Database : MEDLINE
Search on : acute and lung and injury [Words]
References found : 25009 [refine]
Displaying: 1 .. 10   in format [Detailed]

page 1 of 2501 go to page                         

  1 / 25009 MEDLINE  
              next record last record
select
to print
Photocopy
Full text

[PMID]: 29471107
[Au] Autor:Qian M; Lou Y; Wang Y; Zhang M; Jiang Q; Mo Y; Han K; Jin S; Dai Q; Yu Y; Wang Z; Wang J
[Ad] Address:Department of Anesthesia, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, China. Electronic address: qianmeizi1991@163.com.
[Ti] Title:PICK1 deficiency exacerbates sepsis-associated acute lung injury and impairs glutathione synthesis via reduction of xCT.
[So] Source:Free Radic Biol Med;118:23-34, 2018 Feb 20.
[Is] ISSN:1873-4596
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The role of oxidative stress has been well documented in the development of sepsis-induced acute lung injury (ALI). Protein interaction with C-kinase 1 (PICK1) participates in oxidative stress-related neuronal diseases. However, its function in lung infections and inflammatory diseases is not known. We therefore sought to investigate whether PICK1 is involved in sepsis-induced ALI. Cecal ligation and puncture (CLP) was performed in anesthetized wild type (WT) and PICK1 knock out (KO, PICK1 ) mice with C57BL/6 background. At the time of CLP, mice were given fluid resuscitation. Mouse lungs were harvested at 24 and 72 h for Western blot analysis, qRT-PCR, BALF analysis, Hematoxylin and Eosin staining, TUNEL staining, maleimide staining, flow cytometry analysis, GCL, GSH, GSSG and cysteine levels measurement. A marked elevation of PICK1 mRNA and protein level were demonstrated in lung tissue, which was accompanied by increased production of reactive oxygen species (ROS) and reactive nitrogen species (RNS) and consumption of glutathione (GSH). N-acetylcysteine (NAC), buthionine sulfoximine (BSO) and GSH-monoethyl ester (GSH-MEE) were injected into mice via caudal vein to regulate glutathione (GSH) level in lung. Alterations of lung GSH content induced PICK1 level change after CLP challenge. In PICK1 underwent with CLP, lung injury and survival were significantly aggravated compared with wild-type mice underwent with CLP. Concomitantly, CLP-induced lung cell apoptosis was exacerbated in PICK1 mice. The level of xCT, other than PKCα, in lung tissue was significantly lowered in PICK1 but not in wild type that underwent CLP surgery. Meanwhile, Nrf2 activation, which dominating xCT expression, was inhibited in PICK1-/- but not in wild type mice that underwent CLP surgery, as well. Moreover, higher level of PICK1 was detected in PBMCs of septic patients than healthy controls. Taken together, PICK1 plays a pivotal role in sepsis-induced ALI by regulating GSH synthesis via affecting the substrate-specific subunit of lung cystine/glutamate transporter, xCT.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 25009 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29471085
[Au] Autor:Zhu H; Lu X; Ling L; Li H; Ou Y; Shi X; Lu Y; Zhang Y; Chen D
[Ad] Address:Department of Microbiological and Biochemical Pharmacy, School of Pharmacy, Fudan University, Shanghai, China.
[Ti] Title:Houttuynia cordata polysaccharides ameliorate pneumonia severity and intestinal injury in mice with influenza virus infection.
[So] Source:J Ethnopharmacol;218:90-99, 2018 Feb 19.
[Is] ISSN:1872-7573
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:ETHNOPHARMACOLOGICAL RELEVANCE: Hottuynia cordata is an important traditional Chinese medicine for the treatment of respiratory diseases including bacterial and viral infections. Polysaccharides isolated from Houttuynia cordata (HCP), as its main ingredients, have been demonstrated to ameliorate the LPS-induced acute lung injury in mice. The study aimed to determine the protective effects of HCP on multiple organ injury in influenza A virus (IAV) H1N1 infected mice and its primary mechanisms in anti-inflammation and immune regulation. MATERIALS AND METHODS: Mice were inoculated with IAV H1N1 and then treated with 20 or 40 mg/kg/d of HCP for survival test and acute lung-gut injury test. RESULTS: The treatment with HCP resulted in an increase in the survival rate of H1N1 infected mice and the protection from lung and intestine injury, accompanied with the reduced virus replication. HCP markedly decreased the concentration of pulmonary proinflammatory cytokines/chemokines and the number of intestinal goblet cells, and strengthened the intestinal physical and immune barrier, according to the increase of sIgA and tight junction protein (ZO-1) in intestine. At the same time, the inhibition of inflammation in lung and gut was related to the suppressing of the expression of TLR4 and p-NFκB p65 in lung. CONCLUSIONS: These results indicated that HCP ameliorated lung and intestine injury induced by IAV attack. The mechanisms were associated with inhibition of inflammation, protection of intestinal barrier and regulation of mucosal immunity, which may be related to the regulation of gut-lung axis. As an alternative medicine, HCP may have clinical potential to treat IAV infection in human beings.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 25009 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29466698
[Au] Autor:Xu X; Zhi T; Chao H; Jiang K; Liu Y; Bao Z; Fan L; Wang D; Li Z; Liu N; Ji J
[Ad] Address:Department of Neurosurgery, the First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China.
[Ti] Title:ERK1/2/mTOR/Stat3 pathway-mediated autophagy alleviates traumatic brain injury-induced acute lung injury.
[So] Source:Biochim Biophys Acta;1864(5 Pt A):1663-1674, 2018 Feb 18.
[Is] ISSN:0006-3002
