bluuebunny/crossref_metadata_2025_split huggingface dataset:
Electrochemically induced FTIR difference spectroscopy in the mid‐ to far infrared (200 μm) domain: A new setup for the analysis of metal–ligand interactions in redox proteins
Authors: Berthomieu Catherine , Marboutin Laure , Dupeyrat François , Bouyer Pierre 
Published: February 2006

AbstractWe report the setup of an electrochemical cell with chemical–vapor deposition diamond windows and the use of a Bruker 66 SX FTIR spectrometer equipped with DTGS and Si‐bolometer detectors and KBr and mylar beam splitters, to record on the same sample, FTIR difference spectra corresponding to the structural changes associated with the change in redox state of active sites in proteins in the whole 1800–50 cm–1 region. With cytochrome c we show that reliable reduced‐minus‐oxidized FTIR difference spectra are obtained, which correspond to single molecular vibrations. Redox‐sensitive IR modes of the cytochrome c are detected until 140 cm–1 with a good signal to noise. This new setup is promising to analyze the infrared spectral region where metal–ligand vibrations are expected to contribute and to extend the analysis of vibrational properties to metal sites or redox states not accessible to (resonance) Raman spectroscopy. © 2006 Wiley Periodicals, Inc. Biopolymers 82: 363–367, 2006This article was originally published online as an accepted preprint. The “Published Online” date corresponds to the preprint version. You can request a copy of the preprint by emailing the Biopolymers editorial office at biopolymers@wiley.com
The role of ARPC4 in tip growth and alignment of the polar axis in filaments of Physcomitrella patens
Authors: Perroud Pierre‐François , Quatrano Ralph S. 
Published: February 2006

AbstractWhen the actin related protein 2/3 (Arp2/3) complex member arpc4 was deleted in Physcomitrella patens (moss), the resulting null mutant (Δarpc4) was viable and revealed no gross changes during morphogenesis of filaments into gametophores. However, we observed a striking reduction of filamentous tip growth, resulting in smaller, denser colonies. Although polar responses of Δarpc4 filaments to unilateral white light were unaffected, these mutant filaments were defective in their response to polarized white light. These observations strongly suggest a specific role of the Arp2/3 complex as a downstream target for signals regulating oriented tip growth. Insertion of YFP‐ARPC4 into Δarpc4 rescued the mutant phenotypes and localized ARPC4 exclusively to the tip cell of filaments, the site of actin dynamics and polarized growth. The ability of Δarpc4 to perform some but not all cellular responses will allow the study of its function in orientation of tip growth in response to directional cues (e.g. light) in a viable but mutated background. Cell Motil. Cytoskeleton 63: 2006. © 2006 Wiley‐Liss, Inc.
Quality of survival reporting in chemotherapy and surgery trials in patients with metastatic colorectal carcinoma
Authors: Martin Robert C. G. , Augenstein Vedra A. , Scoggins Charles R. , McMasters Kelly M. 
Published: February 2006

AbstractBACKGROUNDPatients with metastatic colorectal carcinoma (MCC) to the liver receive conflicting management recommendations because of the lack of prospective randomized controlled trials (RCTs) clarifying the optimal management in this disease. The oabjective of the current study was to evaluate the reporting of prognostic factors in MCC from chemotherapy and surgery trials and evaluate the ability to compare these results across treatments.METHODSRCTs and retrospective series of greater than 75 MCC patients published between 1980–2004 were reviewed to identify 10 critical prognostic elements of overall survival reported in both types of journals.RESULTSA review 92 RCTs and 116 retrospective reports with 64,898 patients analyzed found 7 (3%) reporting all prognostic factors, with both studies demonstrating no difference in the success of reporting criteria met. The only criterion that was universally reported among both chemotherapy and surgery trials was the mortality rates of the study. All remaining prognostic factors in the evaluation of overall survival were significantly different between both chemotherapy and surgical studies. Considerable variation was observed in the disease‐free interval, number of hepatic metastases, size of hepatic metastases, and performance status, and were significantly different among some of the most significant factors for patients evaluating treatment: complication reporting, surgical margin evaluation, and overall response rate.CONCLUSIONSThe reporting of results in MCC in chemotherapy trials and surgical reports is limited to general outcomes, with a paucity of prognostic factors, which hinders any ability to compare results across treatments. A mandatory reporting criteria of all metastatic colorectal trials is imperative to optimally manage these patients in both academic and community centers. Cancer 2006. © 2006 American Cancer Society.
Occult hepatitis B virus infection is associated with the development of hepatocellular carcinoma in chronic hepatitis C patients
Authors: Squadrito Giovanni , Pollicino Teresa , Cacciola Irene , Caccamo Gaia , Villari Daniela , La Masa Tiziana , Restuccia Tea , Cucinotta Eugenio , Scisca Claudio , Magazzu Domenico , Raimondo Giovanni 
Published: February 2006

