bluuebunny/crossref_metadata_2025_split huggingface dataset:
A Consideration of the Various Types of Songs Popular in England During the Eighteenth Century
Authors: Woods F. Cunningham 
Published: January 2007

It is my duty to commence this lecture with a twofold apology or explanation, if you prefer to call it so.In the first place I would allow myself the usual privilege of construing the term Eighteenth Century in an elastic sense; in the second place I am bound to admit that in many cases it is all but impossible to give a date, even approximately, to some songs to which your attention is to be directed to-day. One may look through numbers of these “broadsides,” or leaflets, and find that not only are composers' and publishers' names wanting, but that the date and price are very seldom given.
A Correction for an Underdispersed Event Count Probability Distribution
Authors: Winkelmann Rainer , Signorino Curtis S. , King Gary 
Published: January 2007

We demonstrate that the expected value and variance commonly given for a well-known probability distribution are incorrect. We also provide corrected versions and report changes in a computer program to account for the known practical uses of this distribution.The probability distribution in question, named the continuous parameter binomial (CPB) by King (1989a), has been known for at least six decades. The publications that reported the moments incorrectly, or were at least unclear about them, include a dated article (Guldberg 1931), a dissertation and several resulting published articles (Katz 1945, 1965), a popular reference book (Johnson and Kotz 1969),' work in political science on event count regression models (King 1989a), and extensions of these event count models in econometrics (Winkelmann and Zimmermann 1991). Event count regression models have become increasingly common in empirical political science research; some recent examples include Wang et al. (1993) and Krause (1994).
Candida albicans inactivation and cell membrane integrity damage by microwave irradiation
Authors: Campanha Nara Hellen , Pavarina Ana Cláudia , Brunetti Iguatemy Lourenço , Vergani Carlos Eduardo , Machado Ana Lucia , Spolidorio Denise Madalena Palomari 
Published: January 2007

SummaryIn indicating the microwave irradiation for disinfecting dentures it is necessary to see how this procedure influences Candida albicans integrity and viability. The aim of this study was to evaluate the ability of microwaves to inactivate C. albicans and damage cell membrane integrity. Two 200‐ml C. albicans (ATCC 10231) suspensions were obtained. A sterile denture was placed in a beaker containing the Experimental (ES) or the Control suspension (CS). ES was microwaved at 650 W for 6 min. Suspensions were optically counted using methylene blue dye uptake as indicative of membrane‐damaged cells; spread on Agar Sabouraud dextrose (ASD) for viability assay; or spectrophotometrically measured at 550 nm. Cell‐free solutions were submitted to content analyses of protein (Bradford and Pyrogallol red methods); Ca++ (Cresolftaleine complexone method); DNA (spectrophotometer measurements at 260 nm) and K+ (selective electrode technique). Data were analysed by Student's t‐ or Wilcoxon z‐tests (α = 0.05). All ES cells demonstrated cell membrane damage. Viable cells were non‐existent in the ES ASD plates. No significant difference in optical density between ES and CS was observed (P = 0.272). ES cells released significantly high protein (P < 0.001, Bradford; P = 0.005, Pyrogallol red), K+ (P < 0.001), Ca++ (P = 0.012) and DNA (P = 0.046) contents. Microwaves inactivated C. albicans and damaged cell membrane integrity.
Sporotrichosis in north‐east India
Authors: Haldar Nibideta , Sharma M. K. , Gugnani H. C. 
Published: January 2007

SummaryReports on the occurrence of sporotrichosis in some parts of north‐east India are scarce. We report here five cases of lymphocutaneous sporotrichosis from north‐east India, including one from Sikkim State and four from distant places in the north‐eastern part of West Bengal. All patients were full or part‐time farmers or gardeners. Diagnosis of sporotrichosis was confirmed by isolation of Sporothrix schenckii in culture and in vitro conversion of the isolates to yeast form. The cases were treated with 50% solution of potassium iodide.
Clonal and Parallel Evolution of Primary Lung Cancers and Their Metastases Revealed by Molecular Dissection of Cancer Cells
Authors: Takahashi Kenji , Kohno Takashi , Matsumoto Shingo , Nakanishi Yukihiro , Arai Yasuhito , Yamamoto Seiichiro , Fujiwara Toshiyoshi , Tanaka Noriaki , Yokota Jun 
Published: January 2007

