Database : MEDLINE
Search on : Myocardial and Ischemia [Words]
References found : 75914 [refine]
Displaying: 1 .. 10   in format [Detailed]

page 1 of 7592 go to page                         

  1 / 75914 MEDLINE  
              next record last record
select
to print
Photocopy
Full text

[PMID]: 29511691
[Au] Autor:Guaricci AI; De Santis D; Carbone M; Muscogiuri G; Guglielmo M; Baggiano A; Serviddio G; Pontone G
[Ad] Address:Institute of Cardiovascular Disease, Department of Emergency and Organ Transplantation, University Hospital Policlinico of Bari, Bari, Italy.
[Ti] Title:Coronary Atherosclerosis Assessment by Coronary CT Angiography in Asymptomatic Diabetic Population: A Critical Systematic Review of the Literature and Future Perspectives.
[So] Source:Biomed Res Int;2018:8927281, 2018.
[Is] ISSN:2314-6141
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The prognostic impact of diabetes mellitus (DM) on cardiovascular outcomes is well known. As a consequence of previous studies showing the high incidence of coronary artery disease (CAD) in diabetic patients and the relatively poor outcome compared to nondiabetic populations, DM is considered as CAD equivalent which means that diabetic patients are labeled as asymptomatic individuals at high cardiovascular risk. Lessons learned from the analysis of prognostic studies over the past decade have challenged this dogma and now support the idea that diabetic population is not uniformly distributed in the highest risk box. Detecting CAD in asymptomatic high risk individuals is controversial and, what is more, in patients with diabetes is challenging, and that is why the reliability of traditional cardiac stress tests for detecting myocardial ischemia is limited. Cardiac computed tomography angiography (CCTA) represents an emerging noninvasive technique able to explore the atherosclerotic involvement of the coronary arteries and, thus, to distinguish different risk categories tailoring this evaluation on each patient. The aim of the review is to provide a wide overview on the clinical meaning of CCTA in this field and to integrate the anatomical information with a reliable therapeutic approach.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.1155/2018/8927281

  2 / 75914 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29511370
[Au] Autor:Seo EH; Song GY; Namgung JH; Oh CS; Lee SH; Kim SH
[Ad] Address:BK21 Plus, Department of Cellular and Molecular Medicine, Konkuk University School of Medicine, Seoul, Korea.
[Ti] Title:Receptor for activated C kinase 1 in rats with ischemia-reperfusion injury: intravenous versus inhalation anaesthetic agents.
[So] Source:Int J Med Sci;15(4):352-358, 2018.
[Is] ISSN:1449-1907
[Cp] Country of publication:Australia
[La] Language:eng
[Ab] Abstract:: The study examined the difference in the expression of the receptor for activated C kinase 1 (RACK1) between anaesthesia with propofol and isoflurane in rats with myocardial ischemia-reperfusion injury (IRI). : Male Sprague-Dawley rats were studied. Anaesthesia was induced with xylazine 20 µg/g by intraperitoneal injection and maintained with propofol or isoflurane. Myocardial IRI was induced by ligating the left anterior descending artery for 1 hour. Reactive oxygen species (ROS), cardiomyocyte apoptosis, the expression of RACK1 and toll-like receptor 4 (TLR4), and the heart injury score were compared between the two groups. : Cardiomyocyte apoptosis with ROS was significantly lower in the propofol group than in the isoflurane group. The propofol group had significantly higher RACK1 expression and lower TLR4 expression, compared with the isoflurane group (RACK1, 1970.50 ± 120.50 . 1350.20 ± 250.30, <0.05; TLR4, 980.50 ± 110.75 . 1275.50 ± 75.35, <0.05). However, the heart injury scores in the two groups did not differ significantly (3.56 ± 0.29 . 4.33 ± 0.23 in the propofol and isoflurane groups, respectively, =0.33). : There were significant differences in inflammation and apoptosis, including the expression of RACK1 and TLR4, after myocardial IRI between the propofol and isoflurane groups. However, both groups had similar heart injury scores.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.7150/ijms.22591