AbstractBACKGROUNDOccult hepatitis B virus (HBV) infection frequently occurs in patients with HBV surface antigen (HBsAg)‐negative chronic liver disease, and much evidence suggests that it is a risk factor for hepatocellular carcinoma (HCC) development. However, to the authors' knowledge, no follow‐up study has been performed to date evaluating HCC occurrence over time in chronic hepatitis patients with or without occult HBV infection.METHODSA cohort of the 380 HBsAg‐negative chronic hepatitis patients attending the study institution between 1991–2000 were evaluated and tested for occult HBV DNA by analysis of liver biopsy specimens.RESULTSThere were 135 patients (35.5%) with occult HBV and 245 patients (64.5%) without occult HBV. Cirrhosis was significantly associated with occult HBV infection (P = 0.01). One hundred thirty‐four of these patients were followed for a minimum of 50 months (median, 82.8 ± 32.6 mos). Fifty‐three patients (39%) were occult HBV carriers and 81 (61%) were not. Nine patients developed HCC during the follow‐up; eight were positive and one was negative for occult HBV (P = 0.002).CONCLUSIONSThe current observational cohort study showed that, among the HBsAg‐negative patients with chronic hepatitis, HCC develops for the most part in carriers of occult HBV. Therefore, the evaluation of HBV genomes in chronic hepatitis patients appears to be a powerful tool for the identification of individuals at higher risk of HCC development. Cancer 2006. © 2006 American Cancer Society.
Decrease in motor performance in children with cancer is independent of the cumulative dose of vincristine
Authors: Hartman Annelies , van den Bos Cor , Stijnen Theo , Pieters Rob 
Published: February 2006

AbstractBACKGROUNDImpaired performance on motor tasks in children treated for acute lymphoblastic leukemia (ALL) after completion of treatment is often attributed to vincristine (VCR). Whether motor problems persist in other children who receive different cumulative doses of VCR is to the authors' knowledge not known. The objective of the current study was to determine the extent of motor problems in children with ALL, Wilms tumor (WT), B‐cell non‐Hodgkin lymphoma (B‐NHL), and malignant mesenchymal tumors (MMT) and whether these motor problems were related to VCR dose.METHODSIn 128 children ages 4–12 years who completed treatment after at least 1 year, motor performance was measured using the Movement Assessment Battery for Children (m‐ABC).RESULTSThe m‐ABC scores of the total study group were significantly lower than those of the normal population (P < 0.001). There were no differences in scores noted between children with ALL, WT, B‐NHL, or MMT. There also were no differences noted between those children with ALL who had received pulses of VCR and steroids during maintenance therapy and those who had not. All groups demonstrated large variability in scores. Scores were not found to be significantly different between those children who had received low (< 20 mg/m2), intermediate (20–40 mg/m2), or high (> 40 mg/m2) cumulative doses of VCR. Cumulative doses of corticosteroids and methotrexate did not affect scores, nor did age at diagnosis and time since the completion of therapy.CONCLUSIONSAlthough motor performance was impaired in all patient groups, no correlation was found between motor performance and the cumulative dose of VCR or other drugs, age, and follow‐up time. Future studies have to address several issues, including whether polymorphisms in drug metabolizing genes or drug target genes explain the significant variability noted in the long‐term motor outcome of children with cancer. Cancer 2006. © 2006 American Cancer Society.
Intranasal interleukin‐12 gene therapy enhanced the activity of ifosfamide against osteosarcoma lung metastases
Authors: Duan Xiaoping , Jia Shu‐Fang , Koshkina Nadezhda , Kleinerman Eugenie S. 
Published: February 2006

