bluuebunny/crossref_metadata_2025_split huggingface dataset:
Statistics atCDC
Authors: Sieber William K. , Stroup Donna F. , Williamson G. David 
Published: October 2006

AbstractThe Centers for Disease Control and Prevention (CDC) is recognized as the lead U.S. Federal agency for protecting the health and safety of people. It accomplishes this mission by promoting health and quality of life with programs preventing and controlling disease, injury, and disability. In this mission CDC is joined by the Agency for Toxic Substances and Disease Registry (ATSDR), which is charged with evaluating the human health effects of exposure to hazardous substances. The National Center for Health Statistics (NCHS), which is a Federal statistical agency with broad responsibilities to monitor the health of the nation, became a part of CDC in 1987. Both CDC and ATSDR are components of the U.S. Department of Health and Human Services (DHHS). An important function of CDC is compilation, analysis, and interpretation of statistical information to guide actions and policies to improve health. Sources of data include vital statistics records, medical records, personal interviews, telephone and mail surveys, physical examinations, and laboratory testing. The integration of statistics and analytic techniques into public health research is also a critical asset to the agency, and has resulted in important applications in various disciplines such as epidemiology, economics, and the behavioral and social sciences. Coordination of statistical activities across CDC and ATSDR is carried out by the CDC/ATSDR Statistical Advisory Group.
Predicting Random Effects in Group Randomized Trials
Authors: Stanek iii Edward J. 
Published: October 2006

AbstractThe main objective in a group‐randomized trial is a comparison between treatments. Often, there is interest in the expected response for a particular group receiving a treatment. Since a random sample of groups is included in the trial, the parameter for such a group is represented as a random effect. In this context, predicting the expected response for a group requires predicting a random effect. We review proposed solutions to this problem focusing on differences in the model assumptions in a simple setting. We conclude that while popular computing solutions exist, fundamental open questions remain that impact interpretation.
Cluster Randomization
Authors: Klar Neil , Donner Allan 
Published: October 2006

AbstractThe purpose of this article is to present a systematic and unified treatment of comparative trials that randomize intact social units, or clusters of individuals, to different intervention groups. Such trials have become particularly widespread in the evaluation of nontherapeutic interventions, including lifestyle modification, educational programmes, and innovations in the provision of health care. Their increasing popularity over the last two decades has led to an extensive body of methodology and a growing, but somewhat scattered, literature that cuts across several disciplines in the statistical, social, and medical sciences.
Experimental and theoretical study of the influence of pressure on SCWO
Authors: Bermejo M. D. , Bielsa I. , Cocero M. J. 
Published: October 2006

AbstractIt is well known that pressure is an important parameter in the SCWO process, because it produces changes in the phase behavior and thermodynamics properties of the system. The influence of pressure on the oxidation efficiency of feeds containing isopropyl alcohol as fuel and acetic acid as waste was studied in an autothermal adiabatic transpiring wall reactor at pilot‐plant scale, at pressures from 13 to 25 Mpa, and temperatures from 600 to 750°C. It was found that reaction temperature decreased between 40 and 100°C, when pressure was lowered, and, subsequently TOC removal decreased. At higher‐temperatures, the decreasing of TOC removal due to pressure difference was reduced. The process was simulated at different pressures using a mathematical model previously developed for the reactor. The Anderko‐Pitzer EoS, especially developed for aqueous systems at high‐temperatures and pressures, was used to have accurate values of the heat capacities of the reaction mixture. It was found that having into account only the effect of pressure in the thermodynamical properties and in the concentration of the reagents, the experimental results could not be explained. Thus, the influence of the pressure in the reaction rate equation had to be considered. Results were qualitatively reproduced considering the reaction rate constant variable with pressure, using a constant volume of activation of −1400 cm3/mol. © 2006 American Institute of Chemical Engineers AIChE J, 2006
Rituximab monotherapy as interim therapy in precursor B‐ALL adults during periods of hepatic toxicity: Report of two cases
Authors: Koren‐Michowitz Maya , Rahimi‐Levene Naomi , Volcheck Yulia , Hardan Izhar , Kornberg Abraham 
Published: October 2006

AbstractPrecursor B‐ALL blasts may be positive for CD20 in up to 50% of cases. There are few reports on the use of the anti CD20 monoclonal antibody, rituximab, in children with B‐ALL. We report on two adult patients with precursor B‐ALL who developed significant hepatic toxicity during induction chemotherapy. Single agent rituximab was given until recovery of liver enzymes was established. Both patients were able to continue further chemotherapy, underwent an Allo BMT and are now 10–12 months after diagnosis in a continuous CR. Am. J. Hematol. 2006. © 2006 Wiley‐Liss, Inc.
Aberrant expression of T‐cell‐associated markers CD4 and CD7 on B‐cell chronic lymphocytic leukemia
Authors: Jani Prashant , Qi Xiao Ying , Chang Hong 
Published: October 2006

