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Articles from this Volume

Christian Ehrnthaller, Anita Ignatius, Florian Gebhard, and Markus Huber-Lang

The complement system was discovered a century ago as a potent defense cascade of innate immunity. Complement has been shown to play a significant role in the pathogenesis of various inflammatory processes such as sepsis, multi-organ dysfunction, ischemia, cardiovascular diseases and many others. The well-known activation pathways of the complement system have been challenged by newer findings demonstrating direct production of central complement effectors. In the case of uncontrolled complement activation, "friendly fire" is generated resulting in the destruction of healthy host tissue. Here, Ehrnthaller et al. review new insights of complement-mediated clinically relevant diseases, the development of complement modulation strategies and current translational research approaches including structure-function-relations of this ancient defense system.

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Posted by Leah Caracappa on Apr 9, 2011 12:00 AM CDT

Nora Sandu, Gabriele Pöpperl, Marie-Elisabeth Toubert, Toma Spiriev, Belachew Arasho, Mikael Orabi, and Bernhard Schaller

Energy metabolism measurements in spinal cord tumors and in osseous spinal tumors are rarely performed using positron emission tomography (PET) molecular imaging. This imaging modality developed from a small number of basic clinical science investigations that influenced the research of others. Molecular imaging represents one of the key technologies in translational molecular neuroscience research and may lead to experimental protocols that may be applied to human patients. In this work, Sandu et al. review the current state-of-the-art spinal positron emission tomography.

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Posted by Leah Caracappa on Apr 8, 2011 12:00 AM CDT

Jochen Grommes and Oliver Soehnlein

Acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) is a lung disease characterized by hypoxemia, non-cardiogenic pulmonary edema, low lung compliance and widespread capillary leakage. ALI/ARDS is primarily caused by sepsis although non-infectious causes may also play a role. Neutrophils are the first cells to be recruited to the site of inflammation and have potent antimicrobial properties consisting of oxidants, proteases and cationic peptides. Under pathological circumstances, dysregulation in the release of these microbicidal compounds into the extracellular space can damage host tissues. In this review, Grommes and Soehnlein focus on the mechanisms of neutrophil recruitment into the lung and their contribution to tissue damage in ALI.

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Posted by Leah Caracappa on Apr 7, 2011 12:00 AM CDT

Alex G Cuenca, Matthew J Delano, Kindra M Kelly-Scumpia, Claudia Moreno, Philip O Scumpia, Drake M LaFace, Paul G Heyworth, Philip A Efron, and Lyle L Moldawer

Myeloid-derived suppressor cells are a heterogenous population of immature myeloid cells whose numbers dramatically increase in chronic and acute inflammatory diseases. Studied originally in cancer, these cells are potently immunosuppressive. Additional properties of these cells, including increased reactive oxygen species and inflammatory cytokine production, as well as their expansion in nearly all inflammatory conditions, suggest that MDSCs may be more of a normal component of the inflammatory response than simply a pathological response to a growing tumor. Although clinical efforts are currently underway to suppress MDSC numbers and function in cancer to improve anti-neoplastic responses, such approaches may not be either desirable or beneficial in other clinical conditions where immune surveillance and antimicrobial activities are required.

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Supplementary Data  PDF

Posted by Leah Caracappa on Apr 6, 2011 12:00 AM CDT

Sara García-Serrano, Inmaculada Moreno-Santos, Lourdes Garrido-Sánchez, Carolina Gutierrez-Repiso, Jose M García-Almeida, Juan García-Arnés, Jose Rivas-Marín, Jose L Gallego-Perales, Eva García-Escobar, Gemma Rojo-Martinez, Francisco Tinahones, Federico Soriguer, Manuel Macias-Gonzalez, and Eduardo García-Fuentes

Animal studies have revealed the association between stearoyl-CoA desaturase 1 (SCD1), obesity and insulin resistance, but few studies have been conducted in humans. Garcia-Serrano et al. studied SCD1 levels in visceral and subcutaneous adipose tissue from morbidly obese patients, and their association with insulin resistance. The insulin resistance was calculated in 40 morbidly obese patients and 11 overweight controls. In visceral adipose tissue of morbidly obese patients, SCD1 protein levels were decreased in those with higher insulin resistance as compared with overweight controls. In contrast, SCD1 protein levels were increased in the subcutaneous adipose tissue of morbidly obese patients with higher insulin resistance. These data suggest that the regulation of SCD1 is altered in morbidly obese persons, that the SCD1 protein has a different regulation in the two adipose tissues, and that SCD1 protein regulation is linked to the degree of insulin resistance.

