bluuebunny/crossref_metadata_2025_split huggingface dataset:
Correlation between vascular endothelial growth factor‐C expression and invasion phenotype in cervical carcinomas
Authors: Ueda Masatsugu , Terai Yoshito , Yamashita Yoshiki , Kumagai Koji , Ueki Ken , Yamaguchi Hiroyuki , Akise Daisuke , Hung Yao‐Ching , Ueki Minoru 
Published: August 2002

AbstractThe correlation between vascular endothelial growth factor (VEGF)‐C gene expression and in vitro invasive activity and matrix metalloproteinase (MMP)‐2 or 9 gene expression and proteolytic activity in 11 cervical carcinoma cell lines, was investigated. Immunohistochemical expression of VEGF‐C in 52 cervical carcinoma tissues was also correlated with tumor aggressiveness with respect to clinicopathologic features, tumor vascularity, MMP‐2 expression and patient outcome. Expression of VEGF‐C mRNA differed remarkably among the cell lines and there was a statistical correlation between VEGF‐C gene expression and the number of invaded tumor cells (p = 0.0009) and MMP‐2 gene expression and activity (p < 0.05). Anti‐VEGF‐C antibody inhibited the invasive and proteolytic activity of tumor cells in a concentration‐dependent manner. VEGF‐C or MMP‐2 expression in clinical tissue samples was well correlated with depth of myometrial invasion, endometrial invasion, pelvic lymphnode metastasis and tumor vascularity (p < 0.05) and there was a close relation between VEGF‐C and MMP‐2 expression (p < 0.0001) in cervical carcinomas. Overall survival rates for 14 patients with strong VEGF‐C staining tumors were lower than those for 38 patients with weak VEGF‐C staining tumors (p = 0.0132) and VEGF‐C tissue status emerged as an independent prognostic parameter (p = 0.0232). These results suggest that VEGF‐C expression is closely related to invasion phenotype and affects the patient's survival in cervical carcinomas. © 2002 Wiley‐Liss, Inc.
Troglitazione affects survival of human osteosarcoma cells
Authors: Lucarelli Enrico , Sangiorgi Luca , Maini Veronica , Lattanzi Giovanna , Marmiroli Sandra , Reggiani Matteo , Mordenti Marina , Gobbi Giuliana Alessandra , Scrimieri Francesca , Zambon Bertoja Annarosa , Picci Piero 
Published: August 2002

AbstractActivation of PPARγ, a transcription factor member of the family of peroxisome proliferator‐activated receptors, induces apoptosis in several normal and tumor cell lines. In our study, we investigated whether treatment with troglitazone (TRO), a known PPARγ agonist, induced apoptosis in the human osteosarcoma (OS) cell lines G292, MG63, SAOS and U2OS that express PPARγ. In our experiments, TRO never induced apoptosis of OS cells; on the contrary, TRO increased cell number, based on MTT proliferation assay. Remarkably, the TRO‐induced cell number increase depended on a decrease of apoptosis that naturally occurred in the culture and was not due to an increased cell proliferation rate. TRO also prevented staurosporin‐induced apoptosis. The TRO‐mediated survival effect correlated with the activation of Akt, a well‐known mediator of survival stimuli. Our work describes a new function for TRO and indicates that the Akt survival pathway may be a mediator of TRO‐induced increase of survival. © 2002 Wiley‐Liss, Inc.
Evidence for an age‐related influence of microsatellite instability on colorectal cancer survival
Authors: Farrington Susan M. , McKinley Aileen J. , Carothers Andrew D. , Cunningham Christopher , Bubb Vivien J. , Sharp Linda , Wyllie Andrew H. , Dunlop Malcolm G. 
Published: August 2002