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Acute lung injury (ALI) is one of several complications in patients with traumatic brain injury (TBI). Autophagy is a primary homeostatic process that promotes cell survival under stress. Accumulating evidence implicates autophagy in the pathogenesis of ALI under various conditions. However, the role of autophagy in TBI-induced ALI remains unknown. The aim of this study was to adjust autophagy with pharmacological agents to determine its functional significance in TBI-induced ALI. Rats were preconditioned with autophagy promoter rapamycin or inhibitor 3-methyladenine before they were challenged with TBI. Extracellular signal-regulated kinase 1/2 (ERK1/2) inhibitor U0126, mechanistic target of rapamycin (mTOR) inhibitor rapamycin, and signal transducer and activator of transcription 3 (Stat3) inhibitor S31-201 were used to test the role of ERK1/2/mTOR/Stat3 signaling pathway in regulating autophagy. Autophagy is activated in lung tissues after TBI. Enhancement of autophagy suppressed apoptosis, inflammation and oxidative stress in lung tissues, which were activated after TBI, whereas inhibition of autophagy aggravated these critical pathological changes. Autophagy also improved TBI-induced impairment in pulmonary barrier function, oxygenation function and static compliance. Furthermore, TBI-induced autophagy was mediated by ERK1/2/mTOR/Stat3 pathway, which may serve to reduce ALI and improve pulmonary barrier function, oxygenation function and static compliance. These findings are important for the prevention and treatment of TBI-induced ALI.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  4 / 25009 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29432911
[Au] Autor:Yang J; Tian H; Huang X
[Ad] Address:Emergency Department, Guizhou Provincial People's Hospital, Guiyang, Guizhou, 550002, China.
[Ti] Title:Tephrosin attenuates sepsis induced acute lung injury in rats by impeding expression of ICAM-1 and MIP-2.
[So] Source:Microb Pathog;117:93-99, 2018 Feb 09.
[Is] ISSN:1096-1208
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Acute lung injury (ALI), a devastating form of respiratory infections, is characterized by increased edema, release of cytokines, weakened arterial oxygenation and infiltration of neutrophils and lymphocytes. The objective of the research envisaged was to reveal protective effects of tephrosin (TP) in ALI. In the present investigation, sepsis was triggered in rats by cecal ligation and puncture (CLP) method, and TP was administered intraperitonially. Five groups - Group A (control), Group B (Sham group) Group C (infected and untreated), and Group D and E (infected and treated with 25 and 50 mg/kg TP respectively) - of ten rats each, were used for the investigation. Evaluation parameters included measurement of arterial oxygenation, lung water content, protein determination, cytokine determination, neutrophil and lymphocyte count in the bronchoalveolar lavage fluid (BALF). As indicated by histopathological examination, the lung injury score was maximum in group C, but indicated reduction in group D and E. Intracellular adhesion molecule (ICAM)-1 and macrophage inflammatory protein-2 (MIP-2) are known to be important mediators responsible for ALI. Reduction in the ICAM-1 and MIP-2 expression was found to reduce after treatment with TP. In comparison to group D, group E reflected higher magnitude of ICAM-1 and MIP-2 suppression due to administration of higher TP dose. Compared to Group A and B, Group E indicated slightly higher expression of ICAM-1 and MIP-2. The research envisaged thus supports that TP attenuates ICAM-1 and MIP-2 expression in sepsis induced ALI rat model.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  5 / 25009 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29523157
[Au] Autor:Sottile PD; Albers D; Moss MM
[Ad] Address:Division of Pulmonary Sciences and Critical Care Medicine, Department of Medicine, University of Colorado School of Medicine, Anschutz Medical Campus, 12700 E. 19th Ave., RC2 9th Floor, C272, Aurora, CO, 80045, USA. peter.sottile@ucdenver.edu.
[Ti] Title:Neuromuscular blockade is associated with the attenuation of biomarkers of epithelial and endothelial injury in patients with moderate-to-severe acute respiratory distress syndrome.
[So] Source:Crit Care;22(1):63, 2018 Mar 10.
[Is] ISSN:1466-609X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Neuromuscular blockade (NMB) is a therapy for acute respiratory distress syndrome (ARDS). However, the mechanism by which NMB may improve outcome for ARDS patients remains unclear. We sought to determine whether NMB attenuates biomarkers of epithelial and endothelial lung injury and systemic inflammation in ARDS patients, and whether the association is dependent on tidal volume size and the initial degree of hypoxemia. METHODS: We performed a secondary analysis of patients enrolled in the ARDS network low tidal volume ventilation (ARMA) study. Our primary predictor variable was the number of days receiving NMB between study enrollment and day 3. Our primary outcome variables were the change in concentration of biomarkers of epithelial injury (serum surfactant protein-D (SP-D)), endothelial injury (von Willebrand factor (VWF)), and systemic inflammation (interleukin (IL)-8). Multivariable regression analysis was used to compare the change in biomarker concentration controlling for multiple covariates. Patients were stratified by treatment arm (12 versus 6 cm /kg) and by an initial arterial oxygen tension (PaO ) to fractional inspired oxygen (FiO ) (P/F) ratio of 120. RESULTS: A total of 446 (49%) patients had complete SP-D, VWF, and IL-8 measurements on study enrollment and day 3. After adjusting for baseline differences, each day of NMB was associated with a decrease in SP-D (-23.7 ng/ml/day, p = 0.029), VWF (-33.5% of control/day, p = 0.015), and IL-8 (-362.6 pg/ml/day, p = 0.030) in patients with an initial P/F less than or equal to 120 and receiving low tidal volume ventilation. However, patients with a P/F ratio of greater than 120 or receiving high tidal volume ventilation had either no change or an increase in SP-D, WVF, or IL-8 concentrations. CONCLUSION: NBM is associated with decreased biomarkers of epithelial and endothelial lung injury and systemic inflammation in ARDS patients receiving low tidal volume ventilation and those with a P/F ratio less than or equal to 120.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Data-Review
[do] DOI:10.1186/s13054-018-1974-4

