bluuebunny/crossref_metadata_2025_split huggingface dataset:
WWOX hypomorphic mice display a higher incidence of B‐cell lymphomas and develop testicular atrophy
Authors: Ludes‐Meyers John H. , Kil Hyunsuk , Nuñez Maria I. , Conti Claudio J. , Parker‐Thornburg Jan , Bedford Mark T. , Aldaz C. Marcelo 
Published: September 2007

AbstractWWOX is a putative tumor suppressor gene encoded within common chromosomal fragile site region FRA16D, in chromosome band 16q23. Multiple studies have demonstrated that WWOX expression is often reduced or lost in various tumor types. WWOX tumor suppressor activity was suggested by re‐expressing WWOX in breast, ovarian, and lung tumor cell lines leading to tumor growth inhibition in vivo. To determine whether loss of Wwox gene expression has a role in tumorigenesis, we generated a mouse strain containing a Wwox gene mutated by a gene‐trap vector. Homozygous Wwox gene‐trap mice (Wwoxgt/gt) had no detectable Wwox protein in most tissues examined, although, a low level could be detected in a minority of tissues. Because of these observations, we concluded that these mice are Wwox hypomorphs. Remarkably, Wwox hypomorphic mice are viable in contrast to the recently reported postnatal lethality of Wwox knockout mice. Testes from Wwoxgt/gt males had high numbers of atrophic seminiferous tubules and reduced fertility when compared with wild‐type counterparts. We observed that the Wwoxgt/gt mice had a significantly shorter lifespan, and female hypomorphs had a higher incidence of spontaneous B‐cell lymphomas. In conclusion, we describe a novel Wwox hypomorphic mouse model that overcomes postnatal lethality that was recently observed in Wwox knockout mice. Therefore, tumorigenesis studies using this model more closely recapitulates the loss of WWOX expression observed in human cancers. Importantly, our observation that Wwox hypomorphs had an increased incidence of B‐cell lymphomas supports a role of Wwox as a tumor suppressor. © 2007 Wiley‐Liss, Inc.
Resident microglia die and infiltrated neutrophils and monocytes become major inflammatory cells in lipopolysaccharide‐injected brain
Authors: Ji Kyung‐Ae , Yang Myung‐Soon , Jeong Hey‐Kyeong , Min Kyoung‐Jin , Kang Seung‐Hee , Jou Ilo , Joe Eun‐Hye 
Published: September 2007

AbstractGenerally, it has been accepted that microglia play important roles in brain inflammation. However, recently several studies suggested possible infiltration of blood neutrophils and monocytes into the brain. To understand contribution of microglia and blood inflammatory cells to brain inflammation, the behavior of microglia, neutrophils, and monocytes was investigated in LPS (lipopolysaccharide)‐injected substantia nigra pars compacta, cortex, and hippocampus of normal and/or leukopenic rats using specific markers of neutrophils (myeloperoxidase, MPO), and microglia and monocytes (ionized calcium binding adaptor molecule‐1, Iba‐1), as well as a general marker for these inflammatory cells (CD11b). CD11b‐immunopositive (CD11b+) cells and Iba‐1+ cells displayed similar behavior in intact and LPS‐injected brain at 6 h after the injection. Interestingly, however, CD11b+ cells and Iba‐1+ cells displayed significantly different behavior at 12 h: Iba‐1+ cells disappeared while CD11b+ cells became round in shape. We found that CD11b/Iba‐1‐double positive (CD11b+/Iba‐1+) ramified microglia died within 6 h after LPS injection. The round CD11b+ cells detected at 12 h were MPO+. These CD11b+/MPO+ cells were not found in leukopenic rats, suggestive of neutrophil infiltration. MPO+ neutrophils expressed inducible nitric oxide synthase, interleukin‐1β, cyclooxygenase‐2, and monocyte chemoattractant protein‐1, but died within 18 h. CD11b+ cells detected at 24 h appeared to be infiltrated monocytes, since these cells were once labeled with Iba‐1 and were not found in leukopenic rats. Furthermore, transplanted monocytes were detectable in LPS‐injected brain. These results suggest that at least a part of neutrophils and monocytes could have been misinterpreted as activated microglia in inflamed brain. © 2007 Wiley‐Liss, Inc.
Differentiation of primary adult microglia alters their response to TLR8‐mediated activation but not their capacity as APC
Authors: Zuiderwijk‐Sick Ella A. , van der Putten Céline , Bsibsi Malika , Deuzing Ilona P. , de Boer Willem , Persoon‐Deen Carla , Kondova Ivanela , Boven Leonie A. , van Noort Johannes M. , 't Hart Bert A. , Amor Sandra , Bajramovic Jeffrey J. 
Published: September 2007

