bluuebunny/crossref_metadata_2025 huggingface dataset:
Tunnel inner lining of bright self‐compacting concrete / Tunnelinnenschale aus hellem selbstverdichtendem Beton
Authors: Krispel Stefan , Strommer Werner
Published: February 2011

Ever more stringent requirements have been specified in recent years for the surfaces of tunnel inner linings with regard to surface porosity (with influence on the ease of cleaning) and lightness. These requirements are normally fulfilled by filling and applying tunnel paint. Recently there have been many cases of damage to paint or coating systems, sometimes only a few weeks after opening for traffic. This often includes the separation of the coating. This flaking leads to increased dirt adhesion and thus to a reduction of lightness and irritation to the field of view of the drivers. The refurbishment work, which is often necessary, leads to traffic obstruction like hold‐ups and diversions. For this reason, the durability of the surface is of great significance, and innovative solutions are also being investigated in the field of concrete technology. The following article presents an alternative and durable method of fulfilling all the requirements placed on the surface of the tunnel inner lining.

In den vergangenen Jahren wurden immer höhere Anforderungen an die Oberflächen von Tunnelinnenschalen betreffend Oberflächenporosität (Einfluss auf Reinigungsfähigkeit) und Helligkeit gestellt. Zur Erfüllung dieser Anforderungen werden meist Tunnelanstriche nach vorheriger Spachtelung verwendet. In letzter Zeit traten jedoch vermehrt Schäden an Anstrichsystemen auf, teilweise schon wenige Wochen nach Verkehrsfreigabe. Hierbei kommt es oftmals zu einem Ablösen der Anstrichschicht. Diese Ablöseerscheinungen führen aufgrund einer verstärkten Schmutzablagerung zu einer Reduktion der Helligkeit und zu Irritationen des Blickfelds der Verkehrsteilnehmer. Die oftmals erforderlichen Instandsetzungsarbeiten am Beschichtungssystem führen zu Verkehrsbehinderungen wie Staus und Umleitungen. Aus diesen Gründen ist die Beständigkeit der Oberfläche von großer Bedeutung, und innovative Lösungswege werden auch im Bereich der Betontechnologie erprobt. Im nachstehenden Beitrag wird eine alternative dauerhafte Methode vorgestellt, die alle Anforderungen an die Oberfläche der Tunnelinnenschale erfüllt.
Fibroblast growth factor 2 regulates astrocyte differentiation in a region‐specific manner in the hindbrain
Authors: Irmady Krithi , Zechel Sabrina , Unsicker Klaus
Published: February 2011

Fibroblast growth factor (FGF)‐2 is known to have important pleiotropic effects in neuronal and glial cells during various physiological and pathological events. To investigate the role of endogenous FGF‐2 in the differentiation of astrocytes, we studied the expression of glial fibrillary acidic protein (GFAP) in the hindbrain of the FGF‐2 null mouse. GFAP was drastically decreased in a region‐specific manner in the hindbrain of the adult and developing FGF‐2 null mouse without an associated change in the expression of alternate markers for astrocytes. The deficit was evident in the astrocytes of pontine and medullary gray matter but not in the white matter. The astrocytes of the gray and white matter were seen to express FGF‐2 and FGF receptors in a distinct pattern. The methylation of histone H3 at lysine 4 residue (H3K4me2) associated with the STAT (signal transducer and activator of transcription)‐binding site of the GFAP promoter was significantly decreased in the gray matter of the FGF‐2 null mouse, suggesting a role for FGF‐2 in the epigenetic regulation of astrocyte differentiation in vivo. These observations underscore the importance of FGF‐2 in astroglial differentiation in the hindbrain and the heterogeneity of astrocytes in their requirement for FGF‐2 as a differentiation inducing signal.© 2011 Wiley‐Liss, Inc.
Mouse schwann cells need both NRG1 and cyclic AMP to myelinate
Authors: Arthur‐Farraj Peter , Wanek Katharina , Hantke Janina , Davis Catherine M. , Jayakar Anuj , Parkinson David B. , Mirsky Rhona , Jessen Kristján R.
Published: February 2011

Genetically modified mice have been a major source of information about the molecular control of Schwann‐cell myelin formation, and the role of β‐neuregulin 1 (NRG1) in this process in vivo. In vitro, on the other hand, Schwann cells from rats have been used in most analyses of the signaling pathways involved in myelination. To correlate more effectively in vivo and in vitro data, we used purified cultures of mouse Schwann cells in addition to rat Schwann cells to examine two important myelin‐related signals, cyclic adenosine monophosphate (cAMP), and NRG1 and to determine whether they interact to control myelin differentiation. We find that in mouse Schwann cells, neither cAMP nor NRG1, when used separately, induced markers of myelin differentiation. When combined, however, they induced strong protein expression of the myelin markers, Krox‐20 and P0. Importantly, the level of cAMP signaling was crucial in switching NRG1 from a proliferative signal to a myelin differentiation signal. Also in cultured rat Schwann cells, NRG1 promoted cAMP‐induced Krox‐20 and P0 expression. Finally, we found that cAMP/NRG1‐induced Schwann‐cell differentiation required the activity of the cAMP response element binding family of transcription factors in both mouse and rat cells. These observations reconcile observations in vivo and on neuron‐Schwann‐cell cultures with studies on purified Schwann cells. They demonstrate unambiguously the promyelin effects of NRG1 in purified cells, and they show that the cAMP pathway determines whether NRG1 drives proliferation or induces myelin differentiation. © 2011 Wiley‐Liss, Inc.
Split central venous sampling of parathyroid hormone: An adjunct to surgical exploration
Authors: Maceri Dennis R. , Kokot Niels , Green Kathrine , Montgomery Vida , Sharifi Jahangir
Published: February 2011

Background

Minimally invasive parathyroid surgery mandates preoperative localization of the adenoma for a targeted operative approach. This technique uses split internal jugular vein parathyroid hormone (PTH) samples to determine a gradient that then directs the surgical exploration.