AbstractBy multiparameter flow cytometry, the T‐cell‐associated markers CD4 and CD7 were aberrantly coexpressed on a case of B‐cell chronic lymphocytic leukemia (CLL). The CLL had an immunophenotype: CD19+, CD20+, CD79b+, CD5+, CD23+, FMC7+, kappa+, CD4+, and CD7+. Molecular analysis confirmed clonal rearrangement of the immunoglobin heavy chain genes and a germline configuration of the T‐cell receptor genes. Fluorescence in situ hybridization showed trisomy 12 anomaly. There was no evidence of deletion 17p (p53), 11q23 (ATM), or 13q14 or translocation t(11:14). The patent was clinically stable without treatment. Although the pathogenesis of such aberrant immunophenotype remains to be determined, the current case illustrates the phenotypic heterogeneity of CLL, and emphasizes the importance of a comprehensive diagnostic approach including clinical, morphologic, immunophenotypic, and molecular cytogenetic studies. Am. J. Hematol. 2006. © Wiley‐Liss, Inc.
Iron status of inner‐city African‐American infants
Authors: Lozoff Betsy , Lu Angelilli Mary , Zatakia Jigna , Jacobson Sandra W. , Calatroni Agustin , Beard John 
Published: October 2006

AbstractThe iron status of African‐American infants continues to be subject to debate. We characterized the iron status of 198 9‐month‐old inner‐city infants (94% fed iron‐fortified formula) using a comprehensive panel of measures and assessing lead and inflammation markers. The proportion with iron deficiency was calculated based on three approaches (≥ 2 abnormal iron measures with or without anemia for MCV model—NHANES II, ferritin model—NHANES III, or Sweden/Honduras study) and a promising new measure—body iron, calculated from ferritin and transferrin receptor (TfR). There were no sex differences for any iron measure. Hb < 110 g/l was observed in 25%; Hb ≤ 105 g/l in 10.1%. Free erythrocyte protoporphyrin (FEP) values were elevated without elevated lead concentrations or an inflammatory response: mean FEP = 86.6 μg/dl red blood cells [75.5 μmol/mol heme]; 52.3% were > 80 μg/dl (1.42 μmol/l), almost half of which were accompanied by a second abnormal iron measure. The estimated prevalence of iron deficiency was 14.4, 5.3, and 2.5% for the MCV model, ferritin model, and Sweden/Honduras cutoffs, respectively, and 4.1% for body iron < 0 mg/kg. Regulation of iron storage is immature at < 1 year of age, making estimates of iron deficiency that depend on ferritin, including body iron, suspect in this age period. Thus, the “true” prevalence of iron deficiency could not be established with confidence due to major differences in the results, depending on the guidelines used. Functional indicators of poor iron status in young infants are urgently needed. Am. J. Hematol. 2006. © 2006 Wiley‐Liss, Inc.
Use of prenatal diagnostic procedures in pregnancies affected with birth defects, Hawaii, 1986–2002
Authors: Forrester Mathias B. , Merz Ruth D. 
Published: October 2006

AbstractBACKGROUNDInformation on the utilization of prenatal ultrasound (US), amniocentesis (AC), and chorionic villus sampling (CVS) in pregnancies affected by birth defects in the United States is limited. The intent of this study was to report on the utilization of these procedures in Hawaii.METHODSCases were all infants and fetuses of any pregnancy outcome with birth defects, included in a Hawaii birth defects registry, and delivered during 1986–2002. The rates of prenatal US, AC/CVS, and prenatal diagnosis were calculated.RESULTSPrenatal US was performed in 76% of the cases and AC/CVS in 14% of the cases. Prenatal diagnosis of a birth defect was made in 16% of the cases. The prenatal US, AC/CVS, and prenatal diagnosis rates in 1998–2002 were 1.5, 1.5, and 1.7 times the rates in 1986–1991, respectively. Among all birth defects, the AC/CVS rate for women aged <35 years was 7% and for women aged ≥35 years was 48%. Among chromosomal abnormalities, the AC/CVS rate for women aged <35 years was 36% and for women aged ≥35 years was 66%.CONCLUSIONSOnly a fraction of the Hawaii birth defects cases was prenatally diagnosed. The rates for prenatal US, AC/CVS, and prenatal diagnosis among pregnancies affected by birth defects were higher in 1998–2002 than in 1986–1991. AC/CVS rates were lower for maternal age <35 years. Birth Defects Research (Part A), 2006. © 2006 Wiley‐Liss, Inc.
Carcinogenicity study of GSM and DCS wireless communication signals in B6C3F1 mice
Authors: Tillmann Thomas , Ernst Heinrich , Ebert Sven , Kuster Niels , Behnke Wolfgang , Rittinghausen Susanne , Dasenbrock Clemens 
Published: October 2006

