Archives of Medical Research Journal Impact Factor & Information

Publisher: Elsevier

Journal description

Archives of Medical Research publishes original peer-reviewed medical research in an attempt to bridge the gaps created by medical specialization. Contributions are grouped into three main categories - biomedical, clinical, and epidemiological. Review articles, outstanding case reports, and preliminary communications will also be considered. As an international publication, the study of diseases is presented from various perspectives to provide the medical community with original investigation from molecular biology to clinical epidemiology within a single publication.

Current impact factor: 2.65

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 2.645
2013 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 2.31
Cited half-life 7.00
Immediacy index 0.41
Eigenfactor 0.00
Article influence 0.54
Website Archives of Medical Research website
Other titles Archives of medical research (Online)
ISSN 0188-4409
OCLC 43351379
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
    • Authors pre-print on any website, including arXiv and RePEC
    • Author's post-print on author's personal website immediately
    • Author's post-print on open access repository after an embargo period of between 12 months and 48 months
    • 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
    • Author's post-print may be used to update arXiv and RepEC
    • Publisher's version/PDF cannot be used
    • Must link to publisher version with DOI
    • 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

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Background and aims: Oxaliplatin is a widely employed platinum-derived chemotherapeutic agent commonly used for the treatment of colorectal cancer. Unfortunately, the benefit of this important drug is compromised by severe side effects such as neuropathy, ototoxicity, gastrointestinal toxicity, and hematological toxicity. Recently, few studies have also suggested the occurrence of hepatotoxicity in oxaliplatin-treated patients. Mitochondria have emerged as targets for anticancer drugs in various kinds of toxicity including hepatotoxicity that can lead to neoplastic disease. Oxidative stress is a well-established biomarker of mitochondrial toxicity. The purpose of this study was to investigate the dose-dependent damage caused by oxaliplatin on isolated liver mitochondria under in vitro conditions. Methods: The study was conducted in mitochondria isolated from liver of Wistar rats. Oxaliplatin was incubated with mitochondria in a dose-dependent manner under in vitro conditions. Oxidative stress indexes and non-enzymatic and enzymatic antioxidants were evaluated, looking at the overall armamentarium against the toxicity induced by oxaliplatin. Results: Oxaliplatin caused a significant rise in the mitochondrial oxidative stress indexes, lipid peroxidation and protein carbonyl. Alterations in the levels of non-enzymatic antioxidants and activities of enzymatic antioxidants were also observed. Conclusion: Oxidative stress plays an important role in the mitochondrial toxicity of oxaliplatin. The integrity of the hepatic tissue is compromised by the reactive oxygen species-mediated lipid peroxidation and protein carbonyl formation.
    Archives of Medical Research 11/2015; DOI:10.1016/j.arcmed.2015.10.002
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    ABSTRACT: Coronary artery disease (CAD) is a common form of vascular disease and is associated with high mortality and morbidity globally. It has been suggested that serum osteopontin (OPN) may be a useful biomarker of atherosclerosis and vascular calcification. The aim of this study was to assess the association between serum OPN levels and severity of CAD. Three hundred and four subjects were studied, 111 with clinically significant angiographically defined CAD (CAD+) (>50% stenosis), 96 with negative angiography (CAD-) (<50% stenosis) and 97 healthy controls. Fasting blood samples were collected from all patients before coronary angiography and serum OPN levels were determined using ELISA. Serum concentrations of OPN were significantly higher in both CAD+ (72.99 [51.05-103.64]) and CAD- (11.11 [8.11-18.23]) (p = 0.001) groups compared with the control group (5.99 [4.26-7.91]) (p = 0.001). CAD+ subjects also had higher serum OPN levels compared with CAD-subjects (p = 0.001). However, OPN levels were comparable between subgroups of CAD+ subjects stratified according to the number of narrowed vessels in angiography. The present results suggest a positive association between circulating OPN concentrations and the presence but not the extent of CAD. Copyright © 2015 IMSS. Published by Elsevier Inc. All rights reserved.
    Archives of Medical Research 03/2015; 46(2). DOI:10.1016/j.arcmed.2015.02.005
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    ABSTRACT: Tumor necrosis factor (TNF)-alpha G308A polymorphism has been reported in the association with susceptibility to Alzheimer's disease (AD); however, results have been contradictory. We conducted an updated meta-analysis to evaluate the role of TNF-alpha G308A in the occurrence of AD. Relevant articles were retrieved from online databases. The combined odds ratio, odds ratio in different genetic models, and the related 95% confidence intervals were calculated. Publication bias and homogeneity among individual studies were estimated. Subgroup analyses and sensitivity analyses were also performed. In overall analyses, no risk of AD was associated with TNF-alpha G308A under different genetic models. However, in the subgroup analyses, a significant association between TNF-alpha G308A and AD risk was observed in Chinese. In addition, a significant protective effect of TNF-alpha -308A was found in the occurrence of AD among North European populations under a dominant model. The result of this meta-analysis suggests that TNF-alpha G308A polymorphism may be associated with the increased risk of AD in Chinese and decreased risk of AD in northern European populations. Copyright © 2015 IMSS. Published by Elsevier Inc. All rights reserved.
