bluuebunny/crossref_metadata_2025_split huggingface dataset:
Blockade of AP‐1 activity by dominant‐negative TAM67 can abrogate the oncogenic phenotype in latent membrane protein 1‐positive human nasopharyngeal carcinoma
Authors: Jin Xin , Song Xin , Li Lili , Wang Zhenlian , Tao Yongguang , Deng Lin , Tang Ming , Yi Wei , Cao Ya 
Published: May 2007

AbstractAlthough activating protein‐1 (AP‐1) transcription factors play an important role in mediating metastasis for nasopharyngeal carcinoma (NPC), the biological and physiological functions of AP‐1, in relation to the oncogenic phenotype of NPC, are not fully understood. Our previous study showed that the latent membrane protein 1 (LMP1) mediated a primary dimer form of c‐jun and jun B. In this study, we used a NPC cell line that express a specific inhibitor of AP‐1, a dominant‐negative c‐jun mutant (TAM67), to investigate the role of AP‐1 in regulating the NPC oncogenic phenotype. First, we observed that TAM67 inhibited cell growth in vitro and in vivo. Next, with Western blotting, we discovered that TAM67 impaired the cyclin D1/cdk4 complex but had little effect on the cyclin E/cdk2 complex, concomitantly with inhibiting Rb phosphorylation. RT‐PCR and luciferase assay results demonstrated that the levels of cyclin D1 mRNA and the promoter activity in TAM67 transfectants were reduced as compared with control cells. Thereby, we show that blockade of AP‐1 transcriptional activity has a negative impact on cyclin D1 transcription. We obtained the first evidence that TAM67 prevented NPC growth both in vitro and in vivo. AP‐1 appears to be a novel target for treating or preventing LMP1‐positive NPC effectively. © 2007 Wiley‐Liss, Inc.
Altered expression of splicing factor, heterogeneous nuclear ribonucleoprotein A2/B1, in mouse lung neoplasia
Authors: Peebles Katherine A. , Dwyer‐Nield Lori D. , Malkinson Alvin M. 
Published: May 2007

AbstractOur previous proteomic investigation of lung neoplasia in vitro demonstrated a high concentration of the lung cancer biomarker and splicing factor, hnRNP A2/B1, in the transformed mouse lung epithelial cell line, E9. Since changes in pre‐mRNA splicing profoundly affect neoplastic progression, we examined hnRNP A2/B1 expression in chemically induced primary mouse lung tumors, an in vivo model of pulmonary adencocarcinoma. Tumor hnRNP A2/B1 content and spatial distribution assessed by immunohistochemistry varied with stage of progression, genetic background, and whether tumors were induced by a single agent (urethane) or by 2‐stage initiation/promotion (3‐methylcholanthrene/butylated hydroxytoluene) carcinogenesis. To address mechanisms governing hnRNP A2/B1 expression changes, we utilized in vitro models. hnRNP A2/B1 protein was overexpressed in E9, the spontaneous tranformant of immortalized but non‐neoplastic E10 cells, but expression was not strictly a function of enhanced proliferative rate in neoplastic cells. Elevated mRNA content was positively associated with cell division in both E10 and E9, but hnRNP A2/B1 protein levels decreased in proliferating E10 cells. The increased mRNA reflected enhanced mRNA stability, as shown by measuring time‐dependent mRNA decay after inhibiting transcription. Dysregulation of hnRNP A2/B1 expression during lung neoplasia in vivo thus depends on complex gene–environmental interactions that affect cell type‐specific changes in mRNA processing and, most probably, the rates of translation and/or protein degradation. © 2007 Wiley‐Liss, Inc.
Ras‐mediated intestinal epithelial cell transformation requires cyclooxygenase‐2‐induced prostaglandin E2 signaling
Authors: Repasky Gretchen A. , Zhou Yixing , Morita Staeci , Der Channing J. 
Published: May 2007