AbstractThe purpose of this study using a total of 1170 B6C3F1 mice was to detect and evaluate possible carcinogenic effects in mice exposed to radio‐frequency‐radiation (RFR) from Global System for Mobile Communication (GSM) and Digital Personal Communications System (DCS) handsets as emitted by handsets operating in the center of the communication band, that is, at 902 MHz (GSM) and 1747 MHz (DCS). Restrained mice were exposed for 2 h per day, 5 days per week over a period of 2 years to three different whole‐body averaged specific absorption rate (SAR) levels of 0.4, 1.3, 4.0 mW/g bw (SAR), or were sham exposed. Regarding the organ‐related tumor incidence, pairwise Fisher's test did not show any significant increase in the incidence of any particular tumor type in the RF exposed groups as compared to the sham exposed group. Interestingly, while the incidences of hepatocellular carcinomas were similar in EMF and sham exposed groups, in both studies the incidences of liver adenomas in males decreased with increasing dose levels; the incidences in the high dose groups were statistically significantly different from those in the sham exposed groups. Comparison to published tumor rates in untreated mice revealed that the observed tumor rates were within the range of historical control data. In conclusion, the present study produced no evidence that the exposure of male and female B6C3F1 mice to wireless GSM and DCS radio frequency signals at a whole body absorption rate of up to 4.0 W/kg resulted in any adverse health effect or had any cumulative influence on the incidence or severity of neoplastic and non‐neoplastic background lesions, and thus the study did not provide any evidence of RF possessing a carcinogenic potential. Bioelectromagnetics 28:173–187, 2007. © 2006 Wiley‐Liss, Inc.
Ataxia‐telangiectasia mutated expression is associated with tobacco smoke exposure in esophageal cancer tissues and benzo[a]pyrene diol epoxide in cell lines
Authors: Jiang Yan , Liang Zheng D. , Wu Tsung T. , Cao Liyu , Zhang Hongfu , Xu Xiao‐Chun 
Published: October 2006

AbstractEsophageal cancer is a substantial health problem because of its usually late stage at diagnosis and poor prognosis. Tobacco smoking and alcohol use are the most important risk factors in the development of esophageal squamous cell carcinoma (SCC). Our previous study demonstrated the binding of benzo[a]pyrene diol epoxide (BPDE), a carcinogen present in tobacco smoke and environmental pollution, to the ataxia‐telangiectasia mutated (ATM) gene. To understand how this binding affects the alteration of ATM expression and to identify biomarkers for the detection of esophageal cancer, we analyzed ATM mRNA expression in tissue specimens from patients with esophageal SCC and premalignant lesions using in situ hybridization. We then performed in vitro experiments to verify and extend our ex vivo observations. We found that ATM expression was increased in esophageal SCC and its premalignant lesions when compared with normal tissues and that increased ATM expression was associated with tobacco smoke exposure and tumor de‐differentiation. Moreover, BPDE induced ATM expression in esophageal SCC cell lines in a time‐dependent manner. In summary, the BPDE in tobacco smoke may be responsible for increased ATM expression in premalignant and malignant esophageal tissues. Our findings suggest that the ATM gene should be further evaluated as a biomarker for the early detection of esophageal cancer and tobacco use in patients. © 2006 Wiley‐Liss, Inc.
Photochemoprevention of UVB‐induced skin carcinogenesis in SKH‐1 mice by brown algae polyphenols
Authors: Hwang Hyejeong , Chen Tong , Nines Ronald G. , Shin Hyeon‐Cheol , Stoner Gary D. 
Published: October 2006

