Fenling Fan
Xi'an Jiaotong University
Network
Latest external collaboration on country level. Dive into details by clicking on the dots.
Publication
Featured researches published by Fenling Fan.
International Journal of Gynecology & Obstetrics | 2009
Fenling Fan; Yuliang Zou; Aiqun Ma; Yafei Yue; Wenjun Mao; Xiancang Ma
To investigate links between psychologic distress and levels of maternal hormones and cortisol during pregnancy and post partum.
Journal of Inflammation | 2014
Fenling Fan; Abby Galvin; Lu Fang; David A. White; Xiao-Lei Moore; Miles Sparrow; F. Cicuttini; Anthony M. Dart
BackgroundInflammation plays an important role in the pathogenesis of atherosclerosis. The link between rheumatoid arthritis (RA) and an increased risk of cardiovascular disease and mortality is well established; however, the association between inflammatory bowel disease (IBD) and cardiovascular risk is controversial. Arterial stiffness is both a marker and risk factor for atherosclerosis. Here we aimed to 1) compare circulating markers of inflammation and endothelial dysfunction, traditional cardiovascular risk factors, and arterial stiffness between RA and IBD to help to understand their different associations with cardiovascular disease; 2) assess the impacts of circulating markers of inflammation and endothelial dysfunction, and traditional risk factors on arterial stiffness.MethodsPatients with RA (n = 43) and IBD (n = 42), and control subjects (n = 73) were recruited. Plasma inflammatory markers and von Willebrand factor (vWF) were measured by Multiplex assays or ELISA. Arterial stiffness was determined by brachial-ankle pulse wave velocity (baPWV) and ankle-brachial index (ABI) was measured. Framingham Risk Score (FRS) was calculated, and other traditional risk factors were also documented.ResultsPlasma levels of several inflammatory markers and vWF were significantly but comparably elevated in RA and IBD compared with controls, except for a higher level of C-reactive protein (CRP) in RA than IBD. Compared to controls, FRS, body mass index, waist circumference, and triglycerides were increased in RA, but not in IBD. baPWV did not significantly differ among 3 groups, while ABI was modestly but significantly lower in IBD than controls. Circulating markers (macrophage migration inhibitory factor, tumour necrosis factor-α, CRP, and vWF) were significantly associated with baPWV. However, traditional risk factors (age, systolic blood pressure, body mass index, diabetes and triglycerides) were the parameters associated with baPWV in multiple regression analyses (overall r = 0.866, p < 0.001).ConclusionsRA has a higher level of CRP and more pronounced traditional cardiovascular risk factors than IBD, which may contribute to the difference in their associations with cardiovascular disease and mortality. Traditional risk factors, rather than inflammation markers, are major predictors of arterial stiffness even in subjects with inflammatory disorders. Our results point to the importance of modifying traditional risk factors in patients with inflammatory disorders.
Inflammatory Bowel Diseases | 2015
Fenling Fan; Piyushkumar A. Mundra; Lu Fang; Abby Galvin; Xiao Lei Moore; Jacquelyn M. Weir; Gerard Wong; David A. White; Jaye Chin-Dusting; Miles Sparrow; Peter J. Meikle; Anthony M. Dart
Background:Inflammatory bowel disease (IBD), which encompasses ulcerative colitis (UC) and Crohns disease (CD), is believed to be caused by abnormal host immune responses to the intestinal microbiome. However, the precise etiology of IBD remains unknown. Lipid metabolism and signaling are suggested to play important roles in inflammation with significant implications for IBD. In this study, we aimed to characterize lipidomic profiles in IBD with comparison between healthy controls, UC, and CD. Methods:Patients with IBD (n = 40, UC: 16 and CD: 24) and age- and gender-matched healthy volunteers (n = 84) were recruited. Plasma lipid profiles containing 333 lipid species were measured using electrospray ionization–tandem mass spectrometry. Results:A total of 86 individual lipid species were significantly changed in CD compared with controls (78 decreased while 8 increased), with the majority belonging to the ether lipids including the alkylphospholipids (alkylphosphatidylcholine and alkylphosphatidylethanolamine) and plasmalogens (alkenylphosphatidylcholine and alkenylphosphatidylethanolamine). Of these 86 lipid species, 33 remained significantly and negatively associated with CD after adjusting for age, sex, waist circumference, current smoking, and diastolic blood pressure in logistic regression. In contrast, only 5 lipid species significantly differed between UC and controls. Conclusions:We demonstrate that a number of ether lipids (alkylphospholipid and plasmalogens) are significantly and negatively associated with CD. These alterations of lipid profiles particularly plasmalogens may contribute to the pathogenesis of IBD.
