Annals of Medicine (ANN MED )

Publisher: Suomalainen lääkäriseura Duodecim, Taylor & Francis


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.

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  • Website
    Annals of Medicine website
  • Other titles
    Annals of medicine (Helsinki, Finland), Annals of medicine, Ann med
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  • Material type
    Periodical, Internet resource
  • Document type
    Journal / Magazine / Newspaper, Internet Resource

Publisher details

Taylor & Francis

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    • Author can archive a pre-print version
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    • Author can archive a post-print version
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    • Some individual journals may have policies prohibiting pre-print archiving
    • On author's personal website or departmental website immediately
    • On institutional repository or subject-based repository after either 12 months embargo for STM, Behavioural Science and Public Health Journals or 18 months embargo for SSH journals
    • 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)
    • The publisher will deposit in on behalf of authors to a designated institutional repository including PubMed Central, where a deposit agreement exists with the repository
    • STM: Science, Technology and Medicine
    • SSH: Social Science and Humanities
    • Publisher last contacted on 25/03/2014
    • 'Taylor & Francis (Psychology Press)' is an imprint of 'Taylor & Francis'
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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: Liquid-assisted ventilation, as an alternative ventilation strategy for respiratory distress, is progressing from theory and basic science research to clinical application. Biochemically inert perfluorochemical liquids have low surface tension and high solubility for respiratory gases. From early immersion experiments, two primary techniques for liquid-assisted ventilation have emerged: total liquid ventilation and partial liquid ventilation. While computer-controlled, time-cycled, pressure/volume-limited total liquid ventilators can take maximum advantage of these liquids by completely eliminating the gas phase in the distressed lung, partial liquid ventilation takes advantage of having these liquids in the lung while maintaining gas ventilation. The benefits of both partial and total techniques have been demonstrated in animal models of neonatal and adult respiratory distress syndrome, aspiration syndromes and congenital diaphragmatic hernia and also in combination with other therapeutic modalities including extracorporeal membrane oxygenation, high-frequency ventilation and nitric oxide. Additionally, nonrespiratory applications have expanding potential including pulmonary drug delivery and radiographic imaging. Since its use in neonates in 1989, liquid-assisted ventilation in humans has progressed to a variety of clinical experiences with different aetiologies of respiratory distress. The future holds the opportunity to clarify and optimize the potential of multiple clinical applications for liquid-assisted ventilation.
    Annals of Medicine 11/2010; 29(6).
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    ABSTRACT: Gene therapy was introduced into clinical practice with great excitement, much publicity and considerable optimism in the early 1990s. Scientific evaluation of the early clinical trials has, however, greatly reduced the initial optimism. Follow-up studies have revealed that many early gene therapy trials mainly represented gene transfer into patients, possibly with short-term effects, but not true gene therapy where the course of the disease is permanently affected. This has lead to critical re-evaluation of the approaches taken. Clearly, more basic understanding is needed of the molecular mechanisms of the diseases treated. For this purpose, better animal models for human diseases are necessary. One of the biggest obstacles for gene therapy has been the lack of adequate vector systems. Development of new vectors for efficient and targeted delivery and uptake of therapeutic genes is a crucial area where progress needs to be made. The rationale for gene therapy depends largely on the type of disease to be treated. Recessively inherited single-gene disorders represent diseases where the concept of gene therapy-addition of a therapeutic gene to restore the lost function of two mutant alleles-is easily understood and rarely questioned. However, most gene therapy protocols are focused on multifactorial diseases such as malignancies where the therapeutic approach is quite different. While gene transfer technologies are being developed into truly effective gene therapy, the fight against inherited single-gene disorders also continues at population level by carrier screening and prenatal diagnostics where rapid methodological developments are taking place.
    Annals of Medicine 11/2010; 29(6):549-551.
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    ABSTRACT: Calcification of extracellular matrix (ECM) can be either physiological or pathological. Physiological calcification (or mineralization) of ECM is restricted to bones, teeth and, to a lesser extent, growth plate cartilages. Pathological calcification appears often in the ECM of arteries where it is a frequent complication of atherosclerosis. However, calcification of the ECM of arteries is not restricted to atherosclerosis. Indeed, human diseases have been described that are characterized by calcification of the aortic media in the absence of any atherosclerotic lesions. The existence of these rare diseases, along with several mouse models recently generated and discussed below, indicates that the formation of atherosclerotic lesions and the calcification of the artery ECM are controlled by different genetic pathways. This emerging knowledge has implications for our understanding of ECM calcification beyond atherosclerosis.
    Annals of Medicine 11/2010; 30(6):538-541.
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    ABSTRACT: The main pathological feature of human T-lymphotropic virus type I (HTLV-1)- associated myelopathy/tropical spastic paraparesis (HAWTSP) is chronic inflammation of the spinal cord characterized by perivascular cuffing of mononuclear cells accompanied by parenchymal lymphocytic infiltration. Although the exact mechanism of the pathogenesis of HAWTSP is still obscure, immunological abnormalities arising from a high HTLV-I proviral load in peripheral blood lymphocytes (PBL) play an important role in the pathological process of spinal cord lesions in HAWTSP patients. The relationship between HLA haplotype and the risk of the occurrence of HAWTSP will be elucidated by results from studies of HLA allele typing. In addition, recent data indicate that HTLV-I and its expression are localized in infiltrated lymphocytes within the spinal cord lesions of HAWTSP patients rather than in resident central nervous system (CNS) parenchymal cells. Although a bystander damage of the surrounding CNS tissues, in which CD8+ HTLV-I-specific cytotoxic T lymphocyte (CTL) attack HTLV-I-infected lymphocytes, might be involved in the pathological events of the spinal cords of HAM/ TSP patients as one of the actual pathogenetic mechanisms, heightened transmigrating activity of HTLV-I-infected CD4+ T lymphocytes to the CNS tissues may have a key role in the development of HAM/TSP. Therefore, although the exact mechanism underlying the high HTLV-I proviral load in PBL in HAWTSP patients is still unknown, we must consider therapeutic approaches in HAM/TSP that eliminate HTLV-I-infected CD4+ T lymphocytes.