Methods

Blood samples were drawn low in the neck from the jugular veins after the neck was opened. The p values for the difference in PTH between the right and left internal jugular veins were calculated with independent sample t tests.

Results

For left‐sided adenomas, the left internal jugular vein mean was significantly higher than the right p = .001). For right‐sided adenomas, the right internal jugular vein mean was significantly higher than the left (p = .004). In hyperplasia, there was no significant difference (p = .43).

Conclusions

This study demonstrates the usefulness of split PTH internal jugular vein samples in patients in whom preoperative localization failed. Eighty percent of these patients with a gradient were treated with site‐directed unilateral exploration. © 2011 Wiley Periodicals, Inc. Head Neck, 2011
Altered metabolism in head and neck squamous cell carcinoma: an opportunity for identification of novel biomarkers and drug targets
Authors: Sandulache Vlad C. , Myers Jeffrey N.
Published: February 2011

Tumor cells were first shown to exhibit a distinct metabolic phenotype over 80 years ago. Since then, it has become clear that multiple oncogenic events contribute to the development of a metabolic phenotype that supports rapid proliferation. Because this phenotype represents an essential component of tumorigenesis and disease progression, it also represents a potential source of biomarkers associated with aggressive disease. In addition, the addiction of tumor cells to specific nutrients and the up‐regulation of key metabolic enzymes provide unique opportunities for pharmacologic manipulation. Despite the use of multimodality treatment, survival rates for patients with advanced head and neck squamous cell carcinoma (HNSCC) remain low, partially attributed to the development of drug resistance. In this review, we evaluate the role of altered HNSCC metabolism as both a source of novel biomarkers and a means to bypass resistance mechanisms to conventional forms of therapy. © 2011 Wiley Periodicals, Inc. Head Neck, 2012
Prognosis: A variable parameter. Dynamic prognostic modeling in head and neck squamous cell carcinoma
Authors: van der Schroeff Marc P. , Steyerberg Ewout W. , Wieringa Marjan H. , Langeveld Ton P. M. , Molenaar Jan , Baatenburg de Jong Robert J.
Published: February 2011

Background

In general, the estimated prognosis of patients with cancer is based on patient characteristics known at the time of diagnosis and presented as if a lifetime verdict. However, the prognosis of patients with cancer who survive the first critical years changes, along with the prognosis for those with local or regional recurrences or distant metastases.

Methods

This study concerns 2927 patients with a primary head and neck squamous cell carcinoma (HNSCC). We developed prognostic models after initial treatment and at different time points during follow‐up.

Results

The developed models show the effects of survival time, recurrences, and distant metastasis during follow‐up. The C‐statistics ranged from 0.76 to 0.69.

Conclusion

Prognosis is dynamic: the passage of time and the occurrence of life events change the predicted probabilities of survival. The models enhance our insight in the effect of recurrences and metastasis during follow‐up and could be used for better patient counseling. © 2011 Wiley Periodicals, Inc. Head Neck, 2012
Novel head and neck cancer survival analysis approach: Random survival forests versus cox proportional hazards regression
Authors: Datema Frank R. , Moya Ana , Krause Peter , Bäck Thomas , Willmes Lars , Langeveld Ton , Baatenburg de Jong Robert J. , Blom Henk M.
Published: February 2011

Background

Electronic patient files generate an enormous amount of medical data. These data can be used for research, such as prognostic modeling. Automatization of statistical prognostication processes allows automatic updating of models when new data is gathered. The increase of power behind an automated prognostic model makes its predictive capability more reliable. Cox proportional hazard regression is most frequently used in prognostication. Automatization of a Cox model is possible, but we expect the updating process to be time‐consuming. A possible solution lies in an alternative modeling technique called random survival forests (RSFs). RSF is easily automated and is known to handle the proportionality assumption coherently and automatically. Performance of RSF has not yet been tested on a large head and neck oncological dataset. This study investigates performance of head and neck overall survival of RSF models. Performances are compared to a Cox model as the “gold standard.” RSF might be an interesting alternative modeling approach for automatization when performances are similar.

Methods

RSF models were created in R (Cox also in SPSS). Four RSF splitting rules were used: log‐rank, conservation of events, log‐rank score, and log‐rank approximation. Models were based on historical data of 1371 patients with primary head‐and‐neck cancer, diagnosed between 1981 and 1998. Models contain 8 covariates: tumor site, T classification, N classification, M classification, age, sex, prior malignancies, and comorbidity. Model performances were determined by Harrell's concordance error rate, in which 33% of the original data served as a validation sample.

Results

RSF and Cox models delivered similar error rates. The Cox model performed slightly better (error rate, 0.2826). The log‐rank splitting approach gave the best RSF performance (error rate, 0.2873). In accord with Cox and RSF models, high T classification, high N classification, and severe comorbidity are very important covariates in the model, whereas sex, mild comorbidity, and a supraglottic larynx tumor are less important. A discrepancy arose regarding the importance of M1 classification (see Discussion).

