bluuebunny/crossref_metadata_2025_split huggingface dataset:
Prevalence of BRCA1 and BRCA2 mutations in Pakistani breast and ovarian cancer patients
Authors: Rashid Muhammad U. , Zaidi Anbreen , Torres Diana , Sultan Faisal , Benner Axel , Naqvi Bilal , Shakoori Abdul R. , Seidel‐Renkert Antje , Farooq Humirah , Narod Steven , Amin Asim , Hamann Ute 
Published: September 2006

AbstractAmong Asian countries, Pakistan has the highest rates of breast and ovarian cancer. To assess the contribution of the BRCA1 and BRCA2 germ line mutations to these high rates, we conducted the first study of 176 Pakistani breast and ovarian cancer patients, selected on family history and on age of diagnosis. Comprehensive BRCA mutation screening was performed using a range of techniques, including denaturing high‐pressure liquid chromatography, single strand conformational polymorphism analysis and protein truncation test, followed by DNA sequencing. Thirty deleterious germ‐line mutations were identified in the 176 families (17.0%), including 23 in BRCA1 and 7 in BRCA2. Four mutations, 185delAG, 185insA, S1503X and R1835X, were recurrent; these accounted for 52% of all identified BRCA1 mutations. Haplotype analyses suggested founder effects for 3 of these. The prevalence of BRCA1 or BRCA2 mutations was 42.8% for families with multiple cases of breast cancer, and was 50.0% for the breast/ovarian cancer families. The prevalence of mutations was 11.9% for single cases of early‐onset breast cancer (≤30 years) and was 9.0% for single cases of early‐onset ovarian cancer (≤45 years). Our findings show that BRCA mutations account for a substantial proportion of hereditary breast/ovarian cancer and early‐onset breast and ovarian cancer cases in Pakistan. © 2006 Wiley‐Liss, Inc.
Oligopeptides impairing the Myc‐Max heterodimerization inhibit lung cancer cell proliferation by reducing Myc transcriptional activity
Authors: D'Agnano Igea , Valentini Alessandra , Gatti Giuliana , Chersi Alberto , Felsani Armando 
Published: September 2006

AbstractDeregulated CMYC gene causes cell transformation and is often correlated with tumor progression and a worse clinical outcome of cancer patients. The transcription factor Myc functions by heterodimerizing with its partner, Max. As a strategy to inhibit Myc activity, we have synthesized three small peptides corresponding to segments of the leucine zipper (LZ) region of Max. The purpose of these peptides is to occupy the site of recognition between Myc and Max located in the LZ and inhibit‐specific heterodimerization between these proteins. We have used the synthesized oligopeptides in two lung cancer cell lines with different levels of Myc expression. Results demonstrate that: (i) the three peptides resulted equally effective in competing the interaction between Myc and Max in vitro; (ii) they were efficiently internalized into the cells and significantly inhibited cell growth in the cells showing the highest Myc expression; (iii) one specific peptide, only nine aminoacids long, efficiently impaired the transcriptional activity of Myc in vivo, showing a more stable interaction with this protein. Our results are relevant to the development of novel anti‐tumoral therapeutic strategies, directed to Myc‐overexpressing tumors. J. Cell. Physiol. 210: 72–80, 2007. © 2006 Wiley‐Liss, Inc.
Methotrexate‐induced mucositis in mucin 2‐deficient mice
Authors: de Koning Barbara A.E. , Sluis Maria van der , Lindenbergh‐Kortleve Dicky J. , Velcich Anna , Pieters Rob , Büller Hans A. , Einerhand Alexandra W.C. , Renes Ingrid B. 
Published: September 2006

