Life sciences

Publisher: Elsevier

Current impact factor: 2.70

Impact Factor Rankings

2016 Impact Factor Available summer 2017
2014 / 2015 Impact Factor 2.702
2013 Impact Factor 2.296
2012 Impact Factor 2.555
2011 Impact Factor 2.527
2010 Impact Factor 2.451
2009 Impact Factor 2.56
2008 Impact Factor 2.583
2007 Impact Factor 2.257
2006 Impact Factor 2.389
2005 Impact Factor 2.512
2004 Impact Factor 2.158
2003 Impact Factor 1.944
2002 Impact Factor 1.824
2001 Impact Factor 1.758
2000 Impact Factor 1.808
1999 Impact Factor 1.774
1998 Impact Factor 1.937
1997 Impact Factor 2.275
1996 Impact Factor 2.352
1995 Impact Factor 2.345
1994 Impact Factor 2.5
1993 Impact Factor 2.381
1992 Impact Factor 2.053

Impact factor over time

Impact factor
Year

Additional details

5-year impact 2.67
Cited half-life >10.0
Immediacy index 0.69
Eigenfactor 0.02
Article influence 0.69
ISSN 1879-0631

Publisher details

Elsevier

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    • Author's post-print must be released with a Creative Commons Attribution Non-Commercial No Derivatives License
    • Publisher last reviewed on 03/06/2015
  • Classification
    green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Aims: The aim of the present study was to investigate the effects and underlying mechanisms of endotoxin (lipopolysaccharide, LPS) on postoperative pain using a rat model of incisional pain. Main methods: Animals were assigned to one of four groups using a 2×2 experimental design: a single intraperitoneal injection of 5mg/kg LPS versus vehicle, by plantar incision versus anesthesia alone. Spontaneous pain and mechanical paw withdrawal threshold (PWT) were evaluated using Rat Grimace Scale (RGS) and von Frey fibers, respectively. Analgesic effects of ketoprofen, morphine, and wound infiltration with ropivacaine, as well as the contribution of the Toll-like receptor (TLR) 4 pathway, were also evaluated. In vivo single fiber recordings were performed to assess the nociceptive afferent signals from the surgical site. Key findings: Systemic administration of LPS significantly increased the pain intensity at 2h after hind paw incision, but did not affect the PWT. The duration of post-incisional pain assessed by both scales did not significantly differ in the presence or absence of LPS. The analgesic efficiency of ketoprofen and morphine was reduced by LPS, while that of wound infiltration with ropivacaine was preserved. On the other hand, in vivo single fiber recording failed to demonstrate any significant effects of LPS on the activity of primary afferents due to mechanical stimuli. Pre-treatment with intrathecal LPS from Rhodobacter sphaeroides, a TLR-4 antagonist, almost completely inhibited LPS-induced exacerbated post-incisional pain, and decreased analgesic responsiveness. Significance: The present results suggested that LPS exacerbates post-incisional pain via the central TLR-4 pathway.
    No preview · Article · Feb 2016 · Life sciences
  • [Show abstract] [Hide abstract]
    ABSTRACT: Aims: Pulmonary fibrosis is a type of chronic lung disease and has characteristics that progress quickly, has a high fatality rate and a poor therapeutic effect. Our previous research showed that interleukin-27(IL-27) potentially attenuates BLM-induced pulmonary fibrosis, but the function of IL-27 in lung fibroblasts (LFs) differentiation pulmonary fibrosis is yet to be known. Main methods: Here we investigated the effect of IL-27 on the proliferation, differentiation and collagen synthesis of lung fibroblasts induced by transforming growth factor-β1 (TGF-β1)using MTT, bromodeoxyuridine(BrdU) staining, real-time quantitative PCR(qPCR), Western blot, cell cycle FACS assay and immunofluorescence. We also examined the expression of the JAK/STAT and TGF-β1/Smad signaling pathway of IL-27 in lung fibroblasts. Key findings: TGF-β1 treated lung fibroblasts showed significantly increased proliferation, differentiation and collagen synthesis as well as overactivated JAK/STAT and TGF-β1/Smad signaling. However, the presence of IL-27 weakened these effects and obviously inactivated the JAK/STAT and TGF-β1/Smad signaling pathways. Significance: Our results indicate that IL-27 may play an anti-fibrotic role in the development, differentiation and collagen synthesis in lung fibroblasts. These data also may provide a target gene therapy method in treating pulmonary fibrosis.
    No preview · Article · Feb 2016 · Life sciences
