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Sun, Xiao-Feng
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Zhang, X., Sun, X.-F., Cao, Y., Ye, B., Peng, Q., Liu, X., . . . Zhang, H. (2018). CBD: a biomarker database for colorectal cancer. Database: The Journal of Biological Databases and Curation, 2018(1 January 2018), Article ID bay046.
Open this publication in new window or tab >>CBD: a biomarker database for colorectal cancer
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2018 (English)In: Database: The Journal of Biological Databases and Curation, ISSN 1758-0463, E-ISSN 1758-0463, Vol. 2018, no 1 January 2018, article id bay046Article in journal (Refereed) Published
Abstract [en]

Colorectal cancer (CRC) biomarker database (CBD) was established based on 870 identified CRC biomarkers and their relevant information from 1115 original articles in PubMed published from 1986 to 2017. In this version of the CBD, CRC biomarker data were collected, sorted, displayed and analysed. The CBD with the credible contents as a powerful and time-saving tool provide more comprehensive and accurate information for further CRC biomarker research. The CBD was constructed under MySQL server. HTML, PHP and JavaScript languages have been used to implement the web interface. The Apache was selected as HTTP server. All of these web operations were implemented under the Windows system. The CBD could provide to users the multiple individual biomarker information and categorized into the biological category, source and application of biomarkers; the experiment methods, results, authors and publication resources; the research region, the average age of cohort, gender, race, the number of tumours, tumour location and stage. We only collect data from the articles with clear and credible results to prove the biomarkers are useful in the diagnosis, treatment or prognosis of CRC. The CBD can also provide a professional platform to researchers who are interested in CRC research to communicate, exchange their research ideas and further design high-quality research in CRC. They can submit their new findings to our database via the submission page and communicate with us in the CBD.

Place, publisher, year, edition, pages
OXFORD UNIV PRESS, 2018
National Category
Bioinformatics (Computational Biology)
Identifiers
urn:nbn:se:liu:diva-149736 (URN)10.1093/database/bay046 (DOI)000436293800001 ()29846545 (PubMedID)
Note

Funding Agencies|Swedish Cancer Foundation; Swedish Research Council

Available from: 2018-07-24 Created: 2018-07-24 Last updated: 2018-08-14
Pathak, S., S, S., Banerjee, A., Marotta, F., Gopinath, M., Murugesan, R., . . . Sun, X.-F. (2018). Review on comparative efficacy of bevacizumab, panitumumab and cetuximab antibody therapy with combination of FOLFOX-4 in KRAS-mutated colorectal cancer patients. OncoTarget, 9(7), 7739-7748
Open this publication in new window or tab >>Review on comparative efficacy of bevacizumab, panitumumab and cetuximab antibody therapy with combination of FOLFOX-4 in KRAS-mutated colorectal cancer patients
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2018 (English)In: OncoTarget, ISSN 1949-2553, E-ISSN 1949-2553, Vol. 9, no 7, p. 7739-7748Article, review/survey (Refereed) Published
Abstract [en]

Colorectal cancer, fourth leading form of cancer worldwide and is increasing in alarming rate in the developing countries. Treating colorectal cancer has become a big challenge worldwide and several antibody therapies such as bevacizumab, panitumumab and cetuximab are being used with limited success. Moreover, mutation in KRAS gene which is linked with the colorectal cancer initiation and progression further interferes with the antibody therapies. Considering median progression free survival and overall survival in account, this review focuses to identify the most efficient antibody therapy in combination with chemotherapy (FOLFOX-4) in KRAS mutated colorectal cancer patients. The bevacizumab plus FOLFOX-4 therapy shows about 9.3 months and 8.7 months of progression free survival for KRAS wild and mutant type, respectively. The overall survival is about 34.8 months for wild type whereas for the mutant it is inconclusive for the same therapy. In comparison, panitumumab results in better progression-free survival which is about (9.6 months) and overall survival is about (23.9 months) for the wild type KRAS and the overall survival is about 15.5 months for the mutant KRAS. Cetuximab plus FOLFOX-4 therapy shows about 7.7 months and 5.5 months of progression-free survival for wild type KRAS and mutant type, respectively. Thus, panitumumab shows significant improvement in overall survival rate for wild type KRAS, validating as a cost effective therapeutic for colorectal cancer therapy. This review depicts that panitumumab along with FOLFOX-4 has a higher response in colorectal cancer patients than the either of the two monoclonal antibodies plus FOLFOX-4.