Conclusion

Both approaches delivered similar error rates. The Cox model gives a clinically understandable output on covariate impact, whereas RSF becomes more of a “black box.” RSF complements the Cox model by giving more insight and confidence toward relative importance of model covariates. RSF can be recommended as the approach of choice in automating survival analyses. © 2011 Wiley Periodicals, Inc. Head Neck, 2012
Randomized trial of lamivudine versus entecavir in entecavir-treated patients with undetectable hepatitis B virus DNA: Outcome at 2 Years
Authors: Fung James , Lai Ching-Lung , Yuen John , Cheng Charles , Wu Ringo , Ka-Ho Wong Danny , Seto Wai-Kay , Hung Ivan Fan-Ngai , Yuen Man-Fung
Published: February 2011

We aimed to determine the 2-year outcomes of entecavir followed by lamivudine in patients with undetectable viral load (<12 IU/mL) and normal alanine aminotransferase (ALT) after initial entecavir treatment for at least 6 months. Patients were randomly assigned 1:1 to continue with entecavir or switch to lamivudine. Liver biochemistry and hepatitis B virus (HBV) DNA were determined at weeks 0, 4, 12, 24, 48, 72, and 96. Mutational analysis using line-probe assay were performed at weeks 0, 24, 48, and 96 and at the time of HBV DNA relapse. There was no elevation of ALT observed in any patients up to 96 weeks. At 96 weeks of follow-up, 19/25 (76%) patients in the lamivudine arm had persistently undetectable HBV DNA, compared with 25/25 (100%) patients in the entecavir arm. Six patients in the lamivudine arm had HBV DNA >20 IU/mL, occurring at a range of 12 to 96 weeks. Of these, four patients had HBV DNA of less than 100 IU/mL during rebound (three had undetectable HBV DNA after switching back to entecavir), and the remaining two patients had HBV DNA levels of 7,973 and 699 IU/mL. Three patients (12%) had evidence of drug-resistant mutations, of which two patients had rtM204I mutation and one patient had rtM204V mutation. One of these three patients had previous lamivudine exposure before entecavir treatment and one patient had questionable drug compliance.

Conclusion:

Sequential therapy using entecavir followed by lamivudine resulted in virological rebound in 24% of patients after 96 weeks. Prior optimal viral suppression with entecavir did not confer any significant advantage in patients who switched to lamivudine. (HEPATOLOGY 2011;)
Lithocholic acid disrupts phospholipid and sphingolipid homeostasis leading to cholestasis in mice
Authors: Matsubara Tsutomu , Tanaka Naoki , Patterson Andrew D. , Cho Joo-Youn , Krausz Kristopher W. , Gonzalez Frank J.
Published: February 2011

Lithocholic acid (LCA) is an endogenous compound associated with hepatic toxicity during cholestasis. LCA exposure in mice resulted in decreased serum lysophosphatidylcholine (LPC) and sphingomyelin levels due to elevated lysophosphatidylcholine acyltransferase (LPCAT) and sphingomyelin phosphodiesterase (SMPD) expression. Global metabolome analysis indicated significant decreases in serum palmitoyl-, stearoyl-, oleoyl-, and linoleoyl-LPC levels after LCA exposure. LCA treatment also resulted in decreased serum sphingomyelin levels and increased hepatic ceramide levels, and induction of LPCAT and SMPD messenger RNAs (mRNAs). Transforming growth factor-β (TGF-β) induced

Lpcat2/4

and

Smpd3

gene expression in primary hepatocytes and the induction was diminished by pretreatment with the SMAD3 inhibitor SIS3. Furthermore, alteration of the LPCs and

Lpcat1/2/4

and

Smpd3

expression was attenuated in LCA-treated farnesoid X receptor-null mice that are resistant to LCA-induced intrahepatic cholestasis.

Conclusion:

This study revealed that LCA induced disruption of phospholipid/sphingolipid homeostasis through TGF-β signaling and that serum LPC is a biomarker for biliary injury. (HEPATOLOGY 2011;)
Interaction between Toll-like receptors and natural killer cells in the destruction of bile ducts in primary biliary cirrhosis
Authors: Shimoda Shinji , Harada Kenichi , Niiro Hiroaki , Shirabe Ken , Taketomi Akinobu , Maehara Yoshihiko , Tsuneyama Koichi , Nakanuma Yasuni , Leung Patrick , Ansari Aftab A. , Gershwin Eric M. , Akashi Koichi
Published: February 2011

Primary biliary cirrhosis (PBC) is characterized by chronic nonsuppurative destructive cholangitis (CNSDC) associated with destruction of small bile ducts. Although there have been significant advances in the dissection of the adaptive immune response against the mitochondrial autoantigens, there are increasing data that suggest a contribution of innate immune mechanisms in inducing chronic biliary pathology. We have taken advantage of our ability to isolate subpopulations of liver mononuclear cells (LMC) and examined herein the role of Toll-like receptors (TLRs), their ligands, and natural killer (NK) cells in modulating cytotoxic activity against biliary epithelial cells (BECs). In particular, we demonstrate that Toll-like receptor 4 ligand (TLR4-L)-stimulated NK cells destroy autologous BECs in the presence of interferon alpha (IFN-α) synthesized by TLR 3 ligand (TLR3-L)-stimulated monocytes (Mo). Indeed, IFN-α production by hepatic Mo is significantly increased in patients with PBC compared to disease controls. There were also marked increases in the cytotoxic activity of hepatic NK cells from PBC patients compared to NK cells from controls but only when the NK cells were prepared following ligation of both TLR3-L- and TLR4-L-stimulated LMC. These functional data are supported by the immunohistochemical observation of an increased presence of CD56-positive NK cells scattered around destroyed small bile ducts more frequently in liver tissues from PBC patients than controls.

