bluuebunny/crossref_metadata_2025_split huggingface dataset:
A new 24 h ELISA culture based method forHelicobacter pylorichemosusceptibility
Authors: Perna Federico , Vaira Dino 
Published: June 2010

BackgroundClarithromycin (CH) and metronidazole (MZ) are routinely used inHelicobacter pyloritreatment regimes. Recently, treatment with these antibiotics has been reported to fail in >30% of patients due to increasing resistance. The common chemosusceptibility methods are cumbersome and take up to 14 days. Chemosusceptibility ofH pyloriis therefore rarely checked.AimTo develop a rapid susceptibility test (RST) forH pylori.MethodsPreliminary experiments were performed to find a broth medium able to support the growth ofH pyloriin 20 h and a reliable detection method to quickly detect the amount ofH pylorigrown in the media. A mixture of different components was the best broth medium; ELISA was chosen as the detection technique. Performance of the new RST was compared to a gold standard (break point agar dilution method). 200 consecutive patients were tested forH pyloriinfection and chemosusceptibility to CH and MZ by the gold standard and RST.Results111 patients were infected withH pylori. 105 of these were positive by both RST and the gold standard culture method; 75/105 and 68/105 strains were susceptible to CH and MZ, respectively. RST misdiagnosed 2 strains of CH and 10 strains of MZ.ConclusionsA new simple and rapid chemosusceptibility test forH pylorihas been validated, which is simple to perform and reduces the procedure time from 6–14 days to 24 h.
Upper Triassic–lowermost Jurassic palynology and palynostratigraphy: a review
Authors: Cirilli Simonetta 
Published: June 2010

Abstract
This review advances understanding of the palynostratigraphy of the Late Triassic–Early Jurassic by correlating the established palynozonations for the northern and southern hemispheres. Previous palynological studies have contributed greatly to our understanding of the biostratigraphy, paleoclimatology and paleogeography of the Upper Triassic. In general, palynology is a good tool for interregional cross-correlation of marine and non-marine successions because palynomorphs, unlike most of other fossils, commonly are present in continental and marine environments. Currently, however, biostratigraphical resolution based on Upper Triassic palynomorph assemblages is rather low, primarily because of the rarity of successions that are independently dated (i.e. via ammonoids, conodonts, isotopes, paleomagnetism) to correlate the palynomorph assemblages, but also for other reasons, such as microfloristic provincialism, palaeoenvironmental conditions and differential preservation of palynomorph assemblages. During the last few decades many palynological studies have attempted to integrate and improve the biostratigraphical correlations and paleoclimatologic reconstructions across the Triassic–Jurassic boundary. Several authors have recognized specific microfloral assemblages with well-defined and recognizable suites of palynomorphs that enhance the importance of palynomorphs in the definition of Triassic–Jurassic stages. Comparison of the palynomorph assemblages from different biostratigraphical stages demonstrates that a change occurred in the palynofloral composition of the Tethyan domain between the Carnian and the earliest Hettangian that was gradual and without abrupt changes.
The Triassic timescale based on nonmarine tetrapod biostratigraphy and biochronology
Authors: Lucas Spencer G. 
Published: June 2010

