bluuebunny/crossref_metadata_2025_split huggingface dataset:
Oxidative stress during leukocyte absorption apheresis
Authors: Hirayama Aki , Nagase Sohji , Ueda Atsushi , Ishizu Takashi , Taru Yoshinori , Yoh Keigyou , Hirayama Kouichi , Kobayashi Masaki , Koyama Akio 
Published: July 2003

AbstractLeukocyte absorption apheresis absorbs leukocytes to the apheresis columns involving leukocyte activation. This process is regarded as bioincompatible and avoided in hemodialysis or other extracorporeal circulation processes. Thus, leukocyte apheresis has a potential risk to exacerbate in vivo oxidative stress. We evaluated the changes in plasma oxidative stress during leukocyte apheresis. Patients diagnosed as ulcerative colitis (UC) and treated with leukocyte apheresis were studied. Adacolumn (celluloseacetate beads) or Cellsorba EX (polyethylenephtarate fiber) was used for the leukocyte absorption device. Oxidative stress was measured by thiobarbituric acid reactive substances (TBARS) and hydroxyl radical (•OH) scavenging activity. Plasma samples were collected from the pre‐ and post‐column sampling port at the start, and from the pre‐column sampling port at the end of the treatment. The •OH signal intensities (OHRI) significantly increased during a column passage, indicating a loss of plasma •OH scavenging activity. However, OHRI was reduced at the end, suggesting a recovery of radical scavenging activity during leukocyte apheresis. Significant decreases of OHRI and TBARS were only observed in the early phase of the therapeutic course. No differences of OHRI and TBARS levels were observed between the two columns. These results indicate that though the plasma antioxidant activity was diminished by a column passage, plasma antioxidant activity recovers during the procedure. This efficient antioxidative effect is limited to the early phase of the therapeutic course. J. Clin. Apheresis 18:61–66, 2003. © 2003 Wiley‐Liss, Inc.
Ubiquitin‐dependent and ‐independent proteasomal degradation of apoB associated with endoplasmic reticulum and golgi apparatus, respectively, in HepG2 cells
Authors: Liao Wei , Chang Benny Hung‐Junn , Mancini Michael , Chan Lawrence 
Published: July 2003

AbstractStudies in hepatocyte cultures indicate that apolipoprotein (apo) B‐100 production is regulated largely by intracellular degradation and the proteasome pathway is a major mechanism for the degradation. In the present study, we have examined the detailed itinerary of apoB degradation through its secretory pathway in HepG2 cells. We found that ubiquitin‐dependent proteasomal degradation of apoB largely occurred on the cytosolic surface of rough and smooth endoplasmic reticulum (ER) and that a small proportion of apoB was dislodged from the secretory organelles into the cytosolic compartment where it underwent ubiquitination for proteasomal degradation. The transmembrane conformation of apoB persisted as the protein was transported through the Golgi apparatus. We further demonstrated that proteasomal degradation of apoB was associated the Golgi apparatus but Golgi‐associated apoB was not ubiquitinated, indicating an ubiquitin‐independent proteasomal degradation of apoB is associated with this organelle. We conclude that apoB undergoes proteasomal degradation while going through different compartments of the secretory pathway; further, ER‐associated proteasomal degradation of apoB in the ER is ubiquitin‐dependent whereas that occurring in the Golgi is ubiquitin‐independent. J. Cell. Biochem. 89: 1019–1029, 2003. © 2003 Wiley‐Liss, Inc.
Enhanced binding of Sp1/Sp3 transcription factors mediates the hyperoxia‐induced increased expression of the lung type I cell gene T1α
Authors: Cao Yu‐Xia , Ramirez Maria I. , Williams Mary C. 
Published: July 2003

