Years and Volumes

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Articles from this Volume

Julieta Panero, Jorge Arbelbide, Dorotea Beatriz Fantl, Hernán García Rivello, Dana Kohan, and Irma Slavutsky

Two of the most common plasma cell disorders are monoclonal gammopathy of undetermined significance (MGUS) and multiple myeloma (MM). Clinical manifestations of MM include osteolytic lesions, anemia, hypercalcemia, immunodeficiency, and renal abnormalities. Telomere length and telomerase activity in cancer development have been extensively studied. Telomeres progressively shorten, lead to dysfunction and contribute to tumorigenesis. While several studies have evaluated telomere length and telomerase activity in MM patients, there is little information regarding this data in presymptomatic MGUS patients. Panero et al. examined mRNA expression in genes encoding telomere binding proteins to investigate the role of telomere dysfunction in the progression of MGUS to MM. Results show evidence of shortened telomeres, changes in telomere maintenance gene expression, and evidence of modified expression in telomere-associated genes between MGUS and MM. Understanding this process may aid in designing therapeutic approaches for patients with plasma cell disorders since many of them may be sensitive to interventions targeting telomere-damage.

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Posted by MolMed Admin on Nov 3, 2010 12:00 AM CDT
Shan-Shan Xing, Xiu-Ping Bi, Hong-Wei Tan, Yun Zhang, Qi-Chong Xing, and Wei Zhang

Metabolic syndrome (MS) is a disorder characterized by a group of metabolic risk factors including obesity, type 2 diabetes, and hypertension, leading to an increased risk of cardiovascular disease. Inflammation plays an important role in the pathophysiology of MS. While it has been suggested that elevated serum levels of the proinflammatory cytokine interleukin-18 (IL-18) are involved in the pathogenesis of MS, the relationship remains unclear. In this work Xing et al. investigated the functional consequences of IL-18 overexpression in MS using an experimental model. Findings indicate overexpression of IL-18 leads to aggravated left ventricular diastolic dysfunction, suggesting an important role of IL-18 in myocardiac fibrosis in MS. Attenuation of the inflammatory process may represent an avenue for therapeutic strategy in treating metabolic cardiomyopathy.

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Posted by MolMed Admin on Nov 2, 2010 12:00 AM CDT
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.

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Posted by MolMed Admin on Nov 1, 2010 12:00 AM CDT
Review Article

Kai Yin, Duan-fang Liao, and Chao-ke Tang

Atherosclerosis, a chronic inflammatory disease of the artery wall, involves numerous cellular and molecular inflammatory components. ATP-binding membrane cassette transporter A1 (ABCA1) is a crucial protein involved in cellular cholesterol efflux and reverse cholesterol transport. Recent studies suggest ABCA1 may be the molecular basis for the interaction between inflammation and RCT. Here, Yin et al. review recent findings on the role of inflammatory cytokines, inflammatory proteins, inflammatory lipids and endotoxin-mediated inflammatory process in expression of ABCA1. Additionally, the authors cover ABCA1's function in modulating immunity and inflammation through direct and indirect anti-inflammatory mechanisms.

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Posted by MolMed Editor on Oct 6, 2010 12:00 AM CDT
Review Article

Nora Sandu and Bernhard Schaller

Neutral stem cells have the potential to become a new and promising treatment modality in different pathologies of the central nervous system, including malignant brain tumors. Novel therapies to eliminate these tumors are already aided by current stem cell research and stem cell regulation monitored by molecular imaging. This review describes the current molecular imaging techniques used on neutral stem cells affected by therapeutic experimental brain tumor models.

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Posted by MolMed Editor on Oct 5, 2010 12:00 AM CDT
Yvonne Wettergren, Elisabeth Odin, Göran Carlsson, and Bengt Gustavsson

Hypermethylation of p16 is associated with reduced survival in patients with colorectal cancer. In this work, Wettergren et al. investigated whether polymorphisms in folate- and methyl-associated genes were linked with p16 hypermethylation in colorectal cancer patients.  Results indicate patients with MTRR gene variants exhibit significantly worse cancer-specific survival when the mucosa is positive for p16 hypermethylation.  The authors hypothesize this may be due to oxidative stress associated with this genotype as well as with p16.  These data begin to unravel a mechanism which may be responsible for increased risk of recurrent disease as well as poor cancer-specific survival.

