Annals of Medicine (ANN MED )

Publisher: Suomalainen lääkäriseura Duodecim, Taylor & Francis

Description

Annals of Medicine is an international, peer-reviewed review journal bridging molecular medicine and clinical practice. It provides current opinions on a wide range of medical specialties focusing on internal medicine. This unique resource enables readers to keep up-to-date with the latest advances in the understanding of the pathogenesis of diseases and how molecular medicine can impact on daily clinical practice. The series on Trends in Clinical Practice and Trends in Molecular Medicine are published regularly. Special Sections feature commissioned, peer-reviewed papers on different aspects of a theme, which in 2001 will include tumorigenesis, obesity, angiogenesis and depression. A new series on the very latest advances in molecular medicine will start with molecular cardiology and molecular endocrinology. Annals of Medicine has an impact factor of 2.566 and is ranked 12/110 in the world in the category of Medicine, General and Internal. This journal is published for The Finnish Medical Society Duodecim.

  • Impact factor
    5.09
    Show impact factor history
     
    Impact factor
  • 5-year impact
    4.64
  • Cited half-life
    7.20
  • Immediacy index
    0.76
  • Eigenfactor
    0.01
  • Article influence
    1.64
  • Website
    Annals of Medicine website
  • Other titles
    Annals of medicine (Helsinki, Finland), Annals of medicine, Ann med
  • ISSN
    0785-3890
  • OCLC
    19550892
  • Material type
    Periodical, Internet resource
  • Document type
    Journal / Magazine / Newspaper, Internet Resource

Publisher details

Taylor & Francis

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 12 month embargo for STM, Behavioural Science and Public Health Journals
    • 18 month embargo for SSH journals
  • Conditions
    • Some individual journals may have policies prohibiting pre-print archiving
    • Pre-print on authors own website, Institutional or Subject Repository
    • Post-print on authors own website, Institutional or Subject Repository
    • Publisher's version/PDF cannot be used
    • On a non-profit server
    • Published source must be acknowledged
    • Must link to publisher version
    • Set statements to accompany deposits (see policy)
    • Publisher will deposit to PMC on behalf of NIH authors.
    • STM: Science, Technology and Medicine
    • SSH: Social Science and Humanities
    • 'Taylor & Francis (Psychology Press)' is an imprint of 'Taylor & Francis'
  • Classification
    ​ yellow