Keywords
KRAS; bevacizumab; cetuximab; colorectal cancer; panitumumab
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:liu:diva-152524 (URN)10.18632/oncotarget.22471 (DOI)29484148 (PubMedID)
Available from: 2019-03-28 Created: 2019-03-28 Last updated: 2019-08-26
Gopinath, M., Di Liddo, R., Marotta, F., Murugesan, R., Banerjee, A., Sriramulu, S., . . . Pathak, S. (2018). Role of Hippo Pathway Effector Tafazzin Protein in Maintaining Stemness of Umbilical Cord-Derived Mesenchymal Stem Cells (UC-MSC). International Journal of Hematology-Oncology and Stem Cell Research, 12(2), 153-165
Open this publication in new window or tab >>Role of Hippo Pathway Effector Tafazzin Protein in Maintaining Stemness of Umbilical Cord-Derived Mesenchymal Stem Cells (UC-MSC)
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2018 (English)In: International Journal of Hematology-Oncology and Stem Cell Research, ISSN 2008-3009, E-ISSN 2008-2207, Vol. 12, no 2, p. 153-165Article, review/survey (Refereed) Published
Abstract [en]

Tafazzin (TAZ) protein has been upregulated in various types of human cancers, although the basis for elevation is uncertain, it has been made definite that the effect of mutation in the hippo pathway, particularly when it is switched off, considerably activates tafazzin transcriptionally and thus this results in tissue or tumor overgrowth. Recent perceptions into the activity of tafazzin, have ascribed to it, a role as stem cell factor in mouse mesenchymal and as well as in neural stem cells. Being a downstream molecule in Hippo signalling, phosphorylation or dephosphorylation of tafazzin gene regulates its transcriptional activity and the stemness of mesenchymal stem cells. Commonly, extracellular matrix controls the stem cell fate commitment and perhaps tafazzin controls stemness through altering the extra cellular matrix. Extracellular matrix is generally made up of prime proteoglycans and the fate stabilization of the resulting lineages is surveilled by engineering these glycans. Tafazzin degradation and addition of proteoglycans affect physical attributes of the extracellular matrix that drives cell differentiation into various lineages. Thus, tafazzin along with major glycans present in the extracellular matrix is involved in imparting stemness. However, there are incoherent molecular events, wherein both tafazzin and the extracellular matrix components, together either activate or inhibit differentiation of stem cells. This review discusses about the role of tafazzin oncoprotein as a stemness factor.

Place, publisher, year, edition, pages
Tehran University of Medical Sciences, 2018
Keywords
Extracellular matrix; Oncoprotein; Proteoglycan; Stemness; Tafazzin
National Category
Cell Biology
Identifiers
urn:nbn:se:liu:diva-155842 (URN)30233778 (PubMedID)
Available from: 2019-03-29 Created: 2019-03-29 Last updated: 2019-03-29
Zhou, Y., Li, Y., Zhou, B., Chen, K., Lyv, Z., Huang, D., . . . Li, Y. (2017). Inflammation and Apoptosis: Dual Mediator Role for Toll-like Receptor 4 in the Development of Necrotizing Enterocolitis. Inflammatory Bowel Diseases, 23(1), 44-56
Open this publication in new window or tab >>Inflammation and Apoptosis: Dual Mediator Role for Toll-like Receptor 4 in the Development of Necrotizing Enterocolitis
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2017 (English)In: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 23, no 1, p. 44-56Article in journal (Refereed) Published
Abstract [en]

