bluuebunny/crossref_metadata_2025_split huggingface dataset:
Osteotome sinus floor elevation technique without grafting material: 3‐year results of a prospective pilot study
Authors: Nedir Rabah , Bischof Mark , Vazquez Lydia , Nurdin Nathalie , Szmukler‐Moncler Serge , Bernard Jean‐Pierre 
Published: March 2009

AbstractObjective: In a prospective pilot study, short≤10 mm ITI‐SLA implants were placed in the resorbed posterior maxilla by means of an osteotome sinus floor elevation (OSFE) procedure without grafting material. This paper presents 3‐year data assessing bone‐level changes around implants.Material and methods: Twenty‐five implants were placed in 17 patients to rehabilitate 16 molar and nine premolar sites. The mean residual bone height (RBH) was 5.4 ± 2.3 mm. A healing period of 3–4 months was allowed before abutment tightening. Most implants (21/25) were 10 mm long, and the others were 8 and 6 mm long. At the 3‐year control, endo‐sinus bone gain, implant length protruding into the sinus and crestal bone loss (CBL) were measured on periapical radiographs.Results: All implants fulfilled the survival criteria. Despite the absence of grafting material, implants were embedded into newly formed bone tissue. All implants gained endo‐sinus bone; the mean gained bone was 3.1 ± 1.5 mm. The residual protrusion length decreased from 4.9 ± 2.1 to 1.8 ± 2.1 mm. CBL was 0.9 ± 0.8 mm.Conclusions: This study confirms that the OSFE procedure without grafting material is sufficient to create bone beyond the natural limit of the sinus. On the mid‐term of 3 years, the technique was found to be predictable in the posterior maxilla when the RBH is limited. Implants gained endo‐sinus bone despite the lack of grafting material. Bone gain was still improving over the first‐year control. No shrinkage of the augmented area was observed.
Investigations of Free Anthraquinones from Rhubarb Against α‐Naphthylisothiocyanate‐induced Cholestatic Liver Injury in Rats
Authors: Zhao Yan‐Ling , Wang Jia‐Bo , Zhou Guang‐De , Shan Li‐Mei , Xiao Xiao‐He 
Published: March 2009

Abstract: The protective effects of anthraquinones from Rhubarb, a Chinese herbal medicine, consisting of the root and rhizome ofRheum palmatumL.,R. tanguticum Maxim. Ex Balf., or R. officinale Baill.(family Polygonaceae) were investigated and compared in rats with liver injury induced by α‐naphthylisothiocyanate. α‐Naphthylisothiocyanate was given intragastrically in rats, liver injury with cholestasis developed within 36 hrs, as indicated by characteristic serum levels of glutamate‐pyruvate transaminase, glutamic oxaloacetic transaminase, total bilirubin, direct bilirubin, alkaline phosphatase, γ‐glutamyltransferase and total bile acid. The intragastrical administration of rhein, aloe‐emodin and physione to α‐naphthylisothiocyanate‐treated rats reduced significantly the serum level of both glutamate‐pyruvate transaminase, glutamic oxaloacetic transaminase and the serum total bilirubin, direct bilirubin, alkaline phosphatase, γ‐glutamyltransferase and total bile acid. For all hepatic biochemical markers and cholestasis index, rhein was most efficient. By comparison, the administration of emodin and chrysophanol did not reduce the serum levels of hepatic enzymes glutamate‐pyruvate transaminase and glutamic oxaloacetic transaminase but decreased the levels of serum total bilirubin, direct bilirubin, alkaline phosphatase, γ‐glutamyltransferase, and total bile acid, showing their partial protective effects on cholestatic liver injury. The liver in α‐naphthylisothiocyanate‐treated rats showed cholangiolitic hepatitis characterized by intrahepatic cholestasis, necrosis of hepatocytes and biliary epithelial cells and bile obstruction. The concurrent intragastrical administration of rhein reduced the severity of all morphological alteration, especially the neutrophil infiltration and sinusoid congestion. Rhein, aloe‐emodin, and physione all exhibited protective effects on hepatocytes and cholangiocytes against α‐naphthylisothiocyanate‐induced damage, whereas emodin and chrystophanol provided partial protection.
Molecular evolution of Na+ channels in teleost fishes
Authors: ZAKON Harold H. , JOST Manda C. , ZWICKL Derrick J. , LU Ying , HILLIS David M. 
Published: March 2009