Abstract
Purpose: Several models of cancer progression, including clonal evolution, parallel evolution, and same-gene models, have been proposed to date. The purpose of this study is to investigate the authenticity of these models by comparison of accumulated genetic alterations between primary and corresponding metastatic lung cancers.
Experimental Design: A whole-genome allelic imbalance scanning using a high-resolution single nucleotide polymorphism array and mutational analysis of the p53, EGFR, and KRAS genes were done on eight sets of primary and metastatic lung cancers. Based on the genotype data, the natural history of each case was deduced, and candidate metastasis suppressor loci were determined.
Results: Five to 20 chromosomal regions showed allelic imbalance in each tumor. Accumulated genetic alterations were similar between primary and corresponding metastatic tumors, and the majority(&gt;67%) of genetic alterations detected in metastatic tumors was also detected in the corresponding primary tumors. On the other hand, in seven of the eight cases, there were genetic alterations accumulated only in metastatic tumors. Among these alterations, allelic imbalances at chromosome 11p15 and 11p11-p13 regions were the most frequent ones (4 of 8, 50%). Likewise, four cases showed genetic alterations detected only in primary tumors.
Conclusions: The natural history of each case indicated that the process of metastasis varies among cases, and that all three models are applicable to lung cancer progression. According to the clonal and parallel evolution models, it is possible that a metastasis suppressor gene(s) for lung cancer is present on chromosome 11p.
Risk of Second Cancer in Nongastric Marginal Zone B-Cell Lymphomas of Mucosa-Associated Lymphoid Tissue: A Population-Based Study from Northern Italy
Authors: Arcaini Luca , Burcheri Sara , Rossi Andrea , Pascutto Cristiana , Passamonti Francesco , Brusamolino Ercole , Paulli Marco , Orlandi Ester , Buelli Maurizio , Viero Piera , Lucioni Marco , Montanari Francesca , Merli Michele , Cortelazzo Sergio , Lazzarino Mario 
Published: January 2007

Abstract
Purpose: The aim of this study was to define the risk of second cancer in nongastric marginal zone lymphomas of mucosa-associated lymphoid tissue (MALT).
Experimental Design: We considered for the analysis 157 patients with a confirmed histology of marginal zone B-cell lymphoma of MALT, presenting with a clinically prevalent extranodal site of disease, except for stomach. All patients came from two hematologic institutions of Northern Italy. We compared the occurrence of second cancer with respect to the general population by calculating the standardized incidence ratio, with the age- and sex-specific incidence rates of a cancer registry of Northern Italy (Lombardia) as a reference.
Results: A history of solid neoplasia was present in 29 (18%) patients for a total number of 30 neoplasms: 25 solid tumors, 2 hematologic diseases (1 Hodgkin's lymphoma and 1 essential thrombocythemia), and 3 nonmelanoma in situ skin cancers. In 4 patients, the site of cancer and lymphoma was the same. In 21 cases the solid tumor preceded the MALToma, in 3 the neoplasm was concomitant, whereas in 6 it was subsequent. For the entire group, the standardized incidence ratio of an additional malignancy was 0.8 [95% confidence interval (95% CI), 0.55-1.17; P = 0.2]. After excluding nonmelanoma skin cancer, the standardized incidence ratio of a second tumor was 0.75 (95% CI, 0.5-1.12; P = 0.2). After excluding all previous malignancies, the standardized incidence ratio of a second cancer was 1.32 (95% CI, 0.69-2.55; P = 0.4). The comparison of risks between males and females was not significant in each group analysis.
Conclusions: Patients with nongastric MALT lymphomas are not at increased risk for other neoplasms compared with the general population of the same geographic area.
The Combi-Targeting Concept: In vitro and In vivo Fragmentation of a Stable Combi-Nitrosourea Engineered to Interact with the Epidermal Growth Factor Receptor while Remaining DNA Reactive
Authors: Qiu Qiyu , Domarkas Juozas , Banerjee Ranjita , Merayo Nuria , Brahimi Fouad , McNamee James P. , Gibbs Bernard F. , Jean-Claude Bertrand J. 
Published: January 2007

