cost-effective and highly controllable strategy and methodology represent an important step toward large-scale platelet production for future biomedical and clinical applications.? | |||
TO cite this article:YANG Yiqing,Liu Cuicui,Lei Xiaohua, et al. 3D rotary culture system augment megakaryopoiesis and thrombopoiesis[OL].[25 November 2015] http://en.paper.edu.cn/en_releasepaper/content/4664369 |
3. Effect of ADH1B Arg48His polymorphism on DNA damage induced by alcohol in esophageal squamous cell lines | |||
Liang Weijun,Wei Zhang,Tian Dongping,Liu Xi,Xu Zexin,Huang Bo,Su Min | |||
Basic Medicine 16 November 2015 | |||
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Abstract:Previous studies reported that ADH1B Arg48His locus was susceptible to esophageal cancer, especially interacting with alcohol drinking, but the mechanism behind the association is not clear. The current study was to explore the effect of ADH1B Arg48His genotypes on alcohol induced DNA damage in esophageal squamous immortalized cell lines. NE2 and NE3 cell lines were performed sanger sequencing to genotype ADH1B Arg48His locus. After treatment with different concentrations of alcohol, DNA double strand breaks (γ-H2AX immunostaining) were detected by immunocytochemistry. We found that higher concentration of alcohol made more serious of DNA damage. In addition, the degree of DNA double strand breaks of NE3 with homozygote His/His genotype were significant serious than that of NE2 with heterozygote Arg/His genotype. These findings provide an important contribution to understanding the role of ADH1B polymorphisms in esophageal susceptibility and carcinogenesis.????? | |||
TO cite this article:Liang Weijun,Wei Zhang,Tian Dongping, et al. Effect of ADH1B Arg48His polymorphism on DNA damage induced by alcohol in esophageal squamous cell lines[OL].[16 November 2015] http://en.paper.edu.cn/en_releasepaper/content/4661634 |
4. Immunoglobulin A Expression Correlated with Aberrant Proliferation of Esophageal Epithelium | |||
Huang Bo,Wang Jihong,Hu Bin,Wu Xianying,Lin Wenting,Tian Dongping,Su Min,Guo Dan | |||
Basic Medicine 16 November 2015 | |||
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Abstract:Many research groups have recently shown that various cancer types can express immunoglobulin, but investigation of immunoglobulin A, the human most abundant isotype of immunoglobulin and the most prominent antibody at mucosa, expression in esophageal squamous cell carcinoma has been lacking. In this study, IgA protein expression was examined by immunohistochemistry in 197 esophageal tissues including normal, precancerous and squamous cancer, and found that IgA protein expressed in all normal and Esophageal Intraepithelial Neoplasia (EIN) and 96.30% of esophageal cancer (EC) (p > 0.05), but the strong expression (++) rate of IgA in cancer (79.01%) was significantly lower than that of normal (90.12%, p = 0.048) and EIN (95%, p = 0.012). Furthermore, the expression pattern changed from cell membrane in normal to cytoplasm in EIN and cancer. From normal, low EIN to high EIN, with increasing of proliferation, IgA expression had an increasing tendency. In EC, IgA expression positively correlated with Ki-67 immunochemically labeled proliferation (rs = 0.223,p = 0.046) but not other clinicopathological parameters. Ki67 labeling index of IgA strong expression (++) group was significantly higher than that of IgA weak expression (+) group (p = 0.011). To avoid the inference of secretory IgA protein from plasma cell, we validated IgA expression by detecting its protein and messenger RNA meanwhile in EC cell lines (EC109) used immunofluorescence and nested Real-time PCR, respectively. Our results indicated that the capability of EC in producing IgA and IgA expression correlated well with aberrant proliferation of EC.) | |||
TO cite this article:Huang Bo,Wang Jihong,Hu Bin, et al. Immunoglobulin A Expression Correlated with Aberrant Proliferation of Esophageal Epithelium[OL].[16 November 2015] http://en.paper.edu.cn/en_releasepaper/content/4661655 |
5. SHIP2 interacts with MLK3 and regulates its tyrosine phosphorylation | |||
WU Zhe,XIE Jingwei | |||
Basic Medicine 09 November 2015 | |||
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Abstract:MLK3, a serine/threonine MAP3K, implicates in various physiological functions as neurodegenerative disease, cell cycle regulation, apoptosis and T-cell activation etc. Phosphorylation of MLK3 is essential for its activation. Ocassionally, in our previous study, MLK3 was found to be phosphorylated at tyrosine site which had not reported yet. Data in the present study show that SHIP2 positively regulated MLK3 tyrosine phosphorylation through SHIP2-MLK3 interaction, and JIP1 showed negative effect on this tyrosine phosphorylation. In addition, SHIP2-MLK3 association was not modulated in response to EGF or TNF-α. Domain tests demonstrate that the catalytic domain of SHIP2 was responsible for the interaction with MLK3. All together, our data may provide a new potential regulating mechaniam of cross-talk between SHIP2 and MLK3-mediated MAPK pathway. | |||