AbstractRas‐mediated transformation is associated with upregulation of cyclooxygenase‐2 (COX‐2), which in turn promotes prostaglandin E2 (PGE2) synthesis and secretion. Although recent studies have identified molecular mechanisms by which Ras mediates upregulation of COX‐2, conflicting observations have been made. Furthermore, while COX‐2 upregulation has been shown to be important for Ras transformation, the signaling pathways initiated by PGE2‐stimulation of EP family of heterotrimeric G protein‐coupled receptors (GPCR) and contribution of PGE2 signaling to Ras‐mediated transformation are issues that remain unresolved. In this study, we first determined that Raf effector pathway activation of the extracellular‐regulated kinase (ERK) mitogen‐activated protein kinase (MAPK) cascade alone was sufficient and necessary for COX‐2 and PGE2 upregulation. However, Raf‐independent regulation of the c‐jun N‐terminal kinase (JNK) and p38 MAPK cascades is also involved in COX‐2 and PGE2 upregulation, with the JNK and p38 pathways exhibiting opposing roles in COX‐2 and PGE2 upregulation. Furthermore, in contrast to previous studies, we found that an epidermal growth factor (EGF) receptor autocrine growth mechanism, another Raf‐independent signaling mechanism, was necessary for COX‐2 and PGE2 upregulation. Second, we determined that inhibition of EP1/2 receptor function blocked growth transformation by Ras, demonstrating that PGE2 upregulation is a key transforming function of COX‐2. Finally, we found that PGE2 stimulated the activation of Ras and ERK, but not Akt, and reduced matrix deprivation‐induced apoptosis, in untransformed epithelial cells. In summary, our studies define additional, multiple signaling mechanisms that promote COX‐2 and PGE2 expression and show that COX‐2‐stimulated PGE2‐EP receptor signaling is required for growth and survival transformation by Ras. © 2007 Wiley‐Liss, Inc.
p63: Defining roles in morphogenesis, homeostasis, and neoplasia of the epidermis
Authors: King Kathryn E. , Weinberg Wendy C. 
Published: May 2007

Abstractp63 is a member of a gene family also including the p53 tumor suppressor and p73. In contrast to p53, p63 is rarely mutated in human cancers. Rather, gene amplification and dysregulated expression of p63 protein have been observed, particularly in squamous cell carcinomas. p63 is essential for development of stratified squamous epithelium, including the epidermis. The p63 gene is expressed as multiple protein isoforms with different functional capacities, and the balance of these isoforms, along with the presence or absence of the other family members, p53 and p73, can impact biological outcome. Both gene silencing and overexpression approaches have been utilized to elucidate the contributions of specific p63 isoforms to normal epidermal morphogenesis and tissue maintenance. While numerous studies have established the essential nature of p63 in the epidermis, the basis of this requirement, and the unique, as well as, overlapping functions of the individual isoforms, remain controversial. In this review, we summarize the current understanding of roles played by specific p63 isoforms within the context of epidermal morphogenesis and homeostasis of the established epidermis, and the potential impact of p63 dysregulation on cancer development. © 2007 Wiley‐Liss, Inc.
The etiology of sunlight‐induced melanoma in Xiphophorus hybrid fish
Authors: Mitchell David , Paniker Lakshmi , Sanchez Guillermo , Trono David , Nairn Rodney 
Published: May 2007

AbstractIn contrast to sunlight‐induced squamous cell carcinoma the etiology of cutaneous malignant melanoma (CMM) is not well understood. In particular, the role that sunlight exposure and DNA damage play in the initiation of this deadly form of cancer is an open question. Early UV carcinogenesis studies in the Xiphophorus backcross hybrid fish model by Richard Setlow indicated that direct DNA damage caused by exposure to the UVB component of sunlight is necessary and sufficient for melanoma formation. Subsequent studies by Setlow suggested that monochromatic UVA radiation that is not directly absorbed by DNA was also sufficient for melanoma induction in Xiphophorus and was, indeed, primarily responsible for initiating human melanoma. These results had significant public health consequences, suggesting that although sunscreens may inhibit UVB‐induced erythema they may actually increase exposure to the UVA wavelengths that cause cancer. An intensive worldwide public debate on sunscreen use and “abuse” ensued. Our data do not support a major role of free radical chemistry in melanoma induction. We find evidence that the direct damage caused by the absorption of UVB wavelengths by DNA (e.g., the cyclobutane pyrimidine dimer or CPD) is required for CMM formation and that the ability to repair these lesions plays a significant role in tumor susceptibility. Using the Xiphophorus backcross hybrid fish we are currently in the process of re‐evaluating the wavelength‐ and DNA damage‐dependence of UV‐induced melanoma and the role nucleotide excision repair and the genes controlling DNA repair and the UV response play in melanoma resistance. From these studies we hope to define the effective solar wavelength boundaries of melanoma, identify the class of critical DNA damage and elucidate the role of DNA repair in tumor suppression. © 2007 Wiley‐Liss, Inc.
Impact of cold preservation on leukocyte adhesion to the transplanted rat lung
Authors: Enomoto Aki , Kikuchi Takeshi , Seo Norimasa , Matsuno Kenjiro , Kobayashi Eiji 
Published: May 2007