AbstractThe mucin Muc2 or Mycin2 (Muc2), which is the main structural component of the protective mucus layer, has shown to be upregulated during chemotherapy‐induced mucositis. As Muc2 has shown to have protective capacities, upregulation of Muc2 may be a counter reaction of the intestine protecting against mucositis. Therefore, increasing Muc2 protein levels could be a therapeutic target in mucositis prevention or reduction. Our aim was to determine the role of Muc2 in chemotherapy‐induced mucositis. Mucositis was induced in Muc2 knockout (Muc2−/−) and wild type (Muc2+/+) mice by injecting methotrexate (MTX). Animals were weighed and sacrificed on Days 2–6 after MTX treatment and jejunal segments were analyzed. Before MTX treatment, the small intestine of Muc2+/+ and Muc2−/− mice were similar with respect to epithelial morphology and proliferation. Moreover, sucrase‐isomaltase and trefoil factor‐3 protein expression levels were comparable between Muc2+/+ and Muc2−/− mice. Up to Day 3 after MTX treatment, percentages of weight‐loss did not differ. Thereafter, Muc2+/+ mice showed a trend towards regaining weight, whereas Muc2−/− mice continued to lose weight. Surprisingly, MTX‐induced intestinal damage of Muc2−/− and Muc2+/+ mice was comparable. Prior to MTX‐injection, tumor necrosis factor‐α and interleukin‐10 mRNAs were upregulated in Muc2−/− mice, probably due to continuous exposure of the intestine to luminal antigens. Muc2 deficiency does not lead to an increase in chemotherapy‐induced mucositis. A possible explanation is the mechanism by which Muc2 deficiency may trigger the immune system to release interleukin‐10, an anti‐inflammatory cytokine before MTX‐treatment. J. Cell. Physiol. 210: 144–152, 2007. © 2006 Wiley‐Liss, Inc.
Exogenous expression of claudin‐5 induces barrier properties in cultured rat brain capillary endothelial cells
Authors: Ohtsuki Sumio , Sato Saori , Yamaguchi Hirofumi , Kamoi Mayu , Asashima Tomoko , Terasaki Tetsuya 
Published: September 2006

AbstractClaudins are thought to be major components of tight junctions (TJs), and claudin‐5 and ‐12 are localized at TJs of the blood‐brain barrier (BBB). Claudin‐5‐deficient mice exhibit size‐selective (<800 Da) opening of the BBB. The purpose of this study was to clarify the expression levels of claudin‐5 and ‐12 in rat brain capillary endothelial cells, and to examine the ability of claudin‐5 to form TJs in cultured rat brain capillary endothelial cells (TR‐BBB). Expression of claudin‐5 mRNA in rat brain capillary fraction was 751‐fold greater than that of claudin‐12. The level of claudin‐5 mRNA in the rat brain capillary fraction (per total mRNA) was 35.6‐fold greater than that in whole brain, while the level of claudin‐12 mRNA was only 13.9% of that in whole brain, suggesting that expression of claudin‐12 mRNA is not restricted to brain capillaries. Transfection of TR‐BBB cells with the claudin‐5 gene afforded TR‐BBB/CLD5 cells, which showed no change in expression of claudin‐12 or ZO‐1, while the expressed claudin‐5 was detected at the cell–cell boundaries. The permeability surface product of [14C]inulin at a TR‐BBB/CLD5 cell monolayer was significantly smaller (P < 0.01) than that for the parental TR‐BBB cells, and the values of the permeability coefficient (Pe) were 1.14 × 10−3 and 11.6 × 10−3 cm/min, respectively. These results indicate that claudin‐5, but not claudin‐12, is predominantly expressed in brain capillaries, and plays a key role in the appearance of barrier properties of brain capillary endothelial cells. J. Cell. Physiol. 210: 81–86, 2007. © 2006 Wiley‐Liss, Inc.
The role of p63 in germ cell apoptosis in the developing testis
Authors: Petre‐Lazar Bétrice , Livera Gabriel , Moreno Stéphanie G. , Trautmann Emilie , Duquenne Clotilde , Hanoux Vincent , Habert René , Coffigny Hervé 
Published: September 2006

AbstractThe fetal and neonatal development of male germ cells (gonocytes) is a poorly understood but crucial process for establishing fertility. In rodents, gonocytes go through two phases of proliferation accompanied by apoptosis and separated by a quiescent period during the end of fetal development. P63 is a member of the P53 gene family that yields six isoforms. We detected only the p63 protein and no p53 and p73 in the nucleus of the gonocytes of mouse testes. We report for the first time the ontogeny of each p63 mRNA isoform during testis development. We observed a strong expression of p63γ mRNA and protein when gonocytes are in the quiescent period. In vitro treatment with retinoic acid prevented gonocytes from entering the quiescent period and was correlated with a reduced production of p63γ isoform mRNA. We investigated the function of p63 by studying the testicular phenotype of P63‐null mice. P63 invalidation slightly, but significantly increased the number of gonocytes counted during the quiescent period. As P63‐null animals die at birth we used an original organ culture that mimicked neonatal in vivo development to study further the testicular development. P63 invalidation resulted in a sharply increased number of gonocytes during the culture period due to a decrease in spontaneous apoptosis with no change in proliferation. P63 invalidation also caused abnormal morphologies in the germ cells that were also found in P63+/− adult male mice. Thus, p63 appears as an important regulator of germ cell development. J. Cell. Physiol. 210: 87–98, 2007. © 2006 Wiley‐Liss, Inc.
SIRT1 interacts with p73 and suppresses p73‐dependent transcriptional activity
Authors: Dai Jin Ming , Wang Zhi Yan , Sun Dao Chun , Lin Ru Xian , Wang Sheng Qi 
Published: September 2006

