Archives of medical research

Publisher: Elsevier

Journal description

Current impact factor: 2.41

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 2.406
2012 Impact Factor 2.079
2011 Impact Factor 1.733
2010 Impact Factor 1.986
2009 Impact Factor 1.884
2008 Impact Factor 1.703
2007 Impact Factor 1.772
2006 Impact Factor 1.275
2005 Impact Factor 1.382
2004 Impact Factor 1.286
2003 Impact Factor 1.277
2002 Impact Factor 0.606
2001 Impact Factor 0.476

Impact factor over time

Impact factor

Additional details

5-year impact 2.00
Cited half-life 4.90
Immediacy index 0.11
Eigenfactor 0.01
Article influence 0.51
Other titles Archives of medical research (En ligne), Archives of medical research
ISSN 1873-5487
OCLC 77547537
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details


  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Pre-print allowed on any website or open access repository
    • Voluntary deposit by author of authors post-print allowed on authors' personal website, or institutions open scholarly website including Institutional Repository, without embargo, where there is not a policy or mandate
    • Deposit due to Funding Body, Institutional and Governmental policy or mandate only allowed where separate agreement between repository and the publisher exists.
    • Permitted deposit due to Funding Body, Institutional and Governmental policy or mandate, may be required to comply with embargo periods of 12 months to 48 months .
    • Set statement to accompany deposit
    • Published source must be acknowledged
    • Must link to journal home page or articles' DOI
    • Publisher's version/PDF cannot be used
    • Articles in some journals can be made Open Access on payment of additional charge
    • NIH Authors articles will be submitted to PubMed Central after 12 months
    • Publisher last contacted on 18/10/2013
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: The IL28B single nucleotide polymorphism (SNP) rs12979860 is a major predictor of treatment outcomes in hepatitis C virus (HCV) infection, but its distribution widely varies among populations and ethnicities. We undertook this study to investigate the distribution of IL28B SNP rs12979860 in Mexican patients with HCV infection and to assess its usefulness in predicting response to pegylated interferon-alpha and ribavirin (PegIFN-α/RVB) therapy. Three hundred and fifty patients with chronic HCV infection were studied. The frequency of sustained virologic response (SVR), non-responders and relapses following a course of standard therapy was longitudinally assessed in 295 of these patients. IL28B SNP rs12979860 was genotyped from genomic DNA using real-time RT-PCR. The number needed to treat (NNT) to achieve a SVR was calculated. Seventy six (22%) patients were CC homozygous, 210 (60%) were heterozygous and 64 (18%) showed TT homozygosity for the IL28B SNP rs12979860. After a standard course of PegIFN-α/RVB, 69% of patients with the CC genotype, 46% of the heterozygous group and 38% of those with the TT genotype (p = 0.001) achieved a SVR. Conversely, the percentage of non-responders was 15, 43, and 48% (p < 0.0001), respectively. The NNT to achieve a SVR was strongly influenced by the IL28B rs12979860 genotype and ranged from 2-10. The IL-28B rs12979860 CC genotype was found in 22% of Mexican patients chronically infected by HCV. Genotyping IL28B SNP rs12979860 is useful to predict the response to a standard regimen with PegIFN-α/RVB, especially in those infected with HCV genotype 1. Copyright © 2015 IMSS. Published by Elsevier Inc. All rights reserved.
    Archives of medical research 07/2015; DOI:10.1016/j.arcmed.2015.07.001
  • Article: Preface.
    Archives of medical research 06/2015; DOI:10.1016/j.arcmed.2015.06.008
  • Archives of medical research 06/2015; DOI:10.1016/j.arcmed.2015.06.007
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    ABSTRACT: The atherosclerotic process in coronary arteries begins with endothelial dysfunction and may provoke thrombotic total occlusion and myocardial infarction. In this state-of-the-art review, we discuss recent evidence of atheroslerosis, vulnerable plaque, and hemodynamic changes in the coronary tree, as well as the current techniques we implement in the catheterization lab to evaluate coronary stenosis. It is clear that atherosclerosis is a chronic inflammatory condition with several consequences in the coronary tree, however, we are able now to characterize the plaque and to select the appropriate treatment for many patients. Copyright © 2015 IMSS. Published by Elsevier Inc. All rights reserved.
