bluuebunny/crossref_metadata_2025_split huggingface dataset:
Eigenvalue‐based model selection during latent semantic indexing
Authors: Efron Miles 
Published: May 2005

AbstractIn this study amended parallel analysis (APA), a novel method for model selection in unsupervised learning problems such as information retrieval (IR), is described. At issue is the selection ofk, the number of dimensions retained under latent semantic indexing (LSI). Amended parallel analysis is an elaboration of Horn's parallel analysis, which advocates retaining eigenvalues larger than those that we would expect under term independence. Amended parallel analysis operates by deriving confidence intervals on these “null” eigenvalues. The technique amounts to a series of nonparametric hypothesis tests on the correlation matrix eigenvalues. In the study, APA is tested along with four established dimensionality estimators on six standard IR test collections. These estimates are evaluated with regard to two IR performance metrics. Additionally, results from simulated data are reported. In both rounds of experimentation APA performs well, predicting the best values ofkon 3 of 12 observations, with good predictions on several others, and never offering the worst estimate of optimal dimensionality.
Secalonic acid D blocks embryonic palatal mesenchymal cell‐cycle by altering the activity of CDK2 and the expression of p21 and cyclin E
Authors: Dhulipala V.C. , Maddali K.K. , Welshons W.V. , Reddy C.S. 
Published: May 2005

AbstractBACKGROUND: The mycotoxin, secalonic acid D (SAD), a known animal and potential human cleft palate (CP)‐inducing agent, is produced by Pencillium oxalicum in corn. SAD selectively inhibits proliferation of murine embryonic palatal mesenchymal (MEPM) cells leading to a reduction in cell numbers. These effects can explain the reduction in shelf size and the resulting CP seen in the offspring of SAD‐exposed mice. Ability of SAD to inhibit proliferation as well as to block the progression of cells from G1‐ to S‐phase of the cell‐cycle were also shown in the human embryonic palatal mesenchymal (HEPM) cells suggesting the potential CP‐inducing effect of SAD in human beings METHODS: Gestation day (GD) 12 mouse embryos and HEPM cells were used to test the hypothesis that the cell‐cycle block induced by SAD results from a disruption of stage‐specific regulatory components both in vivo and in vitro. The effects of SAD on the activity of various cyclin dependent kinases (CDK) and on the levels of various positive (cyclins and CDK) and negative (CDK inhibitors p15, 16, 18, 19, 21, 27, 57) cell‐cycle regulators were assessed by performing kinase assays and immunoblots, respectively. RESULTS: In the murine embryonic palates, SAD specifically inhibited G1/S‐phase‐specific CDK2 activity, reduced the level of cyclin E and tended to increase the level of the CIP/kip CDK inhibitor, p21. In the HEPM cell cultures, exposure to IC50 of SAD significantly affected all of the above targets. In addition, a reduction in the levels/activity of CDK 4/6, a reduction in the levels of cyclins D1, D2, D3, E, A, and all INK4 family proteins, and an increase in the level of the CIP/kip CDK inhibitor, p57, were also seen. CONCLUSIONS: These results suggest that the S‐phase‐specific cell‐cycle proteins CDK2, cyclin E and possibly p21 are the common targets of SAD in murine palatal shelves in vivo and in human embryonic palatal mesenchymal cells in vitro and may be relevant to the pathogenesis of SAD‐induced CP. Birth Defects Res B 2005. © 2005 Wiley‐Liss, Inc.
Control of protein functional dynamics by peptide linkers
Authors: Wriggers Willy , Chakravarty Sugoto , Jennings Patricia A. 
Published: May 2005

AbstractControl of structural flexibility is essential for the proper functioning of a large number of proteins and multiprotein complexes. At the residue level, such flexibility occurs due to local relaxation of peptide bond angles whose cumulative effect may result in large changes in the secondary, tertiary or quaternary structures of protein molecules. Such flexibility, and its absence, most often depends on the nature of interdomain linkages formed by oligopeptides. Both flexible and relatively rigid peptide linkers are found in many multidomain proteins. Linkers are thought to control favorable and unfavorable interactions between adjacent domains by means of variable softness furnished by their primary sequence. Large‐scale structural heterogeneity of multidomain proteins and their complexes, facilitated by soft peptide linkers, is now seen as the norm rather than the exception. Biophysical discoveries as well as computational algorithms and databases have reshaped our understanding of the often spectacular biomolecular dynamics enabled by soft linkers. Absence of such motion, as in so‐called molecular rulers, also has desirable functional effects in protein architecture. We review here the historic discovery and current understanding of the nature of domains and their linkers from a structural, computational, and biophysical point of view. A number of emerging applications, based on the current understanding of the structural properties of peptides, are presented in the context of domain fusion of synthetic multifunctional chimeric proteins. © 2005 Wiley Periodicals, Inc. Biopolymers (Pept Sci) 80: 736–746, 2005This article was originally published online as an accepted preprint. The “Published Online” date corresponds to the preprint version. You can request a copy of the preprint by emailing the Biopolymers editorial office at biopolymers@wiley.com
Engineering mammalian cell factories for improved recombinant monoclonal antibody production: lessons from nature?
Authors: Dinnis Diane M. , James David C. 
Published: May 2005

