bluuebunny/crossref_metadata_2025_split huggingface dataset:
Delineating melanoma using multimodal polarized light imaging
Authors: Tannous Zeina , Al‐Arashi Munir , Shah Sonali , Yaroslavsky Anna N. 
Published: January 2009

AbstractBackground and SignificanceMelanoma accounts for 3% of all skin cancers but causes 83% of skin cancer deaths. The first step in treatment of melanoma is the removal of the lesions, usually by surgical excision. Currently most lesions are removed without intraoperative margin control. Post‐operative methods inspect 1–2% of the surgical margin and are prone to sampling errors. In this study we evaluate the use of reflectance and fluorescence polarization imaging for the demarcation of melanoma in thick fresh skin excisions.Materials and MethodsPigmented lesions clinically suspicious for melanoma were elliptically excised with proper margins. Elliptical surgical excisions were vertically bisected along the short axis of the specimen into two halves in the middle of the pigmented lesions. The vertically bisected tumor face was imaged. After that, one half of the sample was briefly stained in aqueous 2 mg/ml solution of tetracycline, whereas another half was stained in 0.2 mg/ml aqueous solution of methylene blue. Then both specimens were reimaged. Reflectance images were acquired in the spectral range between 390 and 750 nm. Fluorescence images of the tetracycline‐stained tissue were excited at 390 nm and registered between 450 and 700 nm. Fluorescence of the methylene blue‐stained samples was excited at 630 nm and registered between 650 and 750 nm. After imaging, the tissue was processed for standard H&E histopathology. The resulting histological and optical images were compared to each other.Results and ConclusionsOur findings demonstrate that both tetracycline and methylene blue are suitable for imaging dysplastic and benign nevi. Melanoma is better delineated in the samples stained in methylene blue. Accurate and rapid delineation of melanoma in standard fresh surgical excisions appears feasible. Lasers Surg. Med. 41:10–16, 2009. © 2008 Wiley‐Liss, Inc.
Binary Interaction Parameters, Ternary Systems: Realistic Modeling of Liquid/Liquid Phase Separation
Authors: Wolf Bernhard A. 
Published: January 2009

AbstractThe phase behavior of ternary systems (either a polymer solution in a mixed solvent or a polymer blend in a single solvent) was modeled theoretically. The modeling considers two specific features of polymers explicitly: chain connectivity and the ability to respond to changes in the molecular environment by conformational reorientation. Previously, this approach has been applied to polymer solutions in single solvents. Here it is generalized and the number of parameters is reduced to two per binary system. The calculation of the Gibbs energies of the ternary mixtures accounts for the composition dependencies of the binary interaction parameters. The following phenomena are reproduced realistically for polymer solutions in a mixed solvent and for solutions of two polymers in a common solvent: simplicity, co‐solvency, and co‐non‐solvency. The results nourish the hope that the new approach is capable of modeling phase diagrams for ternary systems by means of binary interaction parameters only.magnified image
Transcriptional processing of G4 DNA
Authors: Tornaletti Silvia 
Published: January 2009

AbstractGenomic DNA sequences with the ability to assume non‐B form secondary structures have been recently shown to be particularly susceptible to genetic instability, an early contributing factor in human disease and cancer development. Transcription appears to play a central role in formation of these structures and in promoting instability at these sites. The subpathway of nucleotide excision DNA repair, transcription‐coupled DNA repair (TCR), removes transcription‐arresting damage from the transcribed strands of expressed genes, but little is known about how non‐canonical DNA structures are processed when encountered by the transcription machinery. If such structures arrest transcription, they may elicit “gratuitous” TCR in which the resulting reiterative and futile repair replication might generate a significant level of mutagenesis in a frequently transcribed gene because of faulty processing in the area of transcription arrest. Here we will describe our current understanding of how TCR may be elicited at non‐B DNA structures and summarize recent literature describing the behavior of RNA polymerases when encountering non‐canonical DNA structures, with particular emphasis on quadruplex DNA. © 2009 Wiley‐Liss, Inc.
Regulation of the hedgehog signaling by the mitogen‐activated protein kinase cascade in gastric cancer
Authors: Seto Motoko , Ohta Miki , Asaoka Yoshinari , Ikenoue Tsuneo , Tada Motohisa , Miyabayashi Koji , Mohri Dai , Tanaka Yasuo , Ijichi Hideaki , Tateishi Keisuke , Kanai Fumihiko , Kawabe Takao , Omata Masao 
Published: January 2009