Conclusion:

These data highlight critical differences in the varied roles of Mo and NK cells following TLR3-L and TLR4-L stimulation. (HEPATOLOGY 2011.)
Modulation of hepatitis B virus replication and hepatocyte differentiation by MicroRNA-1
Authors: Zhang Xiaoyong , Zhang Ejuan , Ma Zhiyong , Pei Rongjuan , Jiang Min , Schlaak Joerg F. , Roggendorf Michael , Lu Mengji
Published: February 2011

MicroRNAs (miRNAs) are highly conserved small noncoding RNAs participating in regulation of various cellular processes. Viruses have been shown to utilize cellular miRNAs to increase their replication in host cells. Until now, the role of miRNAs in hepatitis B virus (HBV) replication has remained largely unknown. In this study, a number of miRNA mimics were transfected into hepatoma cell lines with HBV replication. It was noted that microRNA-1 (miR-1) transfection resulted in a marked increase of HBV replication, accompanied with up-regulated HBV transcription, antigen expression, and progeny secretion. However, bioinformatics and luciferase reporter analysis suggested that miR-1 may not target the HBV genome directly but regulate the expression of host genes to enhance HBV replication. Further studies showed that miR-1 was able to enhance the HBV core promoter transcription activity by augmenting farnesoid X receptor α expression. In addition, miR-1 arrested the cell cycle at the G1 phase and inhibited cell proliferation by targeting histone deacetylase 4 and E2F transcription factor 5. Analysis of the cellular gene expression profile indicated that miR-1 transfected hepatoma cells developed a differentiated phenotype of hepatocytes.

Conclusion:

MiR-1 regulates the expression of several host genes to enhance HBV replication and reverse cancer cell phenotype, which is apparently beneficial for HBV replication. Our findings provide a novel perspective on the role of miRNAs in host-virus interactions in HBV infection. (Hepatology 2011;)
From EosFP to mIrisFP: structure‐based development of advanced photoactivatable marker proteins of the GFP‐family
Authors: Wiedenmann Jörg , Gayda Susan , Adam Virgile , Oswald Franz , Nienhaus Karin , Bourgeois Dominique , Nienhaus G. Ulrich
Published: February 2011

Fluorescent proteins from the GFP family have become indispensable imaging tools in life sciences research. In recent years, a wide variety of these proteins were discovered in non‐bioluminescent anthozoa. Some of them feature exciting new properties, including the possibility to change their fluorescence quantum yield and/or color by irradiating with light of specific wavelengths. These photoactivatable fluorescent proteins enable many interesting applications including pulse‐chase experiments and super‐resolution imaging. In this review, we discuss the development of advanced variants, using a structure‐function based, molecular biophysics approach, of the photoactivatable fluorescent protein EosFP, which can be photoconverted from green to red fluorescence by ∼400 nm light. A variety of applications are presented that demonstrate the versatility of these marker proteins in live‐cell imaging. (© 2011 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim)
Successful therapeutic plasma exchange in a 3.2‐kg body weight neonate with atypical hemolytic uremic syndrome
Authors: Jung Sunkyung , Kang Eun‐Suk , Ki Chang‐Seok , Kim Dae‐Won , Paik Kyung‐Hoon , Chang Yun Sil
Published: February 2011

Atypical hemolytic uremic syndrome (aHUS) is a rare form of complement dysregulation disease, and recently various reports have shown that it is associated with one or more mutations in the complement regulatory genes including complement factor H (CFH). Plasma exchange is a therapeutic option for adult patients, but not for a very young infant because of a potential side effect of therapeutic plasma exchange (TPE) itself. Herein, we describe a case of successful treatment of early onset aHUS associated with a novel CFH mutation with total 21 sessions of TPE over a period of 46 days in 3.2 kg 23‐day‐old neonate. J. Clin. Apheresis, 2011. © 2011 Wiley‐Liss, Inc.
RUNX3 in oncogenic and anti‐oncogenic signaling in gastrointestinal cancers
Authors: Ito Kosei
Published: February 2011

The reputation of RUNX3 as a strong candidate for a tumor suppressor originated from studies of gastric carcinogenesis and now extends to a variety of other human cancers. The RUNX3 transcription factor is a downstream effector of the TGF‐β superfamily signaling pathway and has a critical role in the regulation of cell proliferation, cell death by apoptosis, and cell adhesion. Recently, RUNX3 was proposed as a gatekeeper linking oncogenic Wnt and anti‐oncogenic TGF‐β/BMPs signaling pathways in intestinal tumorigenesis in mouse and human. Also, loss of RUNX3 leading to elevated oncogenic Wnt activity was found to be a key event in inducing a precancerous state of the stomach. Chronic Helicobacter pylori infection is reported to inactivate RUNX3 in gastric carcinogenesis by multiple mechanisms. This “Prospect” focuses on our current understanding of the tumor suppressive functions of RUNX3 in the context of gastrointestinal cancer initiation and progression. J. Cell. Biochem. 112: 1243–1249, 2011. © 2011 Wiley‐Liss, Inc.
Synthetic small interfering RNA down‐regulates caspase‐3 and affects apoptosis, IL‐1β, and viability of porcine proximal tubular cells
Authors: Yang Bin , Elias Joshua E. , Bloxham Maureen , Nicholson Michael L.
Published: February 2011

Proximal tubular cells are most vulnerable to ischemia reperfusion injury (IRI) in renal transplantation. Caspase‐3 can be up‐regulated by IRI due to a variety of pathogenic processes such as oxidative damage. This study utilized synthetic small interfering RNA (siRNA) to posttranscriptionally silence target gene, caspase‐3, may represent a feasible approach to produce transient effects, but avoid side actions caused by viral vectors. The porcine proximal tubular cells (LLC‐PK1), with or without the stimulation of hydrogen peroxide (H2O2, an oxidizer), were transfected with synthetic caspase‐3 siRNA using a cationic lipid‐based transfection regent. The expression of caspase‐3 at mRNA and protein level was assessed at different times posttransfection and its downstream biological events were also monitored. The caspase‐3 mRNA was posttranscriptionally silenced by its siRNA up to 50% after 24 h. The active caspase‐3 protein was increased by transfection reagent alone and H2O2 in a dose‐ and time‐dependent manner. Both the precursor and active protein of caspase‐3 were decreased by siRNA after 48 h and maintained up to 96 h at least, with a consistent change in its activity. Consequently, apoptotic cells and active IL‐1β protein expression was reduced by caspase‐3 siRNA; cell viability, especially with H2O2 treatment, was also improved. Taken together, caspase‐3 and apoptosis are sensitive markers for cellular injury; using synthetic siRNA silencing caspase‐3 may provide not only a valid approach for underlying mechanisms of diseases, but also a potential therapeutic intervention for a wide range of acute clinical disorders including IRI in renal transplantation. J. Cell. Biochem. 112: 1337–1347, 2011. © 2011 Wiley‐Liss, Inc.
The role of mechanical stretching in the activation and localization of adhesion proteins and related intracellular molecules
Authors: Boccafoschi F. , Mosca C. , Bosetti M. , Cannas M.
Published: February 2011