AbstractThe tumor suppressor p53‐related p73 shares significant amino‐acid sequence identity with p53. Like p53, p73 recognizes canonical p53 DNA‐binding sites and activates p53‐responsive target genes and induces apoptosis. Moreover, SIRT1 binds to p53 while repressing the expression of their target genes. Here, we report that SIRT1 also binds to p73 and suppresses p73‐dependent transcriptional activity. SIRT1 in human cells reduces the transcriptional activity of p73, and partly inhibits apoptosis induced by p73. Furthermore, SIRT1 can deacetylate p73 protein acetylation both in vivo and in vitro. Collectively, these data suggest that SIRT1 can modulate p73 activity via deacetylation. J. Cell. Physiol. 210: 161–166, 2007. © 2006 Wiley‐Liss, Inc.
ERK1/2 regulates two sequential steps promoting monocyte survival to peroxynitrite
Authors: Cerioni L. , Cantoni O. 
Published: September 2006

AbstractPrevious studies from our laboratory indicate that cytosolic phospholipase A2 (cPLA2)‐released arachidonic acid promotes monocyte/macrophage survival in the presence of peroxynitrite. In particular, the lipid messenger is metabolised by 5‐lipoxygenase (5‐LO) to 5‐hydroxyeicosatetraenoic acid and causes the mitochondrial translocation of protein kinase Cα (PKCα), an event associated with the cytosolic accumulation of Bad and Bax. Here we show that phosphorylation reactions driven by extracellular regulated kinase 1/2 (ERK1/2) critically regulate the activation/nuclear translocation of 5‐LO. Inhibition of ERK1/2 was invariably associated with the cytosolic localisation of PKCα, the mitochondrial accumulation of Bad and Bax and with a rapid mitochondrial permeability transition‐dependent necrosis. All these events were prevented by nanomolar concentrations of 5‐hydroxyeicosatetraenoic acid. Hence, in addition to the previously characterised effects on cPLA2, ERK1/2 critically regulates 5‐LO activity in the absence of additional downstream targets in the survival signalling preventing peroxynitrite toxicity. J. Cell. Physiol. 210: 177–182, 2007. © 2006 Wiley‐Liss, Inc.
Stretch‐activated signaling pathways responsible for early response gene expression in fetal lung epithelial cells
Authors: Copland Ian B. , Post Martin 
Published: September 2006

AbstractHigh‐tidal volume ventilation has been shown to increase the expression of several inflammation‐associated genes prior to overt physiologic lung injury. Herein, using an in vitro stretch system, we investigated the mechanotransduction pathways involved in ventilation‐induced expression of these early response genes (i.e., early growth response gene (Egr)1, heat‐shock protein (HSP)70, and the pro‐inflammatory cytokines interleukin (IL)‐1β, IL‐6, and MIP‐2). Mechanical stretch of fetal lung epithelial cells activated various signaling pathways, resulting in transient or progressive increases in gene expression of the early response genes. The transient increase in Egr1 and IL‐6 expression was mediated via p44/42 mitogen‐activated protein kinase (p44/42 MAPK), while nuclear factor‐kappaB (NF‐κB) was responsible for the sustained and progressive increase in expression of HSP70 and MIP‐2. Blockage of Egr‐1 expression did not affect the upregulation of IL‐6, HSP70, MIP‐2, and itself by stretch. Inhibition of calcium mobilization abolished stretch‐induced p44/42 MAPK activation and NF‐κB nuclear translocation as well as increased expression of all early response genes. Similar results were obtained with an inhibitor of Ras. These results suggest that mechanical stretch of fetal lung epithelial cells evokes a complex network of signaling molecules, which diverge downstream to regulate the temporal expression of a unique set of early response genes, but upstream converge at calcium. Thus, calcium mobilization may be a point of hierarchical integration of mechanotransduction in lung epithelial cells. J. Cell. Physiol. 210: 133–143, 2007. © 2006 Wiley‐Liss, Inc.
Characterization of thromboxane A2 receptor signaling in developing rat oligodendrocytes: Nuclear receptor localization and stimulation of myelin basic protein expression
Authors: Ramamurthy Santosh , Mir Fozia , Gould Robert M. , Breton Guy C. Le 
Published: September 2006

