Years and Volumes

Success! Thank you for subscribing to receive email notifications when new articles are published in Molecular Medicine 2015. Click here to manage your subscriptions.


Articles from this Volume

Gustavo A Nader, Maryam Dastmalchi, Helene Alexanderson, Cecilia Grundtman, Ramkishore Gernapudi, Mona Esbjörnsson, Zuyi Wang, Johan Rönnelid, Eric P Hoffman, Kanneboyina Nagaraju, and Ingrid E Lundberg

Polymyositis (PM) and dermatomyositis (DM) are chronic, autoimmune skeletal muscle disorders characterized by weakness, infiltration by mononuclear inflammatory cells and fibrosis. Despite current pharmacological treatment, many patients are left with impaired muscle function. While recent studies have shown moderate exercise training in combination with immunosuppressive drugs may improve muscle performance, the molecular mechanisms underlying the exercise-associated clinical improvements remain poorly understood. In the present study, Nader et al. investigate the underlying mechanisms responsible for the beneficial effects of resistance exercise in autoimmune inflammatory myopathy (AIM) patients using genome wide mRNA profiles. Changes in gene expression reported are in agreement with performance improvements induced by exercise and suggest resistance exercise training can induce a reduction in inflammation and fibrosis in skeletal muscle. High-throughput analysis of skeletal muscle gene expression may provide useful information for identification of new disease biomarkers and targets for pharmacological intervention of AIM patients.

View article: PDF
Posted by MolMed Admin on Dec 27, 2010 3:15 PM CST
Gianfranco Ferraccioli, Luisa Bracci-Laudiero, Stefano Alivernini, Elisa Gremese, Barbara Tolusso, and Fabrizio De Benedetti

Tumor necrosis factor is the major target of therapeutic approaches in rheumatoid arthritis. A key issue in chronic arthritis is understanding the crucial molecules driving the transition from the acute phase to the chronic irreversible phase of the disease. In this review, Ferraccioli et al. examine five experimental models of rheumatoid arthritis and review cytokines necessary for driving the condition from acute to chronic.

View article: PDF
Posted by MolMed Admin on Dec 5, 2010 12:00 AM CST
Joseph Larner, David L Brautigan, and Michael O Thorner

Classical actions of insulin involve increased glucose uptake from the bloodstream and its metabolism in peripheral tissues. However, non-oxidative and oxidative glucose disposal remain incompletely explained by current models for insulin action. In this work, Larner et al. review the possible role of second messengers in responses and resistance to insulin. The authors postulate that inositol glycans, particularly of the D-chiroinositol class, are insulin mimetic and may serve as insulin second messengers.

View article: PDF
Posted by MolMed Admin on Dec 4, 2010 12:00 AM CST
Antero Salminen, Anu Kauppinen, Juha MT Hyttinen, Elisa Toropainen and Kai Kaarniranta

Age-related macular degeneration (AMD) can cause a progressive loss of central vision in elderly individuals. AMD may be classified into two categories: the atrophic dry form and the exudative wet form. The crucial difference between dry and wet AMD is the development of choroidal neovascularization in the wet form. In this review, Salminen et al. discuss the role of endoplasmic reticulum stress in neovascularization regulation and the conversion of dry age-related macular degeneration to its detrimental wet counterpart.

View article PDF
Posted by MolMed Admin on Dec 3, 2010 12:00 AM CST
Ji Heon Rhim, Jae Hoon Kim, Eui-Ju Yeo, Jae Chan Kim, and Sang Chul Park

Postoperative care for the elderly requires special attention with respect to wound healing time. While several factors have been found to play roles during wound healing, the molecular mechanisms responsible for age-dependent delay in wound healing have not been well defined. Caveolin is a principal structural component of caveolae membranes. Levels of caveolin-1 have been found to increase with aging, and reduction of caveolin-1 using antisense oligonucleotides or siRNA recovers the epidermal growth factor response in senescent cells. Rhim et al. hypothesized that caveolin-1-dependent responses in aged corneal epithelial cells may be responsible for delayed wound healing. The authors evaluated corneal wound healing time after laser epithelial keratomileusis (LASEK) surgery in young, middle aged and elderly patients. Results indicate caveolin-1 status may be responsible for delayed wound healing in the elderly and act as a regulator for wound healing capacity. While downregulation of caveolin-1 may facilitate wound healing in the elderly post LASEK surgery, these results may also be applied to wound healing in other surgeries or traumas.

View article: PDF
Supplementary Data: PDF
Posted by MolMed Admin on Dec 2, 2010 12:00 AM CST
George R Uhl, Tomas Drgon, Catherine Johnson, Marco F Ramoni, Frederique M Behm, and Jed E Rose

Cigarette smoking is a significant cause of premature death and disease. Although abstinence reduces risks to smokers, success rates following attempts to quit smoking remain modest. One year after unaided attempts to quit smoking, abstinence rates are less than 5%. In the current study, Uhl et al. report genome wide association studies of smoking cessation success in individually-genotyped European-American participants in a smoking cessation trial that examined effects of pre-cessation nicotine replacement therapy. Results identified a set of single nucleotide polymorphisms (SNPs) that overlap with prior datasets and likely identify a network of SNPs and genes with true biological relationships. Most of these genes are expressed in the brain and are related to neurotransmission processes, as may be expected for addiction-related traits. These results add to support for personalized approaches to smoking cessation treatment and contribute to studies that document molecular genetic contributions to the ability to quit smoking.