The molecular complexity of the processes which lead to cell adhesion includes membrane and cytoskeletal proteins, involved in the focal adhesion formation, as well as signaling molecules tightly associated with the main intracellular regulatory cascades (Akt/PKB and MAPK/Erk). Dynamic environments, which create substrate deformations at determined frequencies and timing, have significant influences on adhesion mechanisms and in general in cellular behavior. In this work, we investigated the role of mechanical stretching (10% substrate deformation, 1 Hz frequency applied up to 60 min) on adhesion proteins (vinculin and focal adhesion kinase—FAK), related RhoGTPases (Rac1 and RhoA), and intracellular pathways (Akt/PKB and MAPK/Erk) in terms of activation and membrane recruitment in relation with cytoskeletal changes observed (membrane ruffling and filopodia formation). These changes are due to intracellular molecular rearrangements, acting with sequential concerted dynamics, able to modify the cytoskeletal conformation. The observed cellular response adds some important issues for better understanding the cellular behavior in environment which mimic as close as possible the physiological conditions. J. Cell. Biochem. 112: 1403–1409, 2011. © 2011 Wiley‐Liss, Inc.
Pax7‐FKHR transcriptional activity is enhanced by transcriptionally repressed MyoD
Authors: Olguín Hugo C. , Patzlaff Natalie E. , Olwin Bradley B.
Published: February 2011

Alveolar rhabdomyosarcoma (ARMS) are characterized by the expression of chimeric transcription factors Pax3‐FKHR and Pax7‐FKHR, due to chromosomal translocations fusing PAX3 or PAX7 with the FKHR gene. Although ARMS exhibits a muscle lineage phenotype, the cells evade terminal differentiation despite expressing the potent myogenic transcriptional regulator MyoD. Here we show that while Pax7‐FKHR inhibits MyoD‐dependent transcription, MyoD enhances Pax7‐FKHR activity in myogenic cell cultures. Importantly, this effect is not recapitulated by close related transcription factor myogenin and involves specific MyoD functional domains, distinct from those required for Pax7 to regulate MyoD during muscle formation. Together, these results suggest that although repressed as a myogenic regulatory factor, MyoD can play an active role in ARMS by augmenting Pax7‐FKHR function. J. Cell. Biochem. 112: 1410–1417, 2011. © 2011 Wiley‐Liss, Inc.
Comparison of alternative mesenchymal stem cell sources for cell banking and musculoskeletal advanced therapies
Authors: Cavallo Carola , Cuomo Carmela , Fantini Sara , Ricci Francesca , Tazzari Pier Luigi , Lucarelli Enrico , Donati Davide , Facchini Andrea , Lisignoli Gina , Fornasari Pier Maria , Grigolo Brunella , Moroni Lorenzo
Published: February 2011

With the continuous discovery of new alternative sources containing mesenchymal stem cells (MSCs), regenerative medicine therapies may find tailored applications in the clinics. Although these cells have been demonstrated to express specific mesenchymal markers and are able to differentiate into mesenchymal lineages in ad hoc culture conditions, it is still critical to determine the yield and differentiation potential of these cells in comparative studies under the same standardized culture environment. Moreover, the opportunity to use MSCs from bone marrow (BM) of multiorgan donors for cell banking is of relevant importance. In the attempt to establish the relative potential of alternative MSCs sources, we analyzed and compared the yield and differentiation potential of human MSCs from adipose and BM tissues of cadaveric origins, and from fetal annexes (placenta and umbilical cord) after delivery using standardized isolation and culture protocols. BM contained a significantly higher amount of mononuclear cells (MNCs) compared to the other tissue sources. Nonetheless, a higher cell seeding density was needed for these cells to successfully isolate MSCs. The MNCs populations were highly heterogeneous and expressed variable MSCs markers with a large variation from donor to donor. After MSCs selection through tissue culture plastic adhesion, cells displayed a comparable proliferation capacity with distinct colony morphologies and were positive for a pool of typical MSCs markers. In vitro differentiation assays showed a higher osteogenic differentiation capacity of adipose tissue and BM MSCs, and a higher chondrogenic differentiation capacity of BM MSCs. J. Cell. Biochem. 112: 1418–1430, 2011. © 2011 Wiley‐Liss, Inc.
Adiponectin increases MMP‐3 expression in human chondrocytes through adipor1 signaling pathway
Authors: Tong Kwok‐Man , Chen Chao‐Ping , Huang Kui‐Chou , Shieh Dong‐Chen , Cheng Hsu‐Chen , Tzeng Chung‐Yuh , Chen Kun‐Hui , Chiu Yung‐Cheng , Tang Chih‐Hsin
Published: February 2011

