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

Hye-Soon Lee, Annette T Lee, Lindsey A Criswell, Michael F Seldin, Christopher I Amos, John P Carulli, Cristina Navarrete, Elaine F Remmers, Daniel L Kastner, Robert M Plenge, Wentian Li, and Peter K Gregersen

Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease characterized by joint inflammation and progressive joint destruction. Recently, several new genes with modest levels of risk for RA have been identified in various populations. Nevertheless, the MHC remains the strongest region of genetic association with this disease, and until recently this has been assumed to be entirely due to the well-defined allelic associations with the class II HLA-DRB1 locus. However, it is likely that additional risk loci for RA are present WITHIN the major histocompatibility complex (MHC), independent of the HLA-DRB1 locus. Lee et al. (293-300) now provide evidence for several new risk loci for RA located in the Class I region of the MHC, as well as in the region centromeric to the DRB1 locus. These data emphasize the need for more detailed analysis of the MHC in RA, a theme that is also emerging for other autoimmune diseases such as type 1 diabetes.

View article: PDF 
Supplementary Data: PDF

Posted by Leah Caracappa on Jan 28, 2014 8:35 AM CST

Review Article

Ananda S Prasad

Although zinc requirements for plants and animals have been long-known, the role of zinc in human physiology has only recently been recognized. Zinc deficiency is prevalent in the developing world and is responsible for growth retardation in as many as two billion people. In this review, Dr. Prasad (353-357) reviews the evidence that zinc deficiency can lead to immune dysfunction, cognitive impairment, bullous pustular dermatitis, alopecia, diarrhea, weight loss, and a host of other complications.

View article: PDF

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

Review Article

Bart Ferwerda, Matthew BB McCall, Karlijn Verheijen, Bart-Jan Kullberg, André JAM van der Ven, Jos WM Van der Meer, and Mihai G Netea

The innate immune system recognizes a broad range of pathogens and initiates protective responses. Toll-like receptor 4 (TLR4) is an important pathogen recognition receptor that binds lipopolysaccharide of Gram-negative bacteria, structures from fungal and mycobacterial pathogens, and endogenous ligands. Two nonsynonymous polymorphisms of TLR4 may alter the function of the receptor. Ferwerda et al. (346-352) compare studies that assessed the effect of these polymorphisms on susceptibility to Gram-negative infections, and examine the phenotypic consequences of these polymorphisms. In addition, the geographical distribution of the TLR4 polymorphisms is reviewed, and a model for the evolutionary pressures on the TLR4 genetic make-up is presented.

View article: PDF

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

Review Article

Andrew J Vardanian, Ronald W Busuttil, and Jerzy W Kupiec-Weglinski

Ischemia and reperfusion injury represents a complex series of events that result in cellular and tissue damage. Vardanian et al. (337-345) describe the current understanding of molecular mechanisms involved in ischemia and reperfusion injury, primarily in the liver, and their putative therapeutic implications.

View article: PDF

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

Review Article

Michael A Flierl, Daniel Rittirsch, Markus S Huber-Land, J Vidya Sarma, and Peter A Ward

Septic cardiomyopathy is a well-described complication of severe sepsis and
septic shock. However, the interplay of its underlying mechanism remains enigmatic. Flierl et al. (327-336) describe the present understanding of systemic, supracellular and molecular mechanisms involved in sepsis-induced myocardial suppression.

View article: PDF

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

Daniel P Kestler, James S Foster, Sallie D Macy, Charles L Murphy, Deborah T Weiss, and Alan Solomon

Odontogenic ameloblast-associated protein (ODAM) is highly expressed by mature ameloblasts and is present in the enamel organ and junctional epithelial cells of the teeth. In addition to the role of ODAM in odontogenesis, ODAM is upregulated in human cervical and gastric cancer. Kestler et al. (318-326) generated anti-ODAM antibodies to gain further insight into the potential role of ODAM in tissue development and carcinogenesis. The ODAM-specific antibodies recognize ODAM molecules in ameloblasts, as well as certain normal and neoplastic human epithelial tissues. The results indicate that ODAM is a developmental antigen with an essential role in tooth maturation as well as in the pathogenesis of certain odontogenic and other epithelial neoplasms. ODAM may serve as a prognostic biomarker and a potential diagnostic and therapeutic target for patients with breast and other epithelial forms of cancer.

View article: PDF

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

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
< Prev    1 2