AbstractBACKGROUNDCyclophosphamide (CTX) and ifosfamide (IFX) are alkylating agents used to treat osteosarcoma (OS). It was previously demonstrated that the sensitivity of OS cells to 4‐hydroperoxycyclophosphamide (4‐HC, the active metabolite of CTX) is augmented by interleukin (IL)‐12 in vitro through a mechanism involving the Fas/FasL pathway. The purpose of these studies was to determine whether this synergistic effect is operational in vivo.METHODSMice were injected intravenously with human LM7 osteosarcoma cells. Treatment was initiated with IFX (2.5 mg/kg intraperitoneally) with or without intranasal polyethylenimine (PEI):IL‐12 gene therapy given twice weekly for 6 weeks.RESULTSExpression of IL‐12 protein in the lung was demonstrated in all mice receiving intranasal PEI:IL‐12 but not in control mice or those treated with IFX alone. Increased expression of FasL was detected in lungs of all mice receiving IFX. Both IFX and PEI:IL‐12 alone significantly inhibited lung metastasis when compared with control groups (P < 0.05). However, the most significant tumor effect was observed in mice receiving IFX+PEI:IL‐12 (P < 0.01). Immunohistochemical staining for CD31 and basic fibroblast growth factor (bFGF) and the number of proliferating cells as quantified by proliferating cell nuclear antigen (PCNA) staining were also most significantly decreased in mice receiving combination therapy.CONCLUSIONSThese data indicate that combining IFX and IL‐12 may have therapeutic potential and that this increased efficacy may be mediated through a mechanism involving the Fas/FasL pathway. Cancer 2006. © 2006 American Cancer Society
Visual, auditory, sensory, and motor impairments in long‐term survivors of hematopoietic stem cell transplantation performed in childhood
Authors: Gurney James G. , Ness Kirsten K. , Rosenthal Joseph , Forman Stephen J. , Bhatia Smita , Baker K. Scott 
Published: February 2006

AbstractBACKGROUNDBecause of treatment‐related toxicity, research is increasingly being focused on long‐term sequelae secondary to hematopoietic stem cell transplantation (HSCT) in survivor populations.METHODSThis study describes the incidence of auditory, sensory, motor, and visual impairments, including cataracts, among 235 individuals who were treated with HSCT during childhood or adolescence. Outcomes were compared with 705 siblings of childhood cancer survivors. Participants completed a survey with questions on posttransplant organ system impairments. Approximately half of survivors were transplanted when younger than 10 years of age. The median length of followup was 11 years.RESULTSThe cumulative incidence of cataracts was 36% at 15 years post‐HSCT, although cataracts occurred only in those who received total body irradiation as an HSCT conditioning agent or head irradiation before transplant. Persistent pain was reported by 21% of survivors. Loss of hearing in one or both ears, and legal blindness in one or both eyes, each occurred after transplant in 2% of survivors. Occurrences were uncommon, but survivors were 4.3 times (95% confidence interval [CI]: 2.0–9.4) more likely to report coordination problems, 7.7 times (95% CI: 3.2–18.5) more likely to report chewing or swallowing problems, and 3.5 times (3.5; 95% CI: 1.6–7.9) more likely to report muscle weakness than those in the comparison group. Muscle weakness was strongly associated with positive history of chronic graft‐versus‐host disease.CONCLUSIONSIncreased risks were found for motor impairments, hearing loss, vision loss, and persistent pain among study participants. Cataracts were a frequent adverse effect, suggesting that close monitoring with appropriate intervention for preservation of vision, particularly among those who received total body irradiation, should be a primary goal in survivors of HSCT performed in childhood. Cancer 2006. © 2006 American Cancer Society.
Neural activity related to self‐ versus externally generated painful stimuli reveals distinct differences in the lateral pain system in a parametric fMRI study
Authors: Helmchen Christoph , Mohr Christian , Erdmann Christian , Binkofski F. , Büchel Christian 
Published: February 2006

AbstractSelf‐generated sensory stimulation can be distinguished from externally generated stimulation that is otherwise identical. To determine how the brain differentiates external from self‐generated noxious stimulation and which structures of the lateral pain system use neural signals to predict the sensory consequences of self‐generated painful stimulation, we used functional magnetic resonance imaging to examine healthy human subjects who received thermal‐contact stimuli with noxious and non‐noxious temperatures on the resting right hand in random order. These stimuli were internally (self‐generated) or externally generated. Two additional conditions served as control conditions: to account for stimulus onset uncertainty, acoustic stimuli preceding the same thermal stimuli were used with variable or fixed delays but without any stimulus‐eliciting movements. Whereas graded pain‐related activity in the insula and secondary somatosensory cortex (SII) was independent of how the stimulus was generated, it was attenuated in the primary somatosensory cortex (SI) during self‐generated stimulation. These data agree with recent concepts of the parallel processing of nociceptive signals to the primary and secondary somatosensory cortices. They also suggest that brain areas that encode pain intensity do not distinguish between internally or externally applied noxious stimuli, i.e., this adaptive biological mechanism prevents harm to the individual. The attenuated activation of SI during self‐generated painful stimulation might be a result of the predictability of the sensory consequences of the pain‐related action. Hum Brain Mapp, 2006. © 2006 Wiley‐Liss, Inc.
The role of folate receptor α in cancer development, progression and treatment: Cause, consequence or innocent bystander?
Authors: Kelemen Linda E. 
Published: February 2006