AbstractIn this review we consider how cell specific recombinant monoclonal antibody (Mab) production by engineered mammalian cells can be improved. Whilst it is generally recognized that Mab production is limited post‐transcriptionally at folding and assembly reactions, genetic engineering strategies based on overexpression of individual chaperones or foldases in mammalian cells have not reliably increased cell specific Mab production. Given that recent studies have established that chaperones and foldases themselves exist in a large multiprotein complex, which may coordinate the sequential processing of Mabs, we propose that global expansion of all components of the secretory pathway will likely be necessary to generically improve recombinant Mab production by mammalian cells. In this context, what can be learnt from nature? Important recent studies have delineated some of the main cellular pathways involved in the differentiation of B‐cells into nature's own high level Mab producers, plasma cells. This is achieved by a dramatic re‐programming of cellular function where the coordinated expansion of metabolic and secretory machinery precedes Ig production, then is maintained by induction of a key intracellular signaling pathway, the unfolded protein response (UPR). Here we review genetic engineering strategies to increase cell specific production rate and discuss whether manipulation of intracellular signaling systems such as the UPR will provide a novel means to engineer mammalian cells for high level recombinant Mab production. © 2005 Wiley Periodicals, Inc.
The effect of whole cell immobilisation on the biotransformation of benzonitrile and the use of direct electric current for enhanced product removal
Authors: Mustacchi Roberta , Knowles Christopher J. , Li Hong , Dalrymple Ian , Sunderland Garry , Skibar Wolfgang , Jackman Simon A. 
Published: May 2005

AbstractThe nitrilase of Rhodococcus rhodochrous performs a one‐step biotransformation of nitriles to their corresponding carboxylic acids. Application of a direct electric current moves the charged carboxylic acid towards an anode, across an anion exchange membrane, into a separate compartment. Cells encapsulated within alginate beads (2.9 mm diameter) for protection against the current biotransformed benzonitrile to benzoic acid with a 26% reduction in the biotransformation rate, from 0.054 mmol/min/g dcw with free cells to 0.040 mmol/min/g dcw with immobilised cells. When the electric current was applied, the biotransformation rate increased to 0.047 mmol/min/g dcw and product recovery increased from 19% to 79%. © 2005 Wiley Periodicals, Inc.
Clinical outcomes after sirolimus‐eluting stent implantation for de novo saphenous vein graft lesions
Authors: Price Matthew J. , Sawhney Neil , Kao John A. , Madrid Antonio , Schatz Richard A. , Teirstein Paul S. 
Published: May 2005

AbstractThe purpose of this study was to evaluate the clinical outcome of patients undergoing sirolimus‐eluting stent implantation for de novo lesions within saphenous vein grafts (SVGs). Although the incidence of restenosis following sirolimus‐eluting stenting (SES) of native coronary arteries is low, the efficacy of SES to treat de novo lesions within SVGs has not been well studied. A total of 35 patients underwent SES implantation of 39 lesions during 36 procedures. All patients had a minimum follow‐up of 6 months following the index procedure. The mean bypass graft age was 10.1 ± 6.5 years (range, 0–23 years). In‐hospital major adverse cardiac events [death, myocardial infarction, thrombosis, or target vessel revascularization (TVR)] occurred in four patients (11%). Clinical follow‐up was obtained in 100% of patients (mean follow‐up, 7.5 ± 2.2 months). There was one cardiac death, presumed due to stent thrombosis. TVR occurred in only two patients (6%). Myocardial infarction (MI) occurred in four patients (11%), all attributable to a nontarget vessel. The combined endpoint of death, MI, or TVR occurred in seven patients (20%). Freedom from death, nonfatal MI, thrombosis, or any revascularization was 65%. Early experience indicates sirolimus‐eluting stents for de novo saphenous vein graft lesions have a low (6%) rate of clinically driven target vessel revascularization. By 7‐month follow‐up, event‐free survival is limited primarily by disease in nontarget vessels. © 2005 Wiley‐Liss, Inc.
Late distortion of the original Palmaz stent implanted in postoperative lesions associated with congenital heart disease
Authors: Tomita Hideshi , Yazaki Satoshi , Echigo Shigeyuki , Kimura Kohji , Takamuro Motoki , Horita Norihisa , Fuse Shigeto , Tsutsumi Hiroyuki 
Published: May 2005