AbstractThe Triassic timescale based on nonmarine tetrapod biostratigraphy and biochronology divides Triassic time into eight land-vertebrate faunachrons (LVFs) with boundaries defined by the first appearance datums (FADs) of tetrapod genera or, in two cases, the FADs of a tetrapod species. Definition and characterization of these LVFs is updated here as follows: the beginning of the Lootsbergian LVF=FAD ofLystrosaurus; the beginning of the Nonesian=FADCynognathus; the beginning of the Perovkan LVF=FADEocyclotosaurus; the beginning of the Berdyankian LVF=FADMastodonsaurus giganteus; the beginning of the Otischalkian LVF=FADParasuchus; the beginning of the Adamanian LVF=FADRutiodon; the beginning of the Revueltian LVF=FADTypothorax coccinarum; and the beginning of the Apachean LVF=FADRedondasaurus. The end of the Apachean (= beginning of the Wasonian LVF, near the beginning of the Jurassic) is the FAD of the crocodylomorphProtosuchus. The Early Triassic tetrapod LVFs, Lootsbergian and Nonesian, have characteristic tetrapod assemblages in the Karoo basin of South Africa, theLystrosaurusassemblage zone and the lower two-thirds of theCynognathusassemblage zone, respectively. The Middle Triassic LVFs, Perovkan and Berdyankian, have characteristic assemblages from the Russian Ural foreland basin, the tetrapod assemblages of the Donguz and the Bukobay svitas, respectively. The Late Triassic LVFs, Otischalkian, Adamanian, Revueltian and Apachean, have characteristic assemblages in the Chinle basin of the western USA, the tetrapod assemblages of the Colorado City Formation of Texas, Blue Mesa Member of the Petrified Forest Formation in Arizona, and Bull Canyon and Redonda formations in New Mexico. Since the Triassic LVFs were introduced, several subdivisions have been proposed: Lootsbergian can be divided into three sub-LVFs, Nonesian into two, Adamanian into two and Revueltian into three. However, successful inter-regional correlation of most of these sub-LVFs remains to be demonstrated. Occasional records of nonmarine Triassic tetrapods in marine strata, palynostratigraphy, conchostracan biostratigraphy, magnetostratigraphy and radioisotopic ages provide some basis for correlation of the LVFs to the standard global chronostratigraphic scale. These data indicate that Lootsbergian=uppermost Changshingian, Induan and possibly earliest Olenekian; Nonesian=much of the Olenekian; Perovkan=most of the Anisian; Berdyankian=latest Anisian? and Ladinian; Otischalkian=early to late Carnian; Adamanian=most of the late Carnian; Revueltian=early–middle Norian; and Apachean=late Norian–Rhaetian. The Triassic timescale based on tetrapod biostratigraphy and biochronology remains a robust tool for the correlation of nonmarine Triassic tetrapod assemblages independent of the marine timescale.
Triassic conodonts and their role in stage boundary definition
Authors: Orchard Michael J. 
Published: June 2010

Abstract

Conodonts have played an important role in the construction of a Triassic timescale. Each of the stage boundaries is reviewed in the context of their evolving conodont faunas. The base Triassic (Induan) is defined by the appearance of
Hindeodus parvus
, which developed from
H. praeparvus
; a parallel zonation is provided by
Neogondolella
species. For the Induan–Olenekian boundary, the appearance of
Neospathodus waageni sensu lato
within a plexus of similar species is favoured as the defining datum;
Borinella
and
Eurygnathodus
also appear about this time. The base of the Middle Triassic Anisian stage lies close to the appearance of
Chiosella
, with
Triassospathodus
and
Spathicuspus
characterizing the late Olenekian, and
Gladigondolella tethydis
and
Nicoraella
confined to the Anisian. Proxies for the Anisian–Ladinian boundary, which is defined by an ammonoid, are the first
Budurovignathus
species. The basal Carnian, also defined by an ammonoid, lies close to the first metapolygnathids, including
M. polygnathiformis
and
M. tadpole
. The Carnian–Norian boundary interval is characterized by many new taxa in Canada, but only a few species are common to Tethys, notably
Metapolygnathus
ex gr.
M. echinatus
. The Norian–Rhaetian boundary is likely to be based on evolution in
Misikella
in Tethys, with concurrent changes recognized in North American
Epigondolella
.
Triassic radiolarian biostratigraphy
Authors: O'Dogherty Luis , Carter Elizabeth S. , Goričan Špela , Dumitrica Paulian 
Published: June 2010

Abstract
This paper summarizes 30 years of research on the biostratigraphy of Triassic radiolarians and presents a correlation of currently-used radiolarian zonations established in North America, Europe, Japan and Far East Russia. An up-to-date stratigraphic distribution of all hitherto described and still valid Triassic genera is provided. This new range chart consists of 282 genera and allows an accurate dating to substage level. It also clearly manifests general trends in radiolarian evolution through the Triassic. The end-Permian extinction, the most severe extinction in the history of radiolarians, was followed by a long recovery until the early Anisian. The middle and late Anisian were then characterized by a rapid explosion of new morphologies. Maximum generic diversity was attained during the early Carnian, but the first severe extinctions also occurred in the Carnian. A progressive decline of diversity took place through the Norian and Rhaetian, and ended in a mass extinction around the Triassic–Jurassic boundary.
Atoh1 Inhibits Neuronal Differentiation and Collaborates with Gli1 to Generate Medulloblastoma-Initiating Cells
Authors: Ayrault Olivier , Zhao Haotian , Zindy Frederique , Qu Chunxu , Sherr Charles J. , Roussel Martine F. 
Published: June 2010