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    ABSTRACT: Aims: Hemangiosarcoma (HSA) that originates from vascular endothelial cells is the most common splenic malignant neoplasm in dogs, as it accounts for approximately 20% of all canine soft tissue sarcomas. In this study, inhibitory effects of endothelin receptor antagonists on the growth of HSA cells were examined using cell lines established from canine HSA. Main methods: The preproendothelin-1 (PPET-1), endothelin type A receptor (ETA) and endothelin type B receptor (ETB) mRNA expression levels in HSA cell lines (n=5) were analyzed quantitatively by real-time RT-PCR. These levels were compared with those in HSA tissues (n=11) and those in normal splenic tissues (n=6). ETA and ETB protein expression was examined by western blot. The production and secretion of endothelin-1 (ET-1) and big ET-1 by cell lines were analyzed by measuring the levels in the culture medium by ELISA. The inhibitory effects of endothelin receptor antagonists (ambrisentan, BQ788 and bosentan) on cell growth were evaluated by WST-8 assay. Key findings: The PPET1 and ETA mRNA expression levels were elevated in HSA tissues and HSA cell lines compared with normal tissues. In cell lines, the production of ET-1 and big ET-1 peptide as well as the expression of ETA protein were detected, but the levels of ETB were not measured. Ambrisentan and bosentan inhibited growth activity in cell lines. Ambrisentan was more effective than bosentan. Significance: These findings demonstrate the importance of the ETA axis in canine HSA as well as the potential of ETA inhibitors in the treatment of canine HSA.
    No preview · Article · Feb 2016 · Life sciences
  • [Show abstract] [Hide abstract]
    ABSTRACT: Aims: Intracellular calcium (Ca(2+)) is known to play an important role in cancer development and growth. Resveratrol (Res) is a stilbene polyphenol occurring in several plant species and known for various possible beneficial effects, including its ability to inhibit proliferation and to induce apoptosis in cancer cells. This study was designed to determine whether Res affects Ca(2+) signaling in cancer cells. Main methods: We used the REN human mesothelioma cell line, as an in vitro cancer cell model, and the non-malignant human mesothelial MeT5A cell line, as normal cell model. Cytosolic Ca(2+) concentration was measured by the fluorescent indicator Fura-2. Immunofluorescence, Western blot, and siRNA technique were employed to assess the involvement of T-type Ca(2+) channels. Cell viability was determined by the calcein assay. Key findings: REN cells transiently exposed to 1-10μM Res showed increasing peaks of Ca(2+) that were absent in Ca(2+)-free medium and were reduced by non-selective (Ni(2+)), and highly selective (NNC 55-0396) T-type Ca(2+) channels antagonist, and by siRNA knockout of Cav3.2T-type Ca(2+) channel gene. Dose-dependent curve of Res-induced Ca(2+) peaks showed a rightward shift in normal MeT-5A mesothelial cells (EC50=4.9μM) with respect to REN cells (EC50=2.7μM). Moreover, incubation with 3 and 10μM Res for 7days resulted in cell growth inhibition for REN, but not for MeT-5A cells. Significance: Res induces Ca(2+) influx, possibly mediated through T-type Ca(2+) channels, with significant selectivity towards mesothelioma cells, suggesting a possible use as an adjuvant to chemotherapy drugs for mesothelioma clinical treatment.
    No preview · Article · Feb 2016 · Life sciences
  • [Show abstract] [Hide abstract]
    ABSTRACT: Aims: Garlic oil (GO) is used for centuries in folk medicine as a therapy for many diseases including inflammatory disorders. Recently, it has exhibited potent anti-oxidant, anti-inflammatory and immunomodulatory effects. Consequently, we evaluated the possible protective effect of GO in a rat model of colitis, induced by dextran sulfate sodium (DSS). Main methods: Colitis induced by allowing rats a free access to drinking water containing 5% DSS for 7days, from day 1 to day 7. GO was administered orally in doses of 25, 50 and 100mg/kg/day. Mesalazine used as a standard medication in a dose of 15mg/kg/day. All animals fasted for 2h, 1h before and 1h after giving the treatment, which introduced daily for 7days, from day 1 to day 7, at 10:00 to 11:00A.M. Animal body, and colonic weights, colonic myeloperoxidase (MPO), and superoxide dismutase (SOD) activities, colonic reduced-glutathione (GSH), malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-10 levels, macroscopic and microscopic changes of colonic tissues were evaluated. Key findings: GO treatment significantly suppressed the elevated colonic weight, MPO activity, MDA, TNF-α and IL-1β levels. However, it potentiated the decrease body weight, colonic SOD activity, GSH and IL-10 levels. Moreover, it ameliorated the marked macroscopic and microscopic changes of colonic mucosa in a dose dependent manner. Significance: Garlic oil inhibits DSS-induced colitis in rats may be through its anti-oxidant, anti-inflammatory and immunomodulatory properties. Therefore, GO could be a promising protective agent recommended for UC patients.
    No preview · Article · Feb 2016 · Life sciences