AbstractThe transcription factor Sp1 plays an important regulatory role in transactivation of the lung type I cell differentiation gene T1α. Like other lung cells, type I cells may encounter changes in oxygen concentration during the lifetime of the organism. We found that exposure of mice to hyperoxia rapidly increases expression of T1α and other type I cell genes, and that returning the mice to normoxia quickly decreases expression. Likewise hyperoxia increases both endogenous T1α expression in lung epithelial cell lines and transcription of luciferase (Luc) from T1α promoter deletion constructs. Using wild‐type promoter fragments and gel shift assays, we determined that Sp1/Sp3 and a key Sp cis‐element in the proximal promoter mediate the hyperoxic response. Mutations of this element and inhibition of Sp–DNA binding by mithramycin block the hyperoxic response. Western analyses of cell homogenates show that the overall abundance of Sp1 and Sp3 proteins is not altered by hyperoxia. However, the abundance of nuclear Sp1 increases after short hyperoxic exposures, suggesting that signaling pathways activated by hyperoxia lead to Sp protein translocation, perhaps as a result of increased Sp phosphorylation. J. Cell. Biochem. 89: 887–901, 2003. © 2003 Wiley‐Liss, Inc.
NF‐κB activation plays an antiapoptotic role in human leukemic K562 cells exposed to ionizing radiation
Authors: Cataldi Amelia , Rapino Monica , Centurione Lucia , Sabatini Nadia , Grifone Giovanna , Garaci Francesco , Rana Rosalba 
Published: July 2003

AbstractExposure of cells to ionizing radiation (IR) determines cellular lesions, such as DNA and membrane damage, which involve a coordinate network of signal transduction pathways responsible for resistance to or delay of apoptosis, depending on cell type and administered dose. Since, after IR exposure, the apoptotic profile appeared different in the two chosen cell lines K562 and Jurkat along with caspase‐3 activation, we paid attention to the influence exerted by Protein kinase C δ on transcription factor NF‐κB activation. Interestingly, K562 resist to IR carrying out a survival strategy which includes PKC δ/NF‐κB pathway activation, probably mediated by novel IKKs and a role for PI‐3‐kinase in activating PKC δ at Thr 505 by PDK‐1 phosphorylation is suggested. In addition, since caspase‐3 is not activated in these cells upon ionizing radiation exposure, it could be supposed that NF‐κB antagonizes apoptosis induction interfering with pathways which lead to caspase activation, may be by inducing expression of IAP, caspases 3, 7, 9, inhibitor. Thus NF‐κB activation explains the resistance displayed by K562 to IR and drug potential interference directed to this protein could overcome apoptosis resistance in clinical settings. J. Cell. Biochem. 89: 956–963, 2003. © 2003 Wiley‐Liss, Inc.
Constitutive NO synthase regulates the Na+/Ca2+ exchanger in human T cells: Role of [Ca2+]i and tyrosine phosphorylation
Authors: Kiang Juliann G. , McClain David E. , Warke Vishal G. , Krishnan Sandeep , Tsokos George C. 
Published: July 2003

AbstractFor many types of cells, heat stress leads to an increase in intracellular free calcium concentration ([Ca2+]i) that has been shown to trigger a wide variety of cellular responses. In T lymphocytes, for example, heat stress stimulates pathways that make them more susceptible to Fas/CD95‐mediated apoptosis. Because of our interest in understanding more about the response of lymphocytes to various stressors, we used human peripheral and Jurkat T lymphocytes to investigate the effect of heat stress on calcium homeostasis. We found that peripheral and Jurkat T cells both exhibit cNOs activity but not iNOs activity. Heat stress increased NO production, which was inhibited by LNNA (a cNOs inhibitor) but not L‐NIL (an iNOs inhibitor). Heat stress increased [Ca2+]i in Jurkat T cells by decreasing the Km of the cell surface membrane Na+/Ca2+ exchanger for extracellular Ca2+. Heating also increased cNOs phosphorylation at tyrosine residues. In cells incubated with LNNA, heat stress promoted an increase in [Ca2+]i and a decrease in [Na+]i greater than in cells heated without LNNA, a larger decrease in Km of the Na+/Ca2+ exchanger for extracellular Ca2+, and decreased phosphorylation of cNOs. Our results suggest that cNOs plays an important regulatory role after heat stress. Heating appears to increase the phosphorylation of cNOs that is complexed with the Na+/Ca2+ exchanger to decrease its activity. This process is related to increased expression of Fas/CD95 on the cell surface, which might explain the apoptotic diathesis of lymphocytes after heat stress. J. Cell. Biochem. 89: 1030–1043, 2003. Published 2003 Wiley‐Liss, Inc.
Requirement of intracellular free thiols for hydrogen peroxide‐induced hypertrophy in cardiomyocytes
Authors: Tanaka Hiroyuki , Sakurai Koichi , Takahashi Kiyoshi , Fujimoto Yukio 
Published: July 2003