AbstractLittle is known about leukocyte migration in the early phase after ischemia‐reperfusion injury. Recently, there has been much focus on in vivo visualization of cell kinetics. Previously, we established a method for the in vivo visualization of leukocyte circulation using a Green Fluorescent Protein transgenic rat. Herein, we developed a simplified rat heterotopic lung transplantation model that can be mastered by beginners within a few weeks. Using this system, we studied the impact of preservation on adhesion of circulating leukocytes to the transplanted lung. The graft of a fresh group was compared with that of a preserved group. Morphological and immunohistochemical analyses were also performed. We successfully visualized few adherent leukocytes in the fresh graft, whereas adherent cells were attached in the preserved graft within a few minutes. In conclusion, the prolonged cold preservation time promotes leukocyte adhesion, resulting in increased microvascular injury after lung transplantation. © 2007 Wiley‐Liss, Inc. Microsurgery 2007.
Th1/Th2 xenogenic antibody responses are associated with recipient dendritic cells
Authors: Kanai Nobuyuki , Min Wei‐Ping , Ichim Thomas E. , Wang Hao , Zhong Robert 
Published: May 2007

AbstractWe characterized dendritic cells (DC) phenotypically and functionally between C57BL/6 (Th1‐prone) and BALB/c (Th2‐prone) mouse recipients in an in vivo sensitization model. Two strains of mice were presensitized with Lewis rat splenocytes as xenogeneic antigens. We found that BALB/c recipients mounted a significantly higher total IgG response to the xeno‐antigens when compared with C57BL/6 recipients, 10 days after rat splenocyte infusion. A Th2‐mediated antibody response with high ratio of IgG1/IgG2a was seen in the BALB/c recipients, while a Th1 antibody response with low ratio of IgG1/IgG2a was detected in C57BL/6 recipients. CD11c+DC isolated from C57BL/6 recipients possessed increased expression of CD8α+ (DC‐1 type). The administration of bone marrow derived‐DC from IL‐12 knockout mice into C57BL/6 recipients induced a shift of Th‐mediated anti‐xenogeneic antibody responses from Th1 to Th2 domain. Our findings suggest that DC could play an important role to regulate the balance of Th1/Th2 cytokine profiles and rejection patterns in xenotransplantation. © 2007 Wiley‐Liss, Inc. Microsurgery 2007.
Rutin in rat liver ischemia/reperfusion injury: Effect on DDAH/NOS pathway
Authors: Lanteri Raffael , Acquaviva Rosaria , Di Giacomo Claudia , Sorrenti Valeria , Li Destri Giovanni , Santangelo Marco , Vanella Luca , Di Cataldo Antonio 
Published: May 2007

AbstractNitric oxide (NO) plays a key role in the relationship between microcirculatory disorders and I/R injuries. Our results demonstrated a significant modification in the hepatic function of I/R rats compared with the control group; treatment with rutin reported hepatic damage markers to control value. Levels of plasmatic and hepatic thiol groups decreased in the I/R untreated group, and this decrease was inhibited by rutin treatment. In addition, we observed an increase in the iNOS expression in I/R group compared with control and rutin administration attenuated this increase; in post‐ischemic reperfused rutin‐treated rats there was a significant increase in eNOS expression compared with the I/R untreated group. In the same experimental conditions an increase in DDAH 1 expression was observed in I/R group only; rutin treatment also counteracted this increased expression. These data suggest that rutin treatment could be useful for preventing oxidative damage associated with hepatic post‐ischemic reperfusion injury. © 2007 Wiley‐Liss, Inc. Microsurgery 2007.
Microsurgery for treatment of peripheral lymphedema: Long‐term outcome and future perspectives
Authors: Campisi Corradino , Eretta Costantino , Pertile Davide , Da Rin Elisa , Campisi Corrado , Macciò Alberto , Campisi Mirko , Accogli Susanna , Bellini Carlo , Bonioli Eugenio , Boccardo Francesco 
Published: May 2007