    Archives of medical research 06/2015; DOI:10.1016/j.arcmed.2015.06.005
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    ABSTRACT: We targeted to investigate the efficacy and the mechanisms of two gastric bypass surgeries, Roux-en-y Gastric Bypass (RYGB) and Billroth II gastrojejunostomy on managing obese patients with T2DM and nonobese T2DM patients, respectively. Seven nonobese T2DM patients with gastric cancer submitted to Billroth II gastrojejunostomy were compared with nine obese T2DM patients undergoing RYGB about their baseline characteristics, weight loss and glycemic control, 3 months and 2 years after surgery. Meanwhile, β-cell function, glucagon-like peptide 1 (GLP-1), peptide YY (PYY) and gastric inhibitory polypeptide (GIP) levels were also investigated. Significant weight loss and improvement of glycemic control were observed in both groups and in the two follow-up periods. Reduction of body mass index was greater in obese patients with T2DM. The efficacy of Billroth II gastrojejunostomy on controlling blood glucose of nonobese T2DM was similar to that of RYGB on managing obese T2DM. Insulin levels and HOMA-IR were decreased in obese T2DM patients, whereas they remained unchanged in nonobese T2DM patients. Generally, levels of GLP-1 and PYY were increased, whereas GIP levels were decreased in both groups. Glycemic control efficacy of Billroth II gastrojejunostomy on managing nonobese T2DM is similar to that of RYGB on treating obese T2DM in the short- and mid-term. The underlying mechanisms of both surgeries may be related to weight loss and gut hormone modulations. Copyright © 2015 IMSS. Published by Elsevier Inc. All rights reserved.
    Archives of medical research 06/2015; DOI:10.1016/j.arcmed.2015.06.003
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    ABSTRACT: The protective effect of ischemic preconditioning (IP) in liver transplantation (LT) has been studied with controversial results. We undertook this study to investigate whether IP of cadaveric donor livers is protective to allografts. IP (LT + IP, n = 6) was induced by 10-min hilar clamping. These were compared to cadaver donors with no IP (LT, n = 7). Clinical data and blood were obtained in donors and recipients for biochemical and inflammatory mediator (IM) measurements (P-selectin, leukotriene B4, myeloperoxidase, ICAM-1, IL-1, IL-6, and TNF-α). Liver tissue samples were obtained from donors and recipients (90 min after reperfusion). No significant differences were found in demographic characteristics between donors and recipients. When comparing both groups (LT + IP vs. LT only), ICU stay was longer in LT + IP group. For biochemical parameters, a significant difference was found only with a higher total bilirubin at postoperative day 3 in LT + IP group. There was no statistical difference in IM between LT and LT + IP groups at different stages of the study. Histological analysis of donor grafts indicated the presence of steatosis (50%) in one graft from the LT + IP group. However, in post-reperfusion biopsies neither neutrophil infiltration nor grade of necrosis showed significant difference between groups. No incidence of primary graft nonfunction (PGNF) was observed and graft and patient survival was similar in the two groups at 24 months. IP does not seem to protect against I/R injury in cadaveric LT, and no PGNF was seen. Copyright © 2015 IMSS. Published by Elsevier Inc. All rights reserved.
    Archives of medical research 06/2015; DOI:10.1016/j.arcmed.2015.06.002
  • [Show abstract] [Hide abstract]
    ABSTRACT: An assessment was performed of the quality of Pap readings in 19 cytology laboratories (CLs) in Mexico from the Cervical Cancer Screening Program. Nine CLs were affiliated with the Health Ministry (SSA), and ten were affiliated with the Mexican Social Security Institute (IMSS). Two sets of 200 cervical cytology specimens were prepared, one set for each institution. Fourteen percent of the specimens were positive and six were inappropriate for diagnosis (3%). All cervical cytology specimens were processed in the cytopathology laboratory at the General Hospital of Mexico, and histopathology was available for each positive case. Thirty percent of the SSA reading centers had a sensitivity of at least 80%; however, not one of the ten IMSS laboratories evaluated reached this figure. Some reading centers had a sensitivity <65%, meaning that nearly half of the specimens with a cytology consistent with cervical neoplasm were not identified. Given these results, it is a priority to effect a paradigm shift combining various screening tests to improve adherence to standards and enhanced cost-effectiveness of the early detection of cervicouterine cancer (CC) in Mexico. Copyright © 2015 IMSS. Published by Elsevier Inc. All rights reserved.