  6 / 25009 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29522858
[Au] Autor:Soncini R; Vieira J; Ramos Lopes AC; Ruginsk SG; Incerpi EK; Barchuk AR
[Ad] Address:Departamento de Cincias Fisiolgicas, Instituto de Cincias Biomdicas, Universidade Federal de Alfenas, UNIFAL-MG, Alfenas, Minas Gerais, Brazil.
[Ti] Title:Glucocorticoid receptor gene expression in a CLP-induced ARDS-like rat model treated with dexamethasone and metyrapone.
[So] Source:Mol Cell Endocrinol;, 2018 Mar 06.
[Is] ISSN:1872-8057
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:Glucocorticoids (GCs) are used for acute respiratory distress syndrome (ARDS) to improve or prevent lung injury. The mechanisms underlying the effects of GCs involve inadequate GC-receptor (GR)-mediated downregulation of pro-inflammatory factors despite elevated levels of cortisol. Within this context, knowledge of the transcriptional pattern of the GR gene in response to variations in physiological parameters may shed light on this issue. We addressed this problem by measuring plasmatic corticosterone (CCT) levels and assessing GR expression at transcript and protein levels in rats with caecal ligation and puncture (CLP)-induced ARDS-like syndrome treated with dexamethasone and metyrapone. Seventy male rats were randomized into three main groups: Nave (any treatment), Sham (caecum-exposed) and CLP. CLP animals were divided into three groups according to pretreatments performed before surgery: CLP sal (0.9% NaCl ip), CLP metyrapone (50 mg.kg-1 ip) and CLP dexamethasone (0.5 mg.kg-1 ip). Our results showed that CLP sal promotes elevation in CCT levels, which are significantly reduced with metyrapone to levels comparable to untreated animals when dexamethasone is used. In this hormonal milieu, the GR gene transcript levels of both variants, GRα and GR, are produced in comparable levels and in response to caecum-exposing surgery. Nonetheless, the expression of the GRα variant demonstrated positive sensitivity to variations in CCT levels and was downregulated in animals treated with dexamethasone. Moreover, nuclear translocation of GR protein decreased with high levels of plasma CCT and higher GR translocation was found in animals with moderate CCT levels; in either case, the process seemed to be positively associated with the CLP procedure.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  7 / 25009 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29381721
[Au] Autor:von Babo M; Chmiel C; Mggler SA; Rakusa J; Schuppli C; Meier P; Fischler M; Urner M
[Ad] Address:Department of Internal Medicine, Waid City Hospital, Zurich, Switzerland.
[Ti] Title:Transfusion practice in anemic, non-bleeding patients: Cross-sectional survey of physicians working in general internal medicine teaching hospitals in Switzerland.
[So] Source:PLoS One;13(1):e0191752, 2018.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Transfusion practice might significantly influence patient morbidity and mortality. Between European countries, transfusion practice of red blood cells (RBC) greatly differs. Only sparse data are available on transfusion practice of general internal medicine physicians in Switzerland. METHODS: In this cross-sectional survey, physicians working in general medicine teaching hospitals in Switzerland were investigated regarding their self-reported transfusion practice in anemic patients without acute bleeding. The definition of anemia, transfusion triggers, knowledge on RBC transfusion, and implementation of guidelines were assessed. RESULTS: 560 physicians of 71 hospitals (64%) responded to the survey. Anemia was defined at very diverging hemoglobin values (by 38% at a hemoglobin <130 g/L for men and by 57% at <120 g/L in non-pregnant women). 62% and 43% respectively, did not define anemia in men and in women according to the World Health Organization. Fifty percent reported not to transfuse RBC according to international guidelines. Following factors were indicated to influence the decision to transfuse: educational background of the physicians, geographical region of employment, severity of anemia, and presence of known coronary artery disease. 60% indicated that their knowledge on Transfusion-related Acute Lung Injury (TRALI) did not influence transfusion practice. 50% of physicians stated that no local transfusion guidelines exist and 84% supported the development of national recommendations on transfusion in non-acutely bleeding, anemic patients. CONCLUSION: This study highlights the lack of adherence to current transfusion guidelines in Switzerland. Identifying and subsequently correcting this deficit in knowledge translation may have a significant impact on patient care.
[Mh] MeSH terms primary: Blood Transfusion/utilization
General Practice
Hospitals, Teaching/organization & administration
Practice Patterns, Physicians
[Mh] MeSH terms secundary: Cross-Sectional Studies
Humans
Internal Medicine
Switzerland
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180131
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191752