Articular adipose tissue is a ubiquitous component of human joints, and adiponectin is a protein hormone secreted predominantly by differentiated adipocytes and involved in energy homeostasis. The adiponectin is significantly higher in synovial fluid of patients with osteoarthritis and rheumatoid arthritis. Matrix metalloproteinases (MMP)‐3 may contribute to the breakdown of articular cartilage during arthritis. We investigated the signaling pathway involved in MMP‐3 caused by adiponectin in human chondrocytes. Adiponectin increased the secretion of MMP‐3 in cultured human chondrocytes, as shown by qPCR, Western blot, and ELISA analysis. Adiponectin‐mediated MMP‐3 expression was attenuated by AdipoR1 but not AdipoR2 siRNA. Pretreatment with 5′‐AMP‐activated protein kinase (AMPK) inhibitor (araA and compound C), p38 inhibitor (SB203580), and NF‐κB inhibitor (PDTC and TPCK) also inhibited the potentiating action of adiponectin. Activations of p38, AMPK, and NF‐κB pathways after adiponectin treatment were demonstrated. Taken together, our results provide evidence that adiponectin acts through AdipoR1 to activate p38 and AMPK, resulting in the activations of NF‐κB on the MMP‐3 promoter and contribute cartilage destruction during arthritis. J. Cell. Biochem. 112: 1431–1440, 2011. © 2011 Wiley‐Liss, Inc.
Effect of β‐amyloid (25–35) on mitochondrial function and expression of mitochondrial permeability transition pore proteins in rat hippocampal neurons
Authors: Ren Rui , Zhang Yang , Li Benchang , Wu Yanping , Li Baixiang
Published: February 2011

The aim of this study was to assess the effect of the β‐amyloid fragment Aβ25–35 on mitochondrial structure and function and on the expression of proteins associated with the mitochondrial permeability transition pore (MPTP) in rat hippocampal neurons. Ninety clean‐grade Sprague–Dawley rats were randomly assigned to six groups (n = 15 per group). Aβ25–35 (1, 5, or 10 µg/rat) was injected into hippocampal area CA1. Normal saline was injected as a control. The effect of Aβ25–35 injection on hippocampal structure was assessed by transmission electron microscopy. Ca2+‐ATPase activity, [Ca2+]i, and mitochondrial membrane potential were measured. The expression of genes associated with the MPTP, including the voltage‐dependent anion channel (VDAC), adenine nucleotide translocator (ANT), and cyclophilin D (Cyp‐D), were evaluated. Results showed that Aβ25–35 injection damaged the mitochondrial structure of hippocampal neurons, decreased Ca2+‐ATPase activity and mitochondrial membrane potential, and increased [Ca2+]i. The expression levels for VDAC, ANT, and Cyp‐D in all groups were significantly (P < 0.05) higher than those in the normal control group after Aβ25–35 injection. These results indicate that Aβ25–35 damages mitochondria in rat hippocampal neurons and effects mitochondrial dysfunction, as well as increasing the expression of genes associated with the MPTP. Mitochondrial dysfunction may result in increased MPTP gene expression, leading to neurodegenerative effects. J. Cell. Biochem. 112: 1450–1457, 2011. © 2011 Wiley‐Liss, Inc.
Insulin regulates GLUT1‐mediated glucose transport in MG‐63 human osteosarcoma cells
Authors: Cifuentes Manuel , García Maria A. , Arrabal Pilar M. , Martínez Fernando , Yañez María J. , Jara Nery , Weil Bernardo , Domínguez Dolores , Medina Rodolfo A. , Nualart Francisco
Published: February 2011

Osteosarcoma is the most common type of malignant bone cancer, accounting for 35% of primary bone malignancies. Because cancer cells utilize glucose as their primary energy substrate, the expression and regulation of glucose transporters (GLUT) may be important in tumor development and progression. GLUT expression has not been studied previously in human osteosarcoma cell lines. Furthermore, although insulin and insulin‐like growth factor (IGF‐I) play an important role in cell proliferation and tumor progression, the role of these hormones on GLUT expression and glucose uptake, and their possible relation to osteosarcoma, have also not been studied. We determined the effect of insulin and IGF‐I on GLUT expression and glucose transport in three well‐characterized human osteosarcoma cell lines (MG‐63, SaOs‐2, and U2‐Os) using immunocytochemical, RT‐PCR and functional kinetic analyses. Furthermore we also studied GLUT isoform expression in osteosarcoma primary tumors and metastases by in situ hybridization and immunohistochemical analyses. RT‐PCR and immunostaining show that GLUT1 is the main isoform expressed in the cell lines and tissues studied, respectively. Immunocytochemical analysis shows that although insulin does not affect levels of GLUT1 expression it does induce a translocation of the transporter to the plasma membrane. This translocation is associated with increased transport of glucose into the cell. GLUT1 is the main glucose transporter expressed in osteosarcoma, furthermore, this transporter is regulated by insulin in human MG‐63 cells. One possible mechanism through which insulin is involved in cancer progression is by increasing the amount of glucose available to the cancer cell. J. Cell. Physiol. 226: 1425–1432, 2011. © 2011 Wiley‐Liss, Inc.
Coronary stenting after failure of conservative treatment for spontaneous coronary dissection: Usefulness of the intravascular ultrasound
Authors: Marti Vicens , Garcia‐Picart Joan , Balcells Jordi
Published: February 2011

Spontaneous coronary dissection of a coronary artery is a rare cause of acute coronary syndrome. Optimal treatment has not yet been established. We describe a woman with spontaneous dissection of the left anterior descending artery who presented transitory angina and electrocardiographic ST segment elevation in precordial leads. Conservative treatment was carried out. The angina and electrocardiographic changes recurred 3 days later. An intravascular vascular ultrasound was performed and the patient was stabilized following stenting. Stress testing was negative at 6‐month follow‐up and she remained asymptomatic at 18 months. We discuss the usefulness of an intravascular ultrasound study to establish the therapeutic strategy. © 2011 Wiley Periodicals, Inc. J Clin Ultrasound, 2011
Simple and automatic determination of aldehydes and acetone in water by headspace solid‐phase microextraction and gas chromatography‐mass spectrometry
Authors: Kim Hyun‐Ji , Shin Ho‐Sang
Published: February 2011

