bluuebunny/crossref_metadata_2025_split huggingface dataset:
α subunit partners to β1 and β2 integrins during IL‐4‐induced foreign body giant cell formation
Authors: McNally Amy K. , MacEwan Sarah R. , Anderson James M. 
Published: February 2007

AbstractAs β1 and β2 integrins were previously found to mediate adhesion during IL‐4‐induced foreign body giant cell (FBGC) formation, we pursued the identities of the α integrin partners of these adhesion receptors using our in vitro system of human monocyte‐derived macrophage fusion. Immunoprecipitation with β1 and immunoblotting reveal the presence of α5 and αV, as well as α2 and α3. αM and αX immunoprecipitate with β2 but not with β1. Immunocytochemistry coupled with confocal microscopy indicates that α5 and αX are poorly expressed on day 0. However, following the induction of fusion by IL‐4 on day 3, they are each readily detectable in fusing macrophages/FBGC on day 7. In contrast, αM and αV are present throughout the culture period, with very strong αM expression on day 7. We also demonstrate expression and colocalization of α3, α5, or αV with β1 on fusing macrophages/FBGC at this time point as well as strong colocalization of αM and αX with β2 in FBGC and at fusion interfaces. Therefore, IL‐4‐induced FBGC are characterized by the expression of αMβ2, αXβ2, α5β1, αVβ1, α2β1, and α3β1, which indicates potential interactions with fragments of complement C3, fibrin(ogen), fibronectin, Factor X, and vitronectin, and possibly with certain collagens, laminin, and thrombospondin at sites of biomaterial implantation. © 2007 Wiley Periodicals, Inc. J Biomed Mater Res, 2007
Retracted: Overexpression HERG K+ channel gene mediates cell‐growth signals on activation of oncoproteins SP1 and NF‐κB and inactivation of tumor suppressor Nkx3.1
Authors: Lin Huixian , Xiao Jiening , Luo Xiaobin , Wang Huizhen , Gao Huanhuan , Yang Baofeng , Wang Zhiguo 
Published: February 2007

AbstractThe long QT syndrome gene human ether‐a‐go‐go related gene (HERG) encodes a K+ channel critical to cardiac repolarization. It peculiarly overexpresses in cancer cells of different histogenesis and promotes tumorigenesis. To decipher the molecular mechanisms for HERG overexpression, we identified and characterized the promoter region of the HERG gene, which contains cis‐elements for multiple oncoproteins and tumor suppressors. Oncoprotein Sp1 was found to be essential to driving the HERG promoter thereby transcription. Another oncoprotein NF‐κB transactivated, while tumor suppressor Nkx3.1 repressed HERG promoter activity and endogenous HERG transcription. Loss‐of‐function mutations in the corresponding cis‐elements rendered a loss of the ability of the oncoproteins Sp1 and NF‐κB to transactivate, and of the tumor repressor Nkx3.1 to repress, HERG transcription. Either activation of Sp1 and NF‐κB or silencing of Nkx3.1 promoted tumor cell growth, and the effects were abrogated by HERG inhibition or knockdown, but facilitated by overexpression of HERG, indicating that HERG mediates the cell growth signals generated by activation of oncoproteins or inactivation of tumor suppressors. Binding of Sp1, NF‐κB, and Nkx3.1 to their respective cis‐elements in the HERG promoter in vitro and their presence on the HERG promoter in vivo were confirmed. Therefore, the HERG promoter region is characterized by multiple Sp1 binding sites that are responsible for transcription initiation of the HERG gene and by binding sites for multiple other oncogenes and tumor suppressor genes being important for regulating HERG expression. The HERG K+ channel is likely a mediator of growth‐promoting processes induced by oncoproteins and/or by silencing of tumor suppressors. J. Cell. Physiol. 212: 137–147, 2007. © 2007 Wiley‐Liss, Inc.
Flt‐1, but not Flk‐1 mediates hyperpermeability through activation of the PI3‐K/Akt pathway
Authors: Vogel Carsten , Bauer Alexander , Wiesnet Marion , Preissner Klaus T. , Schaper Wolfgang , Marti Hugo H. , Fischer Silvia 
Published: February 2007