AbstractIt is well established that microsatellite instability (MSI), the hallmark of defective DNA mismatch repair (MMR), is associated with prolonged survival in colorectal cancer compared with tumours that are microsatellite stable (MSS). MSI in sporadic colorectal tumours is primarily due to epigenetic silencing of MLH1. However, there are no prospective population‐based studies of survival in patients with germline MMR gene mutations who develop cancer. Although MSI is almost universal in tumours from HNPCC family members, there is a potential confounding effect of ascertainment and other biases that could explain the apparent survival benefit in HNPCC families. Resolving whether germline MMR gene mutations impact on survival is important because it potentially undermines the rationale for surveillance of mutation carriers. Here, we report an investigation of the influence of MSI on survival in cohorts of cancer patients (aged < 30 years at diagnosis, n = 118; non‐age‐selected, n = 181) in the context of clinicopathologic variables. There was a substantial age‐related influence of tumour MSI status on survival. In young patients with tumour MSI, 65% of patients with MSI tumours had germline MSH2 or MLH1 mutations. Clinicopathologic variables and tumour MSI of the cohort were studied with respect to survival and compared with control groups. Young patients had excess MSI tumours (p < 0.000001), mucinous tumours (p < 0.01), advanced disease (p ∼ 0.001) and poorer 5‐year survival compared with older cases. Cox proportional hazard analysis identified Dukes' stage, age at diagnosis and calendar year of treatment as independent predictors of survival. There was no detectable association between tumour MSI and survival in young patients, although we confirmed previous observations that MSI is associated with better prognosis in later onset cohorts. These findings underscore the rationale for surveillance and early identification of tumours in MMR gene carriers as well as refining understanding of the influence of MSI on cancer progression. © 2002 Wiley‐Liss, Inc.
Transmission/disequilibrium tests of androgen receptor and glutathione S‐transferase pi variants in prostate cancer families
Authors: Ho Gloria Y.F. , Knapp Michael , Freije Diha , Nelson William G. , Smith Jeffrey R. , Carpten John D. , Bailey‐Wilson Joan E. , Beaty Terri H. , Petersen Gloria , Xu Jianfeng , Kamensky Victor , Walsh Patrick C. , Isaacs William B. 
Published: August 2002

AbstractPopulation‐based case‐control studies have found relationships between risk of prostate cancer and genetic polymorphisms in the CAG repeat and GGC repeat of the X‐linked androgen receptor gene (AR) as well as the autosomal gene coding for glutathione S‐transferase pi (GSTP1). This family‐based study utilized the transmission disequilibrium test to examine whether there was evidence that these polymorphisms could account for familial aggregation of prostate cancer. Seventy‐nine North American pedigrees were studied. Most of these families had 3 or more affected first‐degree relatives. Genotype information was obtained on 578 individuals. The reconstruction combined transmission disequilibrium test (RC‐TDT) was used to test for linkage. There was no evidence of linkage to the CAG and GGC repeat sequences in the AR gene or the pentanucleotide (ATAAA) repeat in the GSTP1 gene when each allele was analyzed separately or when alleles were grouped by repeat length. Our findings do not support the hypothesis that familial clustering of prostate cancer in high‐risk families is attributable to these genetic variants. © 2002 Wiley‐Liss, Inc.
Nicotine modulates the effects of retinoids on growth inhibition and RARβ expression in lung cancer cells
Authors: Chen Guo‐quan , Lin Bingzhen , Dawson Marcia I. , Zhang Xiao‐kun 
Published: August 2002

AbstractEpidemiological and animal studies have demonstrated that vitamin A and its natural and synthetic derivatives, retinoids, are effective agents in preventing the development of tobacco‐associated cancers. Unfortunately, clinical trials of retinoids on cigarette smokers have shown lack of efficacy in preventing lung cancer. In our study, we investigated the effect of nicotine on the anti‐cancer activity of all trans‐retinoic acid (trans‐RA) in human lung cancer cells. Our results demonstrated that nicotine could abrogate the growth inhibitory effect of trans‐RA by suppressing its ability to induce the expression of RA receptor beta (RARβ), a tumor suppressor. The inhibitory effect of nicotine was accompanied with induction of orphan receptor TR3. Inhibition of TR3 expression by overexpression of TR3 anti‐sense RNA in H460 lung cancer cells strongly prevented the suppressive effect of nicotine on trans‐RA activity. Treatment with nicotine or the cotransfection of TR3 expression vector inhibited the induction of RARβ promoter activity by trans‐RA in transient transfection assays. The inhibition of RARβ promoter activity was due to the interaction of TR3 with orphan receptor COUP‐TF, resulting in inhibition of COUP‐TF DNA binding and transactivation on the RARβ promoter. Furthermore, we found that nicotine failed to suppress the effect of a retinoid X receptor (RXR)‐selective retinoid SR11237 on inducing both growth inhibition and RARβ promoter activity, due to the ability of SR11237 to activate the RARβ promoter through the RXR/TR3 heterodimer. Together, our results demonstrate that nicotine suppresses the growth inhibitory effects of trans‐RA by inhibiting RARβ expression through its induction of TR3 expression and suggest that RXR‐selective retinoids may be more effective than classical retinoids for preventing and treating tobacco‐associated cancers. © 2002 Wiley‐Liss, Inc.
Evaluation of cell survival, DNA double strand breaks, and DNA synthesis during concurrent camptothecin and X‐radiation treatments
Authors: Ng Cheng E. , Mazaheri K. , Payant C. , Raaphorst G. Peter 
Published: August 2002