AbstractActivated microglia are found in a variety of neuroinflammatory disorders where they have attributed roles as effector as well as antigen‐presenting cells (APC). Critical determinants for the multifaceted role of microglia are the differentiation potential of microglia and their mode of activation. In this study, we have investigated the effects of M‐CSF and GM‐CSF‐mediated differentiation of adult primate microglia on their cellular phenotype, antigen presentation, and phagocytic function as well as on Toll‐like receptor (TLR)‐mediated responses. We show that although cell morphology and expression levels of activation markers were markedly different, differentiation with either factor yielded microglia that phenotypically and functionally resemble macrophages. Both M‐CSF and GM‐CSF‐differentiated microglia were responsive to TLR1/2, 2, 3, 4, 5, 6/2, and 8‐mediated activation, but not to TLR7 or 9‐mediated activation. Intriguingly, M‐CSF‐differentiated microglia expressed higher levels of TLR8‐encoding mRNA and protein, and produced larger amounts of proinflammatory cytokines in response to TLR8‐mediated activation as compared to GM‐CSF‐differentiated microglia. While differentiation of adult microglia by growth factors that can be produced endogenously in the central nervous system is thus unlikely to change their APC function, it can alter their innate responses to infectious stimuli such as ssRNA viruses. Resident primate microglia may thereby help shape rather than initiate adaptive immune responses. © 2007 Wiley‐Liss, Inc.
Developmental expression of FMRP in the astrocyte lineage: Implications for fragile X syndrome
Authors: Pacey Laura K. K. , Doering Laurie C. 
Published: September 2007

AbstractOne of the most common causes of mental retardation in humans, Fragile X syndrome, results from the absence of FMRP, the protein product of the FMR1 gene. In the nervous system, expression of FMRP has been thought to be confined mainly to neurons as little research has examined FMRP expression in non‐neuronal lineages. We present evidence that, in addition to neuronal expression, FMRP is expressed in developing CNS glial cells in vitro and in vivo. The neurosphere assay was used to establish cultures of stem and progenitor cells from the brains of wildtype and FMRP knockout (B6.129.FMR1/FvBn) mouse pups. When the neurospheres were differentiated in vitro, ∼50% of the FMRP positive cells also expressed GFAP. Immunocytochemical studies of the embryonic and postnatal mouse brain revealed coexpression of FMRP and GFAP in the developing hippocampus. Prominent coexpression was also observed in ependymal cells surrounding the third ventricle and astrocytes of the glia limitans. No double‐labeled cells were evident in the brains of young adult mice. Cells coexpressing FMRP and the oligodendrocyte precursor marker NG2 were also identified in the hippocampus and corpus callosum of the early postnatal brain. Our results suggest that FMRP is expressed in cells of non‐neuronal lineage(s) during development. This represents potential involvement of glial cells in the neural development of fragile X syndrome. © 2007 Wiley‐Liss, Inc.
Dulxanthone A induces cell cycle arrest and apoptosis via up‐regulation of p53 through mitochondrial pathway in HepG2 cells
Authors: Tian Ze , Shen Jie , Moseman Annie P. , Yang Quanli , Yang Junshan , Xiao Peigen , Wu Erxi , Kohane Isaac S. 
Published: September 2007

AbstractNatural products derived from plants provide a rich source for development of new anticancer drugs. Dulxanthone A was found to be an active cytotoxic component in Garcinia cowa by bioactivity‐directed isolation. Studies to elucidate the cytotoxic mechanisms of dulxanthone A showed that dulxanthone A consistently induced S phase arrest and apoptosis in the most sensitive cell line HepG2. Furthermore, p53 was dramatically up‐regulated, leading to altered expression of downstream proteins upon dulxanthone A treatment. Cell cycle related proteins, such as cyclin A, cyclin B, cyclin E, cdc‐2, p21 and p27 were down‐regulated. Some apoptosis correlated proteins were also altered following the drug treatment. Bcl‐2 family members PUMA was up‐regulated while Bcl‐2 and Bax were down‐regulated. However, the expression ratio of Bax/Bcl‐2 was increased. This resulted in the release of cytochrome C from the mitochondria to the cytosol. Concurrently, Apaf‐1 was stimulated with p53 by dulxanthone A. In result, cytochrome C, Apaf‐1 and procaspase‐9 form an apoptosome, which in turn triggered the activation of caspase‐9, caspase‐3 and downstream caspase substrates. Lamin A/C and PARP were down‐regulated or cleaved, respectively. Moreover, cell cycle arrest and apoptosis in HepG2 cells induced by dulxanthone A were markedly inhibited by siRNA knockdown of p53. In summary, dulxanthone A is an active cytotoxic component of G. cowa. It induces cell cycle arrest at lower concentrations and triggers apoptosis at higher concentrations via up‐regulation of p53 through the intrinsic mitochondrial pathway in HepG2 cells. Dulxanthone A is therefore likely a promising preventive and/or therapeutic agent against Hepatoma. © 2007 Wiley‐Liss, Inc.
A ratings‐based approach to measuring sovereign risk
Authors: Remolona Eli M. , Scatigna Michela , Wu Eliza 
Published: September 2007

