bluuebunny/crossref_metadata_2025_split huggingface dataset:
A multicenter evaluation of the PanLeucogating method and the use of generic monoclonal antibody reagents for CD4 enumeration in HIV‐infected patients in Thailand
Authors: Pattanapanyasat Kovit , Shain Hla , Noulsri Egarit , Lerdwana Surada , Thepthai Charin , Prasertsilpa Varipin , Likanonsakul Sirirat , Yothipitak Prakit , Nookhai Somboon , Eksaengsri Achara 
Published: March 2005

AbstractBackgroundThe current method of CD4 enumeration in Thailand, based on the three‐tube, three‐color method recommended by the Centers for Disease Control and Prevention, is expensive and thus unavailable to most patients who have the human immunodeficiency virus (HIV). Less expensive, simpler protocols (i.e., PanLeucogating and primary CD4 gating) have been described but require more published validation data to gain widespread acceptance. We describe a multicenter evaluation of the PanLeucogating method.MethodsThe PanLeucogating method using generic reagents was evaluated in comparison with the standard three‐tube, three‐color method using commercial reagents. Percentage of CD4+ T cells among lymphocytes and absolute CD4+ T‐cell counts were determined in 611 HIV‐infected individuals recruited from four sites. Linear regression and Bland‐Altman tests were used for statistical analysis.ResultsThe correlation of percentage of CD4+ T cells and absolute CD4+ T‐cell counts obtained with the PanLeucogating strategy and the standard predicate method was high (r2 = 0.96 and 0.95, respectively, for the entire study population and r2 > 0.95 and 0.93, respectively, for each study group). Absolute CD4+ T‐cell counts of the overall study pool and of the two subdivisions of absolute CD4+ T‐cell counts (i.e., 0–250 cells/μl and >250 cells/μl) derived from the two methods demonstrated excellent agreement, with mean biases of +18 cells/μl, +11 cells/μl, and +24 cells/μl, respectively.ConclusionsThese observations demonstrate that CD4 enumeration by PanLeucogating is reliable and can be performed to an identical standard in a quality‐assured network of collaborating laboratories as a new cost‐effective approach to HIV monitoring. © 2005 Wiley‐Liss, Inc.
Improved detection of minimal acute myeloid leukemia cells by the use of the combined parameters of XE‐2100 hematology analyzer
Authors: Tohyama Kaoru , Shiga Shuichi , Itose Yuji , Uchihashi Kinya , Ohkura Mitsugi , Takahashi Keiko , Itoh Mitsuru , Ichiyama Satoshi , Hamaguchi Yukio 
Published: March 2005

AbstractBackgroundFor the diagnosis and therapy of acute leukemia, it is important to detect a small number of leukemic cells precisely. Although several automated hematology analyzers that carry blast‐detecting programs have been developed, they do not exert sufficient detection sensitivity to exceed the sensitivity of manual eye counting method.MethodsWe constructed a new blast‐detecting program by combining the numerical information acquired from five cytometric parameters presented by XE‐2100. The sensitivity and specificity of this blast multi‐scoring program were assessed in comparison with the Blasts flag program equipped originally in XE‐2100.ResultsThe blast‐detecting sensitivity was found to be highly improved in the blast multi‐scoring program as compared with the Blasts flag program without much decreasing the specificity. A small number of leukemic myeloblasts was detected at the better sensitivity than the eye counting method in the clinical course of the patients with acute myeloid leukemia.ConclusionsThe daily practical use of this blast multi‐scoring program will surely contribute to sensitive, objective, and real‐time evaluation of the control of acute myeloid leukemia with a low cost. © 2005 Wiley‐Liss, Inc.
Emission factors for asphalt‐related emissions in roofing manufacturing
Authors: Trumbore David , Jankousky Angela , Hockman Edwin L. , Sanders Ronald , Calkin John , Szczepanik Steve , Owens Roy 
Published: March 2005