  3 / 75914 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29462717
[Au] Autor:Mahalakshmi A; Kurian GA
[Ad] Address:School of Chemical and Biotechnology, SASTRA University, Thanjavur, India.
[Ti] Title:Evaluating the impact of diabetes and diabetic cardiomyopathy rat heart on the outcome of ischemia-reperfusion associated oxidative stress.
[So] Source:Free Radic Biol Med;118:35-43, 2018 Feb 17.
[Is] ISSN:1873-4596
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Earlier literature underlines that oxidative stress plays a major role in the pathology of myocardial ischemia-reperfusion (I/R) injury, diabetic cardiomyopathy (DCM), diabetes mellitus (DM), fibrosis and hypertrophy which could adversely affect the normal cardiac function. However, the contributory role of oxidative stress in I/R pathology of heart with pre-existing abnormalities or diseases like DM and DCM remains to be explored. I/R injury was induced in normal (normal diet), DM (normal diet + streptozotocin: multiple low dose of 30 mg/kg) and DCM (high fat diet (40% fat) + streptozotocin: multiple low dose of 30 mg/kg) rat hearts using Langendorff isolated heart perfusion apparatus. Cardiac physiological recovery after I/R was assessed by hemodynamic parameters like LVDP, and LVSP, whereas cardiac injury was measured by tissue infarct size, and apoptosis, LDH, and CK release in coronary effluent. The oxidative stress was evaluated in myocardial homogenate, mitochondrial subpopulation, and microsomes. Reperfusing the ischemic DCM heart significantly deteriorated cardiac physiological recovery and elevated the cardiac injury (infarct size: 60%), compared to the control. But in DM heart, physiological recovery was prominent in the initial phase of reperfusion but deteriorated towards the end of reperfusion, supported by less infarct size. In addition, elevated lipid peroxidation (70% in DCM-I/R vs Sham) and impaired antioxidant enzymes (% decline vs Sham: GSH - 56% (DM), 63% (DCM); Catalase - 58% (DM), 35% (DCM); GPx - 19% (DM), 27% (DCM) and GR - 28% (DCM)) was observed in myocardial tissue from both DM and DCM. Interestingly, upon reperfusion, only normal heart showed significant deterioration in the antioxidant defense system. Collectively these results demonstrated that I/R induced oxidative stress is minimal in DM and DCM rat heart, despite high infarct size and low cardiac performance. This may be due to the prior adaptive modification in the antioxidant system associated with disease pathology.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  4 / 75914 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29432894
[Au] Autor:Boening A; Assling-Simon L; Heep M; Boengler K; Niemann B; Grieshaber P
[Ad] Address:Department of Cardiovascular Surgery, University Hospital Giessen, Germany.
[Ti] Title:Buckberg's blood cardioplegia for protection of adult and senile myocardium in a rat in vitro model of acute myocardial infarction.
[So] Source:Exp Gerontol;104:98-104, 2018 Feb 10.
[Is] ISSN:1873-6815
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: In patients undergoing surgical myocardial revascularization for acute myocardial infarction, excellent myocardial protection can be achieved by blood cardioplegia. We investigated the influence of age on cardiac function, metabolism, and infarct size using Buckberg's blood cardioplegia (BCP). METHODS: The hearts of male Wistar rats ("adult", age 3 months, n = 8; "senile", age 24 months, n = 8) were excised and mounted on a blood-perfused isolated heart apparatus. An acute myocardial infarction was induced by coronary artery ligation for 30 min before aortic clamping and infusion of Buckberg's BCP. Throughout the experiment, functional parameters were recorded: coronary blood flow (normalized by heart weight), left ventricular peak developed pressure (LVpdP), and positive and negative derived left ventricular pressure over time (dLVPdt and dLVPdt ). Oxygen consumption (MVO ) and lactate production of the hearts were calculated. The infarct size after 90 min of reperfusion (in % of the area at risk) was measured with triphenyl tetrazolium chloride staining of the myocardium. RESULTS: The baseline coronary flow normalized by heart weight was significantly lower in the senile hearts (1.6 ±â€¯0.4 ml/(min ∗ g)) compared with the adult hearts (2.0 ±â€¯0.3 ml/(min ∗ g); p = 0.04). After 90 min of aortic clamping, hemodynamic function of senile hearts recovered better than that of adult hearts: LVpdP (adult 57% of baseline [BL]; senile 88% BL; p = 0.044) and dLVPdt (adult 74% BL, senile 102% BL; p = 0.12). In contrast, myocardial infarct size was similar between the adult (26%) and senile (21%; p = 0.45) hearts, and coronary flow recovered to a similar extent (55% BL and 58% BL, respectively). During reperfusion, MVO (80% BL and 81% BL) and lactate production (1.2 and 1.3 µmol/min) were similar in the two groups. CONCLUSION: After acute myocardial infarction in a rat model, hearts recovered function after reperfusion with Buckberg's BCP solution. Hearts from aged animals recovered better than those from younger animals.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  5 / 75914 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29524006
[Au] Autor:Wider J; Undyala VVR; Whittaker P; Woods J; Chen X; Przyklenk K
[Ad] Address:Cardiovascular Research Institute, Wayne State University School of Medicine, Scott Hall, Room 4356, 540 E Canfield, Detroit, MI, 48201, USA.
[Ti] Title:Remote ischemic preconditioning fails to reduce infarct size in the Zucker fatty rat model of type-2 diabetes: role of defective humoral communication.
[So] Source:Basic Res Cardiol;113(3):16, 2018 Mar 09.
[Is] ISSN:1435-1803
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:Remote ischemic preconditioning (RIPC), the phenomenon whereby brief ischemic episodes in distant tissues or organs render the heart resistant to infarction, has been exhaustively demonstrated in preclinical models. Moreover, emerging evidence suggests that exosomes play a requisite role in conveying the cardioprotective signal from remote tissue to the myocardium. However, in cohorts displaying clinically common comorbidities-in particular, type-2 diabetes-the infarct-sparing effect of RIPC may be confounded for as-yet unknown reasons. To investigate this issue, we used an integrated in vivo and in vitro approach to establish whether: (1) the efficacy of RIPC is maintained in the Zucker fatty rat model of type-2 diabetes, (2) the humoral transfer of cardioprotective triggers initiated by RIPC are transported via exosomes, and (3) diabetes is associated with alterations in exosome-mediated communication. We report that a standard RIPC stimulus (four 5-min episodes of hindlimb ischemia) reduced infarct size in normoglycemic Zucker lean rats, but failed to confer protection in diabetic Zucker fatty animals. Moreover, we provide novel evidence, via transfer of serum and serum fractions obtained following RIPC and applied to HL-1 cardiomyocytes subjected to hypoxia-reoxygenation, that diabetes was accompanied by impaired humoral communication of cardioprotective signals. Specifically, our data revealed that serum and exosome-rich serum fractions collected from normoglycemic rats attenuated hypoxia-reoxygenation-induced HL-1 cell death, while, in contrast, exosome-rich samples from Zucker fatty rats did not evoke protection in the HL-1 cell model. Finally, and unexpectedly, we found that exosome-depleted serum from Zucker fatty rats was cytotoxic and exacerbated hypoxia-reoxygenation-induced cardiomyocyte death.
[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:10.1007/s00395-018-0674-1