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Posted by Leah Caracappa on Apr 5, 2011 12:00 AM CDT

Herbert Schöchl, Cristina Solomon, Arthur Schulz, Wolfgang Voelckel, Alexander Hanke, Martijn van Griensven, Heinz Redl, and Soheyl Bahrami

Standard coagulation tests have a low specificity and sensitivity for diagnosing disseminated intravascular coagulation. The aim of this study was to determine whether whole blood thromboelastometry (TEM) can detect lipopolysaccharide (LPS)-induced changes in coagulation. Blood samples from 10 pigs were drawn at baseline, before, during and after LPS infusion. TEM and simultaneous standard and extended coagulation analyses, including tissue plasminogen activator (t-PA) and plasminogen activator inhibitor 1 (PAI-1) assays, were performed. TEM was superior to standard coagulation tests in reflecting initial activation of coagulation during endotoxemia. TEM analyses suggested consumption of coagulation substrate; at the same time, inhibition of plasminogen activation was accompanied by improved clot stability. Further investigations are necessary to establish the clinical relevance of these findings.

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Posted by Leah Caracappa on Apr 4, 2011 12:00 AM CDT

Maria Galán, Carmen-Maria García-Herrero, Sharona Azriel, Manuel Gargallo, Maria Durán, Juan-Jose Gorgojo, Victor-Manuel Andía, and Maria-Angeles Navas

Mutations in the hepatocyte nuclear factor-1 alpha (HNF-1a) gene result in a type of familial young onset diabetes, also known as maturity-onset diabetes of the young type 3 (MODY3). Clinical phenotypes vary from one family to another and more than 300 different MODY3-causing mutations have been found. Galán et al. functionally characterized six HNF1A mutations identified in diabetic patients. Results suggest that HNF1A mutations may have differential effects on the regulation of specific target genes, which could contribute to the variability of the MODY3 clinical phenotype. Functional characterization of HNF1A mutations may provide insight into molecular defects and help explain variability within the MODY3 phenotype.

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Posted by Leah Caracappa on Apr 3, 2011 12:00 AM CDT

Nan Lu, Chuanxin Wang, Xiaojing Yang, Shengmei Zhao, Xiangdong Li, Xiaoli Li, Hong Jiang, Jinbo Feng, Yi Zhang, and Xiong Zou

Acute graft rejection (AGR) remains the most commonly occurring complication in organ transplantation. While upregulated human leukocyte antigen-g (HLA-G) expression in grafts and plasma correlates with allograft acceptance, expression of the murine homolog, Qa-2, during AGR has not been investigated. Here, Lu et al. use a skin transplantation model to follow changes in Qa-2 expression in allografts with or without immunosuppressive (IS) treatment. The authors reported Qa-2 expression was upregulated during immunosuppressive treatment but decreased during allograft rejection. Serial monitoring of Qa-2 expression after transplantation revealed acceptable diagnostic values suggesting that Qa-2 may be useful as an early predictive marker for acute allograft rejection as well as for monitoring the effects of immunosuppressive treatments.

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Posted by Leah Caracappa on Apr 2, 2011 12:00 AM CDT

Jeffrey K Wickliffe, Sherif Z Abdel-Rahman, Chul Lee, Csilla Kormos-Hallberg, Gagan Sood, Catherine M Rondelli, James J Grady, Robert J Desnick, and Karl E Anderson

Porphyria cutanea tarda (PCT) is the most prevalent of the human porphyrias resulting from decreased hepatic uroporphyrinogen decarboxylase (UROD) activity in the liver. A UROD mutation is only a predisposing factor and is insufficient to cause PCT manifestations on its own. Environmental and genetic factors are also involved in the development of PCT. Wickliffe et al. hypothesized that variants in biotransformation genes could constitute susceptibility factors in this disease and investigated these associations. Positive associations were found indicating functional hepatic biotransformation enzymes are risk factors for the development of this disease.

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Posted by Leah Caracappa on Apr 1, 2011 12:00 AM CDT

Esaki Muthu Shankar, Karlhans Fru Che, Davorka Messmer, Jeffrey D Lifson, and Marie Larsson

Persistent viral infections are characterized by impaired T-cell responses and futile viral control attributes. Functional impairment of T-cells is a key feature of HIV-1 as well as other viral infections. While some of the mechanisms regulating effector T-cell activation have been explored, the molecular factors underlying the fate of naïve T-cells when primed with HIV-pulsed dendritic cells (DCs) remain unknown. Here, Shankar et al. show naïve T-cells primed with monocyte-derived DCs pulsed with HIV had relatively higher expression of negative costimulatory molecules as compared to naïve T-cells primed with mock DCs. This resulted in decreased immune activation possibly due to expression of inhibitory factors. The authors conclude that HIV infection could modulate DCs to generate suppressor T cells, armed by inhibitory molecules with immunoimpairing abilities.

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Supplementary Data  PDF

Posted by Leah Caracappa on Mar 10, 2011 12:00 AM CST
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