Abstract
Purpose: JDA58 (NSC 741282), a “combi-molecule” optimized in the context of the “combi-targeting concept,” is a nitrosourea moiety tethered to an anilinoquinazoline. Here, we sought to show its binary epidermal growth factor receptor (EGFR)/DNA targeting property and to study its fragmentation in vitro and in vivo.
Experimental Design: The fragmentation of JDA58 was detected in cells in vitro and in vivo by fluorescence microscopy and tandem mass spectrometry. EGFR phosphorylation and DNA damage were determined by Western blotting and comet assay, respectively. Tumor data were examined for statistical significance using the Student's t test.
Results: JDA58 inhibited EGFR tyrosine kinase (IC50, 0.2 μmol/L) and blocked EGFR phosphorylation in human DU145 prostate cancer cells. It induced significant levels of DNA damage in DU145 cells in vitro or in vivo and showed potent antiproliferative activity both in vitro and in a DU145 xenograft model. In cell-free medium, JDA58 was hydrolyzed to JDA35, a fluorescent amine that could be observed in tumor cells both in vitro and in vivo. In tumor cells in vitro or in vivo, or in plasma collected from mice, the denitrosated species JDA41 was the predominant metabolite. However, mass spectrometric analysis revealed detectable levels of the hydrolytic product JDA35 in tumor cells both in vitro and in vivo.
Conclusions: The results in toto suggest that growth inhibition in vitro and in vivo may be sustained by the intact combi-molecule plus JDA35 plus JDA41, three inhibitors of EGFR, and the concomitantly released DNA-damaging species. This leads to a model wherein a single molecule carries a complex multitargeted-multidrug combination.
Requirement of Aryl Hydrocarbon Receptor Overexpression for CYP1B1 Up-Regulation and Cell Growth in Human Lung Adenocarcinomas
Authors: Chang Jinghua Tsai , Chang Han , Chen Po-Hung , Lin Shong-Ling , Lin Pinpin 
Published: January 2007

Abstract
Purpose: CYP1B1 and CYP1A1 expression is up-regulated by activation of the aryl hydrocarbon receptor (AhR) through binding of ligands such as cigarette smoke components. We examined the association between AhR, CYP1B1, and CYP1A1 expression in noninvasive bronchioloalveolar carcinomas (BAC) and lung adenocarcinomas and investigated the effects of AhR overexpression on cell physiology.
Experimental Design: AhR, CYP1B1, and CYP1A1 expression was examined in 107 lung adenocarcinomas and 57 BAC by immunohistochemistry. AhR expression in lung adenocarcinoma H1355 cells was stably reduced by RNA interference (RNAi). AhR, CYP1B1, and CYP1A1 expression was examined using real-time reverse transcription-PCR. Cell physiology was evaluated by measuring anchorage-independent growth and intracellular reactive oxygen species.
Results: Expression of AhR and CYP1A1 was associated in smoking adenocarcinoma patients, whereas expression of AhR and CYP1B1 was associated regardless of smoking status. The level of CYP1B1, but not CYP1A1, was positively associated with AhR overexpression in BAC. 2,3,7,8-Tetrachlorobenzo-p-dioxin–induced CYP1A1/1B1 expression was reduced in AhR RNAi clones. In the absence of 2,3,7,8-tetrachlorobenzo-p-dioxin, CYP1B1 mRNA levels were reduced in AhR RNAi clones, whereas CYP1A1 mRNA levels were barely detectable. Furthermore, anchorage-independent growth and intracellular oxidative stress were significantly reduced in AhR RNAi cells.
Conclusions: In the absence of exogenous AhR ligands (such as cigarette smoke components), AhR overexpression up-regulated the expression of CYP1B1 in the early stage of lung adenocarcinoma. Elevated AhR expression in lung adenocarcinoma cells could increase intracellular oxidative stress and promote cell growth, implying that disrupting AhR expression might prevent the early development of lung adenocarcinomas.
Parathyroid Hormone-Related Protein Induces Cachectic Syndromes without Directly Modulating the Expression of Hypothalamic Feeding-Regulating Peptides
Authors: Hashimoto Hirofumi , Azuma Yumiko , Kawasaki Makoto , Fujihara Hiroaki , Onuma Etsuro , Yamada-Okabe Hisafumi , Takuwa Yoh , Ogata Etsuro , Ueta Yoichi 
Published: January 2007