  6 / 75914 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29523921
[Au] Autor:Kido T; Hoashi T; Kitano M; Shimada M; Kurosaki K; Ishibashi-Ueda H; Ichikawa H
[Ad] Address:Department of Pediatric Cardiovascular Surgery, National Cardiovascular and Cerebral Center, 5-7-1, Fujishiro-dai, Suita, Osaka, 565-8565, Japan.
[Ti] Title:Impact of Hybrid Stage 1 Palliation for Hypoplastic Left Heart Syndrome: Histopathological Findings.
[So] Source:Pediatr Cardiol;, 2018 Mar 09.
[Is] ISSN:1432-1971
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The purpose of the study is to analyze the impact of hybrid stage 1 palliation on right ventricular myocardial pathology in hypoplastic left heart syndrome. Sufficient amount of right ventricular biopsies could be obtained from 16 of 32 patients who underwent Norwood operation between 2007 and 2013. Histopathological findings of right ventricle in patients who underwent primary Norwood operation (primary group, n = 5), patients with aortic atresia (HS1P AA group, n = 6) or aortic stenosis (HS1P AS group, n = 5) who underwent staged Norwood palliation following hybrid stage 1 palliation were compared. To eliminate the influence of right ventricular pressure afterload, right ventricular biopsies were obtained from patients with truncus arteriosus communis (TAC group, n = 6) at total correction. The percentage of myocardial fibrosis was significantly higher in both HS1P groups than in TAC group; moreover, it was significantly higher in HS1P AA group than in primary group. Capillary vascular density was significantly lower in all hypoplastic left heart syndrome groups than in TAC group. At the sub-endocardial layer, collagen type I/III ratios were higher in HS1P AA group than in other hypoplastic left heart syndrome groups. The proportions of N-cadherin immunolocalized to myocyte termini were lower in all hypoplastic left heart syndrome groups than in TAC group. Right ventricle in hypoplastic left heart syndrome showed more significant ischemic change and myocardial immaturity than that in truncus arteriosus communis. Hybrid stage 1 palliation for aortic atresia would be a risk factor for further right ventricular myocardial ischemia.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1007/s00246-018-1851-6