Background: Necrotizing enterocolitis (NEC) is the leading cause of neonatal gastrointestinal mortality; effective interventions are lacking with limited understanding of the pathogenesis of NEC. The importance of Toll-like receptor 4 (TLR4) signaling in NEC is well documented; however, the potential mechanisms that regulate enterocyte inflammation and apoptosis remain unclear. The aim of this study was to characterize the role of TLR4-mediated inflammation and apoptosis in the development of NEC and to determine the major apoptotic pathways and regulators in the process. Methods: TLR4-deficient C57BL/10ScNJ mice and lentivirus-mediated stable TLR4-silent cell line (IEC-6) were used. NEC was induced by formula gavage, cold, hypoxia, combined with lipopolysaccharide in vivo or lipopolysaccharide stimulation in vitro. Enterocyte apoptosis was evaluated by TUNEL or Annexin analysis. The expression of TLR4, caspase3, caspase8, caspase9, Bip, Bax, Bcl-2, and RIP was detected by Western blot and immunofluorescence. Inflammatory factors such as tumor necrosis factor-a and interleukin-2 were examined by Luminex. Results: Defect of TLR4 led to suppressed enterocytes apoptosis both in vitro and in vivo; the expression of caspase3, caspase8, Bip, and Bax was decreased; and caspase9 and Bcl-2 were increased. NEC severity was attenuated in TLR4-deficient mice compared with wild-type counterparts, and enterocytes apoptosis was correlated with NEC severity. RIP and cytokine level of tumor necrosis factor-a and interleukin-2 were also decreased. Conclusions: TLR4-induced inflammation and apoptosis play a critical role in the pathogenesis of NEC. TLR4 inhibition, combined with extrinsic (caspase8) and/or endoplasmic reticulum stress (Bip) apoptosis signaling blockade could serve as a potential effective treating strategy for NEC.

Place, publisher, year, edition, pages
LIPPINCOTT WILLIAMS & WILKINS, 2017
Keywords
necrotizing enterocolitis; Toll-like receptor 4; intestinal inflammation; apoptosis; necrosis
National Category
Gastroenterology and Hepatology
Identifiers
urn:nbn:se:liu:diva-136086 (URN)10.1097/MIB.0000000000000961 (DOI)000393897100012 ()27849634 (PubMedID)
Note

Funding Agencies|National Natural Science Fund of China (NSFC) [81470886]

Available from: 2017-03-27 Created: 2017-03-27 Last updated: 2018-05-03
Zhao, S., Sun, H., Jiang, W., Mi, Y., Zhang, D., Wen, Y., . . . Yan, D. (2017). miR-4775 promotes colorectal cancer invasion and metastasis via the Smad7/TGF beta-mediated epithelial to mesenchymal transition. Molecular Cancer, 16, Article ID 12.
Open this publication in new window or tab >>miR-4775 promotes colorectal cancer invasion and metastasis via the Smad7/TGF beta-mediated epithelial to mesenchymal transition
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2017 (English)In: Molecular Cancer, ISSN 1476-4598, E-ISSN 1476-4598, Vol. 16, article id 12Article in journal (Refereed) Published
Abstract [en]

Background: Despite advancements in the diagnosis and treatment of colorectal cancer (CRC), many patients die because of tumor metastasis or recurrence. Therefore, identifying new prognostic markers and elucidating the mechanisms of CRC metastasis and recurrence will help to improve the prognosis of the disease. As dysregulation of microRNAs is strongly related to cancer progression, the aim of this study was to identify the role of miR-4775 in the prognosis of CRC patients and the underling mechanisms involved in CRC progression. Methods: qPCR and in situ hybridization were used to evaluate the expression of miR-4775 in 544 pairs of paraffin-embedded normal and CRC tissues. Kaplan-Meier analysis with the log-rank test was used for survival analyses. Immunohistochemical staining was applied to investigate the expression of miR-4775-regulated Smad7/TGF beta pathway-associated markers. In vitro and in vivo invasion and metastasis assays were used to explore the function of miR-4775 in the progression of CRC. Results: miR-4775 was identified as a high-risk factor for CRC metastasis and recurrence, with high levels predicting poor survival among the 544 studied CRC patients. Furthermore, high miR-4775 expression promoted the invasion of CRC cells as well as metastasis and the epithelial to mesenchymal transition (EMT) via Smad7-mediated activation of TGF beta signaling both in vitro and in vivo. Downregulating miR-4775 or overexpressing Smad7 reversed the tumor-promoting roles of miR-4775/ Smad7/TGF beta in vitro and in vivo. Conclusion: miR-4775 promotes CRC metastasis and recurrence in a Smad7/TGF beta signaling-dependent manner, providing a new therapeutic target for inhibiting the metastasis or recurrence of the disease.