AbstractWe evaluated cell survival, DNA double strand breaks (dsbs), and DNA synthesis following camptothecin (CPT) alone or concurrent CPT and X‐radiation treatments in exponential‐phase cultures of a radioresistant human melanoma cell line. Cell survival was measured by a clonogenic assay. DNA dsbs were measured by pulsed‐field gel electrophoresis. DNA synthesis was measured by incorporation of 3H‐thymidine. We found that (i) concurrent CPT and X‐radiation interacted additively, unlike previous results with plateau‐phase cultures of these cells, which showed synergistic interaction; (ii) there were strong negative correlations (correlation coefficients of at least 0.82) between clonogenic surviving fractions and DNA dsbs following CPT alone or concurrent CPT and radiation treatments; and (iii) concurrent CPT and radiation (10 Gy) treatment did not completely inhibit DNA synthesis, even though addition of radiation to CPT did further decrease DNA synthesis (relative to CPT alone) at CPT concentrations below 20 μM. Our results suggest that during concurrent CPT and radiation treatment residual DNA dsb levels were good indicators of cell killing and that the absence of complete inhibition of DNA synthesis could at least in part explain the additive interaction between CPT and radiation. © 2001 Wiley‐Liss, Inc.
Binary operator design by k‐nearest neighbor learning with application to image resolution increasing
Authors: Kim Hae Yong 
Published: August 2002

AbstractIn a typical office environment, heterogeneous devices and software, each working in a different spatial resolution, must interact. As a result resolution conversion problems arise frequently. This paper addresses the spatial resolution increasing of binary images and documents (e.g., conversion of a 300‐dots per inch [dpi] image into 600 dpi). A new, accurate and efficient solution to this problem is proposed. It makes use of the k‐nearest neighbor learning to design automatically a windowed zoom operator starting from pairs of in‐out sample images. The resulting operator is stored in a look‐up table, which is extremely fast computationally and therefore fit for real‐time applications. It is useful to know a priori the sample complexity (the quantity of training samples needed to get, with probability 1‐δ, an operator with accuracy ε). We use the probably approximately correct (PAC) learning theory to compute sample complexity, for both noise‐free and noisy cases. Because the PAC theory yields an overestimated sample complexity, the statistical estimation is used to estimate, a posteriori, a tight error bound. The statistical estimation is also used to show that the k‐nearest neighbor learning has a good inductive bias that allows reduction of the quantity of training sample images needed. © 2001 John Wiley & Sons, Inc. Int J Imaging Syst Technol, 11, 331–339, 2000
An infant in context: Multiple risks, and a relationship
Authors: Balbernie Robin 
Published: August 2002

AbstractThis article sets out to bring together some of the current thinking on the effect of adverse early experiences on individual development. Although the caregiving relationship is intensely personal, it also reflects a synthesis of surrounding biological and social influences. An exceptional combination of individual characteristics and environmental circumstances may alter the balance between future vulnerability and resilience. These affect the baby via the relationship with the parent. The particular risk factors considered are set within the narrative framework of a single home visit, both to embody them and to emphasize their systemic interrelatedness within a family boundary. ©2002 Michigan Association for Infant Mental Health.
Kojic acid reduces the cytotoxic effects of sulfur mustard on cultures containing human melanoma cells in vitro
Authors: Smith C. N. , Lindsay C. D. 
Published: August 2002

AbstractIn vivo experiments have shown that melanocytes are more sensitive than keratinocytes to the cytotoxic effects of sulfur mustard when it is applied topically to pig skin.1 It has been hypothesized that this is caused by the uncoupling of the melanogenic pathway by depletion of cellular glutathione, resulting in the uncontrolled production of cytotoxic quinone free‐radical species by tyrosinase.2.In the present study, the feasibility of blocking the melanogenic pathway as a means of reducing the cytotoxicity of sulfur mustard was evaluated using kojic acid. Kojic acid is a topically applied depigmenting agent that exerts its effect by acting as a slow‐binding, competitive inhibitor of tyrosinase.3Preincubation of G361 pigmented melanoma cells and mixed cultures of G361 cells and SVK keratinocytes with 2.5 mM kojic acid resulted in significant increases in the viability of these cultures as determined by neutral red (NR) and gentian violet (GV) dye binding assays for up to 48 h following exposure to 50 µM sulfur mustard. The highest levels of protection were seen in the G361 cultures, with a 26.8% increase in culture viability (NR assay) compared with the sulfur‐mustard‐only controls at 24 h. Preincubation of SVK cells alone with kojic acid resulted in lower increases in viability (2.5% at 24 h by the NR assay). Inhibition of the melanogenic pathway reduces the sensitivity of cultures containing pigment cells to sulfur mustard. © Crown copyright 2001. Reproduced with the permission of Her Majesty's Stationery Office. Published by John Wiley & Sons, Ltd.
Changes in concentrations of type IV collagen and tissue inhibitor of metalloproteinase‐1 in patients with paraquat poisoning
Authors: Nakamura Tsukasa , Ushiyama Chifuyu , Shimada Noriaki , Hayashi Kayo , Ebihara Isao , Suzaki Masataka , Koide Hikaru 
Published: August 2002

