bluuebunny/crossref_metadata_2025_split huggingface dataset:
Herpes oncolytic therapy of salivary gland carcinomas
Authors: Reid Vincent , Yu Zhenkun , Schuman Theodore , Li Sen , Singh Paramjeet , Fong Yuman , Wong Richard J. 
Published: August 2007

AbstractOncolytic herpes simplex viruses (HSV) have demonstrated potent antitumoral effects against a variety of human malignancies in preclinical studies and are in early clinical trials. We explored the activity of an attenuated, replication‐competent, oncolytic HSV (NV1023) for the treatment of human salivary gland carcinomas. NV1023 was able to successfully enter into 4 mucoepidermoid carcinoma (H292, H3118, HTB‐41, UT‐MUC‐1) and 2 adenocarcinoma (HSY, HSG) cell lines, as measured by lacZ assays after exposure to 5 viral particles per cell (MOI 5). Viral plaque assays showed variation of viral replication within these cell lines, ranging from a 268‐fold increase (H292) to a 3‐fold increase (HSG) in viral titer. At MOI 5, all cell lines showed >95% cytotoxicity from NV1023 by Day 7, except for HSY (73%). At MOI 0.1, H3118 and UT‐MUC‐1 remained highly sensitive to NV1023, both showing >95% cytotoxicity by Day 7. The mucoepidermoid carcinomas were more sensitive to NV1023 at low viral concentrations compared with the adenocarcinomas. Flank tumors of H3118, HTB‐41 and HSY in nude mice showed significant tumor volume reductions after a single intratumoral injection of NV1023 (2 × 107 plaque‐forming units). These data suggest that oncolytic herpes viruses have significant efficacy entering, replicating within, and lysing human salivary gland carcinomas. These promising biologic agents should be further investigated as novel therapy for patients with salivary carcinomas failing conventional treatment. © 2007 Wiley‐Liss, Inc.
Testicular cancer: Marked birth cohort effects on incidence and a decline in mortality in southern Netherlands since 1970
Authors: Verhoeven Rob , Houterman Saskia , Kiemeney Bart , Koldewijn Evert , Coebergh Jan Willem 
Published: August 2007

AbstractThe aim of our study was to interpret the changing incidence, and to describe the mortality of patients with testicular cancer in the south of the Netherlands between 1970 and 2004. On the basis of data from the Eindhoven Cancer Registry and Statistics Netherlands, 5‐year moving average standardised incidence and mortality rates were calculated. An age‐period‐cohort (APC) Poisson regression analysis was performed to disentangle time and birth cohort effects on incidence. The incidence rate remained stable for all ages at about 3 per 100,000 person‐years until 1989 but increased annually thereafter by 4% to 6 in 2004. This increase can almost completely be attributed to an increase in localised tumours. The largest increase was found for seminoma testicular cancer (TC) patients aged 35–39 and non‐seminoma TC patients aged 20–24 years. Relatively more localised and tumours with lymph node metastases were detected in the later periods. APC analysis showed the best fit with an age‐cohort model. An increase in incidence of TC was found for birth cohorts since 1950. The mortality rate dropped from 1.0 per 100,000 person‐years in 1970 to 0.3 in 2005, with a steep annual decline of 12% in the period 1979–1986. In conclusion, the increase in incidence of TC was strongly correlated with birth cohorts since 1945. The increase in incidence is possibly caused by in utero or early life exposure to a yet unknown risk factor. There was a steep decline in mortality in the period 1979–1986. © 2007 Wiley‐Liss, Inc.
Human papillomavirus genotypes and HPV16 variants in penile carcinoma
Authors: Tornesello Maria Lina , Duraturo Maria Luisa , Losito Simona , Botti Gerardo , Pilotti Silvana , Stefanon Bernardina , Palo Giuseppe De , Gallo Antonio , Buonaguro Luigi , Buonaguro Franco M 
Published: August 2007