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Intracranial aneurysms, also called cerebral aneurysms, are dilatations in the arteries that supply blood to the brain. Rupture of an intracranial aneurysm leads to a subarachnoid hemorrhage, which is fatal in about 50% of the cases. Intracranial aneurysms can be repaired surgically, endovascularly, or by combining these two treatment modalities. They are relatively common with an estimated prevalence of unruptured aneurysms of 2–6% in the adult population, and are considered a complex disease with both genetic and environmental risk factors. Known risk factors include smoking, hypertension, increasing age and positive family history for intracranial aneurysms. Identifying the molecular mechanisms underlying the pathogenesis of intracranial aneurysms is complex. Genome-wide approaches such as DNA linkage and genetic association studies as well as microarray-based mRNA expression studies, provide unbiased approaches to identify genetic risk factors and dissecting the molecular pathobiology of intracranial aneurysms. The ultimate goal of these studies is to use the information in clinical practice to predict an individual’s risk for developing an aneurysm or monitor its growth or rupture risk. Another important goal is to design new therapies based on the information on mechanisms of disease processes to prevent the development or halt the progression of intracranial aneurysms.
    Annals of Medicine 08/2014;
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    ABSTRACT: Abstract Background. Some studies showed an anti-atherogenic effect of TNF-α blockers on lipid profile, but these data have been challenged. Objective. To perform a meta-analysis on lipid profile changes induced by TNF-α blocker treatment. Methods. Prospective studies on rheumatic patients receiving TNF-α blockers and providing before-and-after treatment values of triglycerides (TGs), total cholesterol (TC), HDL-cholesterol (HDLc), LDL-cholesterol (LDLc), and atherogenic index (AI) were included. Standardized mean differences (SMD) in lipid profile were analyzed at short-term (2-12 weeks), middle-term (13-24 weeks), and long-term (25-52 weeks) assessments. Results. Thirty articles (1707 patients) were included. TNF-α blockers determined an increase in TC at short-term, middle-term, and long-term assessments (SMD: 0.20 mmol/L [95% CI: 0.04, 0.35]; SMD: 0.27 mmol/L [95% CI: 0.08, 0.46]; SMD: 0.22 mmol/L [95% CI: 0.01, 0.43]). HDLc increased only at the short-term assessment (SMD: 0.19 mmol/L [95% CI: 0.10, 0.28]), and TGs achieved a significant increase at the long-term assessment (SMD: 0.19 mmol/L [95% CI: 0.04, 0.34]). LDLc and AI were not affected by TNF-α blocker treatment. Conclusions. Slight but significant increases in TC occurred without any significant change in LDLc and AI. Changes in HDLc and TGs were not consistent among the different time point assessments. These quantitative changes in lipid profile do not seem to be able to explain cardiovascular risk improvement reported in patients receiving TNF-α blockers. Further studies on other mechanisms are needed to address this issue.
    Annals of Medicine 01/2014; 46(2):73-83.
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    ABSTRACT: Abstract: Awareness and self reported symptoms among 105 gasoline station workers in the Gaza Strip were assessed. A cross section of workers was asked to fill in a questionnaire. Workers reported high level of knowledge on health effects of leaded gasoline 88 (83.8%) and lead as an environmental pollutant 89 (84.8%). Protective measures were poorly used. Knowledge seems not to have much influence on practice. The most common self reported symptoms were neurological symptoms including headache 78 (74.3%), fatigue 74 (70.5%), irritability 66 (62.9%), concentration difficulties 65 (61.9%), and sleep disturbance 55 (52.4%). The prevalence of symptoms increased with increasing years of work (2 corrected=7.713, P=0.021). Use of respiratory mask in particular can potentially limit such symptoms (2 corrected=8.325, P=0.004).
    Annals of Medicine 01/2010;
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    ABSTRACT: Apolipoprotein A-IV (apoA-IV) is a glycoprotein constituent of triglyceride-rich and high-density lipoproteins (HDL) and may thus play an important role in lipid metabolism. In Finland two common isoforms (A-IV-1 and A-IV-2) of apoA-IV have been found. The isoforms are the result of the G to T substitution in the third base of the codon 360 in the apoA-IV-2 allele of the apoA-IV gene. The purpose of the study was to determine the apoA-IV allele frequencies in the Saami and the Finns, and to relate the apoA-IV phenotypes to serum lipids. The sample was drawn in connection with a Reindeer Herders' Health Survey performed in northern Finland in 1989. The study group included 248 men with known ethnic origin, Saami and Finns, who lived in the area of the nine northernmost municipalities of Finland. ApoA-IV phenotypes from 71 Saami (both parents Saami) and 177 Finns (both parents Finns) were determined by isoelectric focusing and Western blotting. Serum lipids were determined enzymatically. ApoA-IV allele frequencies in the Saami and the Finns were for A-IV-1 0.894 vs 0.944 and for A-IV-2 0.106 vs 0.056, respectively (χ2-test, P < 0.05). The effect of the apoA-IV phenotype on serum HDL-cholesterol levels differed significantly between the Saami and the Finns (two-way ANCOVA, interaction