Share:

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

Rita M Ramalho, Ricardo J S Viana, Rui E Castro, Clifford J Steer, Walter C Low, and Cecilia M P Rodrigues

Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by extracellular plaques of amyloid β and intracellular aggregations of tau. While the exact role of cell death is unclear, apoptosis is increased and caspase-3 is activated in AD. Ramalho et al. (309-317) examined the role of apoptosis in neuronal loss and tau pathology in a mouse model of tauopathy. Results showed that caspase-3 cleaved intermediate tau species early in the course of the disease, and preceded cell loss in amyloid β-exposed cultured neurons. The authors suggest a potential role for apoptosis in neuro- degeneration and underscore the importance of antiapoptotic agents in treating neurodegeneration associated with AD and other tauopathies.

View article: PDF

Posted by Leah Caracappa on Jun 2, 2008 12:00 AM CDT

Per M Humpert, Zdenka Djuric, Ulf Zeuge, Dimitrios Oikonomou, Yuri Seregin, Klaus Laine, Volker Eckstein, Peter P Nawroth, and Angelika Bierhaus

Endothelial progenitor cells (EPC) are involved in vascular regeneration and angiogenesis in experimental diabetes. Insulin therapy mobilizes circulating progenitor cells and in this work Humpert et al.(301-308) examined the effects of insulin on EPC outgrowth in blood from patients with type 2 diabetes. Results show the insulin-like growth factor 1 (IGF-1) receptor mediated the effect of insulin on EPC growth, which was in part dependent on MAP kinases. Insulin-mediated activation of the IGF-1 receptor led to increased clonogenic and angiogenic potential of EPCs in vitro. Specific therapeutic modulation of this signaling pathway may offer potential targets for the treatment of vascular diabetic complications.

View article: PDF

Posted by Leah Caracappa on Jun 1, 2008 12:00 AM CDT

Latifa Hilal, Yassir Hajaji, Marie-Pierre Vie-Luton, Zeina Ajaltouni, Bouchra Benazzouz, Maha Chana, Adelmajid Chraïbi, Abdelkrim Kadiri, Serge Amselem, and Marie-Laure Sobrier

Isolated growth hormone deficiency (IGHD), which can result from altered pituitary functions, may be of genetic origin. To date, five genes have been linked to IGHD, one of which encodes the growth hormone releasing hormone receptor (GHRHR). GHRHR plays a pivotal role in growth hormone synthesis and secretion by the pituitary. In this work, Hilal et al. (286-292) describe the particular phenotypes of two siblings with IGHD, born to a consanguineous union, in whom a novel splice site mutation in the GHRHR gene was identified. These observations broaden the phenotype associated with GHRHR defects and the authors discuss a possible role of GHRHR in the development of extrapituitary structures.

View article: PDF

Posted by Leah Caracappa on May 7, 2008 12:00 AM CDT

Daniel G Maluf, Valeria R Mas, Kellie J Archer, Kenneth Yanek, Eric M Gibney, Anne L King, Adrian Cotterell, Robert A Fisher, and Marc P Posner

With close to 5,000 kidney transplants failing per year in the US returning the recipients to dialysis, kidney transplant failure is a leading cause of end-stage renal disease. Loss of kidney graft function with tubular atrophy (TA) and interstitial fibrosis (IF), a set of findings termed chronic allograft nephropathy (CAN), causes most kidney allograft losses. Maluf et al. (276-285) identified several molecular pathways involved in TA/IF progression.  A distinctive gene expression pattern was observed in TA/IF subjects when compared with normal allografts and kidneys.  Altered gene expression in networks related to immune response, inflammation and cell-to-cell interaction highlight the importance of chronic inflammation in progressive graft deterioration and may lead to the identification of biomarkers or predictors of TA/IF and long term graft function.

View article: PDF 
Supplementary Data 1: PDF 
Supplementary Data 2:
PDF

Posted by Leah Caracappa on May 6, 2008 12:00 AM CDT

Linda Yu, Katrin Saile, Carol D Swartz, Hong He, Xiaolin Zheng, Grace E Kissling, Xudong Di, Shantelle Lucas, Stanley J Robboy, and Darlene Dixon

Uterine leiomyomas (fibroids) are benign neoplasms of the myometrium prevalent in reproductive-aged women. While some leiomyomas are asymptomatic, others cause pelvic pain, menstrual bleeding and infertility. Surgery remains the gold standard of treatment but is a costly and invasive option. Receptor tyrosine kinases (RTKs) play an important role in the enhanced proliferation observed in leiomyomas and in this work, Yu et al. (264-275) used a phospho-RTK array technique to detect RTK activity in leiomyomas. Analysis revealed that overexpression of RTKs and activation of the IGF-IR signaling pathway are important mediators of uterine leiomyoma growth. These data may provide new anti-tumor targets for noninvasive treatment of leiomyomas.