Place, publisher, year, edition, pages
BIOMED CENTRAL LTD, 2017
Keywords
miR-4775; Smad7; TGF beta signaling; Colorectal cancer; EMT
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:liu:diva-135399 (URN)10.1186/s12943-017-0585-z (DOI)000394126300001 ()28095858 (PubMedID)
Note

Funding Agencies|National High Technology Research and Development Program of China [SS2014AA020803]; National Natural Science Foundation of China [81220108021, 81302083, 81272750]; Natural Science Foundation of Shanghai [16ZR1427700]; Project of Shanghai Science and Technology Commission [124119a1700, 14411950502]; Project of Songjiang District [0702 N14001]

Available from: 2017-03-14 Created: 2017-03-14 Last updated: 2018-05-03
Liu, N., Cox, T. R., Cui, W., Adell, G., Holmlund, B., Ping, J., . . . Sun, X.-F. (2017). Nuclear expression of lysyl oxidase enzyme is an independent prognostic factor in rectal cancer patients.. OncoTarget, 8(36), 60015-60024
Open this publication in new window or tab >>Nuclear expression of lysyl oxidase enzyme is an independent prognostic factor in rectal cancer patients.
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2017 (English)In: OncoTarget, ISSN 1949-2553, E-ISSN 1949-2553, Vol. 8, no 36, p. 60015-60024Article in journal (Refereed) Published
Abstract [en]

Emerging evidence has implicated a pivotal role for lysyl oxidase (LOX) in cancer progression and metastasis. Whilst the majority of work has focused on the extracellular matrix cross-linking role of LOX, the exact function of intracellular LOX localisation remains unclear. In this study, we analysed the LOX expression patterns in the nuclei of rectal cancer patient samples and determined the clinical significance of this expression. Nuclear LOX expression was significantly increased in patient lymph node metastases compared to their primary tumours. High nuclear LOX expression in tumours was correlated with a high rate of distant metastasis and increased recurrence. Multivariable analysis showed that high nuclear LOX expression was also correlated with poor overall survival and disease free survival. Furthermore, we are the first to identify LOX enzyme isoforms (50 kDa and 32 kDa) within the nucleus of colon cancer cell lines by confocal microscopy and Western blot. Our results show a powerful link between nuclear LOX expression in tumours and patient survival, and offer a promising prognostic biomarker for rectal cancer patients.

Place, publisher, year, edition, pages
Impact journals, 2017
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:liu:diva-134762 (URN)10.18632/oncotarget.9623 (DOI)000408944300001 ()27231855 (PubMedID)
Note

Funding agencies: Swedish Cancer Foundation; Research Council of South East Sweden; Liu Cancer

Available from: 2017-02-24 Created: 2017-02-24 Last updated: 2018-05-03
Gnosa, S., Capodanno, A., Dahl Ejby Jensen, L. & Sun, X.-F. (2016). AEG-1 knockdown in colon cancer cell lines inhibits radiation-enhanced migration and invasion in vitro and in a novel in vivo zebrafish model. OncoTarget, 7(49), 81634-81644
Open this publication in new window or tab >>AEG-1 knockdown in colon cancer cell lines inhibits radiation-enhanced migration and invasion in vitro and in a novel in vivo zebrafish model
2016 (English)In: OncoTarget, ISSN 1949-2553, E-ISSN 1949-2553, Vol. 7, no 49, p. 81634-81644Article in journal (Refereed) Published
Abstract [en]

Background Radiotherapy is a well-established anti-cancer treatment. Although radiotherapy has been shown to significantly decrease the local relapse in rectal cancer patients, the rate of distant metastasis is still very high. Several studies have shown that radiation enhances migration and invasion both in vitro and in vivo. The aim of this study was to evaluate whether AEG-1 is involved in radiation-enhanced migration and invasion in vitro and in a novel in vivo zebrafish model.

Materials and Methods We evaluated the involvement of AEG-1 in migration and invasion and radiation-enhanced migration and invasion by Boyden chamber assay in three colon cancer cell lines and respective AEG-1 knockdown cell lines. Furthermore, we injected the cells in zebrafish embryos and evaluated the amount of disseminated cells into the tail.

Results Migration and invasion was decreased in all the AEG-1 knockdown cell lines. Furthermore, radiation enhanced migration and invasion, while AEG-1 knockdown could abolish this effect. The results from the zebrafish model confirmed the results obtained in vitro. MMP-9 secretion and expression were decreased in AEG-1 knockdown cells.