AbstractVoltage‐dependent sodium channels are critical for electrical excitability. Invertebrates possess a single sodium channel gene; two rounds of genome duplication early in vertebrates increased the number to four. Since the teleost‐tetrapod split, independent gene duplications in each lineage have further increased the number of sodium channel genes to 10 in tetrapods and 8 in teleosts. Here we review how the occurrence of multiple sodium channel paralogs has influenced the evolutionary history of three groups of fishes: pufferfish, gymnotiform and mormyriform electric fish. Pufferfish (tetraodontidae) produce a neurotoxin, tetrodotoxin, that binds to and blocks the pore of sodium channels. Pufferfish evolved resistance to their own toxins by amino acid substitutions in the pore of their sodium channels. These substitutions had to occur in parallel across multiple paralogs for organismal resistance to evolve. Gymnotiform and mormyriform fishes independently evolved electric organs to generate electricity for communication and object localization. Two sodium channel genes are expressed in muscle in most fishes. In both groups of weakly electric fishes, one gene lost its expression in muscle and became compartmentalized in the evolutionary novel electric organ, which is a muscle derivative. This gene then evolved at elevated rates, whereas the gene that is still expressed in muscle does not show elevated rates of evolution. In the electric organ‐expressing gene, amino acid substitutions occur in parts of the channel involved in determining how long the channel will be open or closed. The enhanced rate of sequence evolution of this gene likely underlies the species‐level variations in the electric signal.
Differentially expressed genes identified by cross‐species microarray in the blind cavefish Astyanax
Authors: STRICKLER Allen G. , JEFFERY William R. 
Published: March 2009

AbstractChanges in gene expression were examined by microarray analysis during development of the eyed surface dwelling (surface fish) and blind cave‐dwelling (cavefish) forms of the teleost Astyanax mexicanus De Filippi, 1853. The cross‐species microarray used surface and cavefish RNA hybridized to a DNA chip prepared from a closely related species, the zebrafish Danio rerio Hamilton, 1822. We identified a total of 67 differentially expressed probe sets at three days post‐fertilization: six upregulated and 61 downregulated in cavefish relative to surface fish. Many of these genes function either in eye development and/or maintenance, or in programmed cell death. The upregulated probe set showing the highest mean fold change was similar to the human ubiquitin specific protease 53 gene. The downregulated probe sets showing some of the highest fold changes corresponded to genes with roles in eye development, including those encoding gamma crystallins, the guanine nucleotide binding proteins Gnat1 and Gant2, a BarH‐like homeodomain transcription factor, and rhodopsin. Downregulation of gamma‐crystallin and rhodopsin was confirmed by in situ hybridization and immunostaining with specific antibodies. Additional downregulated genes encode molecules that inhibit or activate programmed cell death. The results suggest that cross‐species microarray can be used for identifying differentially expressed genes in cavefish, that many of these genes might be involved in eye degeneration via apoptotic processes, and that more genes are downregulated than upregulated in cavefish, consistent with the predominance of morphological losses over gains during regressive evolution.
Doing Culture with Girls Like Me: Why Trying on Gender and Intersectionality Matters
Authors: Williams L. Susan 
Published: March 2009