View article: PDF

Posted by Leah Caracappa on May 5, 2008 12:00 AM CDT

Taka-aki Nakada, Shigeto Oa, Ken-ichi Matsuda, Tomohito Sadahiro, Masataka Nakamura, Ryuzo Abe, and Hiroyuki Hirasawa

Cytokines play a pivotal role in the complex pathophysiology of severe sepsis and septic shock. While cytokine-targeting treatment modalities for these conditions have been devised and tested, few have exhibited beneficial therapeutic effects. Blood purification, originally developed for the treatment of renal failure, has been applied to critical illnesses. Using polymethylmethacrylate-continuous hemodiafiltration (PMMA-CHDF) to remove cytokines, Nakada et al. (257-263) improved hypercytokinemia and dysoxia in patients with septic shock. Their findings suggest that cytokine-oriented therapy using PMMA-CHDF may be an effective strategy for treatment of septic shock.

View article: PDF

Posted by Leah Caracappa on May 4, 2008 12:00 AM CDT

Stefanie B Flohé, Hemant Agrawal, Sascha Flohé, Meenakshi Rani, Jörg M Bangen, and F Ulrich Schade

Sepsis is associated with immunosuppression that prevents host development of an effective immune response against invading microorganisms which may lead to unrestricted spreading of bacteria, multiple organ failure and death.  The impaired capacity of dendritic cells to mount a protective T helper cell type (TH1) response contributes to this immunosuppression. Flohé et al. (247-256) investigated the suppressed cytokine secretion pattern of dendritic cells (DC) during sepsis and analyzed immuno- modulatory approaches for restoration of IL-12 secretion, the key cytokine in TH1 cell development. Results show that the development of immunosuppression during sepsis is associated with an impaired capacity of splenic DC and macrophages to release TH1-promoting cytokines upon stimulation with bacterial products. Immunomodulatory cytokines increased IL-12 synthesis by dendritic cells early during sepsis as well as increased the activity of macrophages. Therapies that modulate the dysfunction of dendritic cells might have beneficial effects on the outcome of sepsis.

View article: PDF


Posted by Leah Caracappa on May 3, 2008 12:00 AM CDT

Mark J Paul-Clark, Rosalinda Sorrentino, Lucy K Bailey, Shiranee Sriskandan, and Jane A Mitchell

Inflammation, which occurs in a number of life-threatening diseases, is associated with an increase in oxidant stress. Oxidants can activate monocytes via Toll-Like Receptor (TLR) 2, however, the functional downstream consequence on immune system bacterial surveillance is unknown. Paul-Clark et al. (238-246) investigated the effects of oxidants on activation of human cells derived from smokers and nonsmokers. Blood from smokers was more sensitive to bacterial stimulation than blood from non-smokers, suggesting that oxidant stress associated with smoking provides an initiating inflammatory signal, potentially via TLR2 or associated transduction pathways, which sensitizes cells to pathogenic stimuli. Such a synergistic relationship between oxidants and pathogen-induced cell activation provides insight to inflammation-associated oxidant stress.

View article: PDF

Posted by Leah Caracappa on May 2, 2008 12:00 AM CDT
Posted by Leah Caracappa on May 1, 2008 12:00 AM CDT

Review Article

Herbert Tilg and Alexander R Moschen

The number of obese and overweight individuals has risen dramatically over the last two decades.  Insulin resistance is the key primary defect underlying the development of type 2 diabetes, and plays an essential role in this and other obesity-related diseases.  Insulin resistance has also frequently been associated with a state of low-grade inflammation and is assumed to contribute to its development. In this review, Tilg et al. (222-231) summarize the link between inflammation, anti-inflammatory strategies and insulin resistance. 

View article PDF

Posted by Leah Caracappa on Apr 8, 2008 12:00 AM CDT
   1 2 3 4 5 6 7 8 9