AbstractThe vast majority of all residential construction in the United States is roofed with asphalt shingles, and asphalt products are also used extensively for commercial roofing. These roofing products are made in roughly 100 manufacturing facilities, by processing about six million tons of asphalt per year. The Asphalt Roofing Manufacturing Association (ARMA) has developed emission factors for asphalt‐related air emissions for all relevant processes in the manufacture of roofing asphalt and fiberglass based roofing products. These processes include asphalt blowing, asphalt storage, and the coating of fiberglass mat with filled asphalt. The emission factors are based on measurements in more than 20 facilities around the country. They replace old, very limited data currently available from the US EPA in their AP‐42 document. In some cases, as with particulate emissions from asphalt blowing, the new emission factors are much lower than the current AP‐42 factors. In other cases, emissions not included in AP‐42 are recognized to be significant, as with SOx emissions from asphalt blowing. Both criteria and hazardous air pollutant (HAP) emissions are covered in this compilation. Roofing asphalt processes are shown to be a very minor contributor to polyaromatic hydrocarbon (PAH) emissions. These data have been submitted to the US EPA for their consideration, and the HAP data presented here constituted the basis for the EPA MACT rulemaking for this industry. © 2005 American Institute of Chemical Engineers Environ Prog, 2005
Oxidation and absorption of nitric oxide in a packed tower with sodium hypochlorite aqueous solutions
Authors: Chen Luke , Hsu Chung‐Hao , Yang Chen‐Lu 
Published: March 2005

AbstractThe oxidation and absorption of nitric oxide (NO) with sodium hypochlorite aqueous (NaClO) solutions were studied to develop a two‐stage chemical scrubbing system for NOx control. In the second stage, the most practical medium for NO2 absorption is sodium sulfite aqueous solution. Although a few two‐stage systems have been installed, there are major gaps in developing NaClO aqueous solutions for NO oxidation in the first stage. Of particular importance is the lack of reliable information on rates of the chemical oxidation. A pilot‐scale research program is initiated to evaluate the oxidation rate of NO with NaClO aqueous solutions in a packed tower. The research is directed toward obtaining the height of a transfer unit (HTU) for NO oxidation and acquiring reasonable operating conditions for the packed‐bed scrubbing system. At pH 5.3, NaClO is an excellent scrubbing medium. The results are consistent with hypochlorous acid (HClO) being the oxidizing agent in the solution. The results also indicate that the liquid mass flow rate is a minor parameter that affects the NO oxidation and absorption in the scrubber. A NaClO concentration of >0.8% is crucial for high NO oxidation. © 2005 American Institute of Chemical Engineers Environ Prog, 2005
Stem/progenitor cell proliferation factors FGF‐2, IGF‐1, and VEGF exhibit early decline during the course of aging in the hippocampus: Role of astrocytes
Authors: Shetty Ashok K. , Hattiangady Bharathi , Shetty Geetha A. 
Published: March 2005

AbstractDentate neurogenesis, important for learning and memory, declines dramatically by middle age. Although studies have shown that this age‐related decrease can be reversed to some extent by exogenous applications of mitogenic factors, it is unclear whether one or more of these factors exhibits decline by middle age. We hypothesize that multiple stem/progenitor cell proliferation factors exhibit early decline during the course of aging in the hippocampus, and some of these declines are linked to age‐related alterations in hippocampal astrocytes. We measured the concentrations of fibroblast growth factor‐2 (FGF‐2), insulin‐like growth factor‐1 (IGF‐1), and vascular endothelial growth factor (VEGF) in the hippocampus of young, middle‐aged, and aged F344 rats, using enzyme‐linked immunosorbent assay (ELISA). In addition, we quantified the total number of FGF‐2 immunopositive (FGF‐2+) and glial fibrillary acidic protein immunopositive (GFAP+) cells in the dentate gyrus and the entire hippocampus. Our results provide new evidence that the concentrations of FGF‐2, IGF‐1, and VEGF decline considerably by middle age but remain steady between middle age and old age. Further, decreased concentrations of FGF‐2 during aging are associated with decreased numbers of FGF‐2+ astrocytes. Quantification of GFAP+ cells, and GFAP and FGF‐2 dual immunostaining analyses, reveal that aging does not decrease the total number of astrocytes but fractions of astrocytes that express FGF‐2 decline considerably by middle age. Thus, dramatically decreased dentate neurogenesis by middle age is likely linked to reduced concentrations of FGF‐2, IGF‐1, and VEGF in the hippocampus, as each of these factors can individually influence the proliferation of stem/progenitor cells in the dentate gyrus. Additionally, the results demonstrate that decreased FGF‐2 concentration during aging is a consequence of age‐related impairment in FGF‐2 synthesis by astrocytes. © 2005 Wiley‐Liss, Inc.
Induction of blood‐brain barrier properties in cultured brain capillary endothelial cells: Comparison between primary glial cells and C6 cell line
Authors: Boveri Monica , Berezowski Vincent , Price Anna , Slupek Stephanie , Lenfant Anne‐Marie , Benaud Christelle , Hartung Thomas , Cecchelli Romeo , Prieto Pilar , Dehouck Marie‐Pierre 
Published: March 2005

