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  • 1
    Article
    Article
    Language: English
    In: Magnetic Resonance Imaging Clinics of North America, 2004, Vol.12(3), pp.487-503
    Description: The high accuracy of renal MR angiography makes it well suited for diagnosing renal vascular disease. A comprehensive examination includes three-dimensional gadolinium MR angiography to assess lumenal anatomy and functional techniques to assess the hemodynamic significance of any stenosis identified. Postprocessing is critical to provide reformations, maximum intensity projections, and optional volume-rendered images to display arteries in an angiographic format for optimal demonstration of any vascular lesions. It is important to review source images to avoid missing pathologic findings. As MR imaging continues to develop, the renal MR angiography examination will likely expand to include extensive functional information about creatinine clearance, flow, and response to pharmacologic agents as well as spectroscopy, diffusion, perfusion, phase contrast, and other techniques.
    Keywords: Medicine
    ISSN: 1064-9689
    E-ISSN: 1557-9786
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  • 2
    Language: English
    In: Radiology, December 2012, Vol.265(3), pp.651-3
    Description: Liu et al (1) have shown that iodinated contrast medium preferentially vasoconstricts the glomerular afferent arterioles by depleting endothelial nitric oxide bioavailability. This potentiates an exaggerated afferent arteriolar vasoconstricting response to angiotensin II and opens possibilities for new methods to prevent or treat nephrotoxicity after contrast medium administration.
    Keywords: Arterioles -- Drug Effects ; Contrast Media -- Pharmacology ; Glomerular Filtration Rate -- Drug Effects ; Triiodobenzoic Acids -- Pharmacology
    ISSN: 00338419
    E-ISSN: 1527-1315
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  • 3
    Language: English
    In: Veterinary Microbiology, 28 June 2013, Vol.164(3-4), pp.212-221
    Description: Porcine epidemic diarrhea (PED) is an acute and highly contagious enteric disease of swine caused by porcine epidemic diarrhea virus (PEDV). The porcine intestinal epithelial cell is the PEDV target cell. In this study, we established a porcine intestinal epithelial cell (IEC) line which can stably express PEDV N protein. We also investigate the subcellular localization and function of PEDV N protein by examining its effects on cell growth, cycle progression, interleukin-8 (IL-8) expression, and survival. The results show that the PEDV N protein localizes in the endoplasmic reticulum (ER), inhibits the IEC growth and prolongs S-phase cell cycle. The S-phase is prolonged which is associated with a decrease of cyclin A transcription level and an increase of cyclin A degradation. The IEC expressing PEDV N protein can express higher levels of IL-8 than control cells. Further studies show that PEDV N protein induces ER stress and activates NF-κB, which is responsible for the up-regulation of IL-8 and Bcl-2 expression. This is the first report to demonstrate that PEDV N protein can induce cell cycle prolongation at the S-phase, ER stress and up-regulation interleukin-8 expression. These findings provide novel information on the function of the PEDV N protein and are likely to be very useful in understanding the molecular mechanisms responsible for PEDV pathogenesis.
    Keywords: Pedv ; N Protein ; S-Phase ; Er Stress ; Il-8 ; Nf-Κb ; Biology ; Veterinary Medicine
    ISSN: 0378-1135
    E-ISSN: 1873-2542
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  • 4
    Language: English
    In: Virology Journal, 01 January 2013, Vol.10(1), p.26
    Description: Abstract Background Porcine epidemic diarrhea virus (PEDV) is an important pathogen in swine and is responsible for substantial economic losses. Previous studies suggest that the PEDV E protein plays an important role in the viral assembly process. However, the subcellular localization and other functions of PEDV E protein still require more research. Methods The subcellular localization and function of PEDV E protein were investigated by examining its effects on cell growth, cell cycle progression, interleukin-8 (IL-8) expression and cell survival. Results The results show that plenty of PEDV E protein is localized in the ER, with small quantities localized in the nucleus. The PEDV E protein has no effect on the intestinal epithelial cells (IEC) growth, cell cycle and cyclin A expression. The cells expressing PEDV E protein express higher levels of IL-8 than control cells. Further studies show that PEDV E protein induced endoplasmic reticulum (ER) stress and activated NF-κB which is responsible for the up-regulation of IL-8 and Bcl-2 expression. Conclusions This study shows that the PEDV E protein is localized in the ER and the nucleus and it can cause ER stress. The PEDV E protein had no effect on the IEC growth and cell cycle. In addition, the PEDV E protein is able to up-regulate IL-8 and Bcl-2 expression.