Abstract
The morphogen and mitogen Sonic Hedgehog (Shh) activates a Gli1-dependent transcription program that drives proliferation of granule neuron progenitors (GNP) within the external germinal layer of the postnatally developing cerebellum. Medulloblastomas with mutations activating the Shh signaling pathway preferentially arise within the external germinal layer, and the tumor cells closely resemble GNPs. Atoh1/Math1, a basic helix-loop-helix transcription factor essential for GNP histogenesis, does not induce medulloblastomas when expressed in primary mouse GNPs that are explanted from the early postnatal cerebellum and transplanted back into the brains of naïve mice. However, enforced expression of Atoh1 in primary GNPs enhances the oncogenicity of cells overexpressing Gli1 by almost three orders of magnitude. Unlike Gli1, Atoh1 cannot support GNP proliferation in the absence of Shh signaling and does not govern expression of canonical cell cycle genes. Instead, Atoh1 maintains GNPs in a Shh-responsive state by regulating genes that trigger neuronal differentiation, including many expressed in response to bone morphogenic protein-4. Therefore, by targeting multiple genes regulating the differentiation state of GNPs, Atoh1 collaborates with the pro-proliferative Gli1-dependent transcriptional program to influence medulloblastoma development. Cancer Res; 70(13); 5618–27. ©2010 AACR.
Calcium Intake Increases Risk of Prostate Cancer among Singapore Chinese
Authors: Butler Lesley M. , Wong Alvin S. , Koh Woon-Puay , Wang Renwei , Yuan Jian-Min , Yu Mimi C. 
Published: June 2010

AbstractConsumption of dairy products, the primary source of calcium in Western diets, has been found to be positively associated with prostate cancer. In an Asian diet, nondairy foods are the major contributors of calcium. Thus, a study of dietary calcium and prostate cancer in Asians can better inform on whether calcium, as opposed to other dairy components, is responsible for the dairy foods–prostate cancer association. We examined calcium intake and prostate cancer risk among 27,293 men in the Singapore Chinese Health Study that was established between 1993 and 1998. As of December 31, 2007, 298 incident prostate cancer cases had been diagnosed among the cohort members. Diet was assessed at baseline with a validated 165-item food-frequency questionnaire. It is hypothesized that there is greater net absorption of calcium in smaller individuals. Therefore, the calcium–prostate cancer association was also assessed in stratified analyses by median body mass index. Vegetables were the largest contributor of daily calcium intake in the study population. Overall, we observed a modest, statistically nonsignificant 25% increase in prostate cancer risk for the 4th (median = 659 mg/d) versus 1st (median = 211 mg/d) quartiles of calcium intake after adjustment for potential confounders. The association became considerably stronger and achieved statistical significance (hazard ratio, 2.03; 95% confidence interval, 1.23–3.34; P for trend = 0.01) for men with a below median body mass index (22.9 kg/m2). Dietary calcium might be a risk factor for prostate cancer even at relatively low intake. Cancer Res; 70(12); 4941–8. ©2010 AACR.
Interaction between Adiponectin and Leptin Influences the Risk of Colorectal Adenoma
Authors: Yamaji Taiki , Iwasaki Motoki , Sasazuki Shizuka , Tsugane Shoichiro 
Published: June 2010

Abstract
Obesity has been associated with an increased risk of colorectal neoplasia, but the mechanisms of this potential association have not been elucidated. We hypothesized that the adipokines adiponectin, leptin, and tumor necrosis factor-α (TNF-α) may mediate an association between obesity and colorectal cancer. We measured plasma concentrations of total and high-molecular-weight (HMW) adiponectin, leptin, and TNF-α in healthy volunteer examinees who underwent total colonoscopy between February 2004 and February 2005, and conducted a case-control study consisting of 778 cases and 735 controls. An inverse association of total and HMW adiponectin was observed with colorectal adenoma (P trend &lt; 0.001 and 0.03, respectively). Further, total adiponectin interacted with leptin, but not TNF-α, in relation to colorectal adenoma (P interaction = 0.007). An inverse association of total adiponectin with colorectal adenoma was apparent in the highest two tertiles of leptin, particularly the middle (P trend &lt; 0.001), whereas a positive association of leptin was obvious in the lowest tertile of total adiponectin (P trend = 0.01) after adjusting for potential confounders and body mass index, which is a major determinant of insulin resistance. Adiponectin may exert an anticarcinogenic effect on the large intestine by interfering with leptin, whereas leptin could conversely exert a carcinogenic effect under conditions of a lower abundance of adiponectin. Our findings provide the first epidemiologic evidence for interactive effects of adiponectin and leptin in the early stage of colorectal tumorigenesis, distinct from their involvement in insulin resistance. Cancer Res; 70(13); 5430–7. ©2010 AACR.
Complement Factor H Autoantibodies Are Associated with Early Stage NSCLC
Authors: Amornsiripanitch Nita , Hong Shaolin , Campa Michael J. , Frank Michael M. , Gottlin Elizabeth B. , Patz Edward F. 
Published: June 2010