We describe a simple and automatic method to determine nine aldehydes and acetone simultaneously in water. This method is based on derivatization with 2,2,2‐trifluoroethylhydrazine (TFEH) and consecutive headspace‐solid‐phase microextraction and gas chromatography‐mass spectrometry. Acetone‐d6 was used as the internal standard. Aldehydes and acetone in water reacted for 30 min at 40°C with TFEH in a headspace vial and the formed TFEH derivatives were simultaneously vaporized and adsorbed on polydimethylsiloxane‐divinylbenzene. Under the established condition, the method detection limit was 0.1–0.5 μg/L in 4 mL water and the relative standard deviation was less than 13% at concentrations of 0.25 and 0.05 mg/L. This method was applied to determine aldehydes and acetone in 5 mineral water and 114 surface water samples. All mineral water samples had detectable levels of methanal (24.0–61.8 μg/L), ethanal (57.7–110.9 μg/L), propanal (11.5–11.7 μg/L), butanal, pentanal (3.3–3.4 μg/L) and nonanal (0.3–0.4 μg/L). Methanal and ethanal were also detected in concentration range of 2.7–117.2 and 1.2–11.9 μg/L, respectively, in surface water of 114 monitoring sites in Korea.
On‐demand photonic crystal resonators
Authors: Kim M.‐K. , Kim J.‐Y. , Kang J.‐H. , Ahn B.‐H. , Lee Y.‐H.
Published: February 2011

Recent progress in the field of re‐locatable photonic crystal resonators is discussed with a particular emphasis on the flexible scheme that employs highly‐curved microfiber. In this scheme a spectrally‐tunable high‐quality‐factor resonator can be defined repeatedly by physically moving a curved microfiber to a new position. When a curved microfiber is placed on top of a photonic crystal waveguide (or photonic crystal), a photonic well is newly created in the vicinity of the contact point. Inside of this photonic well, high‐quality‐factor resonant modes are generated at frequencies below the cutoff edge of the guided mode. The tapered microfiber is an integral part of a single mode optical fiber and efficient out‐coupling is naturally obtained. The sub‐nanometer spectral tuning capability that is available by changing the curvature of the microfiber is also an important characteristic and discussed. This spectrally‐ and spatially‐reconfigurable photonic crystal resonator is expected to be a potential platform for photonic crystal based single photon sources, which enables accurate spatial overlap and spectral overlap with a single quantum dot, together with straightforward photon out‐coupling to the fiber with high efficiency.
Modulation of Material Properties of a Decellularized Myocardial Matrix Scaffold
Authors: Singelyn Jennifer M. , Christman Karen L.
Published: February 2011

Injectable materials offer the potential for minimally invasive therapy for myocardial infarction (MI), either as an acellular scaffold or as a cell delivery vehicle. A recently developed myocardial matrix hydrogel, derived from decellularized porcine ventricular tissue, has the potential to aid in cardiac repair following an MI. Herein, we set out to study the effects of cross‐linking on the cardiac hydrogel stiffness, degradation properties, cellular migration, and catheter injectability in vitro. Cross‐linking increased stiffness, while slowing degradation and cellular migration through the gels. Additionally, the cross‐linked material was pushed through a clinically relevant catheter. These results demonstrate that the material properties of myocardial matrix can be tuned via cross‐linking, while maintaining appropriate viscosity for catheter injectability.

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What Morphologies Do We Want? – TEM Images from Dilute Diblock Copolymer Solutions
Authors: Zhao Hong , Chen Qianjin , Hong Liangzhi , Zhao Lei , Wang Jianfang , Wu Chi
Published: February 2011

The formation of various exotic morphologies of block copolymers in dilute solutions has often been claimed on the basis of TEM imaging. Do they really exist in solutions or are they just some kinetically frozen structures arising from TEM sample preparation? It is shown that different morphologies are formed due to a competition between different time scales. More and more people are realizing that it is necessary to use cryo‐TEM to ascertain a novel morphology in polymer solutions, but not everyone is able to access a modern cryo‐TEM. Our current study serves as an alarm to those who are interested in morphologies in block copolymer solutions that it is necessary to combine different methods, such as LLS, freeze‐drying, and TEM, in their studies.

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Neutral‐State Green Conjugated Polymers from Pyrrole Bis‐Substituted Benzothiadiazole and Benzoselenadiazole for Electrochromic Devices
Authors: Baran Derya , Oktem Gozde , Celebi Selin , Toppare Levent
Published: February 2011

Two donor/acceptor/donor‐type pyrrole‐incorporated monomers, 4,7‐di(1H‐pyrrol‐2‐yl)benzo[c][1,2,5]thiadiazole (M1) and 4,7‐di(1H‐pyrrol‐2‐yl)benzo[c][1,2,5]selenadiazole (M2), were synthesized and polymerized electrochemically. The resulting polymers (P1 and P2) were investigated in terms of their electrochromic and optical properties. Spectroelectrochemistry studies revealed that both polymers show two distinct absorptions in both red and blue regions. The absorptions at around 400 and 700 nm correspond to neutral‐state green polymers P1 and P2, which is a unique property for conjugated polymers. Optical band gaps were calculated as 1.12 and 1.08 eV for P1 and P2, respectively.

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Glia: Initiators and progressors of pathology in Parkinson's disease
Authors: Halliday Glenda M. , Stevens Claire H.
Published: February 2011

Background:

Glia are traditionally known as support cells for neurons, and their role in neurodegeneration has been largely considered secondary to neuronal dysfunction. We review newer concepts on glial function and assess glial changes in Parkinson's disease (PD) at the time of disease initiation when α‐synuclein is accumulating in brain tissue but there is limited neuronal loss, and also as the disease progresses and neuronal loss is evident.