AbstractWe propose a new approach to measuring sovereign default risk. We use sovereign credit ratings and historical default rates provided by credit rating agencies to construct a measure of ratings‐implied expected loss. We compare our measure of expected loss from sovereign defaults with stand‐alone credit ratings and also examine its relationship with credit default swap spreads. We show that our measure is more informative for measuring sovereign risk. We re‐examine the fundamental determinants of sovereign risk and find further evidence to support the debt intolerance and original sin explanations for country risk. This study contributes an improved understanding of the value of sovereign credit rating teams in assessing the long‐term country risks accompanying emerging market investments. Copyright © 2007 John Wiley & Sons, Ltd.
The development of maternal self‐esteem
Authors: Farrow C. , Blissett J. 
Published: September 2007

AbstractAlthough an important theoretical concept, little is known about the development of maternal self‐esteem. This study explores the significance of maternal cognitions, psychopathological symptoms, and child temperament in the prediction of prenatal and postnatal maternal self‐esteem. During pregnancy 162 women completed measures assessing their unhealthy core beliefs, psychopathological symptoms, and self‐esteem. At 1 year postpartum 87 of these women completed measures assessing their self‐esteem and their child's temperament. Overall maladaptive maternal core beliefs and psychopathological symptoms during pregnancy explained 19% of the variance in prenatal maternal self‐esteem. Forty‐two percent of the variance in maternal self‐esteem at 1 year could be explained by a combination of prenatal maternal self‐esteem, mental health symptoms, maternal core beliefs, and more unsociable infant temperament. Underlying maternal cognitive structures may be important in determining the development of maternal self‐esteem.
Caspase‐cleaved cytokeratin 18 and 20 S proteasome in liver degeneration
Authors: Hetz Hubert , Hoetzenecker Konrad , Hacker Stefan , Faybik Peter , Pollreisz Andreas , Moser Bernhard , Roth Georg , Hoetzenecker Wolfram , Lichtenauer Michael , Klinger Markus , Krenn Claus Georg , Ankersmit Hendrik Jan 
Published: September 2007

AbstractApoptosis of epithelial hepatocytes plays a pivotal role in acute as well as in chronic liver diseases. The cleavage of cytokeratin‐18 (CK‐18) by caspases is an early event in the apoptotic process. We therefore sought to investigate serum levels of CK‐18 and 20S proteasome in patients with liver cirrhosis, primary graft dysfunction (PDF), and acute liver failure (ALF), and in healthy volunteers. Enzyme‐linked immunosorbent assay (ELISA) was utilized to measure the concentration of M30, a fragment of CK‐18 cleaved at Asp396 (M30 neoantigen), and the concentration of 20S proteasome. Serum levels of the CK‐18 neoepitope M30 were significantly increased in ALF, primary graft dysfunction, and liver cirrhosis vs. healthy controls (1,993.6±124.7 U/L, 2,238.1±235.9 U/L, and 673.6±86.5 U/L vs. 66.8±29.1 U/L, respectively, P<0.001). Similar results were detected with the evaluation of 20S proteasome (124,014.5±13,235.6 ng/mL, 76,993.2±15,720.1 ng/mL, and 2,395.9±1,098.2 ng/mL vs. 1,074.5±259.4 ng/mL, respectively; P<0.001). Detection of CK‐18 neoepitope M30 and 20S proteasome may represent a novel marker of tracing apoptotic epithelium, respectively mirroring degenerative liver processes in affected patient population. J. Clin. Lab. Anal. 21:277–281, 2007. © 2007 Wiley‐Liss, Inc.
Levels of serum sialic acid and thiobarbituric acid reactive substances in subjects with impaired glucose tolerance and type 2 diabetes mellitus
Authors: Yilmaz Gulsen , Yilmaz Fatma Meric , Aral Yalcin , Yucel Dogan 
Published: September 2007