AbstractVascular endothelial growth factor (VEGF), a potent mediator of endothelial proliferation and migration, has an important role also in brain edema formation during hypoxia and ischemia. VEGF binds to the tyrosine kinase receptors Flt‐1 and Flk‐1. Yet, their relative importance for hypoxia‐induced hyperpermeability is not well understood. We used an in vitro blood‐brain barrier (BBB) model consisting of porcine brain microvascular endothelial cells (BMEC) to determine the role of Flt‐1 in VEGF‐induced endothelial cell (EC) barrier dysfunction. Soluble Flt‐1 abolished hypoxia/VEGF‐induced hyperpermeability. Furthermore, selective antisense oligonucleotides to Flt‐1, but not to Flk‐1, inhibited hypoxia‐induced permeability changes. Consistent with these data, addition of the receptor‐specific homolog placenta‐derived growth factor, which binds Flt‐1 but not Flk‐1, increased endothelial permeability to the same extent as VEGF, whereas adding VEGF‐E, a viral VEGF molecule from the orf virus family activating Flk‐1 and neuropilin‐1, but not Flt‐1, did not show any effect. Using the carcinoma submandibular gland cell line (CSG), only expressing Flt‐1, it was demonstrated that activation of Flt‐1 is sufficient to induce hyperpermeability by hypoxia and VEGF. Hyperpermeability, induced by hypoxia/VEGF, depends on activation of phosphatidylinositol 3‐kinase/Akt (PI3‐K/Akt), nitric oxide synthase (NOS) and protein kinase G (PKG). The activation of the PI3‐K/Akt pathway by hypoxia was confirmed using an in vivo mice hypoxia model. These results demonstrate that hypoxia/VEGF‐induced hyperpermeability can be mediated by activation of Flt‐1 independently on the presence of Flk‐1 and indicate a central role for activation of the PI3‐K/Akt pathway, followed by induction of NOS and PKG activity. J. Cell. Physiol. 212: 236–243, 2007. © 2007 Wiley‐Liss, Inc.
Soft substrate induces apoptosis by the disturbance of Ca2+ homeostasis in renal epithelial LLC‐PK1 cells
Authors: Chiu Wen‐Tai , Wang Yao‐Hsien , Tang Ming‐Jer , Shen Meng‐Ru 
Published: February 2007

AbstractDifferent rigidities of adhesive collagen substrate affect cellular functions with unclear mechanisms. Here, we cultured a renal epithelial cell line (LLC‐PK1) and a tumor cell line (HeLa) on substrates of different rigidities and compared the cell type‐specific responses. The culture dish was coated with a very thin layer of collagen gel (control group) or overlaid with collagen gel (soft substrate). LLC‐PK1 cells contracted as they grew on collagen gel and the apoptotic bodies obviously appeared with time. The protein levels of procaspase‐12 and its downstream target procaspase‐3 were decreased when LLC‐PK1 cells cultured on collagen gel. µ‐calpain was activated on collagen gel. Collage gel also induced the cleavage of α‐spectrin which resulted in the disorganization of actin cytoskeleton. In contrast, there was no significant change in cytochrome c revelation, mitochondrial membrane potential, and the protein levels of procaspase‐8 and procaspase‐9. Moreover, soft substrate caused elevated cytosolic Ca2+, Ca2+ overload in ER and upregulation of capacitative calcium entry. Ca2+ chelator or channel blocker partially rescued the collagen‐gel induced apoptosis by inhibiting µ‐calpain activation. In contrast, for HeLa cells cultured either on collagen gel or on gel‐coated dish, there was no significant change in positive Annexin V staining, no activation of procaspase‐12 and no cleavage of µ‐calpain. Thus, soft substrate induces apoptosis in LLC‐PK1 cells by the disturbance of Ca2+ homeostasis. J. Cell. Physiol. 212: 401–410, 2007. © 2007 Wiley‐Liss, Inc.
Apoptosis of human neutrophils induced by protein phosphatase 1/2A inhibition is caspase‐independent and serine protease‐dependent
Authors: Park Hae‐Young , Song Min‐Gyu , Lee Jun‐Sik , Kim Ja‐Woong , Jin Jun‐O , Park Joo‐In , Chang Young‐Chae , Kwak Jong‐Young 
Published: February 2007