    Archives of medical research 06/2015; DOI:10.1016/j.arcmed.2015.05.013
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    ABSTRACT: Apolipoprotein A-I is the major protein in high-density lipoprotein (HDL) and plays an important role during the process of reverse cholesterol transport (RCT). Knowledge of the high-resolution structure of full-length apoA-I is vital for a molecular understanding of the function of HDL at the various steps of the RCT pathway. Due to the flexible nature of apoA-I and aggregation properties, the structure of full-length lipid-free apoA-I has evaded description for over three decades. Sequence analysis of apoA-I suggested that the amphipathic α-helix is the structural motif of exchangeable apolipoprotein, and NMR, X-ray and MD simulation studies have confirmed this. Different laboratories have used different methods to probe the secondary structure distribution and organization of both the lipid-free and lipid-bound apoA-I structure. Mutation analysis, synthetic peptide models, surface chemistry and crystal structures have converged on the lipid-free apoA-I domain structure and function: the N-terminal domain [1-184] forms a helix bundle while the C-terminal domain [185-243] mostly lacks defined structure and is responsible for initiating lipid-binding, aggregation and is also involved in cholesterol efflux. The first 43 residues of apoA-I are essential to stabilize the lipid-free structure. In addition, the crystal structure of C-terminally truncated apoA-I suggests a monomer-dimer conversation mechanism mediated through helix 5 reorganization and dimerization during the formation of HDL. Based on previous research, we have proposed a structural model for full-length monomeric apoA-I in solution and updated the HDL formation mechanism through three intermediate states. Mapping the known natural mutations on the full-length monomeric apoA-I model provides insight into atherosclerosis development through disruption of the N-terminal helix bundle or deletion of the C-terminal lipid-binding domain. Copyright © 2015 IMSS. Published by Elsevier Inc. All rights reserved.
    Archives of medical research 06/2015; DOI:10.1016/j.arcmed.2015.05.012
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    ABSTRACT: Studies investigating the association between the peptidylarginine deiminase 4 (PADI4) gene polymorphisms and rheumatoid arthritis (RA) reported conflicting results. The aim of this meta-analysis was to assess the association between PADI4 gene polymorphisms and RA. A systematic literature search was conducted to identify relevant studies. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) were used to estimate the strength of the association. A total of 34 studies from 28 articles involving 19859 patients with RA and 25771 healthy controls were included. Significant association of PADI4-94G/A polymorphism and RA was observed (OR = 0.891, 95% CI = 0.833-0.954, p = 0.001) in the overall study population and in the Asian populations (OR = 0.824, 95% CI = 0.759-0.894, p = 0.000) respectively. For the -92C/G polymorphism, a significant association was observed (OR = 1.481, 95% CI = 1.166-1.882, p = 0.001) in Africans. For the -90C/T polymorphism, a significant association was observed (OR = 0.576, 95% CI = 0.381-0.872, p = 0.009) in the Latin American population. The pooled estimates for the other polymorphisms were not statistically significantly associated with RA (PADI4-104C/T, -89A/G, -96T/C). This meta-analysis demonstrates that PADI4-94G/A polymorphism is associated with susceptibility to RA in the overall population and in the Asian population. The PADI4 -92C/G polymorphism confers susceptibility to RA in Africans and the PADI4-90C/T polymorphism was associated with RA in the Latin American population. Copyright © 2015 IMSS. Published by Elsevier Inc. All rights reserved.
    Archives of medical research 06/2015; DOI:10.1016/j.arcmed.2015.05.011