TO cite this article:WU Zhe,XIE Jingwei. SHIP2 interacts with MLK3 and regulates its tyrosine phosphorylation[OL].[ 9 November 2015] http://en.paper.edu.cn/en_releasepaper/content/4660744 |
6. JIP1 negatively regulates SHIP2 catalytic activity through protein-protein interaction | |||
WU Zhe,XIE Jingwei | |||
Basic Medicine 09 November 2015 | |||
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Abstract:SHIP2, a SH2-containing inositol polyphosphate 5-phosphatase 2, plays a role in insulin and growth factor signaling, cytoskeletal organization, neurodegenerative diseases etc. In our previous study, JIP1 (JNK-interacting protein 1) was identified as a new protein partner of SHIP2 and SHIP2 showed negative effect on JIP1-mediated JNK activity. Herein, the region of SHIP2 involved in the interaction with JIP1 and the effect of JIP1 on SHIP2 were inverstigated. Data showd that there existed other region than PR domain of SHIP2 implicating in the association with JIP1, and JIP1 negatively regulated SHIP2 catalytic activity. In addition, SHIP2 might be phosphorylated by JIP1-mediated JNK on serine/threonine sites. Taken together, through JIP1-SHIP2 interaction, JIP1 might be implicated in the signalling functional consequences such as neurodegenerative diseases, cells proliferation and insulin resistance etc. | |||
TO cite this article:WU Zhe,XIE Jingwei. JIP1 negatively regulates SHIP2 catalytic activity through protein-protein interaction[OL].[ 9 November 2015] http://en.paper.edu.cn/en_releasepaper/content/4660362 |
7. The effects of collagen genes col-131, col-150, dpy-5 and col-121 on fertility and development of Caenorhabditis elegans | |||
Lu Zhaolian,Fu Ximei,Zhang Yan,Liang Hongmei,Liu Xin,Chen Gen | |||
Basic Medicine 10 October 2015 | |||
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Abstract:5-Fluorouracil (5-FU) treatment in Caenorhabditis elegans(C.elegans) leads to slow developmental rate, reduces brood size, small body size, and truncates lifespan. Using Digital Gene Expression (DGE) profiling analysis, the potential pathways and genes that could be involved in declining the embryos of C. elegans have identified. Here, when C.elegans treated by 5-FU, three down-regulated genes were identified, including col-131, col-150 and dpy-5, which belong to ECM-receptor interaction pathway and Focal adhesion and one up-regulated gene col-121 which acts in Focal adhesion. Furtherly, RNAi-mediated gene knock down method was used to examine their RNAi phenotypes. The result showed that dpy-5(RNAi) worms were short-body, dumpy, and displaying a serious defect in fertility. col-121(RNAi) worms were slender, long, and slightly altered in body development. In addition, col-121(RNAi) worms displayed abnormal body morphology. Furthermore, knocking down of col-131 has subtle side effect in C.elegans fertility; however, col-131 (RNAi) worms could rescue 5-Fu toxic effect on C.elegans on fertility and lifespan defect. Taken together, the results revealed the essential role for col-150, dpy-5 and col-121 in C.elegans fertility decline. Our data also suggested that col-131 may be an essential gene in ECM-receptor interaction pathway and Focal adhesion and regulate other cuticle collagen genes including col-150, dpy-5, and col-121. | |||
TO cite this article:Lu Zhaolian,Fu Ximei,Zhang Yan, et al. The effects of collagen genes col-131, col-150, dpy-5 and col-121 on fertility and development of Caenorhabditis elegans[OL].[10 October 2015] http://en.paper.edu.cn/en_releasepaper/content/4657315 |
8. Markers in diagnosis of lung cancer: Several common detection methods | |||
LIN Liquan,ZHANG Xi,ZOU Yingchang,LU Yanli,WANG Ping,CHEN Xing | |||
Basic Medicine 09 September 2015 | |||
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Abstract:There's an old saying in China that people turn pale at the mention of a tiger. Today, people will turn pale at the mention of lung cancer because of its high morbidity and high mortality. Fortunately, studies have found lots of markers that can be applied in observational and analytic epidemiology, randomized clinical trials, screening, diagnosis and prognosis of lung cancer. Those markers are including proteins in serum, volatile organic compounds (VOCs) in exhaled breath, exhaled breath condensates (EBCs), gene expression, microRNAs, and medical imaging indices. At the same time, various detection techniques were used to measure the markers. With the effort of researchers, a better detection of lung cancer will be realized by combining different markers in different stages. Developing detection techniques will bring novel machines that are more rapid, more accurate, more robust and more comfort for the diagnosis of lung cancer patient. | |||
TO cite this article:LIN Liquan,ZHANG Xi,ZOU Yingchang, et al. Markers in diagnosis of lung cancer: Several common detection methods[OL].[ 9 September 2015] http://en.paper.edu.cn/en_releasepaper/content/4654285 |