Journal of the American Heart Association | 2016
Fenling Fan; Lu Fang; Xiao-Lei Moore; Xuegang Xie; Xiao-Jun Du; David A. White; Jessica O'Brien; Helen Thomson; Jun Wang; Hans G. Schneider; Andris H. Ellims; Thomas W. Barber; Anthony M. Dart
Background Macrophage migration inhibitory factor (MIF) is a key regulator of inflammatory responses, including in the heart. Plasma MIF is elevated early in the course of acute myocardial infarction. In this study, we hypothesized that plasma MIF may also be increased in acute myocardial ischemia. Methods and Results Patients undergoing cardiac stress test (stress nuclear myocardial perfusion scan or stress echocardiography) were recruited. Twenty‐two patients had a stress test indicative of myocardial ischemia and were compared with 62 patients who had a negative stress test. Plasma MIF was measured by ELISA before and after the stress test. MIF was also measured in patients with peripheral arterial occlusive disease before and after exercise causing claudication. Gene and protein expression of MIF was measured in mouse cardiac and skeletal muscle tissue by real‐time polymerase chain reaction and western blot, respectively. Plasma MIF was elevated at 5 and 15 minutes after stress (relative to before stress) in patients with a positive test, compared with those with a negative test. In contrast, high‐sensitivity troponin T and C‐reactive protein were not altered after stress in either group. MIF was not altered after exercise in PAOD patients, despite the occurrence of claudication, suggesting that plasma MIF is not a marker for skeletal muscle ischemia. This may be explained by a lower gene and protein expression of MIF in skeletal muscle than the heart. Conclusions Our results suggest that plasma MIF is an early marker for acute myocardial ischemia.
Clinical and Experimental Pharmacology and Physiology | 2012
Fenling Fan; Anthony M. Dart
Berberine (natural yellow 18; 5,6-dihydro-9,10-dimethoxybenzo (g)-1,3-benzodioxolo (5,6-a) quinolizinium) is an alkaloid present in plants of the Berberidaceae family, including Coptis chinensis (Huanglian), Rhizoma Coptidis, Hydrastis canadensis (goldenseal), Berberis aquifolium (Oregon grape), Berberis vulgaris (barberry), Berberis aristata (tree turmeric), Tinospora cordifolia, Arcangelisia flava and Cortex Phellodendri. It has supposed antimicrobial effects in traditional Chinese medicine and has been used for centuries in China and Korea to treat diarrhoea and gastrointestinal disorders. However, in recent years this natural isoquinoline alkaloid has received considerable attention because of its wide spectrum of biochemical and pharmacological actions raising the possibility of its use in a broader range of diseases. These potential uses include as an anti-oxidant and an antiinflammatory, as an anticancer agent, as an anti-atherosclerotic and even as an anti-Alzheimer’s disease agent. Preliminary preclinical and clinical studies have highlighted the effects of berberine in modulating metabolic antecedents of atherosclerosis, such as hyperlipidaemia and insulin resistance, as well as affecting vascular smooth muscle proliferation. However, not only does berberine have potential indirect cardiovascular protective effects via modulation of lipid metabolism, glucose homeostasis etc., but it also acts directly on the heart and vessels at various levels. The effects of berberine on blood pressure appear to be due to both vasodilatation and inhibition of adrenal hormone release. In cardiac hypertrophy models, berberine decreased plasma noradrenaline and adrenaline levels, as well as adrenaline content in the ventricular tissue, improved cardiac contractility and reduced the size of the left ventricular myocardium. Intravenous berberine administration increased cardiac output and