AbstractGendering is not a one‐size‐fits‐all process. Girls try on gender. In particular, girls – conditioned to value connections – search their cultural surroundings for ‘girls like me’ to answer the weighty question, Who am I? However, girls are not simply passive beneficiaries of culture, but actively construct their gendered selves by engaging in or ‘doing’ culture; girls activate certain features salient to their experiences. This paper examines how race, ethnicity, and class arbitrate girls’ gendered identities, emphasizing the concept trying on gender to capture the intersectional and experimental character of these processes. As girls try on gender –a local and culturally specific endeavor – they engage in a fluid, multifaceted, and sometimes tentative gendering process. Cross‐over literature by and for girls lends empirical support to how girls accomplish this multi‐constructed sense of self. The article concludes with implications for studies of girls, including a cautionary note about overemphasis on individualistic agency.
Basic Challenges to Prisoner Reentry
Authors: Anderson‐Facile Doreen 
Published: March 2009

AbstractCrime, incarceration and prisoner reintegration are pressing issues facing the United States today. The U.S. prison population has increased from 330,000 in 1980 to over 2.2 million prisoners today. As the prison population grows at record rates so, in turn, does the reentry of prisoners into society. Currently, around 700,000 prisoners are released each year from custody and reenter society – nearly 2,000 inmates per day. The transition from prison to the outside world is often difficult for post‐release prisoners, their families, their communities and the larger society. Many formally incarcerated individuals do not have the skills or support to succeed outside prison walls. Unfortunately, when post‐release prisoners are not successfully reintegrated, they are returned to prison and begin the cycle of incarceration.Practitioners and academics agree that the main components for successful reentry include proper housing, viable employment, and family and community support. However, while there is consensus regarding what post‐release prisoners need for successful reentry there is debate as to which programs and policies work best. This paper examines the basic challenges to reentry and provides a brief summary of the problems with reentry program evaluation.
Bicarbonate Increases Tumor pH and Inhibits Spontaneous Metastases
Authors: Robey Ian F. , Baggett Brenda K. , Kirkpatrick Nathaniel D. , Roe Denise J. , Dosescu Julie , Sloane Bonnie F. , Hashim Arig Ibrahim , Morse David L. , Raghunand Natarajan , Gatenby Robert A. , Gillies Robert J. 
Published: March 2009

Abstract
The external pH of solid tumors is acidic as a consequence of increased metabolism of glucose and poor perfusion. Acid pH has been shown to stimulate tumor cell invasion and metastasis in vitro and in cells before tail vein injection in vivo. The present study investigates whether inhibition of this tumor acidity will reduce the incidence of in vivo metastases. Here, we show that oral NaHCO3 selectively increased the pH of tumors and reduced the formation of spontaneous metastases in mouse models of metastatic breast cancer. This treatment regimen was shown to significantly increase the extracellular pH, but not the intracellular pH, of tumors by 31P magnetic resonance spectroscopy and the export of acid from growing tumors by fluorescence microscopy of tumors grown in window chambers. NaHCO3 therapy also reduced the rate of lymph node involvement, yet did not affect the levels of circulating tumor cells, suggesting that reduced organ metastases were not due to increased intravasation. In contrast, NaHCO3 therapy significantly reduced the formation of hepatic metastases following intrasplenic injection, suggesting that it did inhibit extravasation and colonization. In tail vein injections of alternative cancer models, bicarbonate had mixed results, inhibiting the formation of metastases from PC3M prostate cancer cells, but not those of B16 melanoma. Although the mechanism of this therapy is not known with certainty, low pH was shown to increase the release of active cathepsin B, an important matrix remodeling protease. [Cancer Res 2009;69(6):2260–8]
Epidermal Growth Factor Receptor and PTEN Modulate Tissue Factor Expression in Glioblastoma through JunD/Activator Protein-1 Transcriptional Activity
Authors: Rong Yuan , Belozerov Vladimir E. , Tucker-Burden Carol , Chen Gang , Durden Donald L. , Olson Jeffrey J. , Van Meir Erwin G. , Mackman Nigel , Brat Daniel J. 
Published: March 2009