AbstractThe objective of this study was to report late distortion of a Palmaz stent. Late distortion of an original Palmaz stent, implanted in an extracardiac lesion, is rare. We completed a 1‐year follow‐up of 54 patients who had been implanted with 80 Palmaz stents in extracardiac lesions. Distortion of two stents was detected in two patients. For case 1, we implanted a P188 stent for supravalvar pulmonary stenosis complicating an arterial switch operation in a 14‐year‐old girl. Seven months later, we found compression of the stent. Although we implanted two P308 stents anterior to the distorted stent, distortion of both stents developed after 1 month. Two more P308 stents placed inside each stent were gradually recompressed. A CAT scan showed compression of the stent by a dilated sinus of valsalva. For case 2, we implanted a P308 stent for stenosis of the superior vena cava after Williams operation in an 11‐year‐old boy. A chest X‐ray documented longitudinal compression of the stent 27 months after implantation and a CAT scan showed the ascending aorta was in contact with the stent. A Palmaz stent may be distorted when implanted in a lesion adjacent to a pulsating aorta. © 2005 Wiley‐Liss, Inc.
Risk factors for infections with multidrug‐resistant Pseudomonas aeruginosa in patients with cancer
Authors: Ohmagari Norio , Hanna Hend , Graviss Linda , Hackett Brenda , Perego Cheryl , Gonzalez Virginia , Dvorak Tanya , Hogan Holly , Hachem Ray , Rolston Kenneth , Raad Issam 
Published: May 2005

AbstractBACKGROUNDPseudomonas aeruginosa is responsible for a wide range of infections. In immunocompromised patients with cancer, the emergence of multidrug resistant P. aeruginosa may have grave consequences.METHODSPatients with cancer who were infected with multidrug‐resistant P. aeruginosa with polyclonal DNA restriction patterns were used as the case group. Two control groups were used: one group of cancer patients who were infected with multidrug‐susceptible P. aeruginosa and another group of cancer patients who had the same underlying disease and the same intensive care unit exposure as patients in the case group but who were not infected or colonized by P. aeruginosa.RESULTSRisk factors that were associated significantly with multidrug‐resistant P. aeruginosa infection were the use of carbapenem for ≥ 7 days, a history of P. aeruginosa infection during the preceding year, and a history of chronic obstructive pulmonary disease (P < 0.01).CONCLUSIONSCarbapenems may need to be used more judiciously as first‐line empirical therapy for cancer patients with prior pseudomonal infection or chronic obstructive pulmonary disease who require hospitalization, and alternative, antipseudomonal antibiotic regimens may need to be considered, especially in this patient population. Cancer 2005. © 2005 American Cancer Society.
Theoretical Study of the Magnetic Behavior of Ferric Wheels
Authors: Ruiz Eliseo , Alvarez Santiago 
Published: May 2005

AbstractCalculations of exchange coupling constants (J) based on density functional theory for eight complete, nonmodeled ferric wheels have been performed, and a comparison with the values obtained from magnetic susceptibility data is presented. The calculated J values obtained with a generalized‐gradient approximation (GGA) functional are in good agreement with the experiment probably because the inclusion of pseudopotentials partially compensates the overestimation of the spin delocalization. The magnetostructural correlation obtained shows a strong dependence of the exchange coupling on both the FeOFe bond angle and the FeO bond distance. This correlation holds for both the ferric wheels and the alkoxo‐bridged FeIII dinuclear complexes reported in the literature.
Parathyroid hormone stimulation and PKA signaling of latent transforming growth factor‐β binding protein‐1 (LTBP‐1) mRNA expression in osteoblastic cells
Authors: Kwok Sukyee , Qin Ling , Partridge Nicola C. , Selvamurugan Nagarajan 
Published: May 2005