AbstractThe causative role of human papillomaviruses (HPV) and HPV16 variants has been extensively studied in uterine cervix dysplastic lesions and invasive carcinoma; few such studies, however, have been performed in penile tumors. We have investigated HPV genotype and HPV16 variant distribution on 41 penile cancer biopsies from Italian patients. Cases were extracted from the respective pathology departments databases of National Cancer Institutes in Naples and Milan. HPV sequences were detected by PCR and characterized by direct sequence analysis. Among the 19 HPV‐positive cases (46.3%) 2 viral genotypes were identified (HPV16 and 18) with HPV16 accounting for 94.7% (18 out of 19) of the infections. Sequence analysis of E6, E7 genes and long control region (LCR) of 18 HPV16 isolates allowed the identification of European (E‐G‐350) and non‐European (AA and Af‐1) variants in 44.4% and in 55.6% of the samples, respectively. The AA variant alone represented 44.4% of all HPV16 infections, a significantly higher frequency of that observed in cervical carcinoma from Italian women (Tornesello et al., J Med Virol 2004;74:117‐26). Our results suggest that HPV16 has a very high prevalence among penile cancer patients in Italy and the increased frequency of HPV16 non‐European classes, particularly the AA, suggests that they are more oncogenic than European variants in penile tissue. © 2007 Wiley‐Liss, Inc.
Wnt signaling controls radiosensitivity via cyclooxygenase‐2‐mediated Ku expression in head and neck cancer
Authors: Chang Hyo Won , Roh Jong‐Lyel , Jeong Eun‐Jeong , Lee Sang‐wook , Kim Seung‐Whan , Choi Seung‐Ho , Park Sung‐Kyung , Kim Sang Yoon 
Published: August 2007

AbstractIt has been proposed that Wnt signaling pathway may be a key radioprotective mechanism in irradiated cancer cells; however, the specific radioresistance mechanisms remain not to be fully clarified. Here we elucidate a novel signaling pathway of radioresistance in head and neck cancer (HNC) cell lines involving interactions among the Wnt signaling pathway, cyclooxygenase‐2 (COX‐2) and Ku expression. Activation of the Wnt signaling pathway by (2′Z,3′E)‐6‐bromoindirubin‐3′‐oxime (BIO) resulted in β‐catenin cytoplasmic accumulation and translocation to the nucleus, upregulated Ku expression and increased radioresistance in the COX‐2‐expressing HNC cell line. In contrast, Wnt singaling activation by BIO had no effects on Ku expression and radiosensitivity in a HNC cell line negative for COX‐2. Interactions between Wnt singaling and Ku were indirectly regulated by COX‐2. Blockage of COX‐2 signaling led to the suppression of β‐catenin‐induced Ku expression, and to consequent recovery of the radiosensitivity in HNC cells. Our results conclusively suggest that β‐catenin plays a pivotal role in the regulation of Ku expression via the proposed COX‐2 intracellular pathway, thus supporting a novel radioresistance mechanism of HNC. © 2007 Wiley‐Liss, Inc.
Modulation of viability and maturation of human monocyte‐derived dendritic cells by oncolytic adenoviruses
Authors: Schierer Stephan , Hesse Andrea , Müller Ina , Kämpgen Eckhart , Curiel David T. , Schuler Gerold , Steinkasserer Alexander , Nettelbeck Dirk M. 
Published: August 2007

AbstractAdenoviral oncolysis is a promising new modality for treatment of cancer based on selective viral replication in tumor cells. However, tumor cell killing by adenoviral oncolysis needs to be improved to achieve therapeutic benefit in the clinic. Towards this end, the activation of anti‐tumor immunity by adenoviral oncolysis might constitute a potent mechanism for systemic killing of uninfected tumor cells, thereby effectively complementing direct tumor cell killing by the virus. Knowledge of anti‐tumor immune induction by adenoviral oncolysis, however, is lacking mostly due to species‐specificity of adenovirus replication, which has hampered studies of human oncolytic adenoviruses in animals. We suggest the analysis of interactions of oncolytic adenoviruses with human immune cells as rational basis for the implementation of adenoviral oncolysis‐induced anti‐tumor immune activation. The goal of our study was to investigate how oncolytic adenoviruses affect human dendritic cells (DCs), key regulators of innate and adoptive immunity that are widely investigated as tumor vaccines. We report that melanoma‐directed oncolytic adenoviruses, like replication‐deficient adenoviruses but unlike adenoviruses with unrestricted replication potential, are not toxic to monocyte‐derived immature DCs and do not block DC maturation by external stimuli. Of note, this is in contrast to reports for other viruses/viral vectors and represents a prerequisite for anti‐tumor immune activation by adenoviral oncolysis. Furthermore, we show that these oncolytic adenoviruses alone do not or only partially induce DC maturation. Thus additional signals are required for optimal immune activation. These could be delivered, for example, by inserting immunoregulatory transgenes into the oncolytic adenovirus genome. © 2007 Wiley‐Liss, Inc.
What drives heterogeneity in foreign exchange rate expectations: insights from a new survey
Authors: Dreger Christian , Stadtmann Georg 
Published: September 2007