Abstract
Hypoxia and necrosis are fundamental features of glioblastoma (GBM) and their emergence is critical for the rapid biological progression of this fatal tumor; yet, underlying mechanisms are poorly understood. We have suggested that vaso-occlusion following intravascular thrombosis could initiate or propagate hypoxia and necrosis in GBM. Tissue factor (TF), the main cellular initiator of coagulation, is overexpressed in GBMs and likely favors a thrombotic microenvironment. Epidermal growth factor receptor (EGFR) amplification and PTEN loss are two common genetic alterations seen in GBM but not in lower-grade astrocytomas that could be responsible for TF up-regulation. The most frequent EGFR mutation in GBM involves deletion of exons 2 to 7, resulting in the expression of a constitutively active receptor, EGFRvIII. Here, we show that overexpression of EGFR or EGFRvIII in human glioma cells causes increased basal TF expression and that stimulation of EGFR by its ligand, EGF, leads to a marked dose-dependent up-regulation of TF. In all cases, increased TF expression led to accelerated plasma coagulation in vitro. EGFR-mediated TF expression depended most strongly on activator protein-1 (AP-1) transcriptional activity and was associated with c-Jun NH2-terminal kinase (JNK) and JunD activation. Restoration of PTEN expression in PTEN-deficient GBM cells diminished EGFR-induced TF expression by inhibiting JunD/AP-1 transcriptional activity. PTEN mediated this effect by antagonizing phosphatidylinositol 3-kinase activity, which in turn attenuated both Akt and JNK activities. These mechanisms are likely at work in vivo, as EGFR expression was highly correlated with TF expression in human high-grade astrocytoma specimens. [Cancer Res 2009;69(6):2540–9]
4-Hydroxyestradiol Induces Anchorage-Independent Growth of Human Mammary Epithelial Cells via Activation of IκB Kinase: Potential Role of Reactive Oxygen Species
Authors: Park Sin-Aye , Na Hye-Kyung , Kim Eun-Hee , Cha Young-Nam , Surh Young-Joon 
Published: March 2009

Abstract
Estrogen is converted by cytochrome P450 1B1 to 4-hydroxyestradiol (4-OHE2), a putative carcinogenic metabolite of estrogen. This catechol estrogen metabolite is oxidized further to produce a reactive quinone via semiquinone. Redox cycling between 4-OHE2 and its quinoid generates reactive oxygen species (ROS). ROS not only causes oxidative DNA damage but also promotes neoplastic transformation of initiated cells. In the present study, 4-OHE2 induced anchorage-independent colony formation in human mammary epithelial cells (MCF-10A). MCF-10A cells treated with 4-OHE2 exhibited increased accumulation of intracellular ROS. The antioxidant N-acetyl-l-cysteine inhibited the neoplastic transformation induced by 4-OHE2. ROS overproduced by 4-OHE2 increased the nuclear translocation of nuclear factor-κB (NF-κB) and its DNA binding through induction of IκB kinase α (IKKα) and IKKβ activities. The inhibition of the IKK activities with Bay 11-7082 significantly reduced the anchorage-independent growth induced by 4-OHE2. The 4-OHE2–induced activation of extracellular signal-regulated kinase and Akt resulted in enhanced IKK activities and phosphorylation of IκBα, thereby inducing NF-κB activation and anchorage-independent growth of MCF-10A cells. In conclusion, ROS, concomitantly overproduced during redox cycling of 4-OHE2, activates IKK signaling, which may contribute to neoplastic transformation of MCF-10A cells. [Cancer Res 2009;69(6):2416–24]
MMP13, Birc2 (cIAP1), and Birc3 (cIAP2), Amplified on Chromosome 9, Collaborate with p53 Deficiency in Mouse Osteosarcoma Progression
Authors: Ma Ou , Cai Wei-Wen , Zender Lars , Dayaram Tajhal , Shen Jianhe , Herron Alan J. , Lowe Scott W. , Man Tsz-Kwong , Lau Ching C. , Donehower Lawrence A. 
Published: March 2009