Results:

Of the two main types of astrocytes, only protoplasmic astrocytes are involved in PD, where they become nonreactive and accumulate α‐synuclein. Experimental evidence has shown that astrocytic α‐synuclein deposition initiates the noncell autonomous killing of neurons through microglial signaling. As the disease progresses, more protoplasmic astrocytes are affected by the disease with an increasing microglial response. Although there is still controversy on the role microglia play in neurodegeneration, there is evidence that microglia are activated early in PD and possibly assist with the clearance of extracellular α‐synuclein at this time. Microglia transform to phagocytes and target neurons as the disease progresses but appear to become dysfunctional with increasing amounts of ingested debris. Only nonmyelinating oligodendroglial cells are affected in PD, and only late in the disease process.

Conclusions:

Glial cells are responsible for the progression of PD and play an important role in initiating the early tissue response. In particular, early dysfunction and α‐synuclein accumulation in astrocytes causes recruitment of phagocytic microglia that attack selected neurons in restricted brain regions causing the clinical symptoms of PD. © 2011 Movement Disorder Society
Twitch potentiation induced by stimulated and voluntary isometric contractions at various torque levels in human knee extensor muscles
Authors: Miyamoto Naokazu , Yanai Toshimasa , Kawakami Yasuo
Published: February 2011

The purpose of this study was to compare the extent of twitch potentiation (TP) after stimulated or voluntary contractions at identical intensities for the human knee extensor muscles. Isometric knee extensions of 10 s were performed at 20%, 40%, and 60% of maximal voluntary contraction (MVC) torque level, through percutaneous electrical stimulation of the quadriceps at 80 Hz or voluntary contraction. Twitch responses were evoked by stimulating the femoral nerve percutaneously with supramaximal intensity. The extent of TP after the stimulated contraction was greater than that after the voluntary contraction at the 20% MVC torque level, whereas a stimulated contraction induced a smaller extent of TP than did a voluntary contraction at contraction intensities higher than 40% MVC. We suggest that this contraction intensity dependence of differences in TP after stimulated and voluntary isometric conditioning contractions is responsible for differences in the recruitment pattern of motor units during the conditioning contractions. Muscle Nerve, 2011
Assessment of symptomatic diabetic patients with normal nerve conduction studies: Utility of cutaneous silent periods and autonomic tests
Authors: Koytak Pinar Kahraman , Isak Baris , Borucu Deniz , Uluc Kayihan , Tanridag Tulin , Us Onder
Published: February 2011

Established electrophysiological methods have limited clinical utility in the diagnosis of small‐fiber neuropathy (SFN). In this study, diabetic patients with clinically diagnosed SFN were evaluated with autonomic tests and cutaneous silent periods (CSPs). Thirty‐one diabetic patients with clinically suspected SFN and normal nerve conduction studies were compared with 30 controls. In the upper extremities (UE), the CSP parameters did not differ statistically between the patient and control groups, whereas, in the lower extremities (LE), patients had prolonged CSP latencies (P = 0.018) and shortened CSP durations (P < 0.001). The sensitivity of the CSP duration was 32.6%, and the specificity was 96.7%. The expiration‐to‐inspiration ratios and amplitudes of the sympathetic skin responses in the lower extremities were also reduced. Our findings indicate that the diagnostic utility of CSPs was higher than that of the autonomic tests to support the clinically suspected diagnosis of SFN. Muscle Nerve, 2011
Subacute myopathy in a mature patient due to multiple acyl‐coenzyme a dehydrogenase deficiency
Authors: Kaminsky Pierre , Acquaviva‐Bourdain Cecile , Jonas Jacques , Pruna Lelia , Chaloub Gihan e , Rigal Odile , Grignon Yves , Vianey‐Saban Christine
Published: February 2011

Introduction: Multiple acyl‐coenzyme A dehydrogenase deficiency (MADD), also called glutaric aciduria type II, is an inherited metabolic disorder resulting from a deficiency in electron transfer flavoprotein (ETF) or of its ubiquinone oxidoreductase (ETF‐QO). It usually occurs in the neonatal period or in early infancy and, very rarely, in adolescents and young adult patients. Methods: We report the case of a 55‐year‐old woman who developed a painful subacute myopathy. Results: Lipid accumulation was found at biopsy. MADD was confirmed by plasma acylcarnitine profile and by assessment of ETF‐QO activity in muscle. Conclusions: This study demonstrates that metabolic myopathies usually found in infancy may be also diagnosed in older patients. MADD may be easily treated by riboflavin and coenzyme Q10 and therefore should be included in the differential diagnosis of adult‐onset painful myopathy. Muscle Nerve 43: 444–446, 2011
Electromechanical delay in biceps brachii assessed by ultrafast ultrasonography
Authors: Hug François , Gallot Thomas , Catheline Stefan , Nordez Antoine
Published: February 2011

Using ultrasound we tested the utility of determining the relative contribution of the main muscle structures/mechanisms to the electromechanical delay in the biceps brachii. Nine subjects underwent electrically evoked contractions with the echographic probe maintained over the muscle and the myotendinous junction. No difference was found between the onset of muscle fascicle motion (Dm, 5.57 ± 1.37 ms) and the onset of myotendinous junction motion (Dt, 5.47 ± 1.38 ms), whereas significant differences were found between Dm/Dt and electromechanical delay (approximately 10 ms). Electromechanical delay can be used as a model for studying the effects of neuromuscular disorders or various constraints that affect excitation–contraction coupling and/or muscle force transmission. Muscle Nerve, 2011