    Archives of Medical Research 02/2015; 46(1). DOI:10.1016/j.arcmed.2014.12.006
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    ABSTRACT: Multidrug resistant tuberculosis (MDR-TB) poses problems in treatment, costs and treatment outcomes. It is not known if classically described risk factors for MDR-TB in other countries are the same in Mexico and the frequency of the association between diabetes mellitus (DM) and MDR-TB in our country is not clear. We undertook this study to analyze risk factors associated with the development of MDR-TB, with emphasis on DM. A case-control study in the state of San Luis Potosi (SLP), Mexico Was carried out. All pulmonary MDR-TB patients diagnosed in the state of SLP between 1998 and 2013 (36 cases) evaluated at a state pharmacoresistant tuberculosis (TB) clinic and committee; 139 controls were randomly selected from all pulmonary non-multidrug-resistant tuberculosis (non-MDR-TB) cases identified between 2003 and 2008. Cases and controls were diagnosed and treated under programmatic conditions. Age, gender, malnutrition, being a health-care worker, HIV/AIDS status, and drug abuse were not significantly different between MDR-TB and non-MDR-TB patients. Significant differences between MDR-TB and non-MDR-TB patients were DM (47.2 vs. 28.1%; p = 0.028); previous anti-TB treatments (3 vs. 0, respectively; p < 0.001), and duration of first anti-TB treatment (8 vs. 6 months, respectively; p < 0.001). MDR-TB and DM are associated in 47.2% of MDR TB cases (17/36) in this study. Other recognized factors were not found to be significantly different in MDR-TB compared to non-MDR-TB in this study. Cost-feasible strategies must be implemented in the treatment of DM-TB in order to prevent the selection of MDR-TB. Copyright © 2015 IMSS. Published by Elsevier Inc. All rights reserved.
    Archives of Medical Research 02/2015; 46(2). DOI:10.1016/j.arcmed.2015.01.006
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    ABSTRACT: Wilson's disease (WD), characterized by a disorder of copper metabolism, is an inherited autosomal recessive disease caused by mutations in the ATP7B gene. To explore genotype-phenotype correlations in Chinese WD patients and to evaluate the frequency of the ATP7B mutations, we described 77 clinically and biochemically confirmed WD patients and detected mutations in ten WD families from southwestern China. Clinical features were presented and all the exons of the ATP7B gene were screened. The appearance of Kayser-Fleischer (K-F) rings was closely related to onset age, particularly before 10 years old. For those patients with predominantly neurological symptoms, MRI was the most sensitive and preferred examination. Eight mutations of the ATP7B gene were detected including seven reported mutations (c.2302dup, c.2304delC, c.2333 G>T, c.2621 C>T, c.2755 C>G, c.2975 C>T and c.1366 G>C) and four novel mutations (c.3446 G>A, c.3767insCA, c.3406 G>A and c.3700delG). c.2333 G>T was detected in 6/20 alleles (30%), accounting for the largest proportion, which could be regarded as a mutation hotspot in this region. Our study extends the mutation spectrum of ATP7B and analyzes the relationship between mutations in the ATP7B gene and clinical findings of WD. Copyright © 2015 IMSS. Published by Elsevier Inc. All rights reserved.
    Archives of Medical Research 02/2015; 46(2). DOI:10.1016/j.arcmed.2015.02.001
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    ABSTRACT: Treatment of coronary in-stent restenosis (ISR) is hampered by a high incidence of recurrent ISR. Colchicine is an old drug with known anti-inflammatory and antiproliferative actions. We evaluated the strategy of colchicine combined with conventional balloon angioplasty for the treatment of ISR. Sixty coronary arteries of 60 mini-pigs underwent oversized bare-metal stent implantation to induce ISR. After 28 days, vessels with ISR (≥50% diameter stenosis) were randomly divided into three groups: control (conventional balloon angioplasty combined with placebo), colchicine (conventional balloon angioplasty combined with colchicine) and drug-eluting balloon (DEB). Restenosis and neointima formation were elevated with angiography and histological and morphometric analysis at 28 days after different interventions. Late lumen loss and percent area stenosis at follow-up were lower in colchicine group compared to control group but were similar to those of DEB group. There was no significant difference in proliferating cell nuclear antigen-positive vascular smooth muscle cells and inflammatory score between the colchicine group and the DEB group. The efficacy of colchicine combined with conventional balloon angioplasty for treatment of ISR was comparable to that of DEB. Treatment of ISR might not require a second stent implantation, and colchicine combined with conventional balloon angioplasty seemed to be another consideration. Copyright © 2015 IMSS. Published by Elsevier Inc. All rights reserved.