AbstractCardiovascular disease is a common cause of death for diabetic patients. High sialic acid levels (SA) and increased oxidative stress are important factors for cardiovascular diseases. We aimed to research whether SA and thiobarbituric acid reactive substances (TBARS) levels are associated with the degree of the diabetic regulation and investigate if SA and TBARS levels can be controlled with the regulation of the blood glucose levels. A total of 179 subjects were included in the study. Three groups, which were comprised of subjects with type 2 diabetes mellitus (DM) (DM group [DMG], n=149), impaired glucose tolerance (IGT) (IGT group [IGTG], n=15), and normal oral glucose tolerance (NGT) (NGTgroup [NGTG], n=15) were constituted. Glucose, cholesterol, high‐density lipoprotein (HDL) and glycated hemoglobin (HbA1C), SA, and TBARS were measured in the sera of the patients. SA and TBARS levels were significantly increased in subjects with type 2 DM (P<0.001 for both). SA concentrations showed significant correlation with triglycerides (r=0.229; P<0.05), fasting glucose (r=0.508; P<0.01), 2‐hr postprandial glucose (r=0.455; P<0.01), and HbA1C (r=0.467; P<0.01), and there was a positive correlation between TBARS and HbA1C (r=0.251; P<0.01). Diabetic patients were found to have higher risk for inflammation and oxidative stress. The regulation of blood glucose levels may contribute to the decline of both SA and TBARS levels. J. Clin. Lab. Anal. 21:260–264, 2007. © 2007 Wiley‐Liss, Inc.
Determination of leukocyte counts in cerebrospinal fluid with a disposable plastic hemocytometer
Authors: Yamanishi Hachiro , Imai Nobuko , Suehisa Etsuji , Kanakura Yuzuru , Iwatani Yoshinori 
Published: September 2007

AbstractManual microscopic cell counting in a Fuchs‐Rosenthal (FR) chamber has been the gold standard for quantification of leukocytes in cerebrospinal fluid (CSF). However, for accurate determination of the number and differentiation of cells by chamber counting, hemocytometers must be prepared carefully and kept clean. Improper fitting of the chamber and coverslip changes the volume of sample introduced into the chamber well. Moreover, because conventional hemocytometers are used repeatedly and are breakable, there is a risk of exposure to potentially infectious material. To address these issues, disposable plastic hemocytometers have been developed. However, the accuracy, precision, and clinical usefulness of disposable chambers for CSF cells counting have not been determined. In the present study, we evaluated use of a disposable plastic counting chamber (C‐Chip DHC‐F01) by comparing its performance with that of an FR chamber for counting of CSF specimens and cell suspensions. Within‐run precision of C‐Chip counting was comparable or superior to that of FR chamber counting, and excellent correlation between cell counts obtained with the C‐Chip chamber and FR chamber was observed. However, C‐Chip chambers that were kept at 4°C yielded significantly low cell counts. The disposable hemocytometer will reduce the risk of exposure to potentially infectious material. However, use of C‐Chip chambers should be avoided in cold environments. J. Clin. Lab. Anal. 21:282–285, 2007. © 2007 Wiley‐Liss, Inc.
NA1/NA2 heterozygote of Fcgr3b is a risk factor for progression of IgA nephropathy in Chinese
Authors: Xu Gaosi , He Qiang , Shou Zhangfei , Wang Huiping , Zhang Xiaohui , Wang Yaomin , Chen Ying , Chen Jianghua 
Published: September 2007

AbstractSeveral studies have identified FcgRIIIb (Fcgr3b) polymorphisms that determine susceptibility to autoimmune diseases such as systemic lupus erythematosus and rheumatoid arthritis. The objective of the study was to clarify whether Fcgr3b allele polymorphism influence susceptibility to immunoglobulin A nephropathy (IgAN), clinical features or severity in patients with IgAN. Deoxyribonucleic acid (DNA) fragments were amplified by polymerase chain reaction (PCR) using genomic DNA from 172 unrelated, healthy blood donors and 128 IgAN patients in our Kidney Disease Centre. The present findings showed that Fcgr3b genotype influenced the disease susceptibility and severity of IgAN, although Fcgr3b polymorphism did not affect the age of the disease onset. We found that the genotype frequency of Fcgr3b heterozygote NA1/NA2 in IgAN patients in Chinese significantly higher than that of healthy donors. Furthermore, higher genotype frequency of NA1/NA2 was found also in IgAN patients with glomerulosclerosis or crescent formation than those without it. NA1/NA2 heterozygote of Fcgr3b is a risk factor for progression of IgA nephropathy in Chinese. J. Clin. Lab. Anal. 21:298–302, 2007. © 2007 Wiley‐Liss, Inc.
Development of an ELISA method for detecting immune complexes between tissue‐nonspecific alkaline phosphatase and immunoglobulin G
Authors: Hocchi Kazuo , Ohashi Tatsuya , Miura Toshihide , Sasagawa Kumiko , Sato Yasuhito , Nomura Fumio , Tomonaga Takeshi , Sunaga Masahiko , Kojima Ryo , Katayama Katsuhiro , Kato Toshiyuki , Sato Toyoji , Komoda Tsugikazu , Oda Kimimitsu 
Published: September 2007