AbstractForeign exchange rate expectations play a central role in virtually all monetary models for the open economy. Therefore, it is extremely important to gain empirical insights into the expectations formation process. In this paper, we use a unique disaggregated data set to model the expectations of the Yen/USD exchange rate of about 50 leading foreign exchange rate professionals. The survey includes not only exchange rate projections but also expectations regarding macroeconomic fundamentals, like GDP growth, inflation, and interest rates. Different expectations of fundamentals can lead to different views of exchange rate dynamics. Using panel models, we are able to confirm the heterogeneity of exchange rate expectations often detected in previous studies. More important, we provide strong evidence regarding the likely source of heterogeneity. In line with forward looking models for the exchange rate, expected fundamentals have a substantial impact on exchange rate expectations, thereby challenging the backward looking evidence from previous studies. However, the heterogeneity in the expectations of macroeconomic fundamentals is not sufficient to explain the heterogeneity in exchange rate expectations. Copyright © 2007 John Wiley & Sons, Ltd.
Characterization of anti‐osteopontin monoclonal antibodies: Binding sensitivity to post‐translational modifications
Authors: Kazanecki Christian C. , Kowalski Aaron J. , Ding Tony , Rittling Susan R. , Denhardt David T. 
Published: September 2007

AbstractOsteopontin (OPN) is primarily a secreted phosphoglycoprotein found in a variety of tissues and body fluids. It has a wide range of reported functions, many of which are affected by the degree of post‐translational modification (PTM) of the protein. These PTMs include phosphorylation, glycosylation, and cross‐linking by transglutaminase. Here we describe the generation of unique monoclonal antibodies raised against recombinant OPN utilizing the OPN knockout mouse. The antibodies exhibit differential binding to OPN produced by different cell lines from the same species, as well to the multiple OPN forms in human urine. Most of the antibodies generated are able to recognize OPN produced by ras‐transformed mouse fibroblasts, however only one antibody recognizes the more phosphorylated protein produced by the differentiating pre‐osteoblast murine cell line MC3T3E1. Using a novel biopanning procedure combining T7 phage gene fragment display and protein G precipitation, we have epitope‐mapped these antibodies. Several of the antibodies bind to regions of the OPN molecule that are phosphorylated, and one binds the region of OPN that is glycosylated. Using phosphorylated and non‐phosphorylated peptides, we show that the binding of two antibodies to the C‐terminal end of OPN is inhibited by phosphorylation of this region. In addition, these two antibodies are able to inhibit cell adhesion to recombinant and weakly modified OPN. The antibodies described herein may prove useful in determining the presence of modifications at specific sites and for identifying structural forms of OPN. Also, the sensitivity of these antibodies to PTMs suggests that caution must be taken when choosing anti‐OPN monoclonal antibodies to detect this highly modified protein. J. Cell. Biochem. 102: 925–935, 2007. © 2007 Wiley‐Liss, Inc.
Small non‐embeddable quasi‐derived designs
Authors: Harada Masaaki , Miyabayashi Hiroki 
Published: September 2007

AbstractWe establish the existence of non‐embeddable quasi‐derived 2‐designs with the parameters (13, 4, 3), (15, 6, 5), and (16, 6, 5). © 2007 Wiley Periodicals, Inc. J Combin Designs 16: 364–372, 2008
Focal adhesion targeting of v‐Crk is essential for FAK phosphorylation and cell migration in mouse embryo fibroblasts deficient src family kinases or p130CAS
Authors: Yeo Myeong Gu , Sung Bong Hwan , Oh Hye Jin , Park Zee Yong , Marcantonio Eugene E. , Song Woo Keun 
Published: September 2007

AbstractWe examined the consequences of v‐Crk expression in mouse embryo fibroblasts deficient Src family kinases or p130CAS. We found that Src kinases are essential for p130CAS/v‐Crk signaling leading to FAK phosphorylation and cell migration in which Src is likely to mediate the focal adhesion targeting of v‐Crk. SYF cells showed only low levels of FAK phosphorylation and cell migration, even in the presence of v‐Crk. Expression of v‐Crk restored migration of p130CAS‐deficient cells to the level of wild‐type cells, most likely through the targeting of v‐Crk to focal adhesions by cSrc. In addition, we identified a new v‐Crk‐interacting protein that mediates v‐Crk signaling in p130CAS‐deficient cells. Using RT‐PCR and caspase cleavage assays, we confirmed that this protein is not p130CAS and is responsible for maintaining v‐Crk/Src signaling and migration in these. These findings suggest that focal adhesion targeting of v‐Crk is essential in v‐Crk‐mediated cellular signaling and that v‐Crk must form a complex with p130CAS or a p130CAS substitute to transduce signaling from the extracellular matrix. J. Cell. Physiol. 214: 604–613, 2008. © 2007 Wiley‐Liss, Inc.
Potential conversion of adult clavicle‐derived chondrocytes into neural lineage cells in vitro
Authors: Li Hong‐Yun , Zhou Xin‐Fu 
Published: September 2007