AbstractFolate receptor α (FRα) is a membrane‐bound protein with high affinity for binding and transporting physiologic levels of folate into cells. Folate is a basic component of cell metabolism and DNA synthesis and repair, and rapidly dividing cancer cells have an increased requirement for folate to maintain DNA synthesis, an observation supported by the widespread use of antifolates in cancer chemotherapy. FRα levels are high in specific malignant tumors of epithelial origin compared to normal cells, and are positively associated with tumor stage and grade, raising questions of its role in tumor etiology and progression. It has been suggested that FRα might confer a growth advantage to the tumor by modulating folate uptake from serum or by generating regulatory signals. Indeed, cell culture studies show that expression of the FRα gene, FOLR1, is regulated by extracellular folate depletion, increased homocysteine accumulation, steroid hormone concentrations, interaction with specific transcription factors and cytosolic proteins, and possibly genetic mutations. Whether FRα in tumors decreases in vivo among individuals who are folate sufficient, or whether the tumor's machinery sustains FRα levels to meet the increased folate demands of the tumor, has not been studied. Consequently, the significance of carrying a FRα‐positive tumor in the era of folic acid fortification and widespread vitamin supplement use in countries such as Canada and the United States is unknown. Epidemiologic and clinical studies using human tumor specimens are lacking and increasingly needed to understand the role of environmental and genetic influences on FOLR1 expression in tumor etiology and progression. This review summarizes the literature on the complex nature of FOLR1 gene regulation and expression, and suggests future research directions. © 2006 Wiley‐Liss, Inc.
Regional DNA hypermethylation and DNA methyltransferase (DNMT) 1 protein overexpression in both renal tumors and corresponding nontumorous renal tissues
Authors: Arai Eri , Kanai Yae , Ushijima Saori , Fujimoto Hiroyuki , Mukai Kiyoshi , Hirohashi Setsuo 
Published: February 2006

AbstractTo evaluate the significance of altered DNA methylation during renal tumorigenesis, tumorous tissues (T) and corresponding nontumorous renal tissues (N) from 94 patients with renal tumors, and normal renal tissues (C) from 16 patients without renal tumors were investigated. DNA methylation status on CpG islands of the p16, human MutL homologue 1 (hMLH1), von‐Hippel Lindau (VHL) and thrombospondin‐1 (THBS‐1) genes and the methylated in tumor (MINT) ‐1, ‐2, ‐12, ‐25 and ‐31 clones and DNA methyltransferase (DNMT) 1 expression were examined by bisulfite modification and immunohistochemistry, respectively. The average number of methylated CpG islands was significantly higher in N than in C, and was even higher in T. The average number of methylated CpG islands in N was significantly correlated with a higher histological grade of corresponding conventional renal cell carcinomas (RCCs). The average number of methylated CpG islands in RCCs was significantly correlated with macroscopic configuration with extranodular or multinodular growth, higher histological grade, infiltrating growth pattern and vascular involvement. The recurrence‐free survival rate of patients with RCCs showing accumulation of DNA methylation was significantly lower than that of patients not showing this feature. The incidence of nuclear immunoreactivity for DNMT1 tended to be higher in proximal tubules from N than in those from C, and was significantly higher in RCCs. From the viewpoint of altered DNA methylation, N is at the precancerous stage, and N showing accumulation of DNA methylation may generate more malignant RCCs. Regional DNA hypermethylation may be associated with renal tumorigenesis from a precancerous condition to malignant progression and become a predictor of patient prognosis. © 2006 Wiley‐Liss, Inc.
Hepatocyte growth factor and the Met system as a mediator of tumor–stromal interactions
Authors: Matsumoto Kunio , Nakamura Toshikazu 
Published: February 2006