AbstractThe hedgehog and mitogen‐activated protein kinase (MAPK) signaling pathways regulate growth in many tumors, suggesting cooperation between these two pathways in the regulation of cell proliferation. However, interactions between these pathways have not been extensively studied. We assessed cross‐talk between hedgehog and MAPK signaling in the regulation of cell proliferation in gastric cancer. We showed that PTCH expression was significantly correlated with extracellular signal‐regulated kinase (ERK) 1/2 phosphorylation (P = 0.016) as well as SHH expression (P = 0.034) in the 35 gastric cancers assessed by immunohistochemistry. Indeed, MAPK signaling increased the GLI transcriptional activity and induced the expression of hedgehog target genes in gastric cancer cells. The inductive effect of activated KRAS and mitogen‐activated protein/extracellular signal‐regulated kinase kinase (MEK) 1 was blocked by the suppressor of fused (SUFU), indicating that MAPK signaling regulates GLI activity via a SUFU‐independent process. Moreover, the deletion of the NH2‐terminal domain of GLI1 gene resulted in reduced response to MEK1 stimulation. Our results suggest that the KRAS‐MEK‐ERK cascade has a positive regulatory role in GLI transcriptional activity in gastric cancer. © 2009 Wiley‐Liss, Inc.
Resveratrol enhances cell‐mediated immune response to DMBA through TLR4 and prevents DMBA induced cutaneous carcinogenesis
Authors: Yusuf Nabiha , Nasti Tahseen H. , Meleth Sreelatha , Elmets Craig A. 
Published: January 2009

AbstractToll‐like receptors (TLRs) activate signals that are critically involved in innate immune responses and that contribute to the initiation of adaptive immune responses. Resveratrol (trans‐3,5,4‐trihydroxystilbene), a polyphenol found in red grapes and in several other plant sources, is an effective chemopreventive agent in cutaneous chemical carcinogenesis. In this study, we investigated whether TLR4 was required for the chemopreventive action of resveratrol in DMBA skin carcinogenesis. For this purpose, mice with normal and deficient TLR4 function were compared when pretreated with resveratrol and then subjected to a DMBA‐induced skin carcinogenesis protocol. There were fewer tumors/group (P < 0.001) in resveratrol treated TLR4 competent C3H/HeN mice than in TLR4 deficient C3H/HeJ mice. In addition, the size of tumors in C3H/HeN mice was reduced in vivo and their survival in vitro was inhibited by resveratrol to a significantly greater extent than in C3H/HeJ mice. Resveratrol inhibited angiogenesis to a much greater extent in the TLR4 competent mice than in TLR4 deficient mice. IFN‐γ and IL‐12 levels were also increased in TLR4 competent mice compared to TLR4 deficient mice, and TLR4 competent C3H/HeN mice exhibited a greater increase in the cell‐mediated immune response to DMBA. The results of this study indicate that TLR4 is an important mediator of resveratrol chemoprevention in DMBA skin tumorigenesis. Published 2009 Wiley‐Liss, Inc.
New silicone hydrogels based on interpenetrating polymer networks comprising polysiloxane and poly(vinyl alcohol) networks
Authors: Pavlyuchenko V. N. , Sorochinskaya O. V. , Ivanchev S. S. , Khaikin S. Ya. , Trounov V. A. , Lebedev V. T. , Sosnov E. A. , Gofman I. V. 
Published: January 2009