AbstractReactive oxygen species (ROS) are by‐products of aerobic metabolism and are implicated in the pathogenesis of several diseases. H2O2 produces oxidative stress and acts as a second messenger in several cell types. We tested whether the effect of H2O2 on cellular events could be altered by changes in the intracellular redox status in a cardiomyocyte cell line. Using flow cytometric measurements, we found that adding H2O2 induced hypertrophy in control cells in a time‐dependent manner. Pre‐incubation of the cells with buthionine sulfoximine (BSO), an inhibitor of de novo GSH synthesis, induced increase in the number of cells of small sizes by the addition of H2O2 as compared to non‐BSO pre‐incubated control cells, and exacerbated the decrease in viability. Total thiol and GSH levels in H9c2 cells pre‐incubated with BSO were about 75 and 30% of control, respectively, and GSH levels fell to below the limitation of detection after the addition of H2O2, although total thiol levels were not markedly decreased. In the cells pre‐incubated with BSO, hypertrophy was not observed by the addition of H2O2 at any level of concentration. N‐acetyl‐l‐cysteine and cysteine not only prevented increase in the number of cells of small sizes caused by H2O2 but also induced hypertrophy in cells pre‐incubated with BSO. These results suggest that the intracellular free thiol levels determine whether cell death or hypertrophy occurs in cardiomyocytes in the presence of H2O2. On the other hand, the hypertrophied cells did not become larger by adding H2O2, but had high levels of cellular GSH, suggesting the possibility that the hypertrophied cells have tolerance to oxidative stress. J. Cell. Biochem. 89: 944–955, 2003. © 2003 Wiley‐Liss, Inc.
Paralemnin of the lens
Authors: Bagchi M. , Katar M. , Lo W.‐K. , Maisel H. 
Published: July 2003

AbstractParalemmin was identified in the chicken lens as a protein with mol. wt 65 kDa and a splice variant of 60 kDa, both soluble in Triton X‐100. Paralemmin is localized to the plasma membrane of fiber cells, and was not detected in the annular pad cells. Thus in the chick lens it is another feature of fiber cell differentiation. Its localization to the short side of the fiber cell and the sites of fiber cell interlocking suggests that paralemmin may play a role in the development of such interdigitating processes. J. Cell. Biochem. 89: 917–921, 2003. © 2003 Wiley‐Liss, Inc.
1α, 25‐Dihydroxy‐vitamin D3 alters syk activation through FcγRII in monocytic THP‐1 cells
Authors: Agramonte‐Hevia José , Hallal Claudia , Garay‐Canales Claudia , Guerra‐Araiza Christian , Camacho‐Arroyo Ignacio , Ortega Soto Enrique 
Published: July 2003

AbstractIn monocytes and macrophages, activation of the tyrosine kinase Syk is an essential step in the biochemical cascade linking aggregation of receptors for immunoglobulin G (FcγR) to initiation of effector functions. An increase in Syk activation during differentiation of myeloid cells by different agents has been reported. We studied the activation state of Syk in response to FcγRII crosslinking in monocytic cells before and after in vitro differentiation with 1α, 25‐dihydroxy‐vitamin D3. We show here that while in undifferentiated THP‐1 cells clustering of FcγRII induces significant phosphorylation and activation of Syk, in THP‐1 cells differentiated in vitro by 1α, 25‐dihydroxy‐vitamin D3, FcγRII crosslinking induced a decrease in Syk activity. In vitro differentiation did not induce changes in the expression of FcγRII isoforms. The observed effect on Syk activation though FcγRII could be mediated by differentiation‐induced changes in the expression and basal activation level of Syk, as well as changes in the association of Syk with the tyrosine phosphatase SHP‐1. These results suggest that the biochemical signaling pathways induced by FcγRII could be dependent on the differentiation state of the cell. J. Cell. Biochem. 89: 1056–1076, 2003. © 2003 Wiley‐Liss, Inc.
Proteomics in biomarker discovery and drug development
Authors: He Qing‐Yu , Chiu Jen‐Fu 
Published: July 2003