between ethnicity and apoA-IV phenotype, P < 0.02). In the Saami, HDL-cholesterol levels were significantly higher in the apoA-IV-2/1 than in the apoA-IV-1/1 phenotypes (ANCOVA, P < 0.05). Mean total cholesterol, low-density lipoprotein (LDL)-cholesterol, apolipoprotein B, HDL-cholesterol and triglyceride levels did not differ statistically significantly between the Saami and the Finns. Yet, there was a trend in the Saami of having higher mean total cholesterol, LDL-cholesterol and apolipoprotein B levels than the Finns among the apoA-IV-2/1 phenotypes, while there was only a small difference in these parameters between the Saami and the Finns among the apoA-IV-1/1 phenotypes. In conclusion, the Saami have a higher frequency of the apoA-IV-2 allele than the Finns and most of the other studied populations.
    Annals of Medicine 07/2009; 30(2):218-223.
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    ABSTRACT: The aetiology of simple goitre, affecting up to 5% of a population in iodine-sufficient areas and over 10% in endemic areas, is incompletely understood. It is generally believed that the development of simple goitre, whether endemic or sporadic, depends on complex interactions between genetic, environmental and endogenous factors. The importance of genetic factors is evident from the clustering of simple goitre within families and from a higher concordance rate for goitre in monozygotic than in dizygotic twins. Recently, studies assessing the role of specific candidate genes or genetic markers in the aetiology of simple goitre have given conflicting data in various families. However, there may well be single genes playing a major role within certain families, eg the thyroglobulin (Tg) gene, the thyroid-stimulating hormone receptor (TSHR) gene, the Na+/I- symporter (NIS) gene, and the multinodular goitre marker 1 (MNG1) on chromosome 14, but the genes will vary from family to family. In addition, family and twin studies also indicate a modest to major role for environmental factors in the aetiology of simple goitre. Clearly, iodine deficiency and cigarette smoking are the most important environmental risk factors associated with the genesis of simple goitre. Other suggested risk factors include naturally occurring goitrogens, emotional stress and certain drugs and infections. Ongoing studies focus on whole-genome screening in multiplex families as well as on large population-based case-control studies. However, the possibility that simple goitre is a heterogeneous disease without a single well-defined genotype and phenotype should be left open.
    Annals of Medicine 07/2009; 32(3):153-156.
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    ABSTRACT: Symptoms of infection and tissue pathology are caused by the host response: not by the microbe per se. The same response is also critical for the defence and is needed to clear infection. It is therefore essential to understand how the host response is activated and to identify the critical effector mechanisms of the defence. We have studied these issues in the urinary tract infection (UTI) model. The symptoms of UTI and the host defence both rely on the so-called ‘innate’ immune system, making this one of the best characterized human disease models of ‘innate immunity’. We discuss the critical molecular events that determine whether the host response will be activated by P-fimbriated uropathogenic Escherichio coli as well as factors determining whether the patient develops acute pyelonephritis or asymptomatic bacteriuria. We will describe the glycoconjugate receptors used by the P-fimbriated bacteria adhering to host tissues, the recruitment of TLR4 co-receptors and the signalling pathways that allow progression to symptomatic disease, and discuss how these mechanisms are altered in asymptomatic carriers, presenting the possible genetic basis for unresponsiveness. We have shown that neutrophils are the critical effectors of the host defence and that neutrophil dysfunctions lead to acute pyelonephritis and renal scarring. Here we discuss the mechanisms of neutrophil-mediated, chemokine receptor (CXCR1)-dependent clearance, and the defect in inter-leukin-8 receptor homolog knock-out (IL-8Rh KO) mice and describe the data linking low CXCRI expression to recurrent pyelonephritis in man, as well as the information on the genetic basis for low CXCR1 expression in affected patients. Finally, the mechanisms of renal scarring in IL8Rh KO mice will be discussed in relation to human disease. Our studies hold the promise to provide a molecular and genetic explanation for disease susceptibility in some patients with UTI and to offer more precise tools for the diagnosis and therapy of these infections.
    Annals of Medicine 07/2009; 33(9):563-570.