  • [Show abstract] [Hide abstract]
    ABSTRACT: Aim: Diabetes mellitus associated cardiovascular complications are a leading cause of morbidity and mortality worldwide. Methylglyoxal (MG) is a reactive ketoaldehyde and a byproduct of glucose metabolism and an inducer of advanced glycation endproducts (AGEs). Alagebrium (ALA) is an AGEs crosslink breaker, however, the effects of ALA on MG levels and its consequences in cultured rat cardiomyocytes are not known. The aim of the present study was to examine the effect of high glucose and MG on cultured rat cardiomyocytes and to investigate whether ALA could prevent any deleterious effects of high glucose and MG in these cells. Main methods: MG levels were determined by HPLC. The expression of different genes was measured by RT-PCR. Oxidative stress and AGEs formation was determined by DCF probe and immunocytochemistry respectively. Key findings: High glucose- and MG treated- cardiomyocytes developed a significant increase in MG, and the expression for caspase-3, Bax, RAGE and NF-KB, which were all attenuated after pretreatment with ALA. A significant increase in reactive oxygen species generation and AGEs formation in high glucose- and MG treated- cultured cardiomyocytes was also observed, which was attenuated after pretreatment with ALA. Significance: ALA may have a preventive role against the deleterious effects of high glucose and MG in the heart. Prevention of dicarbonyl-induced AGEs, by safer and specific scavengers of MG is an attractive therapeutic option.
    No preview · Article · Feb 2016 · Life sciences
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    ABSTRACT: Aims: We investigated the effect of the selective sodium-dependent glucose cotransporter 2 inhibitor ipragliflozin on the simultaneous progression of diabetic microvascular complications of retinopathy, nephropathy and neuropathy in individual Spontaneously Diabetic Torii (SDT) fatty rats. Main methods: Ipragliflozin was administered to male SDT fatty rats for 12weeks. Male Sprague-Dawley rats of the same age were used as non-diabetic controls. Non-fasting plasma glucose and glycated hemoglobin levels were measured every 4weeks. Cataract formation was monitored once a week, and the electroretinogram was measured after 6weeks of treatment. After the treatment period, motor nerve conduction velocity was measured and urinalysis was conducted. Tissue samples were then dissected for histopathological examination. Key findings: Treatment with ipragliflozin reduced glycated hemoglobin levels, inhibited the progression of cataract formation, prevented the prolongation of oscillatory potential peaks in the electroretinogram, ameliorated the slowing of motor nerve conduction velocity, and reduced the severity of glomerulosclerosis in SDT fatty rats. Significance: These results suggest that the control of hyperglycemia with ipragliflozin slows the progression of the diabetic complications of retinopathy, nephropathy, and neuropathy.
    No preview · Article · Jan 2016 · Life sciences
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    ABSTRACT: Aims: RB1CC1/FIP200 was essential for autophagosome formation. Therefore, RB1CC1/FIP200 cellular levels are critical for the activation of the autophagy pathways. Following the screen of miRNAs affecting RB1CC1/FIP200 level and rapamycin-induced autophagy, we discovered miR-20a and miR-20b could regulate autophagy by targeting RB1CC1/FIP200. Main methods: Inhibitory effect of miR-20a and 20b on basal and rapamycin-stimulated autophagy was demonstrated using various autophagic tests including GFP-LC3 puncta analysis, LC3II/LC3I gel shift and TEM observation. Key findings: We discovered RB1CC1/FIP200 as cellular targets of miR-20a and miR-20b. Upon miR-20a and miR-20b overexpression, both mRNA and protein levels of RB1CC1/FIP200 decreased. miR-20a and miR-20b target sequences present in the 3' UTR of RB1CC1/FIP200 mRNAs and introduction of mutations abolished the miR-20a and miR-20b responsiveness. In MCF7 and MDA-MB-231 breast cancer cells, miR-20a and miR-20b over-expression attenuated basal and rapamycin-induced autophagy; while suppression of miR-20a or miR-20b by specific antagomir showed normal rapamycin-induced autophagic activity. Significance: To our knowledge, this is the first study showing the significance of miR-20a and miR-20b regulating autophagy by targeting RB1CC1/FIP200.
    No preview · Article · Jan 2016 · Life sciences