AbstractRespiratory failure is one of the major causes of death in patients with paraquat poisoning. In paraquat‐poisoned lungs, abnormal extracellular matrix regulation occurs. The aim of the present study is to determine whether serum concentrations of type IV collagen and tissue inhibitor of metalloproteinase‐1 (TIMP‐1) are altered during the course of paraquat poisoning and whether haemoperfusion therapy affects these concentrations. Twenty‐one patients were admitted within 3 h after ingestion of paraquat and all patients received direct haemoperfusion therapy. Five out of 21 patients survived and 16 patients died within 28 days. Plasma paraquat concentrations in non‐survivors (5740 ± 380 µg l−1) were not significantly different from those in survivors ( 5920 ± 280 µg l−1) before treatment. Haemoperfusion reduced these concentrations in both non‐survivors (120 ± 7 µg l−1) as well as survivors (136 ± 9 µg l−1) on day 5. Serum concentrations of type IV collagen and TIMP‐1 in survivors showed little change between day 1 (type IV collagen, 90.4 ± 3.6 ng ml−1; TIMP‐1, 172.2 ± 7.0 ng ml−1) and day 5 (type IV collagen, 92.6 ± 4.2 ng ml−1; TIMP‐1, 174.2 ± 7.2 ng ml−1). In contrast, these concentrations in non‐survivors on day 5 (type IV collagen, 143.6 ± 7.8 mg ml−1; TIMP‐1, 246.8 ± 13.6 ng ml−1) were significantly higher than those on day 1 (type IV collagen, 88.4 ± 4.2 ng ml−1, P < 0.01; TIMP‐1, 170.6 ± 9.2 ng ml−1, P < 0.05). These data suggest that serum concentrations of type IV collagen and TIMP‐1 may be useful indicators for the development of respiratory failure in patients with paraquat poisoning. Copyright © 2001 John Wiley & Sons, Ltd.
Chelation in metal intoxication: influence of cysteine or N‐acetyl cysteine on the efficacy of 2,3‐dimercaptopropane‐1‐sulphonate in the treatment of cadmium toxicity
Authors: Tandon Sushil K. , Prasad Satgur , Singh Surendra 
Published: August 2002

AbstractThe influence of cysteine or N‐acetyl cysteine administration on the efficacy of 2,3‐dimercaptopropane‐1‐sulphonate (DMPS) in the treatment of cadmium intoxication was investigated in cadmium‐pre‐exposed rats. Cysteine, N‐acetyl cysteine, DMPS, DMPS + cysteine or DMPS + N‐acetyl cysteine were about equal in effectiveness in mobilizing hepatic cadmium mainly from its supernatant cytosolic fraction (SCF) and both of the combinations were more effective than either of them alone in mobilizing cadmium from its nuclear mitochondrial fraction (NMF). The DMPS was apparently more effective than cysteine or N‐acetyl cysteine in mobilizing renal cadmium from its SCF or NMF and it was more effective than even their combinations in mobilizing cadmium from renal SCF. The treatment with cysteine or N‐acetyl cysteine reduced cadmium‐induced hepatic and renal metallothionein (MT) and the treatment with DMPS reduced renal MT only, probably due to removal of hepatic and renal SCF cadmium by these agents. However, MT levels were high in animals treated with DMPS + cysteine or DMPS + N‐acetyl cysteine, despite lowering of cadmium in these tissues, suggesting a contribution of MT induced by cysteine or N‐acetyl cysteine itself. The cadmium exposure increased hepatic and renal zinc and renal copper levels, probably as a result of cadmium‐induced MT, and some of the levels were normalized considerably by the subsequent treatment with cysteine, DMPS or to a lesser extent N‐acetyl cysteine and their combinations, showing their protective effects against cadmium toxicity. The increase in blood cadmium and the decrease in blood zinc and copper levels due to cadmium exposure also were reversed appreciably by some of these treatments. The results have shown a limited benefit of cysteine or N‐acetyl cysteine administration on the efficacy of DMPS in the treatment of cadmium intoxication. Copyright © 2002 John Wiley & Sons, Ltd.
Effects of DMAEMA and 4‐methoxyphenol on gingival fibroblast growth, metabolism, and response to interleukin‐1
Authors: Lapp Carol A. , Schuster George S. 
Published: August 2002