    Annals of Medicine 09/2010; 32(9).
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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: Improvements in detector technology and the development of radioligands for brain receptor imaging have introduced exiting new insights into the pathophysiology of various neuropsychiatric disorders and have improved the possibilities of optimizing the treatment for patients suffering from them. Positron emission tomography (PET) and single-photon emission tomography (SPET) with tailored radiopharmaceuticals provide information on the topographic physiological chemistry of the living human brain. The different patterns of brain receptor densities and distribution can be imaged and modelled with PET and SPET. The normal receptor distribution in the brain is broadly heterogeneous with different cortical layers, which show receptor densities varying from very low to high. Further exploration of the data shows that human neurophysiology and neural architectures possess fractal properties that may be altered during activation and in different neuropsychiatric disorders. This review highlights recent findings in SPET receptor imaging and the use of fractal analysis in the interpretation of images representing various neuropsychiatric disorders.
    Annals of Medicine 08/2009; 30(3).
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    ABSTRACT: Starting from a broad definition of genetic epidemiology, current developments in association, segregation, and linkage analysis of complex inheritance are considered together with integration of genetic and physical maps and resolution of genetic heterogeneity. Mitochondrial inheritance, imprinting, uniparental disomy, pregressive amplification, and gonadal mosaicism are some of the novel mechanisms discussed, with speculation about the future of genetic epidemiology.
    Annals of Medicine 08/2009; 24(6).
  • Annals of Medicine 07/2009; 22(1).
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    ABSTRACT: Serum immunoglobulins and complement factors were investigated retrospectively in 35 splenectomised (n = 28) and autoreplanted (n = 7) patients following trauma. The main deficiency of the immune system following splenectomy was a reduction in the concentrations of serum IgM, C3, and Factor B with normal IgG, IgA and C4 values. These changes were not correlated with the time elapsed after splenectomy. However, patients who had splenic tissue autoreplantation had normal values of immunoglobulins and complement factors compared with healthy controls. Splenic replantation may be able to stop a fall in immunoglobulin and complement factor values after splenectomy.
    Annals of Medicine 07/2009; 21(4).
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    ABSTRACT: The genetic data, implicating mutations framing the beta-amyloid segment of the amyloid precursor protein as causes of Alzheimer's disease are reviewed and integrated with information on the normal processing of the amyloid precursor protein. The data indicating that there is a second and quantitatively major locus for early-onset Alzheimer's disease on the long arm of chromosome 14 are reviewed. The prediction that this second genetic locus will produce a protein intimately involved in the metabolism of the amyloid precursor protein is reiterated, together with the prediction that all causes of Alzheimer's disease will directly involve this process.
    Annals of Medicine 07/2009; 25(5).
  • Annals of Medicine 07/2009; 26(1).
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    ABSTRACT: The prenatal diagnosis of fetal rhesus D (RhD) status is useful for the management of RhD-negative women with partners heterozygous for the RHD gene. Conventional methods for prenatal fetal RhD status determination involve invasive procedures such as fetal blood sampling and amniocentesis. The recent demonstration of the existence of cell-free fetal DNA in maternal plasma and serum opens up the possibility of determining fetal RhD status by analysis of maternal plasma or serum DNA. This possibility has recently been realized by three independent groups of investigators. This development represents an important step towards the routine application of noninvasive fetal blood group diagnosis in sensitized pregnancies and may become a model for developing safer noninvasive prenatal tests for other single-gene disorders.
    Annals of Medicine 07/2009; 31(5).
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    ABSTRACT: Familial adenomatous polyposis is an autosomal dominant disease that includes early development of up to thousands of colorectal adenomas and several extracolonic manifestations. All untreated patients will develop colorectal adenocarcinoma. The treatment of choice is colectomy and ileorectal anastomosis, but restorative proctocolectomy may be considered in selected cases. Polyposis patients treated with ileorectal anastomosis should be followed for life, with regular proctosigmoidoscopy and destruction of new adenomas. Furthermore, regular gastroduodenoscopy should be carried out because of frequent occurrence of premalignant duodenal adenomas. The prognosis is good after prophylactic colectomy in patients without carcinoma. All first degree relatives of affected family members should be examined regularly with proctosigmoidoscopy from the age of ten, and prophylaxis should be organised using a national or regional polyposis register. The recent detection of a specific gene for familial adenomatous polyposis is a long step forward, and several problems may be solved by increasing international cooperation.
    Annals of Medicine 07/2009; 21(4).
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    ABSTRACT: Immunocytochemical studies using antibodies to cytoskeletal proteins have provided conflicting data on the components of paired helical filaments (PHF), due solely to immunological cross-reactivities. To avoid such ambiguity, we developed a protein chemical approach to the identification of the PHF components. After treatment with formic acid, PHF were digested with lysylendopeptidase and the resultant peptides were separated by HPLC. All major peaks were analysed for their amino acid compositions and sequences. From the PHF digest, proteolytic fragments of ubiquitin, tau and β protein were sequenced. Ubiquitin in PHF appears to be in a conjugated form, while its target protein remains unidentified. Tau is integrated into PHF at the site of its carboxyl third. The presence of 0 protein fragments is best interpreted as being due to contamination of amyloid filaments in the PHF preparation. Thus, ubiquitin and tau are the two definite components of PHF.
    Annals of Medicine 07/2009; 21(2).
  • Annals of Medicine 07/2009; 21(1).