AbstractProtein phosphatase (PP) activity is associated with the regulation of apoptosis in neutrophils. However, the underlying regulatory mechanism(s) in apoptosis remain unclear. The type of cell death induced by okadaic acid (OA), the inhibitor of PP1 and PP2A, is characterized by apoptotic morphological changes of the cells and annexin V‐positive staining without DNA fragmentation. The apoptotic effects of OA and calyculin A on neutrophils were observed at concentrations ranging from 50 to 200 nM, or 10 to 50 nM, respectively. Cyclosporine A (a PP2B specific inhibitor), however, did not exhibit any pro‐apoptotic effects. OA and calyculin A, but not cyclosporine A, exhibited significant effects on protein levels and on the electrophoretic mobility of Mcl‐1. zVAD‐fmk, a pancaspase inhibitor, failed to inhibit the effect of OA on the caspase‐3 activity, procaspase‐3 processing, and the apoptotic rate of neutrophils. However, 4‐(2‐aminoethyl) benzenesulfonylfluoride (AEBSF), a general serine protease inhibitor, significantly abrogated the OA‐induced mobility shift in procaspase‐3, caspase‐3 activation, and the apoptotic morphological changes in neutrophils. Moreover, OA enhanced the serine protease activity of the neutrophils. The addition of the proteinase‐3 protein increased the rate of neutrophil apoptosis, which was also blocked by AEBSF but not by zVAD‐fmk. These results suggest that OA induces procaspase‐3 processing but that OA‐induced apoptosis is caspase‐independent and serine protease‐dependent. J. Cell. Physiol. 212: 450–462, 2007. © 2007 Wiley‐Liss, Inc.
The adjuvant effects of co‐stimulatory molecules on cellular and memory responses to HBsAg DNA vaccination
Authors: Du Xiaogang , Zheng Guoxing , Jin Huali , Kang Youmin , Wang Junpeng , Xiao Chong , Zhang Shuo , Zhao Lin , Chen Aoshuang , Wang Bin 
Published: February 2007

AbstractBecause DNA vaccines on their own tend to induce weak immune responses in humans, adjuvant methods are needed in order to improve their efficacy. The co‐stimulatory molecules 4‐1BBL, OX40L, and CD70 have been shown to induce strong T cell activities; therefore, in this study, we investigated whether they may be used as molecular adjuvants for a hepatitis B surface antigen (HBsAg) DNA vaccine (pcDS2) in eliciting strong cellular and memory responses. Compared to mice immunized with pcDS2 alone, addition of the co‐stimulatory molecules increased T cell proliferation and an HBsAg‐specific antibody response that was marked with a higher ratio of IgG2a/IgG1. Importantly, pcDS2 plus these co‐stimulatory molecules elicited a higher level of IFN‐γ and IL‐4 in CD4+ T cells and a higher level of IFN‐γ in CD8+ T cells. In addition, a significantly robust antigen‐specific cytotoxic T lymphocyte (CTL) response and the production of long‐term memory CD8+ T cells were also observed in the groups immunized with pcDS2 plus 4‐1BBL, OX40L, or CD70. Consistently, as late as 100 days after immunization, upregulated expressions of BCL‐2, Spi2A, IL‐7Ra, and IL‐15Ra were still observed in mice immunized with pcDS2 plus these co‐stimulatory molecules, suggesting the generation of memory T cells in these groups. Together, these results suggest that the co‐stimulatory molecules 4‐1BBL, OX40L, or CD70 can enhance the immunogenicity of HBsAg DNA vaccines, resulting in strong humoral, cellular, and memory responses. This approach may lead to an effective therapeutic vaccine for chronic hepatitis B virus (HBV) infection. Copyright © 2007 John Wiley & Sons, Ltd.
Molecular epidemiological studies show that hepatitis A virus is endemic among active homosexual men in Europe
Authors: Stene‐Johansen Kathrine , Tjon Grace , Schreier Eckart , Bremer Viviane , Bruisten Sylvia , Ngui Siew‐Lin , King Mike , Pinto Rosa M. , Aragonès Lluis , Mazick Anne , Corbet Sylvie , Sundqvist Lena , Blystad Hans , Norder Helene , Skaug Kjell 
Published: February 2007