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    ABSTRACT: Cardiovascular disease (CVD) is a universal problem in modern society. Atherosclerosis is the leading cause of CVD resulting in high rate of mortality in the population. Nutrition science has focused on the role of essential nutrients in preventing deficiencies, at the present time, the nutritional strategies are crucial to promote health and intervene with these global noncommunicable diseases. In many cases, diet is a major driving force, which is much easier to change and follow than other factors. It is important to establish that the first strategy to treat atherosclerosis is to modify lifestyle habits, focusing on the beneficial properties of specific nutrients. In the last decades, epidemiological, clinical and experimental studies have demonstrated that diet plays a central role in the prevention of atherosclerosis. In this review we will focus on the effect of specific foods, nutrients and bioactive compounds, including epidemiological facts, potential mechanisms of action and dietary recommendations to reduce the risk of atherosclerosis. In particular, we include information about fiber, plant sterols and stanols, niacin, taurine, olive oil, omega 3 fatty acids, antioxidants, minerals, methyl nutrients and soy. In addition, we also show that dysbiosis of the intestinal microbiota associated with a consumption of certain animal food sources can generate some metabolites that are involved in the development of atherosclerosis and its consequences on CVD. According to the epidemiological, clinical and experimental studies we suggest a recommendation for some dietary foods, nutrients and bioactive compounds to support the complementary clinical management of patients with atherosclerosis. Copyright © 2015 IMSS. Published by Elsevier Inc. All rights reserved.
    Archives of medical research 05/2015; DOI:10.1016/j.arcmed.2015.05.010
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    ABSTRACT: The main atheroprotective mechanism of high-density lipoprotein (HDL) has been regarded as reverse cholesterol transport, whereby cholesterol from peripheral tissues is removed and transported to the liver for elimination. Although numerous additional atheroprotective mechanisms have been suggested, the role of HDL in modulating signal transduction of cell membrane-bound receptors has received little attention to date. This potential was recently highlighted following the identification of a polymorphism in the adenylyl cyclase 9 gene (ADCY9) that was shown to be a determining factor in the risk of cardiovascular (CV) events in patients treated with the HDL-raising compound dalcetrapib. Indeed, ADCY9 is part of the signaling pathway of the β2-adrenergic receptor (β2-AR) and both are membrane-bound proteins affected by changes in membrane-rich cholesterol plasma membrane domains (caveolae). Numerous G-protein-coupled receptors (GPCRs) and ion channels are affected by caveolae, with caveolae composition acting as a 'signalosome'. Polymorphisms in the genes encoding ADCY9 and β2-AR are associated with response to β2-agonist drugs in patients with asthma, malaria and with sickle cell disease. Crystallization of the β2-AR has found cholesterol tightly bound to transmembrane structures of the receptor. Cholesterol has also been shown to modulate the activity of this receptor. Apolipoprotein A1 (ApoA1), the major protein component of HDL, destabilizes and removes cholesterol from caveolae with high affinity through interaction with ATP-binding cassette transporter. Furthermore, β2-AR activity may be affected by ApoA1/HDL-targeted therapies. Taken together, these observations suggest a common pathway that potentially links a primary HDL function to the regulation of signal transduction. Copyright © 2015 IMSS. Published by Elsevier Inc. All rights reserved.
    Archives of medical research 05/2015; DOI:10.1016/j.arcmed.2015.05.008