decreased left ventricular end-diastolic pressure and systemic vascular resistance in animals with ischaemic cardiomyopathy. Moreover, berberine has been shown to increase the cardiac content of high-energy phosphates in experimental heart failure and to prevent ventricular fibrillation because of its actions on ion channels. Berberine blocks ATP-sensitive (KATP) and voltagesensitive K (Kv) channels, indicating that it has a Class III antiarrhythmic effect that results in dose-dependent inhibition of the shortening of action potential duration and effective refractory period induced by hypoxia or cromakalim, as shown in different animal models. Preliminary clinical studies have suggested an anti-arrhythmic effect in humans. For example, 24–48 h ambulatory monitoring of 100 patients with ventricular tachyarrhythmia revealed that berberine caused a > 50% reduction in ventricular premature contractions in 62% of patients and a > 90% reduction in 38% of patients. However, these observations are preliminary and require formal evaluation in multicentre, randomized, blinded studies. Of particular relevance to a therapeutic role for berberine is the recognition of the central role played by inflammation in the initiation and progression of many cardiovascular diseases, including metabolic disorder, hypertension and atherosclerosis. Inflammation is involved in all stages of arterial atherosclerosis, from foam cell and plaque formation to rupture and thrombosis, and to subsequent myocardial ischaemia–reperfusion (I/R) injury, as confirmed by many studies including those from our laboratory. Other findings from our laboratory show that platelets play a pivotal role in promoting systemic and cardiac inflammatory responses after myocardial infarction, contributing to regional inflammation, ventricular remodelling and cardiac wall rupture. During the course of acute coronary syndrome (ACS), platelets can release a range of inflammatory mediators through which they mediate leucocyte activation and infiltration into inflamed tissues in part as platelet–leucocyte conjugates. Berberine has a number of properties relevant to the inflammatory cascade. Not only does berberine suppress pro-inflammatory responses by inhibiting mitogen-activated protein kinase signalling and cellular reactive oxygen species via activation of AMP-activated protein kinase and decrease the mRNA expression of pro-inflammatory genes (e.g. tumour necrosis factor-a, interleukin (IL)-1b, IL-6, monocyte chemotactic protein 1, cyclo-oxygenase 2) in macrophages, but it also reduces levels of human peripheral blood inflammatory mediators, such as matrix metalloproteinase-9, intercellular adhesion molecule-1, vascular cell adhesion molecule-1 and C-reactive protein, as reported by Meng et al. in this issue of the Journal. Meng et al. investigated the anti-inflammatory consequences of berberine in ACS patients after percutaneous coronary intervention (PCI). Oral berberine significantly reduced serum levels of the inflammatory factors compared with levels in ACS patients not treated with supplemental berberine. In addition, other studies on berberine have shown antiplatelet and antiproliferative effects. Together, these observations indicate that berberine has multiple actions likely to be of relevance to the natural history of atherosclerotic vascular disease. See original article on page 406
BMC Pregnancy and Childbirth | 2018
Fenling Fan; Yuliang Zou; Yushun Zhang; Xiancang Ma; Junbo Zhang; Cai Liu; Jie Li; Meili Pei; Yu Jiang; Anthony M. Dart