AbstractA method for the synthesis of a new silicone hydrogel as a biphase material for soft contact lenses is considered. The method is based on the synthesis of sequential interpenetrating polymer networks (IPN) and includes the following stages: (1) cross‐linked silicone synthesis by the reaction of vinyl‐ and hydride‐containing oligosiloxanes; (2) silicone network saturation with vinyl acetate and cross‐linking monomer followed by UV‐initiated polymerization to form an IPN comprising the silicone and cross‐linked poly(vinyl acetate) (PVAc) network; (3) PVAc network alcoholysis with methanol to obtain silicone hydrogels comprising the silicone and cross‐linked poly(vinyl alcohol) (PVAl). A study of hydrophilic, optical, mechanical, and structural features of the silicone hydrogels showed that optical transparency is achieved for materials with the highest density of silicone network cross‐linking where the size of IPN structural units does not exceed 100 nm. The water content in hydrophilic networks of silicone hydrogel is found to be below the values typical of cross‐linked PVAl, leading to non‐additivity of IPN mechanical properties. Indeed, the elasticity moduli (E) of the hydrophilic and silicone networks are 0.4–0.7 and 0.7–1.8 MPa, respectively, whereas for some IPN this value reaches 3.0 MPa. The optimal parameters of synthesis providing the reduction of E to 0.8–1.6 MPa without deterioration of the required performance characteristics (optical transparency 90–92%, water content 20–39 wt%) are determined. Copyright © 2009 John Wiley & Sons, Ltd.
Thermosensitive polylactide‐glycolide delivery systems for treatment of narcotic addictions
Authors: Salehi R. , Nowruzi K. , Entezami A. A. , Asgharzadeh V. , Davaran S. 
Published: January 2009

AbstractEnvironmental switches may be fabricated for the controlled release of pharmaceutical drug using a thermally responsive polymer with the intrinsic chemical and physical nature of stimuli‐sensitive smart materials. Particularly, much attention has been paid to the biomedical applications of poly(N‐isopropyl acrylamide) (PNIPAAm) because of its unique reversible transition at a specific lower critical solution temperature (LCST).Thermally sensitive block copolymers, poly(N‐isopropyl acrylamide‐b‐poly(L‐lactide‐co‐glycolide) (PNIPAAm‐b‐PLGA), and polyethylene glycol‐poly (lactide‐co‐glycolide) (PEG‐PLGA) triblock copolymers with different compositions and length of PLGA block were synthesized via ring‐opening polymerization of lactide and glycolide in the presence of OH‐terminated PNIPAAm or PEG. The composition and structure of the polymer were determined by NMR and FTIR. The effect of important factors, such as ionic strength, pH, and polymer concentration on the phase transition behavior of temperature‐sensitive polymers, were investigated by cloud point measurements. The resulting thermosensitive polymers were used for the entrapment of a narcotic antagonist drug, naltrexone, as the model drug. The loading efficiency and drug release behavior of naltrexone‐loaded hydrogels were investigated. The naltrexone loaded thermosensitive polymers were able to sustain the release of naltrexone for different periods of time, depending on the polymer composition, and concentration. In vitro release studies showed that these thermosensitive polymers are able to deliver naltrexone in biologically active forms at a controlled rate for 3–8 weeks. Copyright © 2009 John Wiley & Sons, Ltd.
Removal of lipopolysaccharide and reactive oxygen species using sialic acid immobilized polysulfone dialyzer
Authors: Chang Jung‐Jhih , Lin Po‐Ju , Yang Ming‐Chien , Chien Chiang‐Ting 
Published: January 2009

AbstractSialic acid (N‐acetylneuraminic acid, NANA) was covalently immobilized onto the surface of a polysulfone (PSF) hollow fiber membrane. Prior to the immobilization, the surface of PSF was treated with ozone, followed by grafting with acrylic acid, and then the esterification of NANA. The surface concentration of NANA was determined by 2‐thiobarbituric acid (TBA) test. Hemocompatibility, the capability of suppressing oxidative stress, and clearance of lipopolysaccharide (LPS) from the resulting hollow fiber membrane were evaluated. The results show that by immobilizing NANA onto PSF hollow fiber, the adhesion of platelet was reduced, while both APTT and PT were little affected. Furthermore, oxidative stress was suppressed by NANA‐immobilized PSF hollow fibers. The level of LPS was also greatly reduced. Copyright © 2009 John Wiley & Sons, Ltd.
Novel AB crosslinked polymer networks from telechelic 4‐vinylbenzyl carbamate terminated polyurethanes and different vinyl monomers
Authors: Venkataramani Sriram , Kannan Tharanikkarasu , Das Palash Jyoti , Radhakrishnan Ganga 
Published: January 2009