AbstractThe present work investigates the role of thromboxane A2 (TXA2) receptors in the development of oligodendrocytes (OLGs). The results demonstrate that the proteins of the TXA2 signaling pathway, i.e., cyclooxygenase (COX‐1), TXA2 synthase (TS), and TXA2 receptor (TPR) are expressed in the developing rat brain during myelination. Furthermore, culture of OLG progenitor cells (OPCs) revealed that the expression levels of these proteins as well as TXA2 synthesis increase during OLG maturation. Separate studies established that activation of TPRs by the agonist U46619 increases intracellular calcium in both OPCs and OLGs as visualized by digital fluorescence imaging. Immunocytochemical staining demonstrated that TPRs are localized in the plasma membrane and perinuclear compartments in OPCs. However, during OLG differentiation, TPRs shift their localization pattern and also become associated with the nuclear compartment. This shift to nuclear localization was confirmed by biochemical analysis in cultured cells and by immunocytochemical analysis in developing rat brain. Finally, it was found that U46619 activation of TPRs in maturing OLGs resulted in enhanced myelin basic protein (MBP) expression. Alternatively, inhibition of endogenous TPR signaling led to reduced MBP expression. Furthermore, TPR‐mediated MBP expression was found to be associated with increased transcription from the MBP promoter using a MBP‐luciferase reporter. Collectively, these findings suggest a novel TPR signaling pathway in OLGs and a potential role for this signaling during OLG maturation and myelin production. © 2006 Wiley‐Liss, Inc.
Positioned to inhibit: Netrin‐1 and netrin receptor expression after spinal cord injury
Authors: Manitt Colleen , Wang David , Kennedy Timothy E. , Howland Dena R. 
Published: September 2006

AbstractNetrin‐1 regulates axon extension during embryonic development and is expressed by neurons and myelinating oligodendrocytes in the adult CNS. To investigate the potential role of netrin‐1 after spinal cord injury, we examined the expression of netrin‐1 and netrin receptors after sagittal myelotomy in adult rats. This lesion targets spinal commissural projections, which respond to netrin‐1 during development. Netrin‐1 mRNA and protein levels were dramatically reduced at the site of injury and reduced expression persisted for at least 7 months. Neither netrin‐1 protein nor mRNA was associated with the glial scar, but netrin‐1 was expressed by neurons and oligodendrocytes immediately adjacent to the lesion. The post‐injury distribution detected is similar to that reported for myelin‐associated inhibitors of axon regeneration, such as Nogo, and is distinct from the distribution of inhibitors associated with a glial scar. DCC and UNC‐5 homologue (UNC5H) expression also was reduced after injury. Although UNC5H levels recovered, DCC expression at the site of injury remained ∼50% of pre‐injury values at 7 months. Increased UNC5H immunoreactivity was associated with fibers in the superficial layers of the dorsal horn and in fibers located in white matter adjacent to the lesion. The dominant expression of UNC5H on axons and neurons in the spinal cord after injury and the persistent expression of netrin‐1 by oligodendrocytes surrounding the lesion are consistent with the hypothesis that netrin‐1 is a myelin‐associated inhibitor of axonal regeneration after spinal cord injury. © 2006 Wiley‐Liss, Inc.
Locus of control at work: a meta‐analysis
Authors: Ng Thomas W. H. , Sorensen Kelly L. , Eby Lillian T. 
Published: September 2006

AbstractThis study meta‐analyzed the relationships between locus of control (LOC) and a wide range of work outcomes. We categorized these outcomes according to three theoretical perspectives: LOC and well‐being, LOC and motivation, and LOC and behavioral orientation. Hypotheses reflecting these three perspectives were proposed and tested. It was found that internal locus was positively associated with favorable work outcomes, such as positive task and social experiences, and greater job motivation. Our findings are discussed in relation to research on core self‐evaluation and the Big Five personality traits. Copyright © 2006 John Wiley & Sons, Ltd.
Maximizing returns on mentoring: factors affecting subsequent protégé performance
Authors: Tonidandel Scott , Avery Derek R. , Phillips McKensy G. 
Published: September 2006

AbstractThis study examined the effects of mentor success, relationship duration, and the amount of mentoring received on protégés' performance after the supervisory mentoring relationship had ended. Data collected from former protégés paired with objective measures of performance indicated that a mentor's success moderated the impact of mentoring functions received on subsequent protégé success. Additionally, the strength of these relationships depended on the length of the mentoring relationship. The present study suggests more emphasis should be placed on the capabilities of the mentor. Copyright © 2006 John Wiley & Sons, Ltd.
High‐temperature Raman spectroscopy of monohydrated L‐asparagine:Cr3+
Authors: Bento I. C. V. , Freire P. T. C. , Bento R. R. F. , Lemos V. , Melo F. E. A. , Filho J. Mendes , Pizani P. S. , Moreno A. J. D. 
Published: September 2006