AbstractAuthors report over 30 years of their own clinical experience in the treatment of chronic peripheral lymphedemas by microsurgical techniques performed at the Center of Lymphatic Surgery of the University of Genoa, Italy. Over 1,500 lymphedema patients were treated with microsurgical techniques. Derivative lymphatic‐venous techniques were most often used. For those cases where a venous disease was associated to lymphedema, reconstructive lymphatic microsurgery techniques were performed (lymphatic‐venous–lymphatic‐plasty). Objective assessment was undertaken by water volumetry and lymphoscintigraphy. Volume changes showed a significant improvement in over 83%, with an average follow‐up of more than 10 years. There was an 87% reduction in the incidence of cellulitic attacks after microsurgery. Microsurgical lymphatic‐venous anastomoses have a place in the treatment of peripheral lymphedema and should be the therapy of choice in patients who are not sufficiently responsive to nonoperative treatment. Improved results can be expected with operations performed at earlier lymphedema stages. © 2007 Wiley‐Liss, Inc. Microsurgery 2007.
Effect of different periods of hyperbaric oxygen on ischemia‐reperfusion injury of rat skeletal muscle
Authors: Vidigal João , José Fagundes Djalma , De Jesus Simões Manuel , Oshima Celina T.F. , Nakao Odashiro Alexandre , Santos SimõEs Ricardo , Tereza Negrini Fagundes Anna , Omar Taha Murched , Frasson De Souza Montero Edna 
Published: May 2007

AbstractThe effect of hyperbaric oxygen (HBO) on ischemia‐reperfusion injury of skeletal muscle, applied during different periods, was studied in 56 male rats. Animals were subjected to 6‐h ischemia by a tourniquet over the major femoral trocanter and 4 (A) or 24 (B) h of reperfusion. HBO was carried out during 1 h in an acrylic chamber at a pressure of 2.0 ATA (100% oxygen): in the last 60 min of ischemia (II), after ischemia, during 1‐h reperfusion time (III), and during the last hour of ischemia plus 1‐h reperfusion (IV). Group I was the control group. After 4‐ or 24‐h reperfusion, samples of the soleus muscle were stained by H&E and analyzed immunohistochemically. No interstitial hemorrhage, neutrophil infiltrate, or cellular necrosis were induced by HBO. The apoptosis index did not differ among the groups. HBO reduced morphologic alterations and promoted better results when administered in the ischemia plus reperfusion period (GIV). © 2007 Wiley‐Liss, Inc. Microsurgery 2007.
Late transplantation period of mice fetal intestine grafts: Morphometric aspects
Authors: De Almeida Carlos Eduardo Saldanha , Artigiani Ricardo , De Oliveira Kátia Ferreira , Navarro Pedro Gabriel Riboli , De Souza Montero Edna Frasson 
Published: May 2007

AbstractMorphometric evaluation of the fetal intestinal graft in the late post‐transplant period was done by using C57BL/6 mice. Under anesthesia, after hysterotomy, a transversal laparotomy was done in the fetus to harvest all intestines. Grafts, cleaned from its mesentery, and divided were transplanted into the preperitoneum space, from male mice, C57BL/6 strain. Thirty days after, mice were killed, and the graft was analyzed with HE stain and S‐100 protein. All grafts as well as fetal and adult intestines were evaluated as controls. All developed grafts showed muscular layer and positivity for S‐100 protein as the adult intestines. The goblet cells, absent in fetal intestines, were in larger number in isogeneic grafts than in adult intestines, even with lower villus. These findings showed sharp progress of the isogeneic graft from fetal to adult intestine, suggesting that they can be viable and might be functionally appropriate in the late period after transplantation. © 2007 Wiley‐Liss, Inc. Microsurgery 2007.
Liver and lung late alterations following hepatic reperfusion associated to ischemic preconditioning or N‐acetylcysteine
Authors: Galhardo Maria Aparecida , Júnior Claudemiro Quireze , Navarro Pedro Gabriel Riboli , Morello Ricardo José , De Jesus Simões Manuel , De Souza Montero Edna Frasson 
Published: May 2007

AbstractThis study aimed the effect of n‐acetylcysteine or ischemic preconditioning in hepatic and pulmonary damage after liver ischemia‐reperfusion injury. Twenty‐four male Wistar‐EPM rats were assigned into four groups: (IR) Hepatic ischemia‐reperfusion; (IPC) IPC achieved before hepatic ischemia; (NAC) Animals received NAC pretreatment; and Sham operated group. After 24 h of hepatic reperfusion, blood, liver, and pulmonary samples were evaluated. Nonparametric tests were used (P ≤ 0.05). Aspartate aminotransferase levels were similar among experimental groups. Lower alanine aminotrasnferase levels were observed in sham group (P = 0.04). IPC and NAC groups prevented from necrosis (P = 0.027), apoptosis (P = 0.003), and microvesicular steatosis (P = 0.0007), but not from neutrophil infiltration in liver tissue. IPC and NAC treatment reduced alveolar septal edema (P = 0.014), but did not prevent from neutrophil infiltration or vascular congestion. In conclusion, IPC and NAC attenuated hepatic and pulmonary damage after hepatic ischemia‐reperfusion injury. © 2007 Wiley‐Liss, Inc. Microsurgery 2007.
Long‐term effect of FTY720 on lymphocyte count and islet allograft survival in mice
Authors: Liu Longshan , Wang Changxi , He Xiaoshun , Shang Wenjun , Bi Ying , Wang Dong 
Published: May 2007