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    ABSTRACT: Aims: Activation of hypoxia inducible factor-1 (HIF) is a hallmark in hypoxia-induced pulmonary hypertension (HPH). microRNAs play a significant role in regulating proliferation of pulmonary arterial smooth muscle cells (PASMCs) in pulmonary hypertension. Previous studies have shown that HIF-1β is a target of miR-103/107. In this present study, we aimed to investigate whether miR-103/107 regulate vascular remodeling in HPH via HIF-1β. Main methods: The HPH model was built by hypoxia exposure in rats. Real-time PCR and western blotting were used to determine the expression of miR-103/107 and HIF-1β. Proliferation of PASMCs was examined by 5-bromo-2´-deoxyuridine (BrdU) incorporation method. The functions of miR-103/107 on PASMCs proliferation, HIF-1α and HIF-1β expression were assessed by transfecting miR-103/107 mimics and inhibitors. Key findings: Significant down-regulation of miR-103/107 was observed in remodeled intrapulmonary vascular in HPH rats and hypoxia exposured PASMCs, whereas HIF-1α and HIF-1β expression were up-regulated. Hypoxia exposure induced significant proliferation of PASMCs, overexpression of miR-103/107 inhibited but miR-103/107 inhibitors exacerbated PASMCs proliferation. Gain-of-function and loss-of-function experiments showed that miR-103/107 expression was inversely correlated with HIF-1β level. No significant changes of HIF-1α expression were observed under miR-103/107 mimic treatment. Significance: Loss of suppression on HIF-1β by miR-103/107 may contribute to excess proliferation of PASMCs and vascular remodeling in hypoxic pulmonary hypertension.
    No preview · Article · Jan 2016 · Life sciences
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    ABSTRACT: Aims: Despite impressive survival benefits from new agents to treat metastasized prostate cancer (PCa), progressive drug resistance hinders long-term response and restricts the efficacy of subsequent therapy. Due to reported antitumor activity of amygdalin and growing popularity for complementary and alternative medicine the potential of this natural, widely used substance to exert antineoplastic effects on prostate cancer cells has been assessed. Main methods: LNCaP (castration-sensitive), DU-145 and PC3 cells (castration-resistant) were exposed to different concentrations of amygdalin for 24h or 2weeks. Cell growth was measured by the MTT test, clonal formation by the clonogenic assay. Flow cytometry served to investigate apoptosis and cell cycle phases. Cell cycle regulating proteins and the mTOR-akt signaling axis were analyzed by western blotting. Key findings: Amygdalin dose-dependently diminished tumor cell growth with maximum effects at 10mg/ml. Apoptosis of PC3 and LNCaP but not of DU-145 cells was reduced, whereas colony formation was suppressed in all cell lines. A decrease in the number of G2/M- and S-phase cells along with an elevated number of G0/G1-phase cells was recorded. The cell cycle proteins cdk 1, cdk 2 and cdk 4 as well as cyclin A, cyclin B and cyclin D3 were modulated by amygdalin after both 24h and 2weeks. Distinct effects on p19 and p27 expression and on Akt, Rictor and Raptor activation became evident only after 2weeks. Significance: Amygdalin exhibits significant antitumor activity in both castration-sensitive and castration-resistant PCa cell lines and merits further evaluation for therapeutic purposes.
    No preview · Article · Jan 2016 · Life sciences
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    ABSTRACT: Aims: The purpose of this study was to assay the role of beta-adrenergic receptor signaling in the regulation of obesity-induced p53 in high fat feeding obese rats. Main methods: The role of beta-adrenergic receptor/cyclic AMP in the regulation of p53 and its downstream mediators was evaluated by western blot and real-time quantitative RT-PCR among diet induced rats. Key findings: Beta-adrenergic receptor agonist, isoproterenol, and an adenylate cyclase activator, forskolin, at a single dose significantly reduced insulin resistance consistent with a decrease in total and phospho-p53 levels in insulin and non-insulin metabolic target tissues. The decrease of p53 signaling was consistent with the elevation of AKT and subsequent activation. Obese rats exposed to fasting also exhibited improvement in insulin action despite a slight effect on p53 level. Significance: Results of the present study obviously showed that beta-adrenergic receptor agonist/cAMP prevented obesity-induced p53 activation. Although this effect in metabolic insulin target tissues tempted us to consider them as insulin sensitizers in obesity-related diabetes, p53 inhibition in non-insulin target tissues warned about the impairment of anti-cancer mechanisms in obese subjects.
    No preview · Article · Jan 2016 · Life sciences