AbstractNeural stem cells (NSC) can be isolated from a variety of adult tissues and become a valuable cell source for the repair of peripheral and central nervous diseases. However, their origin and identity remain controversial because of possible de‐differentiation/trans‐differentiation or contaminations by hematopoietic stem cells (HSCs) or mesenchymal stem cells (MSCs). We hypothesize that the commonly used NSC culture medium can induce committed cartilage chondrocytes to de‐differentiate and/or trans‐differentiate into neural cell lineages. Using a biological isolation and purification method with explants culture, we here show that adult rat clavicle cartilage chondrocytes migrate out from tissue blocks, form sphere‐like structures, possess the capability of self‐renewal, express nestin and p75NTR, markers for neural crest progenitors, and differentiate into neurons, glia, and smooth muscle cells. Comparing with adult cartilage, the spherical‐forming neural crest cell‐like cells downregulate the chondrocytic marker genes, including collagen II, collagen X, and sox9, as well as neural‐lineage repressors/silencers REST and coREST, but upregulate a set of well‐defined genes related to neural crest cells and pro‐neural potential. Nerve growth factor (NGF) and glial growth factor (GGF) increase glial and neuronal differentiation, respectively. These results suggest that chondrocytes derived from adult clavicle cartilage can become neural crest stem‐like cells and acquire neuronal phenotypes in vitro. The possible de‐differentiation/trans‐differentiation mechanisms underlying the conversion were discussed. J. Cell. Physiol. 214: 630–644, 2008. © 2007 Wiley‐Liss, Inc.
Old disease, new culprit: Tumor stem cells in cancer
Authors: Lee John T. , Herlyn Meenhard 
Published: September 2007

AbstractEloquent studies from hematopoietic systems have provided proof that cancer arises from a tumor stem cell that possesses self‐renewing properties. Until recently, it was believed that this tumor stem cell was unique to leukemic disorders; evidence now suggests that solid tumors also harbor cancer stem cells that are capable of initiating tumor growth in immunodeficient animals with as few as 10 cells. Consequently, the term “tumor‐initiating cell” is now gaining favor within the field. Here, we conceptually discuss the current theories regarding tumor‐initiating cells and their involvement in the development and progression of human malignancies. Special attention is given to laboratory techniques and strategies currently exploited to isolate tumor‐initiating cells from larger populations, including their inherent strengths and weaknesses. The biological relevance of a tumor‐initiating subpopulation is also pondered and arguments regarding their origin are presented. The therapeutic promise of targeting tumor‐initiating cells is certainly eminent and we weigh the advantages of targeting this subpopulation. Lastly, the field of cancer stem cells appears to be well‐placed to make significant strides over the next decade and we discuss potential obstacles that must be negotiated to achieve those objectives. The realization of these goals will undoubtedly further our understanding of this complex disease and should eventually lead to improved therapies in the not‐so‐distant future. J. Cell. Physiol. 213:603–609. © 2007 Wiley‐Liss, Inc.
Osteoarthritis
Authors: Goldring Mary B. , Goldring Steven R. 
Published: September 2007