AbstractThe communication between glial cells and brain capillary endothelial cells is crucial for a well‐differentiated blood‐brain barrier (BBB). It has been suggested that in vitro primary glial cells (GCs) be replaced by the glial C6 cell line to standardise the model further. This study compares directly the structural and functional differentiation of bovine brain capillary endothelial cells (BBCECs) induced by co‐culture with rat primary GCs or C6 cells, for the first time. Trans‐endothelial electrical resistance (TEER) measurements showed that under no condition were C6 cells able to reproduce TEER values as high as in the presence of GCs. At the same time, permeability of the BBCECs to both radioactive sucrose and FITC‐inulin was 2.5‐fold higher when cells were co‐cultured with C6 than with GCs. Furthermore, immunocytochemistry studies showed different cell morphology and less developed tight junction pattern of BBCECs co‐cultured with C6 toward GCs. Additionally, studies on P‐glycoprotein (P‐gp) showed much lower P‐gp presence and activity in BBCECs co‐cultured with C6 than GCs. Both VEGF mRNA expression and protein content were dramatically increased when compared with GCs, suggesting that VEGF could be one of the factors responsible for higher permeability of BBB. Our results clearly indicate that, in the presence of the glial C6 cell line, BBCECs did not differentiate as well as in the co‐culture with primary GCs at both structural and functional levels. © 2005 Wiley‐Liss, Inc.
Purkinje cell dendrites grow in alignment with Bergmann glia
Authors: Lordkipanidze Tamar , Dunaevsky Anna 
Published: March 2005

AbstractThe pattern of growth of Purkinje cell dendrites has been analyzed and related to their interactions with Bergmann glial radial processes. In cerebellar slice cultures from mice expressing green fluorescent protein (GFP) under the glial fibrillary acidic protein (GFAP) promoter, Purkinje cells were transfected and imaged with two‐photon microscopy over 2 days. We report that while the Purkinje cell dendritic tree grows, individual dendrites increase or decrease in length. Importantly, we demonstrate that vertical growth of Purkinje cell dendrites occurs primarily in alignment with radial glial processes. These findings suggest that radial glial processes provide a structural substrate for the directional growth of Purkinje cell dendrites, thus influencing the shape of the dendritic tree. © 2005 Wiley‐Liss, Inc.
Melatonin potentiates flavone‐induced apoptosis in human colon cancer cells by increasing the level of glycolytic end products
Authors: Wenzel Uwe , Nickel Alexander , Daniel Hannelore 
Published: March 2005

AbstractMelatonin is a natural compound synthesized by a variety of organs. It has been described to possess cell protecting activity in normal cells but was shown to induce apoptotic cell death in cancer cells. We determined to which extent and based on which molecular mechanisms melatonin is able to cause apoptosis in HT‐29 human colon cancer cells. Induction of apoptosis was assessed by caspase‐3‐like activity, nuclear fragmentation and chromatin condensation. Melatonin, when given alone at a concentration of 1 mM, did not affect any of the apoptosis markers. It potentiated apoptosis induced by the flavonoid flavone significantly. Whereas flavone alone at a concentration of 150 μM led to a 8‐fold increase in caspase‐3‐like activity associated with around 40% of cells displaying DNA‐fragmentation, a combination of flavone and melatonin increased caspase‐3‐like activity 30‐fold and 80% of cells exhibited fragmentation of DNA when compared to untreated controls. Melatonin caused an increase in cytosolic lactate levels that most likely allows the flavone‐induced activation of the mitochondrial pyruvate/lactate importer to deliver more substrates to mitochondrial respiration. The subsequent increased production of mitochondrial O2− · in the presence of flavone was further increased by melatonin. Scavenging mitochondrial O2−. by benzoquinone or blocking the lactate/pyruvate transporter by 5‐nitro‐2‐(3‐phenylpropylamino) benzoate inhibited mitochondrial O2−.‐generation and apoptosis execution mediated by flavone and melatonin. Our study provides evidence that melatonin potentiates flavone‐induced apoptosis in HT‐29 human colon cancer cells by enhancing the level of oxidizable substrates that can be transported into mitochondria in the presence of flavone. © 2005 Wiley‐Liss, Inc.
Recombinant adeno‐associated virus‐mediated TRAIL gene therapy suppresses liver metastatic tumors
Authors: Ma Hong , Liu Yanxin , Liu Shilian , Kung Hsiang‐Fu , Sun Xueying , Zheng Dexian , Xu Ruian 
Published: March 2005