AbstractLarge outbreaks of hepatitis A have occurred in Denmark, Germany, the Netherlands, Norway, Spain, Sweden, and the United Kingdom during the period 1997–2005 affecting homosexual men. A collaborative study was undertaken between these countries to determine if the strains involved in these hepatitis A outbreaks were related genetically. The N‐terminal region of VP1 and the VP1/P2A region of the strains were sequenced and compared. The majority of the strains found among homosexual men from the different European countries formed a closely related cluster, named MSM1, belonging to genotype IA. Different HAV strains circulated among other risk groups in these countries during the same period, indicating that specific strains were circulating among homosexual men exclusively. Similar strains found among homosexual men from 1997 to 2005 indicate that these HAV strains have been circulating among homosexual men for a long time. The homosexual communities are probably too small within the individual countries to maintain HAV in their population over time, whereas the homosexual communities across Europe are probably sufficiently large to sustain continued circulation of homologous HAV strains for years resulting in an endemic situation among homosexual men. J. Med. Virol. 79:356–365, 2007. © 2007 Wiley‐Liss, Inc.
Epstein Barr virus genotypes and LMP‐1 variants in HIV‐infected patients
Authors: Correa Rita Mariel , Dolores Fellner María , Durand Karina , Redini Liliana , Alonio Virginia , Yampolsky Claudio , Colobraro Antonio , Sevlever Gustavo , Teyssié Angélica , Benetucci Jorge , Picconi María Alejandra 
Published: February 2007

AbstractTwo Epstein Barr virus (EBV) genotypes: EBV‐1 and EBV‐2 have been described. A 30‐bp deletion in latent membrane protein‐1 gene (del‐LMP‐1) has been identified in various pathologies. The aim of this study was to determine EBV genotypes and 30‐bp deletion frequency in HIV‐infected patients from Argentina. The study was performed on 258 individuals: Cases: 144 HIV‐infected patients that included: (a) 7 AIDS patients with primary central nervous system lymphoma (PCNSL), (b) 62 AIDS patients, and (c) 75 asymptomatic HIV‐infected patients. Controls: 114 HIV‐negative individuals. EBV genotypes and variants in LMP‐1 gene were detected by polymerase chain reaction (PCR)‐Southern blot on DNA extracted from peripheral blood mononuclear cells and brain biopsies. In PCNSL, the presence of EBV was confirmed by EBER RNA in situ hybridization, and DNA sequencing of 3′ end LMP‐l gene of PCR products was performed. In HIV‐infected patients, EBV‐1 was detected in 48.6%, EBV‐2 in 18.8%, and co‐infection with both genotypes in 32.6%. In control group, EBV‐1 was present in 74.3%, EBV‐2 in 12.4%, and co‐infection in 13.3%. Del‐LMP‐1 was found in 44.4% of HIV‐infected patients samples (20.7% alone and 23.7% co‐infection with non‐deleted form) while it was found in 25.3% (6.3% alone and 19% with co‐infection) in HIV‐negative individuals. In HIV‐infected patients EBV‐2, co‐infection and 30‐bp deletion are more prevalent than in control group. In all, PCNSL brain biopsies samples, del‐LMP‐1 always was detected with EBV‐2, but more cases would have to be included to draw definitive conclusions. J. Med. Virol. 79:401–407, 2007. © 2007 Wiley‐Liss, Inc.
Presence, quantitation and characterization of JC virus in the urine of Italian immunocompetent subjects
Authors: Rossi Andrea , Delbue Serena , Mazziotti Romina , Valli Marilena , Borghi Elisa , Mancuso Roberta , Calvo Maria G. , Ferrante Pasquale 
Published: February 2007