Abstract
Purpose: To discover diagnostic biomarkers associated with early-stage non–small cell lung cancer (NSCLC), we searched for autoantibodies preferentially present in stage I patients compared with patients with advanced-stage disease. Here we describe an autoantibody against complement factor H (CFH) and this autoantibody's association with early-stage NSCLC.
Experimental Design: Immunoblots were used to detect autoantibodies in the sera of stage I NSCLC patients. An autoantibody recognizing a 150 kDa protein was discovered, and the protein was identified by mass spectrometry. The association of the autoantibody with early-stage disease was suggested by the results of immunoblot analysis with sera from 28 stage I patients and 28 stage III/IV patients. This association was confirmed by protein microarray of sera from 125 NSCLC patients of all stages as well as 125 controls matched by age, gender, and smoking history.
Results: The immunoreactive protein was identified as CFH. By immunoblot analysis, anti-CFH autoantibody was found in 50% of stage I NSCLC patients and 11% of late-stage NSCLC patients (P = 0.003). By protein microarray analysis, patients with stage I NSCLC had a significantly higher incidence of anti-CFH antibody than those with late-stage NSCLC (P = 0.0051). The percentage of sera with a positive level of CFH autoantibody was 30.4% in stage I, 21.1% in stage II, 12.5% in stage III, 7.4% in stage IV, and 8.0% in the control group.
Conclusions: These findings suggest that in patients with NSCLC, CFH autoantibody is a molecular marker associated with early-stage disease. Clin Cancer Res; 16(12); 3226–31. ©2010 AACR.
Butein Sensitizes Human Hepatoma Cells to TRAIL-Induced Apoptosis via Extracellular Signal-Regulated Kinase/Sp1–Dependent DR5 Upregulation and NF-κB Inactivation
Authors: Moon Dong-Oh , Kim Mun-Ock , Choi Yung Hyun , Kim Gi-Young 
Published: June 2010

Abstract
Tumor necrosis factor–related apoptosis-inducing ligand (TRAIL) induces cell death in various types of cancer cells but has little or no effect on normal cells. Human hepatoma cells are resistant to TRAIL-induced apoptosis. Although butein is known to mediate anticancer, anti-inflammatory, and antioxidant activities, little is known about the mechanism of butein in terms of TRAIL-induced apoptosis of human hepatoma cells. In this study, we determined that butein enhances TRAIL-induced apoptosis in hepatoma cells through upregulation of DR5. Luciferase analysis showed that a 5′-flanking region containing four Sp1-binding sites within the DR5 promoter was enhanced by butein (−305/−300). Electrophoretic mobility shift assays and chromatin immunoprecipitation studies were used to analyze the elevation of Sp1 binding to DR5 promoter sites by butein. Point mutations of the Sp1-binding site also attenuated promoter activity. Furthermore, pretreatment of the blocking chimeric antibody and small interfering RNA for DR5 significantly suppressed TRAIL-mediated apoptosis by butein in Hep3B cells. Butein also stimulated extracellular signal-regulated kinase (ERK) activation, and the ERK inhibitor PD98059 blocked butein-induced DR5 expression and suppressed binding of Sp1 to the DR5 promoter. Additionally, generation of reactive oxygen species had no effect on cell viability, although pretreatment with N-acetyl-l-cysteine or glutathione inhibited combined treatment-induced reactive oxygen species. Indeed, butein repressed the TRAIL-mediated activation of NF-κB and decreased its transcriptional activity. Our results suggest that butein could sensitize certain human hepatoma cells to TRAIL-induced apoptosis through stimulating its death signaling and by repressing the survival function in these cells. Mol Cancer Ther; 9(6); 1583–95. ©2010 AACR.
A Human Monoclonal Antibody against Insulin-Like Growth Factor-II Blocks the Growth of Human Hepatocellular Carcinoma Cell Lines In vitro and In vivo
Authors: Dransfield Daniel T. , Cohen Edward H. , Chang Qing , Sparrow Lindsay G. , Bentley John D. , Dolezal Olan , Xiao Xiaowen , Peat Thomas S. , Newman Janet , Pilling Patricia A. , Phan Tram , Priebe Ilka , Brierley Gemma V. , Kastrapeli Niksa , Kopacz Kris , Martik Diana , Wassaf Dina , Rank Douglas , Conley Greg , Huang Yan , Adams Timothy E. , Cosgrove Leah 
Published: June 2010