AbstractTo evaluate the tumoricidal activity of tumor necrosis factor (TNF)‐related apoptosis‐inducing ligand (TRAIL) on disseminated liver metastatic tumors, we constructed a recombinant adeno‐associated virus (rAAV) expressing the extracellular domain (95–281aa) of human TRAIL (TRAIL95–281, and the recombinant virus was designated as rAAV‐TRAIL) using the 3‐plasmid, helper‐virus‐free, packaging system. Transduction of mouse lymphoma EL‐4 cells and Jurkat T cells lead to the expression of TRAIL95–281 protein in both virus‐transduced cells and the culture media, along with apoptosis of these cells in vitro. The therapeutic potential of rAAV‐TRAIL was then evaluated in an orthotopic transplanted mouse model mimicking liver cancer metastasis, which was established by injection of EL‐4 cells into the liver of C57BL/6 mice via the hepatic portal veins. Subsequent intraportal vein injection of rAAV‐TRAIL, not the control virus, into the liver of these mice resulted in significant suppression of tumor growth and prolonged survival, while normal hepatocyte toxicity is undetectable. Histological and biochemical analysis in tumor tissue and serum confirmed that TRAIL95–281 was stably expressed in relatively high level in hepatocytes and was secreted into the serum in active trimeric form. Futhermore, the mechanism for rAAV‐TRAIL to inhibit tumor growth was by inducing apoptosis of the tumor cells metastasizing to the livers. These results strongly suggest that the rAAV‐TRAIL‐mediated gene delivery could be a promising approach for the treatment of liver metastasis cancer. © 2005 Wiley‐Liss, Inc.
Activation of human cancer/testis antigen gene, XAGE‐1, in tumor cells is correlated with CpG island hypomethylation
Authors: Lim Jun Hee , Kim Sang‐Pyo , Gabrielson Edward , Park Yong Bok , Park Jong‐Wook , Kwon Taeg Kyu 
Published: March 2005

AbstractExpression of the XAGE‐1 antigen is restricted to germ cells of the testis and a variety of neoplastic tissues. To date, the molecular mechanism for regulating expression of this cancer/testis antigen gene has been unknown. To evaluate methylation as a potential mechanism for regulating expression of this gene, we first correlated gene methylation status (measured by sequencing of bisulfide‐modified DNA and COBRA) to expression of XAGE‐1 mRNA in normal and cancerous cells. This analysis revealed dense methylation of the CpG island in the XAGE‐1 gene promoter for the normal and cancerous cells that do not express this gene but loss of this methylation in normal testis, cancer cell lines and the primary gastric cancers where the gene is highly expressed. Further supporting the role of methylation in regulating expression of XAGE‐1 were observations that treatment of 2 heavily methylated cell lines, SNU620 and HT29, with 5′‐aza‐deoxycytidine resulted in demethylation of XAGE‐1 promoter and corresponding expression of this gene. Finally, we cloned various segments of the CpG‐rich XAGE‐1 gene promoter linked to a luciferase reporter construct and transiently transfected this construct into HCT116 cells. These experiments confirmed transcriptional regulatory activity for the promoter region that incorporates the CpG island and demonstrated that in vitro methylation of this island results in loss of promoter activity. Collectively, these studies indicate that XAGE‐1 expression in normal and cancerous tissues is regulated by methylation of the CpG island in the gene promoter. © 2005 Wiley‐Liss, Inc.
Oral squamous cell carcinoma cells induce osteoclast differentiation by suppression of osteoprotegerin expression in osteoblasts
Authors: Tada Takeyuki , Jimi Eijiro , Okamoto Masato , Ozeki Satoru , Okabe Koji 
Published: March 2005