Abstract
Osteosarcoma is the primary malignant cancer of bone and particularly affects adolescents and young adults, causing debilitation and sometimes death. As a model for human osteosarcoma, we have been studying p53+/− mice, which develop osteosarcoma at high frequency. To discover genes that cooperate with p53 deficiency in osteosarcoma formation, we have integrated array comparative genomic hybridization, microarray expression analyses in mouse and human osteosarcomas, and functional assays. In this study, we found seven frequent regions of copy number gain and loss in the mouse p53+/− osteosarcomas but have focused on a recurrent amplification event on mouse chromosome 9A1. This amplicon is syntenic with a similar chromosome 11q22 amplicon identified in several human tumor types. Three genes on this amplicon, the matrix metalloproteinase gene MMP13 and the antiapoptotic genes Birc2 (cIAP1) and Birc3 (cIAP2), show elevated expression in mouse and human osteosarcomas. We developed a functional assay using clonal osteosarcoma cell lines transduced with lentiviral short hairpin RNA vectors to show that down-regulation of MMP13, Birc2, or Birc3 resulted in reduced tumor growth when transplanted into immunodeficient recipient mice. These experiments revealed that high MMP13 expression enhances osteosarcoma cell survival and that Birc2 and Birc3 also enhance cell survival but only in osteosarcoma cells with the chromosome 9A1 amplicon. We conclude that the antiapoptotic genes Birc2 and Birc3 are potential oncogenic drivers in the chromosome 9A1 amplicon. [Cancer Res 2009;69(6):2559–67
Functional Alteration of the Lymphoma Stromal Cell Niche by the Cytokine Context: Role of Indoleamine-2,3 Dioxygenase
Authors: Maby-El Hajjami Hélène , Amé-Thomas Patricia , Pangault Céline , Tribut Olivier , DeVos John , Jean Rachel , Bescher Nadège , Monvoisin Céline , Dulong Joëlle , Lamy Thierry , Fest Thierry , Tarte Karin 
Published: March 2009

Abstract
Human mesenchymal stem cells (MSC) strongly repress activated T-cell proliferation through the production of a complex set of soluble factors, including the tryptophan-catabolizing enzyme indoleamine 2,3-dioxygenase (IDO), which is induced by IFN-γ. Conversely, MSCs support survival of follicular lymphoma (FL) B cells, in particular after exposure to tumor necrosis factor-α (TNF) and lymphotoxin-α1β2 (LT). The role of MSCs on normal and malignant B-cell growth in steady-state and inflammatory conditions remains to be fully explored. We show here that resting MSCs sustain activated normal B-cell proliferation and survival, whereas IFN-γ–conditioned MSCs mediate IDO–dependent B-cell growth arrest and apoptosis. IFN-γ, TNF, and LT are significantly overexpressed by the microenvironment of invaded FL-lymph nodes, but their relative expression patterns are highly heterogeneous between samples. In vitro, IFN-γ abrogates the B-cell supportive phenotype induced by TNF and LT on MSCs. Moreover, IFN-γ overrules the growth promoting effect of MSCs on primary purified FL B cells. Altogether, these results underline the crucial role of the cytokine context in the local crosstalk between malignant cells and their microenvironment and provide new insights into our knowledge of the FL cell niche that emerges as a new promising target for innovative therapeutic strategies. [Cancer Res 2009;69(7):3228–37]
Antitumor Efficacy of the Novel RAF Inhibitor GDC-0879 Is Predicted by BRAFV600E Mutational Status and Sustained Extracellular Signal-Regulated Kinase/Mitogen-Activated Protein Kinase Pathway Suppression
Authors: Hoeflich Klaus P. , Herter Sylvia , Tien Janet , Wong Leo , Berry Leanne , Chan Jocelyn , O'Brien Carol , Modrusan Zora , Seshagiri Somasekar , Lackner Mark , Stern Howard , Choo Edna , Murray Lesley , Friedman Lori S. , Belvin Marcia 
Published: March 2009