Abstract
Elevated expression of insulin-like growth factor-II (IGF-II) is frequently observed in a variety of human malignancies, including breast, colon, and liver cancer. As IGF-II can deliver a mitogenic signal through both IGF-IR and an alternately spliced form of the insulin receptor (IR-A), neutralizing the biological activity of this growth factor directly is a potential alternative option to IGF-IR–directed agents. Using a Fab-displaying phage library and a biotinylated precursor form of IGF-II (1–104 amino acids) as a target, we isolated Fabs specific for the E-domain COOH-terminal extension form of IGF-II and for mature IGF-II. One of these Fabs that bound to both forms of IGF-II was reformatted into a full-length IgG, expressed, purified, and subjected to further analysis. This antibody (DX-2647) displayed a very high affinity for IGF-II/IGF-IIE (KD value of 49 and 10 pmol/L, respectively) compared with IGF-I (∼10 nmol/L) and blocked binding of IGF-II to IGF-IR, IR-A, a panel of insulin-like growth factor–binding proteins, and the mannose-6-phosphate receptor. A crystal complex of the parental Fab of DX-2647 bound to IGF-II was resolved to 2.2 Å. DX-2647 inhibited IGF-II and, to a lesser extent, IGF-I–induced receptor tyrosine phosphorylation, cellular proliferation, and both anchorage-dependent and anchorage-independent colony formation in various cell lines. In addition, DX-2647 slowed tumor progression in the Hep3B xenograft model, causing decreased tumoral CD31 staining as well as reduced IGF-IIE and IGF-IR phosphorylation levels. Therefore, DX-2647 offers an alternative approach to targeting IGF-IR, blocking IGF-II signaling through both IGF-IR and IR-A. Mol Cancer Ther; 9(6); 1809–19. ©2010 AACR.
Early Changes in Gene Expression Induced by Tobacco Smoke: Evidence for the Importance of Estrogen within Lung Tissue
Authors: Meireles Sibele I. , Esteves Gustavo H. , Hirata Roberto , Peri Suraj , Devarajan Karthik , Slifker Michael , Mosier Stacy L. , Peng Jing , Vadhanam Manicka V. , Hurst Harrell E. , Neves E. Jordao , Reis Luiz F. , Gairola C. Gary , Gupta Ramesh C. , Clapper Margie L. 
Published: June 2010

AbstractLung cancer is the leading cause of cancer deaths in the United States, surpassing breast cancer as the primary cause of cancer-related mortality in women. The goal of the present study was to identify early molecular changes in the lung induced by exposure to tobacco smoke and thus identify potential targets for chemoprevention. Female A/J mice were exposed to either tobacco smoke or HEPA-filtered air via a whole-body exposure chamber (6 h/d, 5 d/wk for 3, 8, and 20 weeks). Gene expression profiles of lung tissue from control and smoke-exposed animals were established using a 15K cDNA microarray. Cytochrome P450 1b1, a phase I enzyme involved in both the metabolism of xenobiotics and the 4-hydroxylation of 17β-estradiol (E2), was modulated to the greatest extent following smoke exposure. A panel of 10 genes were found to be differentially expressed in control and smoke-exposed lung tissues at 3, 8, and 20 weeks (P &lt; 0.001). The interaction network of these differentially expressed genes revealed new pathways modulated by short-term smoke exposure, including estrogen metabolism. In addition, E2 was detected within murine lung tissue by gas chromatography-coupled mass spectrometry and immunohistochemistry. Identification of the early molecular events that contribute to lung tumor formation is anticipated to lead to the development of promising targeted chemopreventive therapies. In conclusion, the presence of E2 within lung tissue when combined with the modulation of cytochrome P450 1b1 and other estrogen metabolism genes by tobacco smoke provides novel insight into a possible role for estrogens in lung cancer. Cancer Prev Res; 3(6); 707–17. ©2010 AACR.
Early Changes in Pulmonary Gene Expression following Tobacco Exposure Shed Light on the Role of Estrogen Metabolism in Lung Carcinogenesis
Authors: Siegfried Jill M. 
Published: June 2010

Abstract
This perspective on Meireles et al. (beginning on p. 707 in this issue of the journal) discusses the increasing evidence for the role of female steroid hormones in lung cancer development and progression. The novel work of Meireles et al. is the first evidence for the rapid upregulation by tobacco smoke of a key cytochrome P450 gene that can metabolize estrogens such as β-estradiol to potentially carcinogenic catechol and quinine forms, as well as the first evidence for the colocalization of β-estradiol and estrogen receptors in murine airway epithelium. Actions of estrogens that contribute to lung carcinogenesis, especially in the presence of tobacco smoke, may involve both reactive intermediates that damage DNA and steroid hormone receptor signaling that promotes growth. Cancer Prev Res; 3(6); 692–5. ©2010 AACR.