AbstractNovel AB crosslinked polymer (ABCP) networks were synthesized from telechelic 4‐vinylbenzyl carbamate terminated polyurethanes and monomers such as styrene, 4‐vinylpyridine, methyl methacrylate and butyl acrylate. Telechelic 4‐vinylbenzyl carbamate terminated polyurethanes were synthesized from polypropylene glycol‐based NCO‐terminated polyurethane and vinylbenzyl alcohol. Effect of changing the molecular weight of polypropylene glycol on the static and dynamic mechanical properties of ABCP networks from polyurethane‐polymethyl methacrylate was studied in detail. Dynamic mechanical thermal analysis results show that polymethyl methacrylate and polystyrene‐based ABCPs have good damping over a broad temperature range. ABCP networks prepared from 4‐vinylbenzyl carbamate terminated polyurethane and different monomers such as methyl methacrylate, butyl acrylate and styrene exhibit single tan δmax value which implies excellent interlocking between the two polymers present in the ABCP networks. Static mechanical studies showed that methyl methacrylate and styrene‐based ABCP networks exhibit better tensile properties compared to other ABCP networks from butyl acrylate and 4‐vinyl pyridine monomers. Thermogravimetric analysis results revealed that the ABCP networks showed an improved thermal stability. Copyright © 2009 John Wiley & Sons, Ltd.
Mechanisms of lymphatic metastasis in human colorectal adenocarcinoma
Authors: Royston Daniel , Jackson David G. 
Published: January 2009

AbstractThe invasion of lymphatic vessels by colorectal cancer (CRC) and its subsequent spread to draining lymph nodes is a key determinant of prognosis in this common and frequently fatal malignancy. Although tumoural lymphangiogenesis is assumed to contribute to this process, review of the current literature fails to support any notion of a simple correlation between lymphatic vessel density and CRC metastasis. Furthermore, attempts to correlate the expression of various lymphangiogenic growth factors, most notably VEGF‐C and VEGF‐D, with the lymphatic metastasis of CRC have provided contradictory results. Recent evidence from animal and human models of tumour metastasis suggests that complex functional and biochemical interactions between the microvasculature of tumours and other cell types within the tumour microenvironment may play a pivotal role in the behaviour of commonly metastasizing tumours. Indeed, previous insights into tumoural blood vessels have provided candidate markers of tumoural angiogenesis that are currently the subject of intense investigation as future therapeutic targets. In this review article we survey the current evidence relating lymphangiogenesis and lymphangiogenic growth factor production to metastasis by CRC, and attempt to provide some insight into the apparent discrepancies within the literature. In particular, we also discuss some new and provocative insights into the properties of tumoural lymphatics suggesting that they have specific expression profiles distinct from those of normal lymphatic vessels and that appear to promote metastasis. These findings raise the exciting prospect of future biomarkers of lymphatic metastasis and identify potential targets for new generation anti‐tumour therapies. Copyright © 2009 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Novel concepts in atherogenesis: angiogenesis and hypoxia in atherosclerosis
Authors: Sluimer Judith C , Daemen Mat J 
Published: January 2009

AbstractThe clinical complications of atherosclerosis are caused by thrombus formation, which in turn results from rupture of an unstable atherosclerotic plaque. The formation of microvessels (angiogenesis) in an atherosclerotic plaque contributes to the development of plaques, increasing the risk of rupture. Microvessel content increases with human plaque progression and is likely stimulated by plaque hypoxia, reactive oxygen species and hypoxia‐inducible factor (HIF) signalling. The presence of plaque hypoxia is primarily determined by plaque inflammation (increasing oxygen demand), while the contribution of plaque thickness (reducing oxygen supply) seems to be minor. Inflammation and hypoxia are almost interchangeable and both stimuli may initiate HIF‐driven angiogenesis in atherosclerosis. Despite the scarcity of microvessels in animal models, atherogenesis is not limited in these models. This suggests that abundant plaque angiogenesis is not a requirement for atherogenesis and may be a physiological response to the pathophysiological state of the arterial wall. However, the destruction of the integrity of microvessel endothelium likely leads to intraplaque haemorrhage and plaques at increased risk for rupture. Although a causal relation between the compromised microvessel structure and atherogenesis or between angiogenic stimuli and plaque angiogenesis remains tentative, both plaque angiogenesis and plaque hypoxia represent novel targets for non‐invasive imaging of plaques at risk for rupture, potentially permitting early diagnosis and/or risk prediction of patients with atherosclerosis in the near future. Copyright © 2009 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Injury‐induced sequential transformation of notochordal nucleus pulposus to chondrogenic and fibrocartilaginous phenotype in the mouse
Authors: Yang Fan , Leung Victor YL , Luk Keith DK , Chan Danny , Cheung Kenneth MC 
Published: January 2009