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    ABSTRACT: BACKGROUND: Tissue injury mediated by matrix metalloproteinases (MMPs) is a hallmark of inflammatory lung diseases. Latent secreted proMMPs must be activated to be catalytically competent. AIM: Our aim was to analyse an involvement of the trypsin-2, trypsin-2-α1-proteinase inhibitor (PI) complex and tumour-associated trypsin inhibitor (TATI) in the in vivo activation of proMMP-8, -9 and -2. METHODS: Concentrations of trypsin-2, trypsin-Z-a,-PI complex and TAT1 in bronchoalveolar lavage fluid (BALF) were analysed by immunofluorometry. Molecular forms and expression of trypsin-2 and trypsin-2-α,-PI complex were identified by Western immunoblot and immunocyto-chemistry. Gelatinolytic and collagenolytic activities were measured by substrate-based activity assays. RESULTS: BALFs from 16 of 43 patients and BALFs from five of 15 healthy controls contained trypsin-2-a,-PI complex. TAT1 was found in all healthy control BALFs (median 0.12 μg/L, range 0.02-0.66 μg/L) whereas 8 of 43 BALFs from patients (median 0, range 0-0.64 μg/L, P = 0.0001) contained TATI. Patient BALFs showed significantly increased activation of MMP-9 and MMP-8 compared with healthy controls. The concentrations of trypsin-2-α,-PI complex correlated with the in vivo activation of MMP-9 and -8 (r = 0.68, P= 0.002 and r = 0.61, P = 0.008) but not with the activation of MMP-2 in BALFs.
    Annals of Medicine 07/2009; 33(6):437-444.
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    ABSTRACT: Phytosterolaemla (sitosterolaemia) is a very rare inherited sterol storage disease characterized by tendon and tuberous xanthomas and by a strong predisposition to premature coronary atherosclerosis. In addition to increased or normal serum cholesterol, patients are found to have markedly elevated concentrations of the phytosterols sitosterol and campesterol. These sterols accumulate in all tissues, except the brain. Increased intestinal absorption of plant sterols, impaired biliary excretion, and decreased cholesterol synthesis are suggested as causes for this disease. However, the primary defect has not yet been identified. As well as dietary restrictions of cholesterol and plant sterols, therapeutic approaches based on interruption of the enterohepatic circulation of bile acids by administration of bile acid-binding resins or ileal bypass surgery have been recommended as therapeutic approaches to reduce all serum sterols. Administration of sitostanol, a nonabsorbable saturated plant sterol, showed a significant reduction of serum plant sterols and cholesterol in two patients with phytosterolaemla, presumably by competitive inhibition of sterol absorption.
    Annals of Medicine 07/2009; 29(3):181-184.
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    ABSTRACT: Improved outcomes of percutaneous coronary interventions (PCI) with drug-eluting stents (DES) have resulted in their expanded use for left main coronary artery (LMCA) stenosis. We compared outcomes of patients undergoing PCI for unprotected LMCA stenosis and patients treated by coronary artery bypass grafting (CABG). Between January 2005 and January 2007, 6705 patients were studied with coronary angiography in northern Finland. All subjects treated with revascularization of LMCA stenosis (n = 287) were included and followed up for a mean of 12+6 months. From 287 patients, 238 underwent CABG, and 49 had PCI with DES. The incidence of 1-year mortality was 4% among the PCI-treated and 11% among CABG-treated patients (P = 0.136). After the first month, mortality among PCI-or CABG-treated patients did not differ statistically significantly (2% versus 7%, P = 0.133). The most significant independent predictor of mortality was reduced left ventricular systolic function (hazard ratio 14.9, 95% CI 5.5-40.0, P < 0.001). PCI with DES for selected LMCA disease patients results in short- and midterm outcomes comparable to results of CABG in general. PCI is a viable therapeutic option in selected patients with LMCA stenosis.
    Annals of Medicine 07/2008; 40(6):437-43.
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    ABSTRACT: Dual antiplatelet treatment with aspirin and clopidogrel is recommended after coronary stenting (PCI-S). There is scant evidence defining optimal post-PCI-S antithrombotic therapy in patients with atrial fibrillation (AF) in whom oral anticoagulation (OAC) is mandated. To evaluate the safety and efficacy of the antithrombotic strategies for this population, we conducted a systematic review of the available evidence in patients treated with OAC undergoing PCI-S. AF was the most frequent indication for OAC. Post-PCI-S management was highly variable, and triple therapy with warfarin, aspirin, and clopidogrel was the most frequent and effective combination. Warfarin plus aspirin alone was not sufficiently effective in the early period after PCI-S and should not be prescribed. While acknowledging that the optimal antithrombotic treatment for patients with AF at medium or high thromboembolic risk undergoing PCI-S is currently undefined, triple therapy of warfarin, aspirin, and clopidogrel is currently recommended, although associated with an increased risk of major bleeding. Restrictive use of drug-eluting stent is also recommended, due to the need for prolonged multiple-drug antithrombotic therapy which may increase the bleeding risk. Whether the combination of warfarin and clopidogrel (without aspirin) will preserve efficacy and produce less bleeding is an important issue still needing to be addressed.
    Annals of Medicine 06/2008; 40(6):428-36.