  7 / 75914 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29523748
[Au] Autor:Durham KK; Chathely KM; Trigatti BL
[Ad] Address:Biochemistry and Biomedical Sciences and Thrombosis and Atherosclerosis Research Institute, McMaster University and Hamilton Health Sciences, 237 Barton st E, HAMILTON, L8L 2X2, Canada.
[Ti] Title:High density lipoprotein protects cardiomyocytes against necrosis induced by oxygen and glucose deprivation, through SR-B1, PI3K, and AKT1 and 2.
[So] Source:Biochem J;, 2018 Mar 09.
[Is] ISSN:1470-8728
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The cardioprotective lipoprotein HDL prevents myocardial infarction and cardiomyocyte death due to ischemia/reperfusion injury The scavenger receptor class B, type 1 (SR-B1) is a high affinity HDL receptor and has been shown to mediate HDL dependent lipid transport as well as signaling in a variety of different cell types.  The contribution of SR-B1 in cardiomyocytes to the protective effects of HDL on cardiomyocyte survival following ischemia has not yet been studied.  Here we use a model of simulated ischemia (oxygen and glucose deprivation; OGD), to assess the mechanistic involvement of SR-B1, PI3K, and AKT in HDL mediated protection of cardiomyocytes from cell death.  Neonatal mouse cardiomyocytes and immortalized human ventricular cardiomyocytes, subjected to OGD for 4 hours, underwent substantial cell death due to necrosis but not necroptosis or apoptosis.  Pretreatment of cells with HDL, but not LDL, protected them against OGD-induced necrosis.  HDL mediated protection was lost in cardiomyocytes from SR-B1 mice or when SR-B1 was knocked down in human immortalized ventricular cardiomyocytes.  HDL treatment induced the phosphorylation of AKT in cardiomyocytes in an SR-B1 dependent manner.  Finally, chemical inhibition of PI3K or AKT, or silencing of either AKT1 or AKT2 gene expression abolished HDL-mediated protection against OGD-induced necrosis of cardiomyocytes.  These results are the first to identify a role of SR-B1 in mediating the protective effects of HDL against necrosis in cardiomyocytes, and to identify AKT activation downstream of SR-B1 in cardiomyocytes.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  8 / 75914 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29523407
[Au] Autor:Potz BA; Scrimgeour LA; Sabe SA; Clements RT; Sodha NR; Sellke FW
[Ad] Address:Division of Cardiothoracic Surgery, Department of Surgery, Cardiovascular Research Center, Rhode Island Hospital, Alpert Medical School of Brown University, Providence, RI.
[Ti] Title:Glycogen synthase kinase 3ß inhibition reduces mitochondrial oxidative stress in chronic myocardial ischemia.
[So] Source:J Thorac Cardiovasc Surg;, 2018 Feb 02.
[Is] ISSN:1097-685X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVES: Glycogen synthase kinase 3ß (GSK-3ß) inhibition has been reported to increase microvascular density and improve myocardial blood flow in a porcine model of chronic myocardial ischemia and metabolic syndrome. Inhibition of GSK-3ß can also be cardioprotective by modulating fibrosis signaling and mitochondrial-induced apoptosis. We hypothesized GSK-3ß inhibition would have a beneficial effect on myocardial fibrosis and oxidative stress in a porcine model of chronic myocardial ischemia and metabolic syndrome. METHODS: Pigs were fed a high fat diet for 4 weeks followed by placement of an ameroid constrictor to the left circumflex coronary artery. Three weeks later animals received either no drug or a GSK-3ß inhibitor. The diets and placebo/GSK-3ß inhibition were continued for an additional 5 weeks, the pigs were then euthanized, and the myocardial tissue was harvested. Collagen expression was analyzed via Picrosirius staining. Oxidative stress was analyzed via Oxyblot analysis. Protein expression was analyzed via Western blot. RESULTS: GSK-3ß inhibition was associated with decreased collagen expression and oxidative stress in the ischemic and nonischemic myocardial tissue compared with control. There was a decrease in profibrotic proteins transforming growth factor-ß, p-SMAD2/3, and matrix metalloproteinase-9, and in proapoptotic and oxidative stress proteins, apoptosis inducing factor, the cleaved caspase 3/caspase 3 protein ratio and phosphorylated myeloid cell leukemia sequence-1 in the GSK-3ß inhibited group compared with the control. CONCLUSIONS: In the setting of metabolic syndrome and chronic myocardial ischemia, inhibition of GSK-3ß decreases collagen formation and oxidative stress in myocardial tissue. GSK-3ß inhibition might be having this beneficial effect by downregulating transforming growth factor-ß/SMAD2/3 signaling and decreasing mitochondrial induced cellular stress.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  9 / 75914 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29501746
[Au] Autor:Kuksal N; Gardiner D; Qi D; Mailloux RJ
[Ad] Address:Department of Biochemistry, Faculty of Science, Memorial University of Newfoundland, St. John's, Newfoundland and Labrador, Canada; Biomedical Sciences, Faculty of Medicine, Memorial University of Newfoundland, St. John's, Newfoundland and Labrador, Canada.
[Ti] Title:Partial loss of complex I due to NDUFS4 deficiency augments myocardial reperfusion damage by increasing mitochondrial superoxide/hydrogen peroxide production.
[So] Source:Biochem Biophys Res Commun;, 2018 Mar 01.
[Is] ISSN:1090-2104
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Recent work has found that complex I is the sole source of reactive oxygen species (ROS) during myocardial ischemia-reperfusion (IR) injury. However, it has also been reported that heart mitochondria can also generate ROS from other sources in the respiratory chain and Krebs cycle. This study examined the impact of partial complex I deficiency due to selective loss of the Ndufs4 gene on IR injury to heart tissue. Mice heterozygous for NDUFS4 (NDUFS4+/-) did not display any significant changes in overall body or organ weight when compared to wild-type (WT) littermates. There were no changes in superoxide (O )/hydrogen peroxide (H O ) release from cardiac or liver mitochondria isolated from NDUFS4 ±â€¯mice. Using selective ROS release inhibitors, we found that complex III is a major source of ROS in WT and NDUFS4 ±â€¯cardiac mitochondria respiring under state 4 conditions. Subjecting hearts from NDUFS4 ±â€¯mice to reperfusion injury revealed that the partial loss of complex I decreases contractile recovery and increases myocardial infarct size. These results correlated with a significant increase in O /H O release rates in mitochondria isolated from NDUFS4 ±â€¯hearts subjected to an IR challenge. Taken together, these results demonstrate that the partial absence of complex I sensitizes the myocardium towards IR injury and that the main source of ROS following reperfusion is complex III.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  10 / 75914 MEDLINE  
              first record previous record
select
to print
Photocopy
Full text