AbstractA convenient method for measuring immune complexes between tissue‐nonspecific alkaline phosphatase (TNSALP) and immunoglobulin G (IgG) (i.e., TNSALP‐IgG) would be highly useful for routine analyses. Here, we identified a surface‐active agent that would dissolve membrane but not dissociate TNSALP‐IgG complexes. Next, we developed an enzyme‐linked immunosorbent assay (ELISA) method for detecting TNSALP‐IgG complexes with two monoclonal antibodies (MoAbs): 3‐29‐3R was coated on assay plates and captured TNSALP‐IgG from a specimen; an horseradish peroxidase (HRP)‐conjugated anti‐human IgG1 then reacted with captured TNSALP‐IgG to form an “immunocomplex sandwich.” The immunocomplex was detected via the absorbance of an HRP substrate, resulting in a semiquantitative assay. The mean absorbance of 0.195 (n=5) measured in sera from healthy donors was designated as an arbitrary unit (AU/mL) of TNSALP‐IgG concentration. The ELISA values of patient sera known to contain TNSALP‐IgG complexes were greater than those of normal sera (normal, 1.86 plusmn; 0.61; patient, 9.30 plusmn; 5.44), and these data were confirmed by electrophoresis. Thus, the ELISA could detect TNSALP‐IgG complexes. The intraassay coefficient of variation (CV) was within 7.4% and analytical recovery was excellent. There was no significant interference from hemolytic, lipemic, or icteric serum. In summary, an ELISA using 3‐29‐3R MoAb and HRP‐conjugated anti‐human IgG1 constitutes a reliable and convenient method for the semiquantitative detection of TNSALP‐IgG complexes in human serum. J. Clin. Lab. Anal. 21:322–329, 2007. © 2007 Wiley‐Liss, Inc.
The average degree of an edge‐chromatic critical graph II
Authors: Woodall Douglas R. 
Published: September 2007

AbstractA graph G with maximum degree Δ and edge chromatic number $\chi\prime({G}) > \Delta$ is edge‐Δ‐critical if $\chi\prime{(G-e)} = \Delta$ for every edge e of G. It is proved that the average degree of an edge‐Δ‐critical graph is at least ${2\over 3}{(\Delta+1)}$ if $\Delta \geq 2$, at least ${2\over 3}\Delta + 1$ if $\Delta \geq 8$, and at least ${2\over 3}(\Delta + 2)$ if $\Delta \geq 15$. For large Δ, this improves on the best bound previously known, which was roughly ${1\over 2}(\Delta+\sqrt{2\Delta})$. © Wiley Periodicals, Inc. J. Graph Theory 56: 194–218, 2007
Self‐organization versus Watchmaker: ambiguity of molecular recognition and design charts of cellular circuitry
Authors: Kurakin Alexei 
Published: September 2007

AbstractA large body of experimental evidence indicates that the specific molecular interactions and/or chemical conversions depicted as links in the conventional diagrams of cellular signal transduction and metabolic pathways are inherently probabilistic, ambiguous and context‐dependent. Being the inevitable consequence of the dynamic nature of protein structure in solution, the ambiguity of protein‐mediated interactions and conversions challenges the conceptual adequacy and practical usefulness of the mechanistic assumptions and inferences embodied in the design charts of cellular circuitry. It is argued that the reconceptualization of molecular recognition and cellular organization within the emerging interpretational framework of self‐organization, which is expanded here to include such concepts as bounded stochasticity, evolutionary memory, and adaptive plasticity offers a significantly more adequate representation of experimental reality than conventional mechanistic conceptions do. Importantly, the expanded framework of self‐organization appears to be universal and scale‐invariant, providing conceptual continuity across multiple scales of biological organization, from molecules to societies. This new conceptualization of biological phenomena suggests that such attributes of intelligence as adaptive plasticity, decision‐making, and memory are enforced by evolution at different scales of biological organization and may represent inherent properties of living matter. Copyright © 2007 John Wiley & Sons, Ltd.