AbstractChronic exposure of the skin to ultraviolet B (UVB) radiation induces oxidative stress, which plays a crucial role in the induction of skin cancer. In this study, the effect of dietary feeding and topical application of brown algae polyphenols on UVB radiation‐induced skin carcinogenesis in SKH‐1 mice was investigated. SKH‐1 hairless mice were randomly divided into 9 groups, including control, UVB control and treatment groups. They were treated orally (0.1% and 0.5% with AIN‐76 diet, w/w) and topically (3 and 6 mg/0.2 ml of vehicle) with brown algae polyphenols and irradiated with UVB for 26 weeks. Dietary feeding (0.1% and 0.5%) of brown algae polyphenols significantly reduced tumor multiplicity (45% and 56%) and tumor volume (54% and 65%), and topical administration (3 and 6 mg) significantly decreased tumor multiplicity (60% and 46%) and tumor volume (66% and 57%), respectively, per tumor‐bearing mouse. Dietary feeding and topical administration of the polyphenols also inhibited tumor incidence by 6% and 21%, respectively, but the results were not significant. Dietary and topical administration of the polyphenols markedly inhibited cyclooxygenase‐2 activity and cell proliferation. These observations show that brown algae polyphenols have an antiphotocarcinogenic effect which may be associated with the prevention of UVB‐induced oxidative stress, inflammation, and cell proliferation in the skin. © 2006 Wiley‐Liss, Inc.
Annexin‐I as a potential target for green tea extract induced actin remodeling
Authors: Xiao Gui‐Shan , Jin Yu‐Sheng , Lu Qing‐Yi , Zhang Zuo‐Feng , Belldegrun Arie , Figlin Robert , Pantuck Allan , Yen Yun , Li Frederick , Rao JianYu 
Published: October 2006

AbstractUsing a multistep human urothelial model, we previously showed that green tea extract (GTE) selectively modulates actin remodeling in transformed cells (MC‐T11), which resulted in increased cell adhesion and reduced cell motility (Lu et al., Clin Cancer Res 2005;11:1675–83). This study further analyzed which actin binding proteins (ABPs) might be involved in this process. Proteomic profiles of GTE treated and untreated MC‐T11 cells using two‐dimensional gel electrophoresis coupled with liquid chromatography tandem mass spectrometry (LC/MS/MS) and matrix‐assisted laser desorption and ionization time‐of‐flight (MALDI‐TOF) identified 20 GTE‐induced proteins. Among them, 3 were ABPs (tropomodulin, cofilin and annexin‐I), and only annexin‐I showed a dose‐ and time‐dependent expression. The increased annexin‐I correlated with actin remodeling, and was the result of transcription level up‐regulation, as determined by RT‐PCR, pull‐down immunoblot and siRNA analyses. 5‐Azacytidine, a DNA methylation inhibitor, exhibited no effect on annexin‐I expression when used alone, but had an additive effect for GTE‐induced annexin‐I expression. Immunohistochemistry of bladder cancer tissue array showed a decrease of annexin‐I expression in carcinoma in situ and low grade papillary carcinoma (n = 32, 0% positive) compared to nontumor urothelium (n = 18, 89% positive) (p < 0.001 by Fisher exact test), but increased in some (6 of 15, 40%) high‐grade tumors. Together, GTE induced annexin‐I expression plays a role in regulating actin remodeling and decreased annexin‐I expression is a common event in early stage of bladder cancer development. © 2006 Wiley‐Liss, Inc.
Dietary intake of calcium, fiber and other micronutrients in relation to colorectal cancer risk: Results from the Shanghai Women's Health Study
Authors: Shin Aesun , Li Honglan , Shu Xiao‐Ou , Yang Gong , Gao Yu‐Tang , Zheng Wei 
Published: October 2006

AbstractWe evaluated the associations of dietary intake of calcium, fiber and vitamins with colorectal cancer risk in a population‐based prospective cohort study conducted among Chinese women in Shanghai. Subjects were recruited in urban Shanghai from March 1997 to May 2000. All subjects were interviewed in‐person to obtain information on demographic and lifestyle factors and anthropometric measurement was conducted. Usual dietary intake, using a validated food frequency questionnaire was assessed at the baseline survey. After following a total of 73,314 women for a median of 5.74 years, 283 incident colorectal cancer cases were recorded. Excluding the first 2 years of follow‐up, a high intake of calcium was associated with a decreased risk of colorectal cancer. Comparing the highest quintile of nutrients intake to the lowest, the adjusted relative risk for colorectal cancer was 0.6 (p value for trend = 0.023) for calcium. No apparent associations were found for fiber, total vitamin A, carotene, vitamins B1, B2, B3, C and E with colorectal cancer risk. Our results suggest that calcium may be protective against colorectal cancer development even at a lower consumption level compared to Western populations. © 2006 Wiley‐Liss, Inc.
Inhibition of carcinoma cell‐derived VEGF reduces inflammatory characteristics in xenograft carcinoma
Authors: Salnikov Alexei V. , Heldin Nils‐Erik , Stuhr Linda B. , Wiig Helge , Gerber Hanspeter , Reed Rolf K. , Rubin Kristofer 
Published: October 2006