    Keywords: Pedv ; E Protein ; Er Stress ; Il-8 ; Nf-Κb ; Bcl-2 ; Medicine ; Biology
    ISSN: 1743-422X
    E-ISSN: 1743-422X
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  • 5
    Language: English
    In: Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan, April 2014, Vol.34(2), pp.173-7
    Description: To investigate how the pretreatment of mice with Ganoderma spores affected the apoptosis of their splenic lymphocytes induced by dexamethasone after 19 days treatment. Sixty Kunming mice were randomly divided into six groups: blank control groupdrenched with normal saline; a drug control group drenched with 150 mg/mL Ganoderma spores; a model group treated with saline; a low dose group with 50 mg/mL Ganoderma spores; a moderate dose group with 100 mg/mL Ganoderma spores; and a high dose group with 150 mg/mL Ganoderma spores. The effect of Ganoderma spores on apoptosis in spleen lymphocytes was analyzed. All groups were treated for 19 days. On day 20, the model group and the 3 treatment groups were intraperitoneally injected dexamethasone to induce apoptosis. Splenic index and apoptosis indes were employed to measure cell apoptosis. The results showed that Ganoderma spores reduced the splenic index to different degrees in each group and the best effect was seen in the high dose group (P 〈 0.05).Terminal dexynucleotidyl transferase (TdT)-mediated 2'-Deoxyuridine 5'-Triphosphate nick end labeling staining revealed that the apoptotic index in all groups administered Ganoderma spores differed significantly from the model group, and a dose-response was observed. Flow cytometric analysis indicated that spleen lymphocyte apoptosis in the model group was extensive. Each dose of Ganoderma spores inhibited dexamethasone-induced apoptosis in spleen lymphocytes, and a dose-response was observed as well. The highest dose of Ganoderma spores decreased Malondialdehyde content in serum induced by dexamethasone (P 〈 0.05). The findings imply that the pretreatment of the mice with Ganoderma spores could reduce the apoptosis rate induced by dexamethasone in their splenic lymphocytes.
    Keywords: Apoptosis -- Drug Effects ; Drugs, Chinese Herbal -- Pharmacology ; Lymphocytes -- Cytology ; Protective Agents -- Pharmacology ; Reishi -- Chemistry ; Spleen -- Cytology ; Spores, Fungal -- Chemistry
    ISSN: 0255-2922
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  • 6
    Language: English
    In: Virology Journal, 01 September 2012, Vol.9(1), p.202
    Description: Abstract Background Bovine herpesvirus type 1 (BHV-1) is an important pathogen in cattle that is responsible for substantial economic losses. Previous studies suggest that BHV-1 may induce apoptosis in Madin-Darby bovine kidney (MDBK) cells via a mechanism only involving caspases and p53. However, the mechanism for BHV-1-induced MDBK cell apoptosis still requires more research. Methods MDBK was used as a model to study the precise signaling pathways of apoptosis induced by BHV-1 infection. Results BHV-1 infection activated a Fas/FasL-mediated apoptotic pathway, resulting in activation of caspase-8 and cleavage of Bid. In addition, BHV-1 infection down-regulated Bcl-2 and up-regulated Bax expression, thereby initiating the release of cytochrome c followed by caspase-9 activation. The combined activation of the extrinsic and intrinsic pathways resulted in activation of downstream effecter caspase-3 and poly ADP-ribose polymerase (PARP), leading to apoptosis. Furthermore, blocking apoptosis using caspase inhibitors improved BHV-1-infected MDBK cell viability to different extent. BHV-1 infection did not induce significant DNA fragmentation in MDBK cells pretreated with ammonium chloride (NH4Cl) or cells infected with UV-inactivated BHV-1. Blocking caspases activation increased BHV-1 replication. Conclusions BHV-1 induces apoptosis in MDBK cells through extrinsic and intrinsic pathways and there might be cross-talk between the two pathways. In addition, BHV-1 replication may be necessary for the induction of apoptosis in BHV-1-infected cells, and prolonged cell viability benefits BHV-1 replication.