  8 / 25009 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29366758
[Au] Autor:Yuhong L; Tana W; Zhengzhong B; Feng T; Qin G; Yingzhong Y; Wei G; Yaping W; Langelier C; Rondina MT; Ge RL
[Ad] Address:Research Center for High Altitude Medicine, Qinghai University, Xining 810001, China; Department of Respiratory Medicine, The Affiliated Hospital of Qinghai University, Xining 810001, China.
[Ti] Title:Transcriptomic profiling reveals gene expression kinetics in patients with hypoxia and high altitude pulmonary edema.
[So] Source:Gene;651:200-205, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:OBJECTIVE: High altitude pulmonary edema (HAPE) is a life threatening condition occurring in otherwise healthy individuals who rapidly ascend to high altitude. However, the molecular mechanisms of its pathophysiology are not well understood. The objective of this study is to evaluate differential gene expression in patients with HAPE during acute illness and subsequent recovery. METHODS: Twenty-one individuals who ascended to an altitude of 3780 m were studied, including 12 patients who developed HAPE and 9 matched controls without HAPE. Whole-blood samples were collected during acute illness and subsequent recovery for analysis of the expression of hypoxia-related genes, and physiologic and laboratory parameters, including mean pulmonary arterial pressure (mPAP), heart rate, blood pressure, and arterial oxygen saturation (SpO ), were also measured. RESULTS: Compared with control subjects, numerous hypoxia-related genes were up-regulated in patients with acute HAPE. Gene network analyses suggested that HIF-1α played a central role in acute HAPE by affecting a variety of hypoxia-related genes, including BNIP3L, VEGFA, ANGPTL4 and EGLN1. Transcriptomic profiling revealed the expression of most HAPE-induced genes was restored to a normal level during the recovery phase except some key hypoxia response factors, such asBNIP3L, EGR1, MMP9 and VEGF, which remained persistently elevated. CONCLUSIONS: Differential expression analysis of hypoxia-related genes revealed distinct molecular signatures of HAPE during acute and recovery phases. This study may help us to better understand HAPE pathogenesis and putative targets for further investigation and therapeutic intervention.
[Mh] MeSH terms primary: Altitude Sickness/genetics
Hypertension, Pulmonary/genetics
Pulmonary Edema/genetics
[Mh] MeSH terms secundary: Acute Lung Injury/etiology
Acute Lung Injury/genetics
Adult
Case-Control Studies
Cohort Studies
Gene Expression Profiling
Humans
Up-Regulation
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180126
[St] Status:MEDLINE