Abstract
Purpose: Parathyroid hormone-related protein (PTHrP) is a causative factor of humoral hypercalcemia of malignancy (HHM) and concurrent anorexia and wasting. Because changes in the expression of hypothalamic feeding-regulating peptides can directly affect appetites and thereby can cause anorexia and wasting, we addressed whether the cachectic syndromes induced by PTHrP rely on the action of hypothalamic feeding-regulating peptides.
Experimental Design: Rats were inoculated with a LC-6 human cancer xenograft that secreted PTHrP, and the mRNA levels of the hypothalamic feeding-regulating peptide genes and serum leptin levels were examined before and after the development of HHM by in situ hybridization histochemistry and ELISA, respectively. Some rats were given the anti-PTHrP antibody.
Results and Conclusion: The mRNA levels for the orexigenic peptides, such as the agouti-related protein and the neuropeptide Y in the arcuate nucleus (Arc), were significantly increased after the development of HHM, whereas the mRNA levels for the anorexigenic peptides, such as the proopiomelanocortin in the Arc, the cocaine and amphetamine-regulated transcript in the Arc, and the corticotropin-releasing factor in the paraventricular nucleus, were significantly decreased after the development of HHM. Plasma leptin levels were also reduced in cachectic rats, and the administration of anti-PTHrP antibody to the cachectic rats not only improved the cachectic symptoms but also restored the mRNA levels of these orexigenic and anorexigenic peptides, except for orexin. Thus, PTHrP induces HHM and concurrent cachectic syndromes by mechanisms other than directly modulating the leptin or hypothalamic feeding-regulated peptides.
Reciprocal Modifications of CLIC4 in Tumor Epithelium and Stroma Mark Malignant Progression of Multiple Human Cancers
Authors: Suh Kwang S. , Crutchley John M. , Koochek Arash , Ryscavage Andrew , Bhat Kiran , Tanaka Takemi , Oshima Akira , Fitzgerald Peter , Yuspa Stuart H. 
Published: January 2007

AbstractPurpose: CLIC4, a member of a family of intracellular chloride channels, is regulated by p53, c-Myc, and tumor necrosis factor-α. Regulation by factors involved in cancer pathogenesis, together with the previously shown proapoptotic activity of CLIC4, suggests that the protein may have a tumor suppressor function. To address this possibility, we characterized the expression profile, subcellular localization, and gene integrity of CLIC4 in human cancers and determined the functional consequences of CLIC4 expression in tumor epithelium and stromal cells.Experimental Design: CLIC4 expression profiles were analyzed by genomics, proteomics, bioinformatics, and tissue microarrays. CLIC4 expression, as a consequence of crosstalk between stroma and epithelium, was tested in vitro by coculture of breast epithelial tumor cells and normal fibroblasts, and the functional consequences of CLIC4 expression was tested in vivo in xenografts of human breast tumor cell lines reconstituted with CLIC4 or mixed with fibroblasts that overexpress CLIC4 transgenically.Results: In cDNA arrays of matched human normal and tumor tissues, CLIC4 expression was reduced in renal, ovarian, and breast cancers. However, CLIC4 protein levels were variable in tumor lysate arrays. Transcript sequences of CLIC4 from the human expressed sequence tag database and manual sequencing of cDNA from 60 human cancer cell lines (NCI60) failed to reveal deletion or mutations in the CLIC4 gene. On matched tissue arrays, CLIC4 was predominantly nuclear in normal human epithelial tissues but not cancers. With advancing malignant progression, CLIC4 staining became undetectable in tumor cells, but expression increased in stromal cells coincident with up-regulation of α-smooth muscle actin, suggesting that CLIC4 is up-regulated in myofibroblasts. Coculture of cancer cells and fibroblasts induced the expression of both CLIC4 and α-smooth muscle actin in fibroblasts adjacent to tumor nests. Introduction of CLIC4 or nuclear targeted CLIC4 via adenovirus into human breast cancer xenografts inhibited tumor growth, whereas overexpression of CLIC4 in stromal cells of xenografts enhanced tumor growth.Conclusion: Loss of CLIC4 in tumor cells and gain in tumor stroma is common to many human cancers and marks malignant progression. Up-regulation of CLIC4 in tumor stroma is coincident with myofibroblast conversion, generally a poor prognostic indicator. Reactivation and restoration of CLIC4 in tumor cells or the converse in tumor stromal cells could provide a novel approach to inhibit tumor growth.
Reversing Hepatocellular Carcinoma Progression by Using Networked Biological Therapies
Authors: Epstein Richard J. , Leung Thomas W. 
Published: January 2007

Abstract
The liver is distinguished from other tissues by (a) its detoxifying function, (b) its resistance to apoptosis, and (c) its regenerative response to damage. Hepatocellular carcinoma arises when chronic insults, such as hepatitis or iron overload, constitutively activate this regenerative program. Here, we propose that the proliferative response of the liver to damage underlies the resistance of hepatocellular carcinoma to cytotoxic therapy, and that hepatocellular carcinoma growth should therefore be more readily controlled by using a networked combination of noncytotoxic interventions to interrupt the damage-inducible regenerative pathway. To this end, hepatocellular carcinoma boasts a wealth of potential drug targets, including viral replication, the antiapoptotic immunosuppressant α-fetoprotein, hepatic iron overload, inflammatory signaling, extracellular proteases, and growth factors. By blocking these positive feedback loops in parallel, and so returning the host environment to a more normal state, epigenetic repression of tumor-suppressor gene function may be reversed and tumor dormancy restored. Noncytotoxic maneuvers that short circuit damage resistance loops may thus represent an indirect form of gene therapy meriting incorporation into hepatocellular carcinoma clinical trials.
Probable Statin-Induced Testicular Pain
Authors: Linnebur Sunny A , Hiatt William H 
Published: January 2007