AbstractParathyroid hormone (PTH) regulates bone remodeling and calcium homeostasis by acting on osteoblasts. Recently, the gene expression profile changes in the rat PTH (1–34, 10−8M)‐treated rat osteoblastic osteosarcoma cell line, UMR 106‐01, using DNA microarray analysis showed that mRNA for LTBP‐1, a latent transforming growth factor (TGF‐β)‐binding protein is stimulated by PTH. Latent TGF‐β binding proteins (LTBPs) are required for the proper folding and secretion of TGF‐β, thus modifying the activity of TGF‐β, which is a local factor necessary for bone remodeling. We show here by real time RT‐PCR that PTH‐stimulated LTBP‐1 mRNA expression in rat and mouse preosteoblastic cells. PTH also stimulated LTBP‐1 mRNA expression in all stages of rat primary osteoblastic cells but extended expression was found in differentiating osteoblasts. PTH also stimulated TGF‐β1 mRNA expression in rat primary osteoblastic cells, indicating a link between systemic and local factors for intracellular signaling in osteoblasts. An additive effect on LTBP‐1 mRNA expression was found when UMR 106‐01 cells were treated with PTH and TGF‐β1 together. We further examined the signaling pathways responsible for PTH‐stimulated LTBP‐1 and TGF‐β1 mRNA expression in UMR 106‐01 cells. The PTH stimulation of LTBP‐1 and TGF‐β1 mRNA expression was dependent on the PKA and the MAPK (MEK and p38 MAPK) pathways, respectively in these cells, suggesting that PTH mediates its effects on osteoblasts by several intracellular signaling pathways. Overall, we demonstrate here that PTH stimulates LTBP‐1 mRNA expression in osteoblastic cells and this is PKA‐dependent. This event may be important for PTH action via TGF‐β in bone remodeling. © 2005 Wiley‐Liss, Inc.
Inhibition of extracellular signal regulated kinase (ERK) leads to apoptosis inducing factor (AIF) mediated apoptosis in epithelial breast cancer cells: The lack of effect of ERK in p53 mediated copper induced apoptosis
Authors: Ostrakhovitch Elena A. , Cherian M. George 
Published: May 2005

AbstractRecent studies have shown that MEK/ERK‐mediated signals play a major role in regulation of activity of p53 tumor suppressor protein. In this study, we investigated whether or not there is functional interaction between p53 and MEK/ERK pathways in epithelial breast cancer cells exposed to copper or zinc. We demonstrated that expression of wild‐type p53 induced by copper or zinc significantly reduced phosphorylation of extracellular signal regulated kinase (ERK) in epithelial breast cancer MCF7 cells. Mutation or suppression of p53 in MDA‐MB231 and MCF7‐E6 cells, respectively, resulted in a strong ERK phosphorylation in the presence of metals. Weak ERK phosphorylation in MCF7 cells induced by copper or zinc was linked to mitochondrial disruption and apoptosis. Furthermore, inhibition of ERK through addition of PD98059 stimulated p53 activation in MCF7 cells and also led to upregulation of p53 downstream targets, p21 and Bax, which is a proapototic member of Bcl‐2 family triggering mitochondrial pore opening. Moreover, blockage of the MEK/ERK pathway caused a breakdown of the mitochondrial membrane potential accompanied by an elevation in the ROS production. Disruption of p53 expression attenuated the depolarization of the mitochondrial membrane and ROS generation. Furthermore, PD98059 initiated apoptosis inducing factor (AIF) translocation from mitochondria to the nucleus in MCF7 cells; which are depleted in caspase 3. Interestingly, repression of MEK/ERK pathway did not intensify the cell stress caused by metal toxicity. Therefore, these findings demonstrate that MEK/ERK pathway plays an important role in downregulation of p53 and cell survival. Inhibition of ERK can lead to apoptosis via nuclear relocation of AIF. However, metal‐induced activation of p53 and mitochondrial depolarization appears to be independent of ERK. Our data suggest that copper induces apoptosis through depolarization of mitochondrial membrane with release of AIF, and this process is MEK/ERK independent. © 2005 Wiley‐Liss, Inc.
Osteogenic oxysterols inhibit the adverse effects of oxidative stress on osteogenic differentiation of marrow stromal cells
Authors: Shouhed Daniel , Kha Hoa Ton , Richardson Jennifer A. , Amantea Christopher M. , Hahn Theodore J. , Parhami Farhad 
Published: May 2005