AbstractOsteoarthritis (OA) is characterized by degeneration of articular cartilage, limited intraarticular inflammation with synovitis, and changes in peri‐articular and subchondral bone. Multiple factors are involved in the pathogenesis of OA, including mechanical influences, the effects of aging on cartilage matrix composition and structure, and genetic factors. Since the initial stages of OA involve increased cell proliferation and synthesis of matrix proteins, proteinases, growth factors, cytokines, and other inflammatory mediators by chondrocytes, research has focused on the chondrocyte as the cellular mediator of OA pathogenesis. The other cells and tissues of the joint, including the synovium and subchondral bone, also contribute to pathogenesis. The adult articular chondrocyte, which normally maintains the cartilage with a low turnover of matrix constituents, has limited capacity to regenerate the original cartilage matrix architecture. It may attempt to recapitulate phenotypes of early stages of cartilage development, but the precise zonal variations of the original cartilage cannot be replicated. Current pharmacological interventions that address chronic pain are insufficient, and no proven structure‐modifying therapy is available. Cartilage tissue engineering with or without gene therapy is the subject of intense investigation. There are multiple animal models of OA, but there is no single model that faithfully replicates the human disease. This review will focus on questions currently under study that may lead to better understanding of mechanisms of OA pathogenesis and elucidation of effective strategies for therapy, with emphasis on mechanisms that affect the function of chondrocytes and interactions with surrounding tissues. J. Cell. Physiol. 213:626–634. © 2007 Wiley‐Liss, Inc.
Experimental manipulation of ovary activation and gene expression in honey bee (Apis mellifera) queens and workers: testing hypotheses of reproductive regulation
Authors: Thompson Graham J. , Yockey Heather , Lim Julianne , Oldroyd Benjamin P. 
Published: September 2007

AbstractA fundamental issue in sociobiology is to understand how social insect females regulate their individual reproduction to maximize colony and personal fitness. Although the social cues mediating reproductive output within castes of the honey bees (Apis mellifera) are understood at a basic level, the underlying gene regulatory networks are not. In this study, we investigate the expression of 25 genes whose function suggests a role in the gene networks that regulate ovary activation—a functional determinant of reproductive skew. To this end, we used CO2 narcosis to manipulate ovary activation in queens and workers, and then quantified concomitant changes in gene expression using quantitative polymerase chain reaction. Of the 25 genes studied, ten were differentially expressed between treated and control groups in at least one caste. Two of these genes, a ribosomal protein and a tyramine receptor, were differentially expressed between treatments and controls in both castes. We use the expression pattern of all differentially expressed genes to test hypotheses for the caste‐specific regulation of ovary activation in honey bees. J. Exp. Zool. 307A:600–610, 2007. © 2007 Wiley‐Liss, Inc.
Relationships among household saving, public saving, corporate saving and economic growth in India
Authors: Sinha Dipendra , Sinha Tapen 
Published: August 2007

AbstractThis paper examines the relationship between the growth rates of household saving, public saving, corporate saving and economic growth in India using multivariate Granger causality tests. The conventional wisdom suggests that the causality flows from saving to economic growth. We show that the causality goes in the opposite direction for India. Hence, higher saving is the consequence of higher economic growth and not a cause. Such evidence is consistent with models of habit formation. Copyright © 2007 John Wiley & Sons, Ltd.
Increased hepatic cytochrome P4503A activity decreases the risk of developing steroid‐induced osteonecrosis in a rabbit model
Authors: Masada Toshiaki , Iwakiri Kentaro , Oda Yutaka , Kaneshiro Yasunori , Iwaki Hiroyoshi , Ohashi Hirotsugu , Takaoka Kunio 
Published: September 2007

AbstractLow hepatic cytochrome P4503A (CYP3A) activities might play an important role for inducing osteonecrosis of the femoral head (ONFH) by corticosteroids. However, the relationship between hepatic CYP3A activity and steroid‐induced ONFH is unknown. We have examined the relationship between hepatic CYP3A activity and the inducibility of ONFH in a rabbit model. Sixty rabbits were divided into three groups. Hepatic CYP3A inducer (phenobarbital, group P; n = 15), inhibitor (itraconazole, group I; n = 15), or saline (group C, n = 30) was administrated for 3 weeks before intramuscular methylprednisolone. In groups P and I, hepatic CYP3A levels were measured by midazolam clearance before treatment (baseline) and before methylprednisolone injection. All animals were sacrificed 3 weeks after methylprednisolone injection and both femurs were harvested and examined histologically for osteonecrosis. Midazolam clearance was significantly increased and decreased, compared with baseline in groups P and I respectively (p < 0.0005, p < 0.002). The incidence of osteonecrosis in group P (33%) was significantly lower than in group I (100%) and group C (83%; p < 0.001 for both). The percentage necrotic area to whole bone marrow area on cross sections in group P (8.2 ± 5.9%) was significantly lower than in group I (69.8 ± 20.8%) and group C (51.5 ± 30.7%; p < 0.005 for both). Hepatic CYP3A activity inversely correlated with the incidence of osteonecrosis and extent of the necrotic area caused by the same dose of corticosteroids, suggesting possible prevention of the steroid‐induced osteonecrosis by reducing steroid dose in poor corticosteroid metabolizers. © 2007 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 26:91–95, 2008