AbstractIntervertebral disc degeneration has been widely studied in different animal models. To test the hypothesis that needle puncture could induce progressive biochemical and molecular changes in murine discs, we established a mouse tail model to investigate the pathogenesis and molecular mechanism of puncture‐induced disc degeneration. Caudal discs in mouse tails were punctured using a 31G gauge needle at controlled depth under microscopic guidance. The progress of the disc degeneration was evaluated by radiographic analysis of disc height, histological grading and glycosaminoglycan (GAG) quantification pre‐operation and 1, 2, 6 and 12 weeks post‐puncture. Gene and protein expression of the extracellular matrix (ECM) was analysed by RT–PCR, in situ hybridization and immunohistochemistry. Histological study and disc height analysis revealed progressive degenerative changes in the punctured discs. Compared with the pre‐operation control group, total GAG content decreased 40% (p < 0.05) and aggrecan (Acan), decorin (Dcn) and versican (Vcan; Cspg2) expression was down‐regulated at 12 weeks post‐puncture. A transient increase of Col2a1‐expressing cells and elevation of collagen II protein in the nucleus pulposus (NP) was detected. Fibronectin (Fn1) expression was up‐regulated 50% and deposition of collagen I in NP was observed at 12 weeks post‐puncture. This study is the first to use an injury‐induced model to study disc degeneration in mouse. The disc degeneration involves a transient transformation of NP from notochordal to chondrogenic and eventually into fibrocartilaginous phenotype. The degenerative changes have some similarity to human disc degeneration, suggesting that this model may potentially be used in future to study the molecular mechanism and dissect the pathways of disc degeneration. Copyright © 2009 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Current smoking‐specific gene expression signature in normal bronchial epithelium is enhanced in squamous cell lung cancer
Authors: Boelens Mirjam C , van den Berg Anke , Fehrmann Rudolf SN , Geerlings Marie , de Jong Wouter K , te Meerman Gerard J , Sietsma Hannie , Timens Wim , Postma Dirkje S , Groen Harry JM 
Published: January 2009

AbstractCigarette smoking is the main risk factor for the development of squamous cell lung carcinoma (SCC). However, the smoking‐related molecular changes in SCC have not been studied. Gene expression studies in both histologically normal bronchial epithelium and SCC epithelial samples identified genes differentially expressed between current and ex‐smokers. Subsequently, expression levels of the smoking‐related genes in normal bronchial epithelium were compared with those in SCC cells, since we hypothesized that the smoking‐induced changes would be also deregulated in SCC. Gene expression profiles were generated using Agilent whole human genome microarrays on laser‐microdissected normal bronchial epithelium and SCC samples. Expression levels of 246 genes, mainly related to oxidative stress response, were significantly different between normal bronchial epithelium of current and ex‐smokers. Such a differential gene expression profile did not exist in SCC cells of smokers and ex‐smokers. Interestingly, when comparing SCC and normal bronchial epithelium from ex‐smokers, the vast majority of these 246 genes were also deregulated in SCC. When comparing SCC with normal epithelium from smokers, 22% of the up‐regulated genes showed a similar high expression in SCC whereas 79% of the down‐regulated genes were even further reduced in SCC as compared to current smokers. The down‐regulated genes included several tumour suppressor genes, such as C9orf9, INHBB, LRIG1, SCGB3A1, SERPINI2, STEAP3 and ZMYND10. Thus, our study shows that the majority of genes up‐regulated in normal bronchial epithelium of current smokers show similar high expression levels in SCC, while down‐regulated genes are even further repressed in SCC. Our data indicate that smoking‐related changes in normal bronchial epithelial cells persist in malignant transformed squamous cells. Copyright © 2009 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.