    Keywords: Bhv-1 ; Mdbk Cells ; Apoptosis ; Caspase Cascades ; Fas ; Mitochondria ; Medicine ; Biology
    ISSN: 1743-422X
    E-ISSN: 1743-422X
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  • 7
    Language: English
    In: Inflammation, 2017, Vol.40(4), pp.1319-1330
    Description: Acute lung injury (ALI) is a major complication soon after paraquat poisoning and rapidly progresses with high mortality. However, the specific mechanism underlying paraquat-induced ALI is still unclear. In this study, the mechanism underlying the protective effects of SP600125 on paraquat-induced ALI was investigated according to oxidative stress, inflammation, and apoptosis. The rats were randomly assigned into the control group (CON), the paraquat poisoning group (PQ), and the PQ + SP600125 group (SP). A549 cells were divided into the Con group, Pq group, and Sp group. H&E staining and detection of lung wet/dry ratio were employed to evaluate lung injury. Annexin V-PI staining was done to evaluate A549 cell apoptosis. Dihydroethidium fluorescence was used to measure reactive oxygen species (ROS) in the lungs and A549 cells. ELISA was performed to detect TNF-α and IL-6 in the supernatant of bronchoalveolar lavage fluid (BALF) and A549 cells. RT-qPCR was done to measure the messenger RNA (mRNA) expression of TNF-α and IL-6 in the lungs and A549 cells. Western blotting assay was performed to detect the protein expression of phospho-JNK, total JNK, and cleaved caspase-3. Electrophoretic mobility shift assay was employed to detect the DNA binding activities of AP-1 and P-p65. JNK inhibitor SP600125 reduced JNK phosphorylation, downregulated cleaved caspase-3 protein level, decreased AP-1 transcriptional activity and ROS level, and reduced the transcription and expression of TNF-α and IL-6, which improved ALI and cell apoptosis after paraquat poisoning. Our results indicate that JNK/AP-1 mediates ALI as well as oxidative stress and inflammation deterioration secondary to paraquat poisoning.
    Keywords: acute lung injury ; c-Jun N-terminal kinase ; paraquat ; apoptosis
    ISSN: 0360-3997
    E-ISSN: 1573-2576
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  • 8
    Language: English
    In: PLoS ONE, 2012, Vol.7(1), p.e29347
    Description: Acute respiratory distress syndrome (ARDS) induced by pandemic 2009 H1N1 influenza virus has been widely reported and was considered the main cause of death in critically ill patients with 2009 H1N1 infection. However, no animal model has been developed for ARDS caused by infection with 2009 H1N1 virus. Here, we present a mouse model of ARDS induced by 2009 H1N1 virus. ; Mice were inoculated with A/swine/Shandong/731/2009 (SD/09), which was a 2009 H1N1 influenza variant with a G222D mutation in the hemagglutinin. Clinical symptoms were recorded every day. Lung injury was assessed by lung water content and histopathological observation. Arterial blood gas, leukocyte count in the bronchial alveolar lavage fluid and blood, virus titers, and cytokine levels in the lung were measured at various times post-inoculation. Mice infected with SD/09 virus showed typical ARDS symptoms characterized by 60% lethality on days 8–10 post-inoculation, highly edematous lungs, inflammatory cellular infiltration, alveolar and interstitial edema, lung hemorrhage, progressive and severe hypoxemia, and elevated levels of proinflammatory cytokines and chemokines. ; These results suggested that we successfully established an ARDS mouse model induced by a virulent 2009 H1N1 variant without previous adaptation, which may be of benefit for evaluating the pathogenesis or therapy of human ARDS caused by 2009 H1N1 virus.
    Keywords: Research Article ; Biology ; Medicine ; Virology ; Infectious Diseases ; Physiology ; Respiratory Medicine
    E-ISSN: 1932-6203
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  • 9
    Language: English
    In: Cellular and Molecular Life Sciences, 2010, Vol.67(8), pp.1371-1381
    Description: The N-myc downstream-regulated gene 2 (NDRG2) is involved in cell differentiation and apoptosis, but its function in the pancreas remains to be established. Herein we examine the expression and function of NDRG2 in the endocrine pancreas. NDRG2 immunoreactivity was localized mainly in the cytoplasm of pancreatic β cells. When β-TC3 cells were exposed chronically to high levels of free fatty acid (FFA), cell viability was impaired, and Akt and NDRG2 phosphorylation were reduced. NDRG2 is a potential substrate of protein kinase Akt. Overexpression of constitutively active Akt enhanced NDRG2 phosphorylation and abolished the apoptosis induced by FFA in β-TC3 cells, whereas NDRG2 knock-down attenuated Akt-mediated protection of β cells against fatty acid-triggered apoptosis. Collectively, these data indicate that NDRG2 acts as a key molecule in pancreatic β cells and is involved in the Akt-mediated protection of β cells against lipotoxicity.
    Keywords: NDRG2 ; Pancreatic β cell ; Protein kinase Akt ; Free fatty acid ; Apoptosis
    ISSN: 1420-682X
    E-ISSN: 1420-9071
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  • 10
    Language: English
    In: 2014, Vol.9(12), p.e115422
    Description: Avian leukosis virus subgroup J (ALV-J) has induced serious clinical outbreaks and has become a serious infectious disease of chickens in China. We describe here the creation of a recombinant ALV-J tagged with the enhanced green fluorescent protein (named rHPRS-103EGFP). We successfully utilize the rHPRS-103EGFP to visualize viral infection and for development of a simplified serum-neutralization test.
    Keywords: Research Article ; Biology And Life Sciences
    E-ISSN: 1932-6203
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