AbstractHuman polyomavirus JC (JCV) infects the worldwide population, remains latent in the kidney, and is excreted in the urine. A longitudinal study was performed in order to evaluate JCV excretion, to characterize molecularly the virus and to determine if its presence in urine is a consequence of viral reactivation or merely of epithelial squamous cell shedding. The presence of cellular sediment and the JCV genome were examined in 333 urine samples collected periodically for 3 months from 17 healthy subjects; molecular characterization, and quantitation of the virus were also undertaken. JCV DNA was detected in 40.2% of the samples, with a significant difference (P < 0.001) observed between males and females. JCV shedding was independent of the presence of cellular sediment in every individual. JCV genotype 1 was the genome detected most frequently, while all of the amplified strains showed archetypal organization of the transcriptional control region (TCR). No clinical symptoms have been associated with JCV excretion and no microbial load was detected in the urine samples. The lack of correlation between JCV DNA detection and the presence of squamous cells in urine sediment indicates that viruria is regulated by the life cycle of JCV. Thus, the virus is eliminated as consequence of its reactivation. J. Med. Virol. 79:408–412, 2007. © 2007 Wiley‐Liss, Inc.
Matrix metalloproteinase‐9 and tissue inhibitor of matrix metalloproteinase‐1 in the respiratory tracts of human infants following paramyxovirus infection
Authors: Elliott Matthew B. , Welliver Robert C. , Laughlin Todd S. , Pryharski Karin S. , LaPierre Natisha A. , Chen Tong , Souza Victor , Terio Nicole B. , Hancock Gerald E. 
Published: February 2007

AbstractRespiratory syncytial (RSV) and parainfluenza (PIV) viruses are primary causes of acute bronchiolitis and wheezing illnesses in infants and young children. To further understand inflammation in the airways following infection, we tested for the presence of matrix metalloproteinases (MMP) and natural tissue inhibitors of MMP (TIMP) in primary and established human cell lines, and in the nasopharyngeal secretions (NPS) of human infants infected with RSV or PIV. Using ELISA and multiplex‐based assays, MMP‐9 and TIMP‐1 proteins were, respectively, detected in 66/67 and 67/67 NPS. During PIV or RSV infection TIMP‐1 concentrations were associated with hypoxic bronchiolitis. TIMP‐1 amounts were also negatively correlated with O2 saturation, and positively correlated with IL‐6, MIP‐1α, and G‐CSF amounts following RSV infection. IL‐6, MIP‐1α, and G‐CSF were negatively correlated with O2 saturation during RSV infection. Acute respiratory tract disease was not associated with MMP‐9 protein/protease activity. Additional studies using real‐time quantitative PCR suggested that MMP‐9 mRNA copy numbers were elevated in normal human bronchial epithelial (NHBE) cells infected with RSV, while TIMP‐1 and TIMP‐2 were not increased. However, ELISA did not reveal MMP‐9 protein in the NHBE cell culture supernatants. Hence, the data implied that airway epithelial cells were not the primary source of MMP or TIMP following paramyxovirus infection. Taken together, the data suggested that paramyxovirus infection perturbs MMP‐9/TIMP‐1 homeostasis that in turn may contribute to the severity of respiratory tract disease. J. Med. Virol. 79:447–456, 2007. © 2007 Wiley‐Liss, Inc.
Hypophysectomy for disseminated prostatic carcinoma
Authors: Murphy G. P. , Boctor Z. N. , Gailani S. , Belmusto L. 
Published: February 2007