BackgroundTo determine the relationship between maternal anxiety and cortisol values and birth weight at various stages of pregnancy.MethodsTwo hundred sixteen pregnant Chinese women were assessed for anxiety and depression and had measurement of morning fasting serum cortisol. Women were assessed either in the first (71), second (72) or third (73) trimester. Birth weights of all children were recorded.ResultsThere were significant negative correlations between anxiety level and birth weight of − 0.507 (p < 0.01) and − 0.275 (p < 0.05) in trimesters 1and 2. In trimester 3 the negative relation between anxiety and birth weight of −.209 failed to reach significance (p = 0.070). There was no relation between depression and birth weight in any trimester (p > 0.5 for all). Maternal cortisol was significantly inversely related to birth weight in trimester 1 (r = − 0.322) and with borderline significance in trimester 2 (r = − 0.229). Anxiety score and maternal cortisol were significantly correlated in each trimester (r = 0.551, 0.650, 0.537). When both anxiety score and maternal cortisol were simultaneously included in multiple regression analyses only anxiety score remained significant.ConclusionWhilst both maternal anxiety score and maternal cortisol are inversely related to birth weight the associations with anxiety score were more robust perhaps indicating the importance of mechanisms other than, or in addition to, maternal cortisol in mediating the effects of anxiety. The findings indicate the importance of measures to reduce maternal anxiety, particularly of a severe degree, at all stages of pregnancy.Trial registrationThe study was approved by the Ethics Committee of the 1st Affiliated Hospital of Xi’an Jiaotong University.
Clinical Therapeutics | 2017
Fenling Fan; Yuliang Zou; Songlin Zhang; Yushun Zhang; Beidi Lan; Qiang Song; Meili Pei; Lu He; Huili Wu; Yajuan Du; Anthony M. Dart
PURPOSE Peripherally inserted central catheters (PICCs) are frequently used for prolonged drug administration, but their use is commonly complicated by the development of upper extremity deep venous thrombosis (UEDVT) requiring anticoagulation. Here, we compared the efficacy and safety profile of rivaroxaban (20 mg/d) with low molecular weight (LMW) heparin and vitamin K antagonists in the treatment of PICC-associated UEDVT. METHODS Patients (N = 84) with PICC-associated UEDVT were studied. All had UEDVT identified by ultrasound scanning. Further ultrasound images were obtained at 1, 2, and 3 months after the start of treatment. Forty-four patients were treated with rivaroxaban and 40 with initial LMW heparin and vitamin K antagonist with continuation of vitamin K antagonists alone once international normalized ratio was therapeutic FINDINGS: In the rivaroxaban group mean (SD) age was 51 (16) years and 57% were men, whereas in the other group respective values were 50 (16) years and 56%. All patients were receiving treatment for cancer. Resolution of thrombus had occurred in 53.5% at 1 month, 76.1% at 2 months, and 92.6% at 3 months in the rivaroxaban-treated patients. Corresponding values in the LMW heparin/vitamin antagonist-treated patients were 34.2%, 55.5%, and 88.5%, respectively. Differences between groups were significant at 1 month (P < 0.01) and 2 months (P < 0.05). There were no major bleeds in either group, and cumulative bleeding rates by 3 months were 7.3% in the rivaroxaban group and 11.4% in the LMW heparin/vitamin K antagonist group. IMPLICATIONS Rivaroxaban led to faster resolution of PICC-associated UEDVT than LMW/vitamin K antagonists without any increase in bleeding.
Metabolomics | 2016
Lu Fang; Piyushkumar A. Mundra; Fenling Fan; Abby Galvin; Jacquelyn M. Weir; Gerard Wong; Jaye Chin-Dusting; F. Cicuttini; Peter J. Meikle; Anthony M. Dart
Circulation | 2014
Fenling Fan; Yuliang Zou; Hongyan Tian; Yushun Zhang; Junbo Zhang; Xiancang Ma; Ya Liu; Yan Meng; Yafei Yue; Kai Liu; Anthony M. Dart
International Journal of Gynecology & Obstetrics | 2009
Yuliang Zou; Fenling Fan; Aiquin Ma; Yafei Yue; Wenjun Mao; Xiancang Ma