AbstractThe osteoporosis that occurs with aging is associated with reduced number and activity of osteoblastic cells. Aging, menopause, and osteoporosis are correlated with increased oxidative stress and reduced antioxidant defense mechanisms. We previously demonstrated that oxidative stress induced by a variety of compounds such as xanthine/xanthine oxidase (XXO) and minimally oxidized LDL (MM‐LDL) inhibit the osteogenic differentiation of osteoprogenitor cells. Oxysterols are a family of products derived from cholesterol oxidation that have important biological activities. Recently, we reported that a specific oxysterol combination consisting of 22(S)‐ or 22(R)‐hydroxycholesterol and 20(S)‐hydroxycholesterol has potent osteogenic properties in vitro when applied to osteoprogenitor cells including M2‐10B4 (M2) marrow stromal cells. We now demonstrate that this osteogenic combination of oxysterols prevents the adverse effects of oxidative stress on differentiation of M2 cells into mature osteoblastic cells. XXO and MM‐LDL inhibited the osteogenic differentiation of M2 cells, demonstrated by the inhibition of markers of osteogenic differentiation: alkaline phosphatase activity, osteocalcin expression and mineralization. Treatment of M2 cells with osteogenic oxysterol combination 22(S)‐ and 20(S)‐hydroxycholesterol both blocked and reversed the inhibition of osteogenic differentiation produced by XXO and MM‐LDL in these cells. The protective effect of the oxysterols against oxidative stress was dependent on cyclooxygenase 1 and was associated with the osteogenic property of the oxysterols. These findings further demonstrate the ability of the osteogenic oxysterols to positively regulate osteogenic differentiation of cells, and suggests that the use of these compounds may be a novel strategy to prevent the adverse effects of oxidative stress on osteogenesis. © 2005 Wiley‐Liss, Inc.
Theoretical studies on the electronic and optical properties of two new alternating fluorene/carbazole copolymers
Authors: Yang Li , Feng Ji‐Kang , Ren Ai‐Min 
Published: May 2005

AbstractPoly(fluorene)‐type materials are widely used in polymer‐based emitting devices. During operation there appears, however, an additional emission peak at around 2.3 eV, leading to both a color instability and reduced efficiency. The incorporation of the carbazole units has been proven to efficiently suppress the keto defect emission. In this contribution, we apply quantum‐chemical techniques to investigate two series of alternating fluorene/carbazole oligomers and copolymers poly[2,7‐(N‐(2‐methyl)‐carbazole)‐co‐alt‐2,7‐m(9,9‐dimethylfluorene)], namely, PFmCz (m = 1,2) and gain a detailed understanding of the influence of carbazole units on the electronic and optical properties of fluorene derivatives. The electronic properties of the neutral molecules, HOMO‐LUMO gaps (ΔH‐L), in addition to the positive and negative ions, are studied using B3LYP functional. The lowest excitation energies (Egs) and the maximal absorption wavelength λabs of PFmCz (m = 1,2) are studied, employing the time‐dependent density functional theory (TD‐DFT). The properties of the two copolymers, such as ΔH‐L, Eg, IPs, and EAs were obtained by extrapolating those of the oligomers to the inverse chain length equal to zero (1/n = 0). The outcomes showed that the carbazole unit is a good electron‐donating moiety for electronic materials, and the incorporation of carbazole into the polyfluorene (PF) backbone resulted in a broadened energy gap and a blue shift of both the absorption and photoluminescence emission peaks. Most importantly, the HOMO energies of PF1Cz and PF2Cz are both a higher average (0.4 eV) than polyfluorene (PF), which directly results in the decreasing of IPs of about 0.2 eV more than PF, indicating that the carbazole units have significantly improved the hole injection properties of the copolymers. In addition, the energy gap tends to broaden and the absorption and emission peaks are gradually blue‐shifted to shorter wavelengths with an increase in the carbazole content in the copolymers. This is due to the interruption of the longer conjugation length of the backbone in the (F1Cz)n series. © 2005 Wiley Periodicals, Inc. J Comput Chem 26: 969–979, 2005
Gicerin/CD146 is involved in neurite extension of NGF‐treated PC12 cells
Authors: Taira Eiichi , Kohama Keiko , Tsukamoto Yasuhiro , Okumura Shigeki , Miki Naomasa 
Published: May 2005

AbstractGicerin/CD146 is a cell adhesion molecule, which belongs to the immunoglobulin (Ig) superfamily. We have reported that it has a homophilic binding activity, which participates in the neurite extension from embryonic neurons. To elucidate how gicerin is involved in the neurite extension mechanism, we employed PC12 cells, which expresses gicerin/CD146. PC12 cells extend longer neurites by nerve growth factor (NGF) on gicerin substrate than on without gicerin substrate, which indicates that gicerin participates in neurite extension by NGF. We also found that the expression of gicerin in PC12 cells is induced by NGF. Over‐expression of gicerin also promotes neurite extension by gicerin–gicerin homophilic interaction. These findings suggested that increase of gicerin expression by NGF promotes the gicerin–gicerin homophilic interaction resulting in the neurite extension. © 2005 Wiley‐Liss, Inc.