AbstractSome components of resins used in restorative dentistry have been shown to alter metabolism in cultured oral epithelial cells. Here we have extended such studies to the underlying supportive tissue, composed of gingival fibroblasts (GF). Primary cultures of human GF were transferred to serum‐free, defined medium and exposed to either 2‐(dimethylamino)ethyl methacrylate (DMAEMA) or 4‐methoxyphenol (MEHQ) for 24–72 h. At a DMAEMA concentration of 6.4 mM, which was well tolerated by epithelial cells, GF numbers, as estimated by crystal violet, and metabolic activity, as indicated by MTT, were reduced at least 60% within 24 h of exposure. Between 1.6 and 6.4 mM, there were dose‐related reductions in cell numbers; however, at lower doses (0.32–0.64 mM), proliferation was stimulated. MEHQ, between 8 and 16 μM, did not stimulate cellular protein production. To examine the capacity of GF to respond to an inflammatory stimulus, interleukin‐6 (IL‐6) production by confluent cells was estimated without or with these compounds. DMAEMA (1.6– 6.4 mM) virtually eliminated the acute IL‐6 response of these cells to an interleukin‐1β challenge; only at 0.32 mM DMAEMA was the response restored. MEHQ (1.6–16 μM) reduced the IL‐6 response by >50%. In summary, both growth and the innate immune responsivity of GF were affected by DMAEMA and MEHQ in vitro; thus, these compounds deserve careful evaluation for biocompatibility. © 2002 Wiley Periodicals, Inc. J Biomed Mater Res 60: 30–35, 2002
Interleukin‐4 regulates connective tissue growth factor expression in human lung fibroblasts
Authors: Rishikof David C. , Ricupero Dennis A. , Kuang Ping‐Ping , Liu Hanqiao , Goldstein Ronald H. 
Published: August 2002

AbstractTransforming growth factor‐β (TGF‐β) and interleukin‐4 (IL‐4) have fibrogenic properties and induce extracellular matrix production in a variety of lung diseases. Connective tissue growth factor (CTGF) is a matrix signaling molecule stimulated by TGF‐β that in part mediates α1(I) collagen mRNA expression. In these studies, the regulation of CTGF expression by IL‐4 in human lung fibroblasts was examined. Following 6 h of stimulation with IL‐4, basal CTGF mRNA levels were unchanged as assessed by Northern blot analysis. However, IL‐4 attenuated the TGF‐β‐stimulated induction of CTGF mRNA expression by 50%. This effect was selective because IL‐4 did not affect fibronectin or α1(I) collagen mRNA expression induced by TGF‐β. Experiments employing the transcriptional inhibitor actinomycin D suggest that IL‐4 did not affect the stability of the CTGF mRNA. Transient transfection assays with 3TP‐Lux, a luciferase gene controlled by a TGF‐β inducible promoter, and with a CTGF promoter construct indicate that IL‐4 interfered with the TGF‐β‐induced transcriptional activation of the CTGF gene. J. Cell. Biochem. 85: 496–504, 2002. © 2002 Wiley‐Liss, Inc.
Evidence for a pre‐restriction point Cdk3 activity
Authors: Keezer Susan M. , Gilbert David M. 
Published: August 2002

AbstractWe have examined the activity of cyclin‐dependent kinase 3 (cdk3) during G1‐phase of the cell cycle in Chinese Hamster Ovary (CHO) fibroblasts. Histone H1 kinase activity associated with anti‐cdk3 immunoprecipitates peaked during a brief window of time, 2–3 h prior to the restriction point. In vitro cdk3 activity was sensitive to roscovitine, a drug previously shown to inhibit cdks 1, 2, and 5, but not cdk4 or 6. Early G1‐phase activation of cdk3 was downregulated by treatment of cells with MG132, an inhibitor of the proteasome, and by the protein synthesis inhibitor cycloheximide. These results provide evidence for a pre‐restriction point cdk3 activity that requires both the synthesis of a regulatory subunit and degradation of an inhibitor. J. Cell. Biochem. 85: 545–552, 2002. © 2002 Wiley‐Liss, Inc.