AbstractA series of 15 patients with disseminated prostatic carcinoma were treated with open or cryosurgical hypophysectomy, following relapse from conventional forms of hormonal therapy. Six of 15 patients (40%) had objective and subjective signs of clinical and chemical response. To date, however, patients in remission have not demonstrated a significant prolongation in survival. Human growth hormone (HGH) levels were used to test the degree of functional suppression of pituitary function posthypophysectomy. Cryosurgical hypophysectomy, although an admittedly anatomically incomplete procedure, can induce marked reduction in activity of the anterior pituitary as judged by the HGH responses. The levels of plasma growth hormone suggested some residual pituitary tissue (hypofunction) rather than complete ablation. The decreased operative mortality and present results with cryosurgical hypophysectomy for disseminated prostatic carcinoma are encouraging and may permit the application of this form of therapy to a greater number of patients.
Purified roswell park cultured antilymphocytie globulin RPMI‐CALG: Preparation and clinical trial
Authors: Moore G. E. , Murphy G. P. , Papermaster B. W. , Amiraian K. , Kenny G. M. , Moore R. H. 
Published: February 2007

AbstractPurified human antilymphocytic globulin (RPMI‐CALG) has been prepared in bulk quantities by immunization of horses with purified normal lymphocytes maintained in continuous cell culture at the Roswell Park Cell Plant. The characterization studies herein described reveal RPMI‐CALG to be purified, nontoxic, and nonpyrogenic with specific in vitro immunosuppressive activity. Contamination with hemolysins and hemagglutinins is minimal and in marked contrast to other available preparations. Initial clinical trials with a lyophilized preparation reveal that it can be safely administered intravenously to humans without untoward effects. Comparison of hematological data was made on patients receiving RPMI‐CALG pretransplant without other immunosuppressive agents to the same patients post‐transplant receiving RPMI‐CALG plus azathioprine and prednisone. No significant depressive hematological effect was apparent. Platelets were not depressed. Eosinophilia was not seen acutely or on follow‐up examination. Urticaria was not evident. Follow‐up studies up to 6 months after allografting failed to reveal any specific toxicity in the measured hematological parameters. This purified preparation merits further clinical trial.
The effects of uremia on erythropoietin activity
Authors: Mirand Edwin A. , Murphy Gerald P. 
Published: February 2007

AbstractErythropoietin (ESF) activity was determined during acute and chronic uremic states with and without evidence of excretory renal function in humans. These observations demonstrated that detectable endogenous levels of ESF were absent in humans during an acute and chronic uremic state. Unlike the humans, the experimental animals produced ESF at a diminished rate. Also, in experimental animals, factors appear by 48–60 hr which make the bone marrow and spleen less responsive to exogenous ESF. Therefore, the human and nonhuman data show that the anemia of the uremic state can be explained by two factors: (1) an initial inhibition of end‐organ ESF responsiveness, and (2) a failure in ESF production. The temporal difference in the effect of these two aspects of erythropoietin activity is perhaps the basis for the variability in measured ESF activity in acute and chronic uremic states.
Simultaneous bilateral radical neck dissection following high‐level radiation therapy
Authors: Mooney Charles S. , Jewell William , Greenlaw Robert , Rush Benjamin F. 
Published: February 2007

AbstractTwenty‐two patients with advanced cancer in the area of the head and neck were treated by combining major curative radiation (5000‐8000 rads) and a composite operation including excision of the primary lesion and bilateral radical neck dissection. The mortality and morbidity of combining these two treatment methods was quite acceptable and did not exceed mortality and complication rates for this type of operation done without prior radiation.