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    ABSTRACT: Aims: Sweetme Sweet Pumpkin™ (SSP, baked Cucurbita moschata Duch.) has been used to treat patients with depression in Korea. However, the role of SSP in improving depression has not been elucidated yet. Thus, we assessed the antidepressant-like effect of SSP and its active compound, β-carotene, with the forced swimming test (FST). Main methods: SSP and β-carotene were orally administered once a day for 28days. The levels of brain-derived neurotrophic factor (BDNF), phosphorylated extracellular signal-regulated kinase (pERK), and estrogen receptor-beta (ER-β) were analyzed by Western blotting and quantitative real-time-polymerase chain reaction. Key findings: After 28days, treatment with SSP and β-carotene significantly decreased the immobility time during the FST. SSP significantly increased the levels of serotonin and norepinephrine in the brain. The levels of BDNF, pERK, and ER-β were significantly increased in the SSP- and β-carotene-administered groups compared with the control group. In addition, the groups treated with SSP and β-carotene showed significantly reduced levels of tumor necrosis factor-alpha and interleukin-6 compared with the control group. Significance: In conclusion, these findings suggest the potential of SSP and β-carotene as a novel therapeutic agent for the treatment of depression.
    No preview · Article · Jan 2016 · Life sciences
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    ABSTRACT: Aims: Liver cirrhosis is the common pathological histology manifest among a number of chronic liver diseases and liver cancer. Circulating levels of insulin growth factor-1 (IGF-1) have been recently linked to liver cirrhosis and the development of liver cancer. Herein, we hypothesized that IGF-1R overexpression combining the activation of GSK-3β and FOXO3a were involved in the development of human and murine chronic liver cirrhosis. Methods: Liver samples of patients were screened from the Tissue Bank of the China-Japan Union Hospital of Jilin University. Mice liver fibrosis model was performed using intraperitoneal injection of carbon tetrachloride (CCl4) for 12weeks. Serum IGF-1 levels were detected by enzyme-linked immunosorbent assays (ELISA). Microscopical examination of liver parenchyma was performed using conventional H&E and Masson's staining. Moreover, we investigated the IGF-1 receptor (IGF-1R) signaling pathway at different period after CCl4 administration. Results: Serum IGF-1 levels were significantly decreased in patients with liver cirrhosis, which is concomitant with the declined circulating levels of IGF-1 in 8 to 12weeks CCl4-treated mice. Furthermore, the expression of IGF-1R was significantly higher at 12w compared with control group. In addition, activation of the GSK-3β and FOXO3a were activated during the process of murine chronic liver injury. Conclusion: The present study demonstrates that decreased circulating IGF-1 levels are involved in human and murine chronic liver disease. Interestingly, overexpression of the IGF-1R, and activation of GSK3β and FOXO3a might be the molecular mechanisms underlying the development of liver cirrhosis.
    No preview · Article · Jan 2016 · Life sciences
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    ABSTRACT: Aims: One of the most popular beverages worldwide, green tea, was investigated for its potential protective effect in a rat model of gentamicin-induced nephrotoxicity by monitoring functional and morphological changes in kidneys. Main methods: The study was conducted on four groups of rats: control group (C), treated with only gentamicin (GM), treated with only green tea (GT) and treated with both gentamicin and green tea (GT+GM). Kidney function, oxidant and antioxidant parameters of renal tissue, as well as histopathological studies were assessed. Morphometric analysis was used to quantify these histopathological changes. Key findings: Gentamicin caused significant elevations in serum creatinine and urea and oxidative stress parameter (AOPP), while antioxidative enzyme catalase was significantly decreased. Histological sections of kidneys in GM group revealed necrosis of proximal tubules, vacuolation of cytoplasm and massive mononuclear inflammatory infiltrates in interstitium. Coadministration of green tea with gentamicin histologically showed renoprotective effect. Histological results were confirmed and quantified by morphometric analysis. Also in this group we measured ameliorated parameters of renal functions and antioxidative defense. Significance: Regenerative potential of green tea after renal injury induced by gentamicin could be explained through the decrease of oxidative stress and lipid peroxidation. Green tea is a natural antioxidant, with many health promoting effects, widely available and in accordance to that affordable. Because of the established habits, people largely consume it as a beverage. It could be beneficial in the reduction of oxidative stress and changes caused by it primarily in renal tubules and interstitium.
    No preview · Article · Jan 2016 · Life sciences