    Archives of Medical Research 02/2015; 46(2). DOI:10.1016/j.arcmed.2015.01.004
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    ABSTRACT: Nutrition during critical periods of development is one of the pivotal factors in establishing a lifelong healthy metabolism. Different nutritional deficiencies such as a low availability of proteins in the maternal diet produce alterations in offspring that include changes in insulin and glucose metabolism, a decrease in the size and number of cells of pancreatic islets of Langerhans, and premature ageing of the secretory function of pancreatic β cells. Moreover, it has been reported that chronic nutritional stress is associated with epigenetic alterations in mechanisms of gene regulation during pancreatic development and function. These alterations can lead to dysfunctional states in pancreatic β cells, which in the long run are responsible for the onset of metabolic diseases like type 2 diabetes. The present review summarizes the most important evidence in relation to the participation of epigenetic mechanisms in the regulation of gene expression during the intrauterine programming of the endocrine pancreas in animal models. Such mechanisms include DNA methylation as well as modifications of histones and microRNAs (miRNAs). Copyright © 2015 IMSS. Published by Elsevier Inc. All rights reserved.
    Archives of Medical Research 02/2015; 46(2). DOI:10.1016/j.arcmed.2015.01.005
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    ABSTRACT: β-Catenin and adenomatous polyposis coli (APC) are major components of the Wnt pathway. This study aimed to investigate the expression of β-catenin and APC in tumors and lymph nodes in colorectal cancer (CRC) patients and the mutational spectrum of the genes coding these proteins. Expression of APC and β-catenin was examined in 124 tumors and 41 lymph nodes. Exon 3 of CTNNB1 and the mutation cluster region (MCR) in exon 15 of the APC gene were screened for mutation by PCR-sequencing. Nuclear/cytoplasmic immunostaining of β-catenin was detected in 58.1 and 48.8% in tumors and lymph nodes, respectively. In tumors, abnormal expression of β-catenin correlated with tumor size and with those in lymph nodes. Membranous β-catenin expression occurred in 41.9 and 14.6% of tumors and lymph nodes, respectively. In tumors, lack of membranous β-catenin correlated with high invasiveness and metastatic potential. Positive immunostaining for APC was observed in 2 and 14% of tumors and lymph nodes, respectively. Overexpression in nucleus/cytoplasm and lack of membranous β-catenin significantly correlated with a reduced overall survival. Among 25 tumors, four harbour mutation in Ser33 and Ser47 and overexpress the β-catenin in the nucleus/cytoplasm. Mutations were identified in the APC gene in 13 tumors and six mutations were novel. Positive association between aberrant expression of β-catenin in the nucleus/cytoplasm of tumors and lymph nodes was observed. Nucleus/cytoplasmic accumulation of β-catenin and loss of membranous expression are related to reduced survival and could serve as a candidate prognostic predictor. Copyright © 2015 IMSS. Published by Elsevier Inc. All rights reserved.
    Archives of Medical Research 02/2015; 46(1). DOI:10.1016/j.arcmed.2015.01.001
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    ABSTRACT: We undertook this study to detect if there is a relationship between lactate production in the myocardium and the presence or absence of chest pain in patients with coronary artery disease (CAD). Forty six patients with significant CAD including left anterior descending artery were undergone echocardiography study, coronary angiography and pacing-induced ischemia. Serum lactate levels were determined in four blood samples, from mid-LV cavity and from coronary sinus before and after pacing-induced ischemia. Twenty eight patients comprised angina group and 18 patients comprised silent myocardial ischemia (SMI) group during pacing-induced ischemia. Eighteen patients (64.3%) of angina group had lactate production during ischemia. Eighteen patients of SMI group (100%) had diminished lactate extraction, and none had lactate production. The novel finding of this study is that the major difference in metabolism during SMI and angina pectoris is in the state of lactate production, which is absent during SMI and present during angina. We assume that lactate is the stimulus of cardiac ischemic pain and when its level increases, it stimulates pain receptors leading to chest pain. Copyright © 2015 IMSS. Published by Elsevier Inc. All rights reserved.