Abstract
Oncogenic activation of the BRAF serine/threonine kinase has been associated with initiation and maintenance of melanoma tumors. As such, development of pharmacologic agents to target RAF proteins or their effector kinases is an area of intense investigation. Here we report the biological properties of GDC-0879, a highly selective, potent, and orally bioavailable RAF small-molecule inhibitor. We used extracellular signal-regulated kinase (ERK)-1/2 and mitogen-activated protein kinase/ERK kinase (MEK)-1/2 phosphorylation as biomarkers to explore the relationship between tumor outcome and pharmacodynamic inhibition of the RAF-MEK-ERK pathway. In GDC-0879–treated mice, both cell line– and patient-derived BRAFV600E tumors exhibited stronger and more sustained pharmacodynamic inhibition (&gt;90% for 8 hours) and improved survival compared with mutant KRAS–expressing tumors. Despite the involvement of activated RAF signaling in RAS-induced tumorigenesis, decreased time to progression was observed for some KRAS-mutant tumors following GDC-0879 administration. Moreover, striking differences were noted for RAF and MEK inhibition across a panel of 130 tumor cell lines. Whereas GDC-0879–mediated efficacy was associated strictly with BRAFV600E status, MEK inhibition also attenuated proliferation and tumor growth of cell lines expressing wild-type BRAF (81% KRAS mutant, 38% KRAS wild type). The responsiveness of BRAFV600E melanoma cells to GDC-0879 could be dramatically altered by pharmacologic and genetic modulation of phosphatidylinositol 3-kinase pathway activity. These data suggest that GDC-0879–induced signaling changes are dependent on the point of oncogenic activation within the RAS network. Taken together, these studies increase our understanding of the molecular determinants for antitumor efficacy resulting from RAF pathway inhibition and have implications for therapeutic intervention in the clinic. [Cancer Res 2009;69(7):3042–51]
GD3, an Overexpressed Tumor-Derived Ganglioside, Mediates the Apoptosis of Activated but not Resting T Cells
Authors: Sa Gaurisankar , Das Tanya , Moon Christina , Hilston Cynthia M. , Rayman Patricia A. , Rini Brian I. , Tannenbaum Charles S. , Finke James H. 
Published: March 2009

Abstract
We previously elucidated an important role for gangliosides in renal cell carcinoma–mediated T lymphocyte apoptosis, although the mechanism by which they mediated lymphocyte death remained unclear. Here, we show that when added in purified form, GD3 is internalized by activated T cells, initiating a series of proapoptotic events, including the induction of reactive oxygen species (ROS), an enhancement of p53 and Bax accumulation, an increase in mitochondrial permeability, cytochrome c release, and the activation of caspase-9. GD3-induced apoptosis of activated T cells was dose dependent and inhibitable by pretreating the lymphocytes with N-acetylcysteine, cyclosporin A, or bongkrekic acid, emphasizing the essential role of ROS and mitochondrial permeability to the process. Ganglioside-induced T-cell killing was associated with the caspase-dependent degradation of nuclear factor-κB–inducible, antiapoptotic proteins, including RelA; this suggests that their loss is initiated only after the cascade is activated and that their disappearance amplifies but not triggers GD3 susceptibility. Resting T cells did not internalize appreciable levels of GD3 and did not undergo any of the proapoptotic changes that characterize activated T lymphocytes exposed to the ganglioside. RelA overexpression endows Jurkat cells with resistance to GD3-mediated apoptosis, verifying the role of the intact transcription factor in mediating protection from the ganglioside. [Cancer Res 2009;69(7):3095–104]