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    ABSTRACT: Aims: Methylmercury (MeHg) exposure results in increased risk of hypertension and cardiovascular diseases. In this study, we aimed to investigate whether the in vivo exposure of MeHg in mice affects blood pressure and basilar arterial responses to angiotensin II (Ang II) and acetylcholine (ACh), which are important modulators of cerebrovascular autoregulation. Main methods: Mice were exposed to MeHg (40ppm) in drinking water for 21days. Blood pressure was measured in conscious mice by an indirect tail-cuff method. Functional studies of the isolated arteries' response to vasoactive substances were performed using a micro-organ-bath system. Key findings: Systolic and mean blood pressures were significantly increased after 2 and 3weeks of treatment with MeHg, respectively. Ang II-induced contraction in an isolated basilar artery, which is mediated via Rho-kinase activation, was increased in MeHg-treated mice. ACh-induced relaxation, which is dependent on NO production from the endothelial cells, was decreased in MeHg-treated mice. However, alterations of vascular responses to Ang II and ACh were not observed in the isolated thoracic aorta. Significance: This study demonstrated that the cerebral vasculature appears to be particularly sensitive to in vivo exposure of MeHg. Our results suggest that in vivo MeHg increases blood pressure and causes alterations in the cerebrovascular reactivity in response to Ang II and ACh through enhancement of Rho-kinase activity and inhibition of NO bioavailability, respectively.
    No preview · Article · Jan 2016 · Life sciences
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    ABSTRACT: Aims: Anaphylactic shock sometimes accompanies pulmonary vaso- and broncho-constriction. We previously reported the hemodynamic features of mouse anaphylaxis (Life Sci. 2014; 116: 98-105). However, the effects of anaphylactic chemical mediators on the hemodynamics of in vivo mice are not well known. Furthermore, it is uncertain whether the mediators exert the same directional actions. Therefore, we determined their effects systematically on total peripheral resistance (TPR), pulmonary vascular resistance (PVR), or airway pressure (AWP) in anesthetized mice. Main methods: We measured directly pulmonary arterial pressure, left atrial pressure, systemic arterial pressure, central venous pressure and aortic blood flow to determine PVR and TPR, as well as AWP, following injections of platelet-activating factor (PAF), histamine, serotonin, leukotriene (LT) C4, and prostaglandin (PG) D2 in anesthetized open-chest artificially ventilated BALB/c mice. Key findings: Consecutive administration of any agents increased PVR dose-dependently with the maximal responsiveness being PAF>LTC4>serotonin>histamine=PGD2. Histamine caused a biphasic PVR response, an initial decrease, which was abolished by L-NAME, followed by an increase at high doses. PAF, serotonin, and histamine decreased TPR dose-dependently, while LTC4 or PGD2 yielded an increase or no change in TPR, respectively. Serotonin, but not the other agents, increased AWP. Significance: Anaphylactic mediators exert non-uniform actions on the pulmonary and systemic circulation and airway in anesthetized BALB/c mice: PAF, LTC4 and serotonin cause substantial pulmonary vasoconstriction, while histamine biphasic responses of the initial nitric oxide dependent vasodilation followed by vasoconstriction; PAF, serotonin, and histamine, but not LTC4 or PGD2, evoke systemic vasodilatation; only serotonin induces airway constriction.
    No preview · Article · Jan 2016 · Life sciences
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    ABSTRACT: Aldehyde dehydrogenase 2 (ALDH2), an important mitochondrial enzyme governing ethanol metabolism, displays polymorphism in human. Recent evidence suggested that genetic polymorphism in ALDH2 gene may be significantly correlated with the susceptibility to cancer, such as colorectal cancer, esophageal cancer, and liver cancer. To investigate the correlation between ALDH2 mutant gene and the risk of a certain cancer, many studies have been done by testing the ALDH2 genotype in patients with cancers. Here, we summarized 84 ALDH2 gene single nucleotide polymorphism (SNP) sites in human cancer, which focus primarily on the rs671 SNP site. As a novel biological marker, ALDH2 displays a very attractive prospect in the screening, diagnosis and evaluation of the prognosis of many diseases. Moreover, much attention has been attracted to the studies of the biological functions and potential value of ALDH2 in the human cancer treatment. This review will provide an overview about the clinical prospects of ALDH2 based on the available information.
    No preview · Article · Jan 2016 · Life sciences