AbstractThe stroma of carcinomas shares several characteristics with inflamed tissues including a distorted vasculature, active angiogenesis and macrophage infiltration. In addition, the tumor interstitial fluid pressure (PIF) of the stroma is pathologically elevated. We show here that bevacizumab [rhuMab vascular endothelial growth factor (VEGF), Avastin], a monoclonal antibody to VEGF, at a dose of 5 mg/kg modulated inflammation in KAT‐4 xenograft human anaplastic thyroid carcinoma tissue. At this dose, bevacizumab reduced the density of macrophages, MHC class II antigen expression by macrophages and IL‐1β mRNA expression. Furthermore, bevacizumab lowered tumor extracellular fluid volume, plasma protein leakage from tumor vessels, the number of CD31‐positive structures and tumor PIF. The tumor plasma volume and the number of α‐smooth muscle actin‐positive vessels, however, remained unchanged. Our data suggest that carcinoma cell‐derived VEGF either directly or indirectly participates in maintaining an inflammatory microenvironment in experimental KAT‐4 carcinoma. Furthermore, our data indicate that the reduction of inflammation resulting in reduced vascular permeability and decrease in the tumor extracellular fluid volume by bevacizumab contributes to reduced tumor PIF. © 2006 Wiley‐Liss, Inc.
Pentose phosphate cycle oxidative and nonoxidative balance: A new vulnerable target for overcoming drug resistance in cancer
Authors: Ramos‐Montoya Antonio , Lee Wai‐Nang P. , Bassilian Sara , Lim Shu , Trebukhina Raisa V. , Kazhyna Maria V. , Ciudad Carlos J. , Noé Véronique , Centelles Josep J. , Cascante Marta 
Published: October 2006

AbstractThe metabolic network of cancer cells confers adaptive mechanisms against many chemotherapeutic agents, but also presents critical constraints that make the cells vulnerable to perturbation of the network due to drug therapy. To identify these fragilities, combination therapies based on targeting the nucleic acid synthesis metabolic network at multiple points were tested. Results showed that cancer cells overcome single hit strategies through different metabolic network adaptations, demonstrating the robustness of cancer cell metabolism. Analysis of these adaptations also identified the maintenance of pentose phosphate cycle oxidative and nonoxidative balance to be critical for cancer cell survival and vulnerable to chemotherapeutic intervention. The vulnerability of cancer cells to the imbalance on pentose phosphate cycle was demonstrated by phenotypic phase plane analysis. © 2006 Wiley‐Liss, Inc.
Ursodeoxycholic acid modulates histone acetylation and induces differentiation and senescence
Authors: Akare Sandeep , Jean‐Louis Samira , Chen Wemin , Wood Daniel J. , Powell Ashley A. , Martinez Jesse D. 
Published: October 2006

AbstractAgents that can modulate colonic environment and control dysregulated signaling are being evaluated for their chemopreventive potential in colon cancer. Ursodeoxycholate (UDCA) has shown chemopreventive potential in preclinical and animal models of colon cancer, but the mechanism behind it remains unknown. Here biological effects of UDCA were examined to understand mechanism behind its chemoprevention in colon cancer. Our data suggests that UDCA can suppress growth in a wide variety of cancer cell lines and can induce low level of apoptosis in colon cancer cells. We also found that UDCA treatment induces alteration in morphology, increased cell size, upregulation of cytokeratin 8, 18 and 19 and E‐cadherin, cytokeratin remodeling and accumulation of lipid droplets, suggesting that UDCA induces differentiation in colon carcinoma cells. Our results also suggest significant differences in UDCA and sodium butyrate induced functional differentiation. We also report for the first time that UDCA can induce senescence in colon cancer cells as assessed by flattened, spread out and vacuolated morphology as well as by senescence marker β‐galactosidase staining. We also found that UDCA inhibits the telomerase activity. Surprisingly, we found that UDCA is not a histone deacytylase inhibitor but instead induces hypoacetylation of histones unlike hyperacetylation induced by sodium butyrate. Our results also suggest that, although UDCA induced senescence is p53, p21 and Rb independent, HDAC6 appears to be important in UDCA induced senescence. In summary, our data shows that UDCA modulates chromatin by inducing histone hypoacetylation and induces differentiation and senescence in colon cancer cells. © 2006 Wiley‐Liss, Inc.