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    ABSTRACT: Allogeneic hematopoietic stem cell transplantation (allo-HSCT) remains the only proven curative therapy for chronic myeloid leukemia (CML), but lack of human leukocyte antigen (HLA)-matched sibling or unrelated donors has restricted its application. Recently, we developed an effective method for haploidentical allo-HSCT achieving comparable outcomes to HLA-identical transplantation. To evaluate the outcomes of CML patients who underwent haploidentical allo-HSCT. Ninety-three patients were treated with a modified busulfan (BU)/cyclophosphamide (CY) 2 regimen, including antithymocyte globulin followed by unmanipulated blood and marrow transplantation. Our data showed that the cumulative incidence of acute graft-versus-host disease (GVHD) was 64.52%, and grade III-IV was 26.45%, 61.79% had chronic GVHD, and 28.93% had extensive chronic GVHD. Non-relapse mortality varied at 8.72% (100 days), 20.72% (1 year) and 20.72% (2 years). Probability of 1-year and 4-year leukemia-free survival was similar in chronic phase (CP) 1, CP2/CR2, accelerated phase, and blast crisis patients. Probability of 4-year overall survival varied as 76.5% (CP1), 85.7% (CP2/CR2), 73.3% (accelerated phase), and 61.5% (blast crisis). Multivariate analysis indicated that factors affecting transplantation outcomes were HLA-B+DR mismatches versus others for II-III acute GVHD and III-IV acute GVHD, the stage of disease at transplantation for relapse, and the time from diagnosis to transplantation for leukemia-free survival, overall survival, and transplantation-related mortality. In our protocol, survival of HSCT for advanced CML was similar to stable stage. For patients lacking an HLA-identical related donor, haploidentical relatives are alternative HSCT donors.
    Annals of Medicine 04/2008; 40(6):444-55.
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    ABSTRACT: Prolyl 4-hydroxylases (P4Hs) have central roles in the synthesis of collagens and the regulation of oxygen homeostasis. The 4-hydroxyproline residues generated by the endoplasmic reticulum (ER) luminal collagen P4Hs (C-P4Hs) are essential for the stability of the collagen triple helix. Vertebrate C-P4Hs are alpha2beta2 tetramers with three isoenzymes differing in their catalytic alpha subunits. Another P4H family, the HIF-P4Hs, hydroxylates specific prolines in the alpha subunit of the hypoxia-inducible transcription factor (HIF), a master regulator of hypoxia-inducible genes, and controls its stability in an oxygen-dependent manner. The HIF-P4Hs are cytoplasmic and nuclear enzymes, likewise with three isoenzymes in vertebrates. A third vertebrate P4H type is an ER transmembrane protein that can act on HIF-alpha but not on collagens. All P4Hs require Fe2+, 2-oxoglutarate, O2, and ascorbate. C-P4Hs are regarded as attractive targets for pharmacological inhibition to control excessive collagen accumulation in fibrotic diseases and severe scarring, while HIF-P4H inhibitors are believed to have beneficial effects in the treatment of diseases such as myocardial infarction, stroke, peripheral vascular disease, diabetes, and severe anemias. Studies with P4H inhibitors in various animal models of fibrosis, anemia, and ischemia and ongoing clinical trials with HIF-P4H inhibitors support this hypothesis by demonstrating efficacy in many applications.
    Annals of Medicine 02/2008; 40(6):402-17.
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    ABSTRACT: Calcium (Ca(2+)) and phosphate (P(i)) are essential to many vital physiological processes. Consequently the maintenance of Ca(2+) and P(i) homeostasis is essential to a healthy existence. This occurs through the concerted action of intestinal, renal, and skeletal regulatory mechanisms. Ca(2+) and P(i) handling by these organs is under tight hormonal control. Disturbances in their homeostasis have been linked to pathophysiological disorders including chronic renal insufficiency, kidney stone formation, and bone abnormalities. Importantly, the kidneys fine-tune the amount of Ca(2+) and P(i) retained in the body by altering their (re)absorption from the glomerular filtrate. The ion transport proteins involved in this process have been studied extensively. Recently, new key players have been identified in the regulation of the Ca(2+) and P(i) balance. Novel regulatory mechanisms and their implications were introduced for the antiaging hormone klotho and fibroblast growth factor member 23 (FGF23). Importantly, transgenic mouse models, exhibiting disturbances in Ca(2+) and P(i) balance, have been of great value in the elucidation of klotho and FGF23 functioning. This review highlights the current knowledge and ongoing research into Ca(2+) and P(i) homeostasis, emphasizing findings from several relevant knockout mouse models.
    Annals of Medicine 02/2008; 40(2):82-91.
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    ABSTRACT: Stress-responsive adrenocortical function is the final physiological response to the cascade of events that occurs when the interaction between individuals and their environment takes place. Glucocorticoids are produced in response to perturbance of homeostasis and are necessary for the energy required to restore this homeostasis. Genetics contributes to the individual variation in basal and stimulated plasma glucocorticoid levels and also to adrenal gland mass that increases in response to prolonged adrenal stimulation. This review briefly describes regulation of the adrenocortical axis, summarizes the linkage studies carried out so far in humans and in model organisms, and discusses the potential candidate genes that might contribute to the variation. The significance of individual variations in the glucocorticoid stress-responsiveness, with particular attention to their potential role in the recent explosion of obesity and the prevalence of metabolic syndrome X, is commented upon.
    Annals of Medicine 02/2008; 40(2):139-48.

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