AbstractRaman scattering of L‐asparagine:Cr3+ was studied over the complete range of wavenumbers at temperatures from ambient to ∼410 K. A qualitative change in the spectrum occurs when the temperature approaches 400 K. In the region of the spectrum corresponding to lattice vibrations of the crystal some bands disappear, as they do in the intermediate range of wavenumbers 200 cm−1 < ν < 1000 cm−1, where some new peaks also appear. Similar changes also occur in the highest spectral region, for wavenumbers >3000 cm−1, which is associated with water molecule vibrations. The changes indicate a modification of the crystal structure with irreversible loss of water molecules during the heating process. Copyright © 2006 John Wiley & Sons, Ltd.
Raman scattering study of molecules adsorbed on ZnS nanocrystals
Authors: Wang Yanfei , Sun Zhihua , Hu Hailong , Jing Shengyu , Zhao Bing , Xu Weiqing , Zhao Chun , Lombardi John R. 
Published: September 2006

AbstractThe adsorption of 4‐mercaptopyridine (4‐Mpy) molecules on ZnS nanocrystals was investigated by means of Raman spectroscopy. We compared the Raman signals of 4‐Mpy molecules adsorbed on ZnS nanocrystals and Ag substrate. The differences in the adsorption of 4‐Mpy molecules on the semiconductor and the metal substrate were noted. The results demonstrated that adsorbed species on the semiconductor ZnS nanocrystals can be detected by Raman spectroscopy. Copyright © 2006 John Wiley & Sons, Ltd.
Thermal micro‐Raman spectroscopic study of polymorphic transformation of famotidine under different compression pressures
Authors: Lin Shan‐Yang , Cheng Wen‐Ting , Wang Shun‐Li 
Published: September 2006

AbstractThe objective of this study was to investigate the effect of pressure and/or temperature on the polymorphic transformation of famotidine from form B to form A by using a thermal confocal Raman microspectroscopy. A compact with a wide transparent zone in the center and an opaque zone surrounding it was prepared by compressing a conical mass of famotidine form B. Two unique Raman peaks at 2897 and 2920 cm−1 for famotidine forms B and A, respectively, were used as markers. The result indicates that the opaque zone in each compact was composed of famotidine from B, and it did not undergo any polymorphic transformation by preparing with higher compression pressure and/or by heating. The Raman peak intensity ratio of the 2920 cm−1 and 2897 cm−1 bands markedly increased starting from 120 °C for the transparent zone prepared by compressing with 19.61 × 104 kPa pressure, but increased from 100 °C with 49.03 × 104 kPa pressure, indicating the occurrence of thermally induced polymorphic transformation of famotidine from form B to form A. However, the transparent zone prepared by 9.81 × 104 kPa compression pressure retained the same Raman spectrum as that of the famotidine form B, revealing that the thermally induced polymorphic transformation of famotidine was dependent on the pressure applied. There was no polymorphic transformation of famotidine in the transparent zone when it was prepared by a higher compression pressure at a lower temperature or by a lower pressure at a higher temperature. The combined effect of compression and temperature was found to accelerate the polymorphic transformation from form B to form A in the transparent zone of famotidine. Copyright © 2006 John Wiley & Sons, Ltd.
The hydrates and deuterates of ferrous sulfate (FeSO4): a Raman spectroscopic study
Authors: Chio Chi Hong , Sharma Shiv K. , Muenow David W. 
Published: September 2006

AbstractA comparative analysis has been carried out on the Raman spectra of FeSO4·nH2O (n = 1, 4, 7) including the 2D‐analogs. The effects of changing the degrees of hydration have been found from the lattice, SO42− internal, and H2O internal modes. Increasing degrees of hydration shift the intense ν1(SO4) peak to lower wavenumbers and reduce the amount of splitting on the ν3(SO4) peaks. Some of the water librational bands cause the broadening of the ν4(SO4) peaks in FeSO4·7H2O and the ν2(SO4) peaks in FeSO4·7D2O. The ν2(H2O) band in FeSO4·H2O is red‐shifted in excess of 100 cm−1 relative to the unperturbed H2O band. Between 240 and 190 K and between 140 and 90 K in the spectra of FeSO4.4H2O, two potential phase transitions have been identified from the changes in the lattice and water‐stretching regions. The resolution of the ν1(H2O) and ν3(H2O) bands in FeSO4·4H2O and FeSO4·H2O also improved sharply at low temperatures. The capability of distinguishing various forms of FeSO4 hydrates unambiguously makes the Raman technique a potential analytical tool for the identification of sulfate minerals on planetary surfaces. Copyright © 2006 John Wiley & Sons, Ltd.