    Archives of Medical Research 01/2015; 46(2). DOI:10.1016/j.arcmed.2015.01.003
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    ABSTRACT: Obesity is associated with increased adipose tissue inflammation as well as with the development of type 2 diabetes (T2D). Syntaxin 8 (STX8) is a protein required for the transport of endosomes. In this study we analyzed the relationship of STX8 with the presence of T2D in the context of obesity. With this purpose, 21 subjects (seven lean [LN], eight obese normoglycemic [OB-NG] and six obese with type 2 diabetes [OB-T2D]) were included in the study. Gene and protein expression levels of STX8 and GLUT4 were analyzed in visceral adipose tissue (VAT). mRNA (p = 0.008) and protein (p <0.001) expression levels of STX8 were significantly increased in VAT of OB-T2D patients. Moreover, gene expression levels of SLC2A4 (GLUT4) were downregulated (p = 0.002) in VAT of obese patients. We found that STX8 was positively correlated (p <0.05) with fasting glucose concentrations, plasma glucose 2 h after an OGTT and C-reactive protein. Interestingly, the expression of STX8 was negatively correlated (p <0.05) with the expression of SLC2A4 in VAT. Increased STX8 expression in VAT appears to be associated with the presence of T2D in obese patients through a mechanism that may involve GLUT4. Copyright © 2014 IMSS. Published by Elsevier Inc. All rights reserved.
    Archives of Medical Research 12/2014; 46(1). DOI:10.1016/j.arcmed.2014.12.003
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    ABSTRACT: Influenza virus infections are serious public health concerns worldwide that cause considerable mortality and morbidity. Moreover, the emergence of resistance to anti-influenza viral agents underscores the need to develop new anti-influenza viral agents and novel treatment strategies. Recently, we identified anti-influenza viral activity of manuka honey. Therefore, we hypothesized that methylglyoxal (MGO), a key component of manuka honey, may impart anti-influenza viral activity. The aim of this study was to evaluate the anti-influenza viral activity of MGO and its potential in combination treatments with neuraminidase (NA) inhibitors. MDCK cells were used to evaluate anti-influenza viral activity. To evaluate the mechanism of MGO, plaque inhibition assays were performed. The synergistic effects of MGO and viral NA inhibitors were tested. MGO inhibited influenza virus A/WSN/33 replication 50% inhibitory concentration = 240 ± 190 μmol; 50% cytotoxic concentration = 1.4 ± 0.4 mmol; selective index (SI) = 5.8, which is related to its virucidal effects. Moreover, we found that MGO showed promising activity against various influenza strains. A synergistic effect was observed by a marked increase in SI of NA inhibitors at ∼1/100(th) of their single usage. A synergistic effect of MGO and oseltamivir was also observed against oseltamivir-resistant virus. Our results showed that MGO has potent inhibitory activity against influenza viruses and also enhanced the effect of NA inhibitors. Thus, the co-administration of MGO and NA inhibitors should be considered for treatment of influenza virus infections. Copyright © 2014 IMSS. Published by Elsevier Inc. All rights reserved.
    Archives of Medical Research 12/2014; 46(1). DOI:10.1016/j.arcmed.2014.12.002
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    ABSTRACT: The SNP rs662 in the paraoxonase 1 gene (PON1 Q192R) has been associated with obesity, dyslipidemia and cardiovascular risk. In this study, DNA samples of 117 children aged 6 to 12 years from San Luis Potosí, México were genotyped for Q192R polymorphism of the PON1 gene. Genotypic frequencies were determined by allelic discrimination assay by real-time PCR using TaqMan fluorogenic probes. Anthropometry, lipid profile, glucose and insulin were analyzed by genotype. The distribution of allele frequency in the population was Q = 65 and R = 35 following the Hardy Weinberg equilibrium (χ(2) = 3.15, p = 0.076). The Homeostasis Model Assessment for Insulin Resistance (HOMA-IR) index showed statistically significant differences among QQ/QR/RR genotypes (p = 0.032). The odds ratio for the carriers of the RR genotype was associated with HOMA-IR corresponding to the 95(th) percentile or higher for Mexican children based on sex and age (OR = 4.68; 95% confidence intervals, 1.23-17.8; p = 0.016). When the absolute mean of HOMAR-IR was set as the cutoff, an increased odds was observed (OR = 6.52; 95% confidence intervals, 1.68-25.3; p = 0.008). According to our results, PON1 Q192R polymorphism is a risk marker for insulin resistance, a pathological factor involved in the development of metabolic syndrome. Copyright © 2014 IMSS. Published by Elsevier Inc. All rights reserved.
    Archives of Medical Research 12/2014; 46(1). DOI:10.1016/j.arcmed.2014.12.001