Objective: To describe a case of a patient experiencing testicular pain on 3 occasions after taking 3 different statins. Case Summary: A 54-year-old man with hyperlipidemia was started on lovastatin therapy. His other medications included aspirin, levothyroxine, buspirone, and atenolol. Seven months after starting lovastatin, the patient experienced testicular discomfort that resolved upon discontinuation of the drug. Afterward, he started simvastatin and again experienced testicular discomfort. The simvastatin was changed to atorvastatin, and the pain resolved. However, 3 months after starting atorvastatin, the patient developed testicular pain, which resolved after the drug was stopped. During each of the episodes, the patient's pain increased when he was sitting, driving, or wearing tight clothing. The Naranjo probability scale indicates that statins probably caused the patient's pain. Discussion: Testicular pain is rarely caused by medications. Product labeling for statins does not list urinary adverse events as common. However, labeling for atorvastatin and pravastatin lists rare urologic adverse effects. A literature search did not reveal any previously reported cases of testicular adverse effects from statins. However, statins have been shown to inhibit cholesterol synthesis in the testis. Some data indicate that statins reduce serum testosterone concentrations, but other data indicate that statins have no effect on sex hormones or spermatogenesis. Data are also available indicating that aspirin might affect testosterone concentrations and testicular function. It is difficult to know whether either of the above hormonal mechanisms was associated with our patient's testicular discomfort, but the time course and challenge/rechallenge aspects of the case suggest that the statins were the cause. Conclusions: Urologic adverse effects of statins rarely occur but should not be overlooked by medical providers.
Barriers to the Identification and Management of Psychosocial Issues in Children and Maternal Depression
Authors: Horwitz Sarah McCue , Kelleher Kelly J. , Stein Ruth E.K. , Storfer-Isser Amy , Youngstrom Eric A. , Park Elyse R. , Heneghan Amy M. , Jensen Peter S. , O'Connor Karen G. , Hoagwood Kimberly Eaton 
Published: January 2007

CONTEXT. Child psychosocial issues and maternal depression are underidentified and undertreated, but we know surprisingly little about the barriers to identification and treatment of these problems by primary care pediatricians.OBJECTIVES. The purpose of this work was to determine whether (1) perceived barriers to care for children's psychosocial issues and maternal depression aggregate into patient, physician, and organizational domains, (2) barrier domains are distinct for mothers and children, and (3) physician, patient, and practice/organizational characteristics are associated with different barrier domains for children and mothers.METHODS. We conducted a cross-sectional survey of the 50818 US nonretired members of the American Academy of Pediatrics. Of a random sample of 1600 members, 832 (745 nontrainee members) responded. This was a mailed 8-page survey with no patients and no intervention. We measured physician assessment of barriers to providing psychosocial care for children's psychosocial problems and maternal depression.RESULTS. Pediatricians frequently endorse the lack of time to treat mental health problems (77.0%) and long waiting periods to see mental health providers (74.0%) as the most important barriers to the identification and treatment of children's psychosocial problems. For maternal depression, pediatricians most often endorsed lack of training in treatment (74.5%) and lack of time to treat (64.3%) as important barriers. Pediatricians' reports of barriers clustered into physician and organizational domains. Physician domains were distinct for children and mothers, but organizational domains were not. Several physician and practice characteristics are significantly associated with the 4 barrier scales, and different characteristics (eg, sociodemographic, attitudinal, and practice features) were related to each barrier area.CONCLUSIONS. Pediatricians endorse a wide range of barriers with respect to the diagnosis and treatment of children's mental health problems and maternal depression. The specificity of factors relating to various barrier areas suggests that overcoming barriers to the identification and treatment of child mental health problems and maternal depression in primary care pediatrics is likely to require a multifaceted approach that spans organizational, physician, and patient issues. In addition, comprehensive interventions will likely require social marketing approaches designed to engage diverse audiences of clinicians and their patients to participate.