AbstractProteomics is a research field aiming to characterize molecular and cellular dynamics in protein expression and function on a global level. The introduction of proteomics has been greatly broadening our view and accelerating our path in various medical researches. The most significant advantage of proteomics is its ability to examine a whole proteome or sub‐proteome in a single experiment so that the protein alterations corresponding to a pathological or biochemical condition at a given time can be considered in an integrated way. Proteomic technology has been extensively used to tackle a wide variety of medical subjects including biomarker discovery and drug development. By complement with other new technique advances in genomics and bioinformatics, proteomics has a great potential to make considerable contribution to biomarker identification and to revolutionize drug development process. This article provides a brief overview of the proteomic technologies and their application in biomarker discovery and drug development. J. Cell. Biochem. 89: 868–886, 2003. © 2003 Wiley‐Liss, Inc.
Co‐detection of PTH/PTHrP receptor and tartrate resistant acid phosphatase in osteoclasts
Authors: Gay Carol V. , Zheng Betty , Gilman Virginia R. 
Published: July 2003

AbstractSerial sections of rat metaphyses were prepared from paraffin embedded tissue blocks and analyzed in sets of three. The central section was stained for tartrate resistant acid phosphatase (TRAP) in order to identify osteoclasts, one adjacent section was immunostained with an affinity purified antibody to a 15 amino acid sequence unique to rat PTH/PTHrP receptor, and the other adjacent section in the set served as an immunostaining control. This allowed each of the 110 osteoclasts examined to be identified by TRAP and to be tested for the presence or absence of PTH/PTHrP receptor. All antibody solutions and rinses contained 1% donkey serum and 0.5% Tween 20 to ensure antibody integrity and good rinsing procedure. Confocal microscopy was used to evaluate fluorescence intensity of the immunostained osteoclasts. Pixel intensities of 58 osteoclasts from young (4 month) rats and 52 osteoclasts from old (15 month) rats were obtained. Pixel intensities were similar (P = 0.89) for both young and old animals. However, the number of PTH/PTHrP receptor deficient osteoclasts was greater for the older animals (14.29% vs. 7.24%). This provides direct evidence of PTH/PTHrP receptors in osteoclasts. J. Cell. Biochem. 89: 902–908, 2003. © 2003 Wiley‐Liss, Inc.
1α,25‐Dihydroxyvitamin D3‐3β‐(2)‐bromoacetate, an affinity labeling derivative of 1α,25‐dihydroxyvitamin D3 displays strong antiproliferative and cytotoxic behavior in prostate cancer cells
Authors: Swamy Narasimha , Persons Kelly S. , Chen Tai C. , Ray Rahul 
Published: July 2003

AbstractIn this report we describe that 1,25(OH)2D3‐3‐BE, a VDR‐affinity labeling analog of 1,25(OH)2D3, showed strong and dose‐dependent growth‐inhibitory effect in several epithelial cells, i.e., keratinocytes (primary cells), MCF‐7 breast cancer, PC‐3, and LNCaP prostate cancer and PZ‐HPV‐7 immortalized normal prostate cell‐lines. Furthermore, 10−6 M of 1,25(OH)2D3‐3‐BE induced apoptosis specifically in LNCaP and PC‐3 cells; and the effect was much less pronounced at lower doses. We also showed that the effect (of 1,25(OH)2D3‐3‐BE) was not due to probable degradation (hydrolysis) of 1,25(OH)2D3‐3‐BE or random interaction of this molecule with cellular proteins. Tissue‐ or cell‐specific action of 1,25(OH)2D3 and its mimics is not common due to the ubiquitous nature of VDR. Furthermore, variable effects of 1,25(OH)2D3 and its analogs in various cell‐lines potentially limits their application as anticancer agents. We showed that 1,25(OH)2D3‐3‐BE displayed similar growth‐inhibitory and cytotoxic activities towards androgen sensitive LNCaP and androgen‐independent PC‐3 cell‐lines. Therefore, these results raise the possibility that 1,25(OH)2D3‐3‐BE or similar VDR‐cross linking analogs of 1,25(OH)2D3 might be considered for further development as potential candidates for prostate cancer. J. Cell. Biochem. 89: 909–916, 2003. © 2003 Wiley‐Liss, Inc.
Induced subgraphs of prescribed size
Authors: Alon Noga , Krivelevich Michael , Sudakov Benny 
Published: July 2003