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    ABSTRACT: Although reducing low-density lipoprotein-cholesterol (LDL-C) levels with lipid-lowering agents (statins) decreases cardiovascular disease (CVD) risk, a substantial residual risk (up to 70% of baseline) remains after treatment in most patient populations. High-density lipoprotein (HDL) is a potential contributor to residual risk, and low HDL-cholesterol (HDL-C) is an established risk factor for CVD. However, in contrast to conventional lipid-lowering therapies, recent studies show that pharmacologic increases in HDL-C levels do not bring about clinical benefits. These observations have given rise to the concept of dysfunctional HDL where increases in serum HDL-C may not be beneficial because HDL loss of function is not corrected by or even intensified by the therapy. Chronic kidney disease (CKD) increases CVD risk, and patients whose CKD progresses to end-stage renal disease (ESRD) requiring dialysis are at the highest CVD risk of any patient type studied. The ESRD population is also unique in its lack of significant benefit from standard lipid-lowering interventions. Recent studies indicate that HDL-C levels do not predict CVD in the CKD population. Moreover, CKD profoundly alters metabolism and composition of HDL particles and impairs their protective effects on functions such as cellular cholesterol efflux, endothelial protection, and control of inflammation and oxidation. Thus, CKD-induced perturbations in HDL may contribute to the excess CVD in CKD patients. Understanding the mechanisms of vascular protection in renal disease can present new therapeutic targets for intervention in this population. Copyright © 2015 IMSS. Published by Elsevier Inc. All rights reserved.
    Archives of medical research 05/2015; DOI:10.1016/j.arcmed.2015.05.009
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    ABSTRACT: Atherosclerosis is a chronic disease hallmarked by chronic inflammation, endothelial dysfunction and lipid accumulation in the vasculature. Although lipid modification and deposition are thought to be a major source of the continuous inflammatory stimulus, a large body of evidence suggests that infectious agents may contribute to atherosclerotic processes. This could occur by either direct effects through infection of vascular cells and/or through indirect effects by induction of cytokine and acute phase reactant proteins by infection at other sites. Multiple bacterial and viral pathogens have been associated with atherosclerosis by seroepidemiological studies, identification of the infectious agent in human atherosclerotic tissue, and experimental studies demonstrating an acceleration of atherosclerosis following infection in animal models of atherosclerosis. This review will focus on those infectious agents for which biological plausibility has been demonstrated in animal models and on the challenges of proving a role of infection in human atherosclerotic disease. Copyright © 2015 IMSS. Published by Elsevier Inc. All rights reserved.
    Archives of medical research 05/2015; DOI:10.1016/j.arcmed.2015.05.006
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    ABSTRACT: Ulcerative colitis (UC) is a chronic idiopathic inflammatory disease in which reducing pro-inflammatory and/or increasing anti-inflammatory molecules is the mainstay of treatment. The aim of this study was to evaluate the effects of supplementation with resveratrol as an antiinflammatory and antioxidant agent on inflammation and quality of life in patients with active UC. In this randomized, double-blind, placebo-controlled study, 50 eligible patients with active mild to moderate UC were supplemented with either a 500-mg resveratrol or placebo capsule for 6 weeks. Serum inflammatory markers, activity of NF-κB in peripheral blood mononuclear cells (PBMC) and quality of life were assessed at baseline and at the end of the study. Resveratrol supplementation led to a significant reduction in plasma levels of TNF-α (19.70 ± 12.80 to 17.20 ± 10.09 pg/mL) and hs-CRP (4764.25 ± 2260.48 to 2584.50 ± 1792.80 ng/mL) and activity of NF-κB in PBMCs (0.19 ± 0.05 to 0.10 ± 0.04 OD) (p < 0.001), whereas there were no significant changes of these factors in placebo group. Also, the score of inflammatory bowel disease questionnaire -9 (IBDQ-9) increased, whereas the clinical colitis activity index score decreased significantly in the resveratrol group (32.72 ± 7.52 to 47.64 ± 8.59) (p < 0.001) and when compared with the placebo group (35.54 ± 9.50 to 41.08 ± 6.59) (p < 0.001). Our results indicate that 6 weeks supplementation with 500 mg resveratrol can improve quality of life and disease clinical colitis activity at least partially through inflammation reduction in patients with UC. Whether these effects will be continued in longer duration of treatment remains to be determined. Copyright © 2015 IMSS. Published by Elsevier Inc. All rights reserved.
    Archives of medical research 05/2015; DOI:10.1016/j.arcmed.2015.05.005