9. 17β-Estradiol Up-Regulates NRF2 via PI3k/AKT and Estrogen Receptor Signaling Pathways to Suppress Light-Induced Retinal Degeneration in Rat | |||
ZHU Chunhui,LI Hongbo,WANG Shaolan,WANG Baoying,HU Chenghu,DU Fangying,ZHAO Panpan,LI Ang,YU Xiaorui | |||
Basic Medicine 17 June 2015 | |||
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Abstract:Human age-related retinal diseases, such as age-related macular degeneration (AMD), are intimately associated with decreased tissue oxygenation and hypoxia. Different antioxidants have been investigated to reverse AMD. In the present study, we describe the antioxidant 17β-estradiol (βE2) and investigate its protective effects on retinal neurons. Fourteen days after ovariectomy, adult Sprague-Dawley rats were exposed to 8000-lux light for 12 h to induce retinal degeneration. Reactive oxygen species (ROS) levels were assessed by confocal fluorescence microscopy using 2, 7-dichlorofluorescein diacetate. Nuclear factor erythroid 2-related factor 2 (Nrf2) and antioxidant enzyme mRNA expression were detected by real-time PCR. Western blotting was used to evaluate NRF2 activation. NRF2 translocation was determined by immunohistochemistry, with morphological changes monitored by hematoxylin and eosin staining. Following light exposure, βE2 significantly reduced ROS production. βE2 also up-regulated NRF2 mRNA and protein levels, with maximal expression at 4 and 12h post-exposure, respectively. Interestingly, following βE2 administration, NRF2 was translocated from the cytoplasm to the nucleus, primarily in the outer nuclear layer. βE2 also up-regulated NRF2, which triggered phase-2 antioxidant enzyme expression (superoxide dismutases 1 and 2, catalase, glutaredoxins 1 and 2, and thioredoxins 1 and 2), reduced ROS production, and ameliorated retinal damage. However, the beneficial effects of βE2 were markedly suppressed by pretreatment with LY294002 or ICI182780, specific inhibitors of the phosphotidylinositol 3-kinase-Akt (PI3K/AKT), and estrogen receptor (ER) signaling pathways, respectively. Taken together, these observations suggest that βE2 exerts antioxidative effects following light-induced retinal degeneration potentially via NRF2 activation. This protective mechanism may depend on two pathways: a rapid, non-genomic-type PI3K/AKT response, and a genomic-type ER-dependent response. Our data provides evidence that βE2 is potentially effective for treatment of retinal degeneration diseases. | |||
TO cite this article:ZHU Chunhui,LI Hongbo,WANG Shaolan, et al. 17β-Estradiol Up-Regulates NRF2 via PI3k/AKT and Estrogen Receptor Signaling Pathways to Suppress Light-Induced Retinal Degeneration in Rat[J]. |
10. Enhanced Colonic Hypersensitivity and Sensitization of Voltage-gated Sodium Channel in Primary Sensory Neurons in Diabetic Rats | |||
Song Zhenyuan,Hu Ji,Zhang Honghong,Xu Guangyin | |||
Basic Medicine 18 May 2015 | |||
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Abstract:Background: Patients with long-standing diabetes often demonstrate intestinal dysfunction and abdominal pain. However, the pathophysiology of abdominal pain in diabetic patients remains elusive. This study was designed to determine roles of voltage-gated sodium channels (VGSCs) in dorsal root ganglion (DRG) in colonic hypersensitivity of diabetic rats. Methods: Diabetic models were induced by a single intraperitoneal injection of Streptozotocin (STZ; 65 mg/kg i.p.) in adult female rats. Behavioral responses to colorectal distention (CRD) were used to determine colonic sensitivity in rats. Colon-specific DRG neurons labeled with DiI were acutely dissociated for measuring excitability and sodium channel currents by whole-cell patch clamp recordings. Western blot analysis was employed to measure the expression of NaV1.7 and NaV1.8 of colon DRGs. Results: STZ injection produced a significantly lower distention threshold than control rats in responding to CRD. STZ injection also depolarized the resting membrane potentials, hyperpolarized action potential threshold, decreased rheobase and increased number of action potentials evoked by 2 and 3 times rheobase stimulation and ramp current stimulation. Furthermore, STZ injection enhanced neuronal sodium current densities of DRG neurons innervating the colon. STZ injection also led to a significant upregulation of NaV1.7 and NaV1.8 expression in colon DRGs compared with age and sex-matched control rats. Conclusion: Our results suggest that enhanced neuronal excitability following STZ injection, which might be mediated by upregulation of NaV1.7 and NaV1.8 expression in primary sensory neurons, may play an important role in diabetic colonic hypersensitivity. | |||
TO cite this article:Song Zhenyuan,Hu Ji,Zhang Honghong, et al. Enhanced Colonic Hypersensitivity and Sensitization of Voltage-gated Sodium Channel in Primary Sensory Neurons in Diabetic Rats[OL].[18 May 2015] http://en.paper.edu.cn/en_releasepaper/content/4644279 |
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