AbstractA subgraph of a graph G is called trivial if it is either a clique or an independent set. Let q(G) denote the maximum number of vertices in a trivial subgraph of G. Motivated by an open problem of Erdős and McKay we show that every graph G on n vertices for which q(G)≤ C log n contains an induced subgraph with exactly y edges, for every y between 0 and nδ (C). Our methods enable us also to show that under much weaker assumption, i.e., q(G) ≤ n/14, G still must contain an induced subgraph with exactly y edges, for every y between 0 and $e^{\Omega} (\sqrt { \log\, n})$. © 2003 Wiley Periodicals, Inc. J Graph Theory 43: 239–251, 2003
Off‐diagonal and asymptotic results on the Ramsey number r(K2,m,K2,n)
Authors: Lortz Roland , Mengersen Ingrid 
Published: July 2003

AbstractAn upper bound on the Ramsey number r(K2,n‐s,K2,n) where s ≥ 2 is presented. Considering certain r(K2,n‐s,K2,n)‐colorings obtained from strongly regular graphs, we additionally prove that this bound matches the exact value of r(K2,n‐s,K2,n) in infinitely many cases if $s \approx 2\sqrt n$ holds. Moreover, the asymptotic behavior of r(K2,m,K2,n) is studied for n being sufficiently large depending on m. We conclude with a table of all known Ramsey numbers r(K2,m,K2,n) where m,n ≤ 10. © 2003 Wiley Periodicals, Inc. J Graph Theory 43: 252–268, 2003
A 2‐factor with two components of a graph satisfying the Chvátal‐Erdös condition
Authors: Kaneko Atsushi , Yoshimoto Kiyoshi 
Published: July 2003

AbstractChvátal and Erdös showed that a k‐connected graph with independence number at most k and order at least three is hamiltonian. In this paper, we show that a graph contains a 2‐factor with two components, i.e., the graph can be divided into two cycles if the graph is k(≥ 4)‐connected with order at least six and independence number at most k. © 2003 Wiley Periodicals, Inc. J Graph Theory 43: 269–279, 2003
Decreasing the diameter of cycles
Authors: Grigorescu Elena 
Published: July 2003

AbstractAlon, Gyárfás, and Ruszinkó 1 established a bound for the minimum number of edges that have to be added to a graph of n ≥ n0 vertices in order to obtain a graph of diameter 2. Alon et al. approximated n0 by a polynomial function of the maximum degree of the initial graph. They conjectured that the minimum value for n0 is 12 for the case of Cn, as opposed to n0 = 274 obtained by calculations for the general case. In this paper we prove their conjecture. For the reduction to diameter 3 of a cycle, we also improve the bounds from 1 showing that the minimum number of edges that need to be added to the cycle Cn is between n − 59 and n − 8. © 2003 Wiley Periodicals, Inc. J Graph Theory 43: 299–303, 2003
Tumor necrosis factor‐α‐induced cell death in U373 cells overexpressing α‐synuclein
Authors: Stefanova Nadia , Schanda Kathrin , Klimaschewski Lars , Poewe Werner , Wenning Gregor K. , Reindl Markus 
Published: July 2003