[PMID]: 29470977
[Au] Autor:Wang X; Xu L; Gillette TG; Jiang X; Wang ZV
[Ad] Address:Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China; Division of Cardiology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA.
[Ti] Title:The unfolded protein response in ischemic heart disease.
[So] Source:J Mol Cell Cardiol;117:19-25, 2018 Feb 20.
[Is] ISSN:1095-8584
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Ischemic heart disease is a severe stress condition that causes extensive pathological alterations and triggers cardiac cell death. Accumulating evidence suggests that the unfolded protein response (UPR) is strongly induced by myocardial ischemia. The UPR is an evolutionarily conserved cellular response to cope with protein-folding stress, from yeast to mammals. Endoplasmic reticulum (ER) transmembrane sensors detect the accumulation of unfolded proteins and stimulate a signaling network to accommodate unfolded and misfolded proteins. Distinct mechanisms participate in the activation of three major signal pathways, viz. protein kinase RNA-like ER kinase, inositol-requiring protein 1, and activating transcription factor 6, to transiently suppress protein translation, enhance protein folding capacity of the ER, and augment ER-associated degradation to refold denatured proteins and restore cellular homeostasis. However, if the stress is severe and persistent, the UPR elicits inflammatory and apoptotic pathways to eliminate terminally affected cells. The ER is therefore recognized as a vitally important organelle that determines cell survival or death. Recent studies indicate the UPR plays critical roles in the pathophysiology of ischemic heart disease. The three signaling branches may elicit distinct but overlapping effects in cardiac response to ischemia. Here, we outline the findings and discuss the mechanisms of action and therapeutic potentials of the UPR in the treatment of ischemic heart disease.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher


page 1 of 7592 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