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Posted by MolMed Editor on Oct 4, 2010 12:00 AM CDT
Jing Zhang, Selena Wei Shan Sio, Shabbir Moochhala, and Madhav Bhatia

Patients with severe burns are susceptible to sepsis, a systemic inflammatory condition that may lead to multiple organ failure and shock, which are common causes of morbidity and mortality. Full-thickness burns exceedin 25% of the total body surface area produce a profound systemic inflammatory reaction characterized by leukocyte activation and plasma leakage in the microvasculature of tissues and organs remote from the wound. Endogenous hydrogen sulfide (H2S) is naturally synthesized in many types of mammalian cells and plays a proinflammatory role in various experimental models. Here, Zhang et al. investigate the effect of local burn injury on H2S release in distant organs. Burn injury significantly increased plasma and liver H2S levels. Prophylactic as well as therapeutic administration of an inhibitor of H2S synthesis significantly reduced systemic inflammation. These findings highlight the role of H2S in contributing to inflammatory damage after burn injury and contribute to our understanding of this process. 

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Posted by MolMed Editor on Oct 3, 2010 12:00 AM CDT
Kirti Bhatt, Li Zhou, Qing-Sheng Mi, Shuang Huang, Jin-Xiong She, and Zheng

Acute Kidney Injury (AKI) may occur in cancer patients due to the potent chemotherapy drug Cisplatin, which accumulates in renal tubular cells resulting in cell injury and death.  MicroRNAs, small non-coding RNAs produced endogenously, have emerged as important regulators in pathophysiological conditions such as development and tumorigenesis.  Little is known regarding the role of microRNAs in renal diseases such as AKI.  Here, Bhatt et al. examine the regulation of microRNA-34a (miR-34a), a target gene of p53, in experimental models of Cisplatin-induced AKI or nephrotoxicity.  Results demonstrate microRNA regulation in a model of acute kidney injury and indicate that Cisplatin-induced miR-34a may play a cytoprotective role in cell survival. 

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Posted by MolMed Editor on Oct 2, 2010 12:00 AM CDT
Pei-Fen Chen, Ya-ling Luo, Wei Wang, Jiang-xin Wang, Wen-yan Lai, Si-ming Hu, KaiFan Cheng, and Yousef Al-Abed

Asthmatic airway remodeling, characterized by structural and morphometric changes of the airway epithelium, is believed to be the result of chronic inflammation in the bronchial wall. Since macrophage migration inhibitory factor (MIF) is required for allergic asthma, Chen et al. investigated its effects on the development of airway remodeling using a small molecule MIF antagonist called ISO-1. Results demonstrate MIF small-molecule antagonism has significant antiinflammatory effects on allergen-induced lung inflammation and can prevent changes in airway remodeling in experimental models. This suggests that MIF antagonism may be an attractive alternative therapy for asthmatic patients.

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Posted by MolMed Editor on Oct 1, 2010 12:00 AM CDT
Gie Ken-Dror, Philippa J Talmud, Steve E Humphries, and Fotios Drenos

While the role of common Apolipoprotein E (APOE) variants on Coronary Heart Disease (CHD) is well known, the influence of other nearby apolipoprotein genes is unclear. Ken-Dror et al. examined the association between gene cluster variations of apolipoproteins in the genotypes of over 2700 middle-aged men, including 275 CHD events, over a 15-year follow-up period. Results indicate carriers of the APOE ε2 and APOC2 single nucleotide polymorphisms (SNPs) had a significantly lower risk of CHD when compared with non-carriers, while carriers of the APOC1 SNP had higher risk of CHD. The common APOE polymorphism may explain the majority of the locus genetic determinants of plasma lipid levels; however, additional SNPs in the APOC1/C2 region may contribute to CHD risk. This work exposes the potential of non-APOE SNPs as potential risk factors for CHD.

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Posted by MolMed Editor on Sep 6, 2010 12:00 AM CDT
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