View article: PDF
Posted by MolMed Admin on Dec 1, 2010 12:00 AM CST
Wei Wang, Haoting Yen, Chih-Hung Chen, Nitesh Jasani, Rimabahen Soni, Karen Koscica, and Sandra E Reznik

Premature birth is an increasing health problem and is the major cause of neonatal mortality in developed countries. Intrauterine infection is often associated with preterm labor. The matrix metalloproteinases (MMPs) are a family of zinc-dependant endopeptidases that aid in the degradation of the extracellular matrix, allowing for cell movement and tissue reorganization thereby supporting the growing fetus. Endothelin-1 (ET-1), an extremely potent vasoconstrictor peptide, has been shown to increase myometrial smooth muscle tone. Blockade of ET-1 through endothelin-converting enzyme 1 (ECE-1) inhibitor or endothelin receptor antagonists prevents preterm labor and delivery in mice. Wang et al. demonstrate that LPS-induced preterm labor is associated with increased levels of MMP-1. Using ECE-1 RNAi, they show that silencing the ECE-1/ET-1 pathway prevents both the onset of preterm labor and MMP-1 upregulation. Their data indicate that ET-1 and MMP-1 act in the same molecular pathway in preterm labor.

View article: PDF
Posted by MolMed Admin on Nov 7, 2010 12:00 AM CDT
Martin Ploder, Katharina Kurz, Andreas Spittler, Gabriele Neurauter, Erich Roth, and Dietmar Fuchs

Hyperhomocysteinaemia, or increased levels of homocysteine in the blood, is an established risk factor for coronary artery disease, which occurs when dietary supply with folate and/or vitamin B12 is inadequate. Increased homocysteine in the blood may lead to formation of blood clots, resulting in heart attack or stroke. Homocysteine also acts as a proinflammatory mediator and may therefore play a role when the immune system is stimulated, such as in trauma or sepsis. Since no major studies have investigated homocysteine concentrations in septic patients, Ploder et al. investigated whether hyperhomocysteinemia may develop in this cohort despite administration of enteral nutrition. Results indicate increased levels of homocysteine are associated with poor patient outcomes. This may be due to the increased demand of B-vitamins associated with immunopathogenetic mechanisms. Although preliminary, this work suggests B-vitamin supplementation during inflammatory conditions should be further explored.

View article: PDF
Posted by MolMed Admin on Nov 6, 2010 12:00 AM CDT
Jennifer M Kaplan, Paul W Hake, Alvin Denenberg, Marchele Nowell, Giovanna Piraino, and Basilia Zingarelli

Sepsis, an overwhelming inflammatory response to infection or injury, may lead to shock, multiple organ failure and death. Peroxisome proliferator-activated receptor-γ (PPARγ) is a transcription factor which regulates inflammation. Post-translational modifications to PPARγ regulate its function, potentially affecting inflammation. In this work, Kaplan et al. investigated the kinetics of altered PPARγ expression and activation in a model of polymicrobial sepsis. Data demonstrate PPARγ is reduced in immunomodulatory and parenchymal cells during polymicrobial sepsis. Restoration of PPARγ correlates with an increase in levels of the antiinflammatory adipokine, adiponectin. These results provide a mechanism through which a decrease in PPARγ in sepsis may be partially explained and support the notion that additional studies investigating the molecular link between adipokines and the inflammatory response in sepsis are warranted.

View article: PDF
Posted by MolMed Admin on Nov 5, 2010 12:00 AM CDT
Daniel James Antoine, Dominic P Williams, Anja Kipar, Hugh Laverty, and B Kevin Park

Drug induced liver injury (DILI) is a major clinical concern and a leading cause of acute liver failure (ALF). Acetaminophen is a widely used analgesic which is safe at therapeutic doses. Acetaminophen hepatotoxicity following overdose contributes to a significant proportion of cases of ALF worldwide. While biochemical events leading to acetaminophen hepatotoxicity are well-defined, little is known about the cellular mechanism linking metabolic activation to clinical outcome. In this study, Antoine et al. investigated the effect of dietary restriction on cellular mechanisms during acetaminophen hepatotoxicity. Their findings indicate the inhibition of caspase driven apoptosis and HMGB1 oxidation by ATP depletion from fasting, promotes an inflammatory response during drug-induced hepatotoxicity. This work may aid the development of intervention therapies for cases of acetaminophen overdose and could improve the clinical management of drug induced liver injury.

View article: PDF
Posted by MolMed Admin on Nov 4, 2010 12:00 AM CDT
< Prev    1 2 3 4 5 6 7