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Sökning: L773:0012 6667 OR L773:1179 1950 > (2015-2019)

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1.
  • Skillgate, Eva, et al. (författare)
  • Healthy lifestyle behavior and risk of long duration troublesome neck pain or low back pain among men and women : results from the Stockholm Public Health Cohort
  • 2017
  • Ingår i: Clinical Epidemiology. - 1179-1349 .- 1179-1349. ; 9, s. 491-500
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: The role of healthy lifestyle behavior (HLB) in terms of physical activity, alcohol intake, smoking, and diet put together has not yet been explored for the risk of low back pain (LBP) and neck pain (NP). Our aim was to study if an HLB is protective against the onset of long duration troublesome LBP and NP in men and women.Methods: Two cohorts from the Stockholm Public Health Cohort, free from LBP (n=12,483) and NP (n=10,539), respectively, in 2006, were surveyed with questionnaires. Baseline information about physical activity, alcohol intake, diet, and smoking were dichotomized into being healthy/not healthy and combined in a categorical variable according to the number of healthy behaviors present. Binomial regression analyses were used to evaluate the role of HLB for the outcomes 4 years later.Results: When men with three or four healthy lifestyles were compared to men with none or one, the risk ratio (RR) of LBP was 0.63 (95% confidence interval [CI]: 0.39-1.02). The corresponding RR for LBP in women was 0.86 (95% CI: 0.56-1.32). When men with three or four healthy lifestyles were compared to men with none or one, the RR for NP was 1.13 (95% CI: 0.74-1.71). The corresponding RR for NP in women was 0.52 (95% CI: 0.35-0.77).Conclusion: An HLB seems to be protective for long duration troublesome LBP in men, and for long duration troublesome NP in women.
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  • Eapen, Mathew Suji, et al. (författare)
  • Chronic Obstructive Pulmonary Disease and Lung Cancer : Underlying Pathophysiology and New Therapeutic Modalities
  • 2018
  • Ingår i: Drugs. - : Springer Science and Business Media LLC. - 0012-6667 .- 1179-1950. ; 78:16, s. 1717-1740
  • Tidskriftsartikel (refereegranskat)abstract
    • Chronic obstructive pulmonary disease (COPD) and lung cancer are major lung diseases affecting millions worldwide. Both diseases have links to cigarette smoking and exert a considerable societal burden. People suffering from COPD are at higher risk of developing lung cancer than those without, and are more susceptible to poor outcomes after diagnosis and treatment. Lung cancer and COPD are closely associated, possibly sharing common traits such as an underlying genetic predisposition, epithelial and endothelial cell plasticity, dysfunctional inflammatory mechanisms including the deposition of excessive extracellular matrix, angiogenesis, susceptibility to DNA damage and cellular mutagenesis. In fact, COPD could be the driving factor for lung cancer, providing a conducive environment that propagates its evolution. In the early stages of smoking, body defences provide a combative immune/oxidative response and DNA repair mechanisms are likely to subdue these changes to a certain extent; however, in patients with COPD with lung cancer the consequences could be devastating, potentially contributing to slower postoperative recovery after lung resection and increased resistance to radiotherapy and chemotherapy. Vital to the development of new-targeted therapies is an in-depth understanding of various molecular mechanisms that are associated with both pathologies. In this comprehensive review, we provide a detailed overview of possible underlying factors that link COPD and lung cancer, and current therapeutic advances from both human and preclinical animal models that can effectively mitigate this unholy relationship.
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  • Källén, Bengt, et al. (författare)
  • Ongoing Pharmacological Management of Chronic Pain in Pregnancy
  • 2016
  • Ingår i: Drugs. - : Springer Science and Business Media LLC. - 0012-6667 .- 1179-1950. ; 76:9, s. 915-924
  • Tidskriftsartikel (refereegranskat)abstract
    • The article discusses possible effects of the use of analgesics during pregnancy. It summarizes the pertinent literature and reports some previously unpublished data from the Swedish Medical Birth Register. Most likely the use of analgesics does not cause spontaneous abortion. Only small malformation risk increases are seen after the use of opioids and perhaps non-steroid anti-inflammatory drug (NSAID) use. If possible, the latter should be avoided during the first trimester. If exposure has occurred there is no reason to consider an interruption of the pregnancy. Continued use of analgesics may increase the risk of preeclampsia and of preterm birth, especially valid for opioids. Use of acetylsalicylic acid (ASA) in late pregnancy should be avoided because of the risk of bleeding and (valid also for NSAIDs) premature closure of the ductus arteriosus. A small risk for neonatal abstinence syndrome may exist after the use of opioids for chronic pain, notably during the third trimester and long-lasting effects on child development can possibly occur. For a woman with chronic pain, adequate use of pain killers during pregnancy is needed. It is prudent to avoid ASA and NSAIDs towards the end of the pregnancy, while acetaminophen is an acceptable option all through pregnancy. If continued use of opioids is necessary, the associated risks are low. Triptans can be used for migraine during pregnancy. If possible sumatriptan is preferable to other triptans as data for the latter are largely lacking. Ergots are preferably avoided as not enough data are available.
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  • Ludvigsson, Johnny (författare)
  • Therapies to Preserve beta-Cell Function in Type 1 Diabetes
  • 2016
  • Ingår i: Drugs. - : ADIS INT LTD. - 0012-6667 .- 1179-1950. ; 76:2, s. 169-185
  • Forskningsöversikt (refereegranskat)abstract
    • In spite of modern techniques, the burden for patients with type 1 diabetes mellitus will not disappear, and type 1 diabetes will remain a life-threatening disease causing severe complications and increased mortality. We have to learn of ways to stop the destructive process, preserve residual insulin secretion or even improve the disease via beta-cell regeneration. This will give a milder disease, a more stable metabolism, simpler treatment and perhaps even cure. Therapies based on single drugs have not shown sufficient efficacy; however, there are several treatments with encouraging efficacy and no apparent, or rather mild, adverse events. As the disease process is heterogeneous, treatments have to be chosen to fit relevant subgroups of patients, and step by step efficacy can possibly be improved by the use of combination therapies. Thus immunosuppressive therapies like anti-CD3 and anti-CD20 monoclonal antibodies might be combined with fusion proteins such as etanercept [tumor necrosis factor (TNF)-alpha inhibitor] and/or abatacept (CTLA4-Ig) early after onset to stop the destructive process, supported by beta-cell protective agents. The effect may be prolonged by using autoantigen therapy [glutamate decarboxylase (GAD) proinsulin], and by adding agents facilitating beta-cell regeneration [e.g. glucagon-like peptide-1 (GLP-1)] there should be a good chance to make the disease milder, perhaps leading to cure in some patients.
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