AbstractThis study was performed to observe the long‐term effect of FTY720 on lymphocyte count change and islet allograft survival. Diabetic C57BL/6 mice were given FTY720 (group 1, 0.5 mg/kg/day; group 2, 1.0 mg/kg/day) or its vehicle (group 3, controls) after transplantation. Median graft survival time was prolonged in a dose‐dependent manner (group 1, 84.5 days; group 2, >100 days, and group 3, 10 days, P < 0.01). Peripheral blood lymphocytes in groups 1 and 2 decreased to 23.81% and 12.59% compared with control group after FTY720 treatment. Lymphocytes from mesenteric lymph nodes and axillary nodes in groups 1 and 2 significantly increased on day 5, but decreased on day 14. Lymphocyte infiltration to the graft site was attenuated in groups 1 and 2. In conclusion, continuous FTY720 administration can induce and maintain lymphopenia, and inhibit lymphocytes from infiltrating the graft site so as to prolong islet allograft survival in mice. © 2007 Wiley‐Liss, Inc. Microsurgery 2007.
Administration of dendritic cells modified by RNA interference prolongs cardiac allograft survival
Authors: Xiang Jianbin , Gu Xiaodong , Zhou Yiming , Gong Xun , Qian Shiguang , Chen Zongyou 
Published: May 2007

AbstractSystemic administration of immature donor‐dendritic cells (DC) that are deficient in co‐stimulatory molecules delays the onset of allograft rejection. However, it is not easy to control culture condition and guarantee that the administered DC are in the immature stages, which obviously affects their therapeutic effect. In this study, we attempted to inhibit expression of CD86 on DC using an RNA interference technology. The function of CD86low DC was determined by the influence on their capacity to stimulate T cell proliferation and by the effect of DC systemic administration on survival of cardiac allografts. CD86low DC stimulated low T cell proliferative responses in vitro and administration of CD86low DC prolonged survival of heart allografts in vivo. These results suggest that RNA interference is a useful approach to modify DC function, which has potentials for clinical application. © 2007 Wiley‐Liss, Inc. Microsurgery 2007.
Stability of the steady state for the Falk model system of shape memory alloys
Authors: Suzuki Takashi , Yoshikawa Shuji 
Published: May 2007

AbstractIn this article a stability result for the Falk model system is proven. The Falk model system describes the martensitic phase transitions in shape memory alloys. In our setting, the steady state is a nonlocal elliptic problem. We show the dynamical stability for the linearized stable critical point of the corresponding functional. Copyright © 2007 John Wiley & Sons, Ltd.
On the minimum path problem in Knödel graphs
Authors: Harutyunyan Hovhannes A. , Morosan Calin D. 
Published: May 2007

AbstractThe Knödel graphs Wd,n are regular graphs, of even order n and degree d ≤ ⌊log n⌋. They have been introduced by W. Knödel as gossip graphs for d = ⌊log n⌋. A logarithmic algorithm for the minimum path problem in Knödel graphs is an open problem despite the fact that they are bipartite and highly symmetric. In this paper, we describe a logarithmic time two‐approximation algorithm for the shortest path in the Knödel graph on 2d vertices with degree d. We also prove that for a subset of the set of vertices, the algorithm gives a minimum length path. © 2007 Wiley Periodicals, Inc. NETWORKS, Vol. 50(1), 86–91 2007
Multiperiod network design with incremental routing
Authors: Lardeux Benoit , Nace Dritan , Geffard Jérôme 
Published: May 2007

AbstractIn this paper, we study a special case of multiperiod network design (MPND) problems, multiperiod network design with incremental routing (MPNDI), as applied to the transmission layer of an optical network. We optimize simultaneously the network architecture and the link dimensioning under discrete cost functions in order to route all traffic demands in line with traffic growth over a discrete time horizon. Because of operational requirements, routing paths used at a given period to route some traffic demands have to be preserved over subsequent periods; this is called incremental routing with respect to incremental flow. To handle the high dimensionality, a compact formulation omitting explicitly written flow variables is given. We examine the dominant polyhedron of the incremental multicommodity flow and provide a polyhedral study of it. Finally, a solution approach taking advantage of the polyhedral structure of MPNDI is proposed, and computational results for a range of instances with 8 and 10 nodes are provided. © 2007 Wiley Periodicals, Inc. NETWORKS, Vol. 50(1), 109–117 2007