  9 / 25009 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29191391
[Au] Autor:Prevotat A; Rouyer C; Gosset P; Kipnis E; Faure K; Guery B
[Ad] Address:Recherche translationnelle: relations hte pathognes, universit de Lille, CHU de Lille, EA7366, 59000 Lille, France.
[Ti] Title:Biphasic lung injury during Streptococcus pneumoniae infection in a murine model.
[So] Source:Med Mal Infect;48(2):103-113, 2018 Mar.
[Is] ISSN:1769-6690
[Cp] Country of publication:France
[La] Language:eng
[Ab] Abstract:OBJECTIVES: Streptococcus pneumoniae is the leading cause of community-acquired pneumonia. We aimed to analyze the epithelial response to S.pneumoniae-induced lung injury. METHODS: Using an in vitro model with 16HBE cells and experimental in vivo murine model of acute lung injury, we analyzed the epithelial response to S.pneumoniae. Lung epithelial cell monolayers were exposed to S.pneumoniae and permeability was assessed by transepithelial resistance (TER) measurement and organization and expression of junction proteins. Functional consequences were studied with an in vivo murine model measuring alveolar permeability, distal alveolar fluid clearance (DAFC), and the alveolar inflammatory response. RESULTS: In vitro, S.pneumoniae induced a dose-dependent decrease in transepithelial resistance, which was associated with significant modifications in the organization of junction proteins assessed by immunofluorescence staining and expression after 6hours of exposure. In vivo, S.pneumoniae induced a transient increase in alveolar permeability with an adequate increase in DAFC 6hours post infection. In a second phase, a permanent increased permeability was associated with a major decrease in DAFC. CONCLUSION: Overall, the epithelial response to S.pneumoniae followed a biphasic pattern with an initial reversible increase in permeability related to the alteration of tight and adherens junctions and a second phase associated with an epithelial injury with a major increase in permeability with a decreased DAFC reflecting an injured alveolar capillary barrier.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Process

  10 / 25009 MEDLINE  
              first record previous record
select
to print
Photocopy
Full text

[PMID]: 29522258
[Au] Autor:Wang B; Xiao Y; Yang X; He Y; Jing T; Wang W; Zhang J; Lin R
[Ad] Address:Department of Pharmacology, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, P. R. China.
[Ti] Title:Protective effect of dihydromyricetin on LPS-induced acute lung injury.
[So] Source:J Leukoc Biol;, 2018 Mar 09.
[Is] ISSN:1938-3673
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Dihydromyricetin (DHM), a bioactive flavonoid component isolated from Ampelopsis grossedentata, is known to have anti-inflammatory effect, but the effect of DHM on acute lung injury (ALI) is largely unknown. Here, we investigated the effect of DHM on ALI and the underlying mechanism by bioinformatic analyses and animal experiments. We found that pretreatment with DHM ameliorated lung pathological changes and suppressed the inflammation response in lung tissues after LPS challenge. The potential targets of DHM were predicted by DDI-CPI and DRAR-CPI tools and analyzed using the STRING server to predict the functionally related signaling pathways, such as MAPK signaling. Molecular docking calculations indicated that DHM could be embedded tightly into the binding pocket of ERK, JNK, and p38. Furthermore, the activation of MAPK signaling induced by LPS was inhibited by DHM. In conclusion, these findings suggest that DHM may exert its protective effect on ALI by inhibiting MAPK signaling. The present study supports a potential clinical application for DHM in treating ALI and provides a novel design that combines in silico methods with in vivo experiments for drug research.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher
[do] DOI:10.1002/JLB.3MA0317-101RRR


page 1 of 2501 go to page                         
   


Refine the search
  Database : MEDLINE Advanced form   

    Search in field  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/PAHO/WHO - Latin American and Caribbean Center on Health Sciences Information