Conclusion Our results demonstrate that AEG-1 knockdown inhibits migration and invasion, as well as radiation-enhanced migration and invasion. We speculate that this is done via the downregulation of the intrinsic or radiation-enhanced MMP-9 expression. The zebrafish model can be used to study early events in radiation-enhanced invasion.

Place, publisher, year, edition, pages
Impact Journals, 2016
Keywords
AEG-1, MTDH, LYRIC, Colon cancer, Zebrafish, Transwell migration and invasion, Radiation
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:liu:diva-121866 (URN)10.18632/oncotarget.13155 (DOI)000389877500121 ()27835571 (PubMedID)
Note

The previous status of this publication was manuscript

Funding agencies: Swedish Cancer Foundation; Swedish Research Council; Health Research Council in South-East Sweden; Onkologiska klinikernas i Linkoping

Available from: 2015-10-12 Created: 2015-10-12 Last updated: 2017-12-01Bibliographically approved
Li, Y., Zhang, X., Ge, J., Liu, X., Xu, S., Zhu, Z., . . . Sun, X.-F. (2016). Can Nup88 expression be associated with atypical endometrial hyperplasia and endometrial cancer? A preliminary study. Pathology, Research and Practice, 212(4), 274-278
Open this publication in new window or tab >>Can Nup88 expression be associated with atypical endometrial hyperplasia and endometrial cancer? A preliminary study
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2016 (English)In: Pathology, Research and Practice, ISSN 0344-0338, E-ISSN 1618-0631, Vol. 212, no 4, p. 274-278Article in journal (Refereed) Published
Abstract [en]

Background: Nup88 is overexpressed in a number of types of carcinomas and is associated with myometrial invasion, but its exact expression pattern in endometrial cancer and premalignant lesions is unknown. Aims: To evaluate the role of Nup88 in endometrial cancers and atypical endometrial hyperplasia and its clinicopathological significance. Methods: Nup88 expression was examined by immunohistochemistry in samples from 104 endometrial cancers, 21 atypical endometrial hyperplasia lesions, and 40 normal endometria. All samples were from patients who underwent surgery at the First Hospital of Hebei Medical University (Shijiazhuang, China) between April 2006 and December 2009. Nup88 expression was compared between the groups and associations were assessed between Nup88 and clinicopathological characteristics of the subjects. Results: Nup88 expression in cancer (76% of samples) and atypical hyperplasia (91%) was significantly higher compared to normal endometrium (33%, both P < 0.001), but there was no significant difference between endometrial cancer and atypical hyperplasia (P = 0.237). The expression of Nup88 increased significantly with increasing exposure time to estrogen (P = 0.033). Conclusions: Nup88 may be related to the occurrence of endometrial cancers and premalignant lesions. Nup88 might be a useful biomarker for pre-malignant lesions and early-stage endometrial cancer. (C) 2016 Elsevier GmbH. All rights reserved.

Place, publisher, year, edition, pages
ELSEVIER GMBH, URBAN & FISCHER VERLAG, 2016
Keywords
Nup88; Nuclear pore complexes; Endometrial cancer; Atypical endometrial hyperplasia; Immunohistochemistry; Biomarker
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-128983 (URN)10.1016/j.prp.2016.01.003 (DOI)000375500300006 ()26839161 (PubMedID)
Note

Funding Agencies|Natural Science Foundation General Program of Hebei Province [H2012206040]

Available from: 2016-06-09 Created: 2016-06-07 Last updated: 2017-11-30
Gnosa, S., Ticha, I., Haapaniemi, S. & Sun, X.-F. (2016). MTDH genetic variants in colorectal cancer patients. Scientific Reports, 6
Open this publication in new window or tab >>MTDH genetic variants in colorectal cancer patients
2016 (English)In: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 6Article in journal (Refereed) Published
Abstract [en]