AbstractThe invasion of oral squamous cell carcinoma (SCC) cells into the mandibular bone is a common clinical problem. It has been reported that BHY cells, a human oral SCC cell line, are capable of invading mandibular bone of nude mice. These results led us to examine possible mechanisms of osteoclastogenesis induced by BHY cells using in vitro culture systems. When BHY cells were cocultured with mouse bone marrow cells (BMCs), only few osteoclasts were formed, even though BHY cells express the receptor activator of NF‐κB ligand (RANKL). However, adding BHY cells to a coculture of mouse primary osteoblasts (POBs) and BMCs markedly induced osteoclastogenesis in the absence of osteotropic factors. Furthermore, another oral SCC cell line, HSC‐2, which does not express RANKL, also induced osteoclastogenesis in our cocultures. These effects were significantly, but not completely, inhibited by adding osteoprotegerin (OPG). In addition, we also found that TNFα released from these cells partially contributes to osteoclastogenesis via a RANKL‐independent mechanism. Adding BHY or HSC‐2 cells suppressed mouse OPG mRNA expression and protein production by POBs in cocultures of POBs and human oral SCC cells. This finding is consistent with the result that BHY cells and HSC‐2 cells did not enhance osteoclastogenesis in cocultures of BMCs and POBs from OPG‐deficient mice. Immunohistochemical analysis showed a reduction of OPG expression in osteolytic lesions as compared to normal lesions from oral SCC patients. Therefore, oral SCC‐induced suppression of OPG expression in POBs appears critical for osteoclastogenesis, rather than expression of RANKL in SCC cells. © 2005 Wiley‐Liss, Inc.
Herceptin‐induced inhibition of ErbB2 signaling involves reduced phosphorylation of Akt but not endocytic down‐regulation of ErbB2
Authors: Longva Karianne E. , Pedersen Nina Marie , Haslekås Camilla , Stang Espen , Madshus Inger H. 
Published: March 2005

AbstractThe anti‐proliferative effect of the ErbB2 specific antibody Herceptin in cells overexpressing ErbB2 has previously been explained by endocytic downregulation of ErbB2. However, in the following, we demonstrate that Herceptin inhibited proliferation of ErbB2 overexpressing cells without downregulating ErbB2. Herceptin did also not induce endocytosis of ErbB2. Herceptin was found to blunt proliferation of SKBr3 cells overexpressing EGFR, ErbB2, and ErbB3 and expressing functional PTEN, probably by recruiting PTEN to the plasma membrane. Akt was found to be constitutively phosphorylated both in SKBr3 cells overexpressing EGFR, ErbB2 and ErbB3, and in SKOv3 cells, overexpressing EGFR and ErbB2. However, phosphorylation of Akt was inhibited by Herceptin only in SKBr3 cells. SKOv3 cells, which lack the tumour suppressor protein Ras homolog member I, was found to have constitutively phosphorylated mitogen activated protein kinase and functionally increased Ras activity. SKOv3 cells further had low expression levels of PTEN. We thus confirm that the anti‐proliferative effect of Herceptin in SKBr3 cells is due to recruitment of PTEN to the plasma membrane and conclude that Herceptin does not blunt phosphatidyl inositol 3 kinase‐induced growth in cells with constitutive Ras activity. We further conclude that endocytic downregulation of ErbB2 does not contribute to Herceptin's antiproliferative effect. © 2005 Wiley‐Liss, Inc.
Polymorphisms of XRCC1 gene, alcohol consumption and colorectal cancer
Authors: Hong Yun‐Chul , Lee Kwan‐Hee , Kim Woo‐Chul , Choi Sun‐Keun , Woo Ze‐Hong , Shin Soo‐Kyung , Kim Ho 
Published: March 2005

AbstractTo evaluate contribution of polymorphisms of the XRCC1 gene to the risk of colorectal cancer, we conducted a case‐control study of 209 colorectal cancer cases and 209 age‐ and gender‐matched controls in the Korean population. We tested the hypothesis by constructing allele combinations with known SNP. Allelic variants of the XRCC1 gene at codons 194, 280 and 399 were analyzed in lymphocyte DNA by PCR‐RFLP. We observed an increased risk of colorectal cancer associated with the 399Gln allele. The odds ratio (OR) was 1.61 (95% confidence interval [CI] 1.09–2.39) for the 399Gln allele. When combined allele‐specific OR were calculated after estimating frequencies, 3 common allele combinations were found to be associated with an increased risk of colorectal cancer. The OR for the 194Trp‐280Arg‐399Arg was 1.48 (95% CI = 1.06–2.07) using 194Arg‐280Arg‐399Arg as the reference. The OR for the 194Arg‐280His‐399Arg and the 194Arg‐280Arg‐399Gln were 1.78 (95% CI = 1.09–2.89) and 1.78 (95% CI = 1.23–2.59), respectively. Analysis after controlling for smoking, exercise and dietary habits indicated that alcohol consumption (≥80 g/week) is a significant risk factor of colorectal cancer (OR = 2.60, 95% CI = 1.46–4.62). An increased risk for colorectal cancer was identified in alcohol drinkers with the risky allele combinations. Our results suggest that polymorphisms in the XRCC1 genes may contribute to colorectal cancer susceptibility, and some evidence was obtained of a genetic modification for the relationship between alcohol intake and colorectal cancer. © 2005 Wiley‐Liss, Inc.