AbstractIntracellular α‐synuclein inclusion formation in glial cells is frequently seen in Parkinson's disease and multiple system atrophy. Microglial activation in these neurodegenerative disorders suggests that neuroinflammatory responses might interact with α‐synuclein and contribute to the pathogenesis of these disorders. To study the role of tumor necrosis factor‐α (TNF‐α), an important proinflammatory cytokine produced by microglia, on cells overexpressing α‐synuclein we have used the astrocytoma cell line U373 engineered to express C‐terminally truncated α‐synuclein as a fusion protein with red or green fluorescent proteins. We demonstrate that α‐synuclein overexpression augmented TNF‐α‐induced apoptotic cell death in U373 cells by induction of caspase activation. Furthermore, TNF‐α exposure was associated with significant cytoskeletal changes characterized by altered inclusion composition with loss of cytoskeletal proteins and elevation of high‐molecular‐weight α‐synuclein species. We conclude that α‐synuclein overexpression significantly increases the vulnerability of U373 cells to apoptosis through TNF‐α‐mediated pathways. © 2003 Wiley‐Liss, Inc.
Effect of salt stress on crotonobetaine and D(+)‐carnitine biotransformation into L(−)‐carnitine by resting cells of Escherichia coli
Authors: Cánovas Manuel , Torroglosa Tomás , Kleber Hans‐Peter , Iborra Jose Luis 
Published: July 2003

AbstractThe biotransformation of crotonobetaine and D(+)‐carnitine into L(−)‐carnitine is affected by salt stress in the resting cells of E. coli O44 K74 and the transformed E. coli K38 pT7‐5KE32. A yield of 65 and 80% of L(−)‐carnitine, respectively, were obtained with 0.5 M NaCl with the wild and transformed strain compared with the 40% obtained with the control. Higher salt levels reduced the conversion. In L(−)‐carnitine transport studies using both strains, the transformed strain presented slightly lower apparent Km and V values. Arsenate reduced both the transport and biotransformation of crotono‐betaine in the presence or absence of 0.5 M NaCl, whereas vanadate only inhibited these processes under salt stress conditions. Hg(II) inhibited both the transport and biotransformation and Pb(II) reduced the biotransformation only under salt stress conditions. Cu(II) produced a significantly higher decrease than Pb(II) in the biotransformation with both substrates in the absence of salt stress condi‐tions, but only affected transport in the presence of such conditions. Furthermore, salt stress affected the CaiT transporter for L(−)‐carnitine and crotonobetaine and induced ProU and ProP in the absence of the inducer of the L(−)‐carnitine metabolism. It is highly likely that the increase in L(−)‐carnitine production was not only due to improved transport but also to the permeabilization effect caused by NaCl, as transport and 1‐N‐phenylnaphthylamine uptake studies revealed.
Xylanolytic complex from Aspergillus giganteus: production and characterization
Authors: Coelho Glauciane Danusa , Carmona Eleonora Cano 
Published: July 2003

AbstractAn Aspergillus giganteus strain was isolated as an excellent producer of xylanase associated with low levels of cellulase. Optimal xylanase production was obtained in liquid Vogel medium containing xylan as carbon source, pH 6.5 to 7.0, at 25 °C and under shaking at 120 rpm during 84h. Among the several carbon sources tested, higher xylanase production was verified in xylan, xylose, sugar‐cane bagasse, wheat bran and corn cob cultures, respectively. Optimal conditions for activity determination were 50 °C and pH 6.0. The xylanolytic complex of A. giganteus showed low thermal stability with T50 of 2 h, 13 min and 1 min when it was incubated at 40, 50 and 60 °C, respectively, and high stability from pH 4.5 to 10.5, with the best interval between 7.0 to 7.5. This broad range of stability in alkali pH indicates a potential applicability in some industrial processes, which require such condition. Xylanolytic activity of A. giganteus was totally inhibited by Hg+2, Cu+2 and SDS at 10 mM. The analysis of the products from the oat spelts xylan hydrolysis through thin‐layer chromatography indicated endoxylanase activity, lack of debranching enzymes and β‐xylosidase activity in assay conditions.