Colorectal cancer (CRC) is the second most common cancer worldwide and accounts for around 8.5% of all cancer related death. The colorectal carcinogenesis is a complex process of genetic alterations. For better prognosis it is very important to understand the composition of genetic alterations in a tumor. Astrocyte elevated gene-1 (AEG-1) has been shown to be overexpressed in CRC and had prognostic significance. The aim of this study was to determine the frequency and the spectrum of MTDH variants, and their relationship to clinicopathological variables in CRC patients. The study included tumors from 356 unselected CRC patients. Mutation analysis of the MTDH gene, including coding region and adjacent intronic sequences, was performed by direct DNA sequencing. We detected 42 intronic variants, whereby 25 were novel. Furthermore, we found eight exonic variants of which four, one missense (c.977C>G) and three frameshift mutations (c.533delA, c.1731delA, c.1340dupA), were novel. In silico prediction analyses revealed that four variants c.232G>T, c.533delA, c.1340dupA and c.1731delA were deleterious. There were no correlations between the MTDH variants and tumor stage, differentiation or patient survival. The detection of pathogenic mutations and alterations in functional protein domains suggest their involvement in tumorigenesis, although none of the variants had prognostic potential.

Place, publisher, year, edition, pages
Nature Publishing Group, 2016
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:liu:diva-121865 (URN)10.1038/srep23163 (DOI)000372164500001 ()
Note

Funding agencies:  Swedish Cancer Foundation; Swedish Research Council, and the Health Research Council in South-East Sweden; Ministry of Health, Czech Republic [RVO 64165]

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Available from: 2015-10-12 Created: 2015-10-12 Last updated: 2017-12-01Bibliographically approved
Liu, Y., Zhou, D., Long, F.-W., Chen, K.-L., Yang, H.-W., Lv, Z.-Y., . . . Zhou, Z.-G. (2016). Resolvin D1 protects against inflammation in experimental acute pancreatitis and associated lung injury. American Journal of Physiology - Gastrointestinal and Liver Physiology, 310(5), G303-G309
Open this publication in new window or tab >>Resolvin D1 protects against inflammation in experimental acute pancreatitis and associated lung injury
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2016 (English)In: American Journal of Physiology - Gastrointestinal and Liver Physiology, ISSN 0193-1857, E-ISSN 1522-1547, Vol. 310, no 5, p. G303-G309Article in journal (Refereed) Published
Abstract [en]

Acute pancreatitis is an inflammatory condition that may lead to multisystemic organ failure with considerable mortality. Recently, resolvin D1 (RvD1) as an endogenous anti-inflammatory lipid mediator has been confirmed to protect against many inflammatory diseases. This study was designed to investigate the effects of RvD1 in acute pancreatitis and associated lung injury. Acute pancreatitis varying from mild to severe was induced by cerulein or cerulein combined with LPS, respectively. Mice were pretreated with RvD1 at a dose of 300 ng/mouse 30 min before the first injection of cerulein. Severity of AP was assessed by biochemical markers and histology. Serum cytokines and myeloperoxidase (MPO) levels in pancreas and lung were determined for assessing the extent of inflammatory response. NF-kappa B activation was determined by Western blotting. The injection of cerulein or cerulein combined with LPS resulted in local injury in the pancreas and corresponding systemic inflammatory changes with pronounced severity in the cerulein and LPS group. Pretreated RvD1 significantly reduced the degree of amylase, lipase, TNF-alpha, and IL-6 serum levels; the MPO activities in the pancreas and the lungs; the pancreatic NF-kappa B activation; and the severity of pancreatic injury and associated lung injury, especially in the severe acute pancreatitis model. These results suggest that RvD1 is capable of improving injury of pancreas and lung and exerting anti-inflammatory effects through the inhibition of NF-kappa B activation in experimental acute pancreatitis, with more notable protective effect in severe acute pancreatitis. These findings indicate that RvD1 may constitute a novel therapeutic strategy in the management of severe acute pancreatitis.

Place, publisher, year, edition, pages
AMER PHYSIOLOGICAL SOC, 2016
Keywords
acute pancreatitis; resolvin D1; inflammation; nuclear factor-kappa B; lung injury
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-126827 (URN)10.1152/ajpgi.00355.2014 (DOI)000371303400002 ()26702138 (PubMedID)
Note

Funding Agencies|National Natural Science Fund of China (NSFC key project) [30830100, 81170439, 81470886, 81500486]; Scientific Research Foundation for the Returned Overseas Chinese Scholars, State Education Ministry [20101174-4-2]

Available from: 2016-04-07 Created: 2016-04-05 Last updated: 2017-11-30
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