AbstractCrosstalk between carcinoma cells and host stromal cells such as fibroblasts has a great deal of influence on the invasive and metastatic behavior of cancer cells. The oncogenic action of fibroblasts has been demonstrated through genetic alterations that occur specifically in fibroblasts. Hepatocyte growth factor (HGF), a ligand for the Met receptor tyrosine kinase, plays a definitive role, particularly in the progression to invasive and metastatic cancers, predominantly as a stroma‐derived paracrine mediator. Many types of cancer cells secrete molecules that enhance HGF production in fibroblasts, while fibroblast‐derived HGF, in turn, is a potent stimulator of the invasion of cancer cells. Fibroblast‐specific genetic alterations leading to an overexpression of HGF are associated with the development of epithelial neoplasia and invasive carcinoma. Strategies for targeting the HGF–Met axis are being pursued, in attempts to block the malignant behavior of cancers. In normal tissues, the HGF–Met axis plays diverse roles in organogenesis and in wound healing. The simile that “cancer is a never‐healing wound” appears to be pertinent here. © 2006 Wiley‐Liss, Inc.
Development of a reinforced porcine elastin composite vascular scaffold
Authors: Hinds Monica T. , Rowe Rebecca C. , Ren Zhen , Teach Jeffrey , Wu Ping‐Cheng , Kirkpatrick Sean J. , Breneman Kathryn D. , Gregory Kenton W. , Courtman David W. 
Published: February 2006

AbstractElastin, a principal structural component of native arteries, has distinct biological and mechanical advantages when used as a biomaterial; however, its low ultimate tensile strength has limited its use as an arterial conduit. We have developed a scaffold, consisting of a purified elastin tubular conduit strengthened with fibrin bonded layers of acellular small intestinal submucosa (aSIS) for potential use as a small diameter vascular graft. The addition of aSIS increased the ultimate tensile strength of the elastin conduits nine‐fold. Burst pressures for the elastin composite vascular scaffold (1396 ± 309 mmHg) were significantly higher than pure elastin conduits (162 ± 36 mmHg) and comparable to native saphenous veins. The average suture pullout strength of the elastin composite vascular scaffolds was 14.612 ± 3.677 N, significantly higher than the pure elastin conduit (0.402 ± 0.098 N), but comparable to native porcine carotid arteries (13.994 ± 4.344 N). Cyclic circumferential strain testing indicated that the composite scaffolds were capable of withstanding physiological loading conditions for at least 83 h. Implantation of the elastin composites as carotid interposition grafts in swine demonstrated its superiority to clinically acceptable ePTFE with significantly longer average patency times of 5.23 h compared to 4.15 h. We have developed a biologically based elastin scaffold with suitable mechanical properties and low thrombogenicity for in vivo implantation, and with the potential for cellular repopulation and host integration reestablishing an appropriate elastic artery. © 2006 Wiley Periodicals, Inc. J Biomed Mater Res, 2006
Substrate specificity of soluble and membrane‐associated ADP‐ribosyltransferase ART2.1
Authors: Zheng Xuexiu , Morrison Alan R. , Chung An‐Sik , Moss Joel , Bortell Rita 
Published: February 2006

AbstractADP‐ribosyltransferases (ARTs) are a family of enzymes that catalyze the covalent transfer of an ADP‐ribose moiety, derived from NAD, to an amino acid of an acceptor protein, thereby altering its function. To date, little information is available on the protein target specificity of different ART family members. ART2 is a T‐cell‐specific transferase, attached to the cell surface by a glycosylphosphatidylinositol (GPI) anchor, and also found in serum. Here we investigated the role of ART2 localization in serum or on the cell surface, or solubilized with detergents or enzymes, on its target protein specificity. We found that detergent solubilization of cell membranes, or release of ART2 by phosphoinositide‐specific phospholipase C treatment, altered the ability of ART2 to ADP‐ribosylate high or low molecular weight histone proteins. Similarly, soluble recombinant ART2 (lacking the GPI anchor) showed a different histone specificity than did cell‐bound ART2. When soluble ART2 was incubated with serum proteins in the presence of [32P]‐labeled NAD, several serum proteins were ADP‐ribosylated in a thiol‐specific manner. Mass spectrometry of labeled proteins identified albumin and transferrin as ADP‐ribosylated proteins in serum. Collectively, these studies reveal that the membrane or solution environment of ART2 plays a pivotal role in determining its substrate specificity. J. Cell. Biochem. 98: 851–860, 2006. © 2006 Wiley‐Liss, Inc.