bluuebunny/crossref_metadata_2025_split huggingface dataset:
Does L‐Arginine induce intestinal adaptation by epithelial growth factor?
Authors: Camli Alparslan , Barlas Meral , Yagmurlu Aydin 
Published: March 2005

Background:  To evaluate whether L‐Arginine has an effect on endogenous epidermal growth factor secretion and intestinal adaptation in massive small bowel resection an experimental study was performed.Methods:  Fourteen albino Wistar rats weighing 250−300 g were used for the study. After performing 50% small bowel resection and anastomosis the rats were randomly divided into two groups. The first group received 500 mg/kg/day of L‐Arginine intraperitoneally for 14 days just after the surgical procedure. The control group received isotonic saline instead. Body weight measurement was preformed daily. At the end of the second postoperative week all rats underwent relaparotomy. Small bowel was resected for histopathological examination. Levels of epidermal growth factor were measured by enzyme‐linked immunosorbent assay in serum, saliva, and urine at the end of second postoperative week in both groups.Results:  The weight gain was higher in the L‐Arginine treated group (P < 0.05). Serum, saliva and urinary epidermal growth factor levels were significantly higher at the end of the second week compared to the control group (P < 0.05). The villus height was higher on histopathological examination in L‐Arginine treated group compared to the control group (P < 0.05).Conclusion:  L‐Arginine resulted in a better intestinal adaptation after massive bowel resection. The high levels of epidermal growth factor in body fluids of L‐Arginine treated rats could be the explanation for this effect.
Effects of humidity and temperature on the fatigue behaviour of an extruded AZ61 magnesium alloy
Authors: SAJURI Z. B. , MIYASHITA Y. , MUTOH Y. 
Published: March 2005

ABSTRACTLoad‐controlled fatigue tests were performed at 20 and 50 °C using two relative humidity levels of 55 and 80% to characterize the influence of humidity and temperature on the fatigue behaviour of an extruded AZ61 magnesium alloy. Fatigue tests were also conducted at 150 °C. No significant variation in fatigue properties was noticed with respect to temperature over the range from 20 to 50 °C for both the humidity levels. Fatigue limits in the range 140–150 MPa were observed for relative humidity of 55%. Fatigue strength decreased significantly with increase in temperature to 150 °C. Further, a significant reduction in fatigue strength with a fatigue limit of ∼110 MPa was observed with increase in relative humidity to 80% at 20 and 50 °C. The crack initiation and propagation remained transgranular under all test conditions. The fatigue fracture at low stress amplitudes and high relative humidity of 80% results from the formation of corrosion pits at the surface and their growth to a critical size for fatigue‐crack initiation and propagation. The observed reduction in fatigue strength at high humidity is ascribed to the effects associated with fatigue–environment interaction.
Fatigue failure of adhesively patched 2024‐T3 and 7075‐T6 clad and bare aluminium alloys
Authors: DUQUESNAY D. L. , UNDERHILL P. R. , BRITT H. J. 
Published: March 2005

ABSTRACTThe fatigue behaviour of adhesive patches used for repairing aircraft components was investigated. Adhesive patches were simulated using single‐lap shear specimens on clad and bare 7075‐T6 and 2024‐T3 aluminium alloy substrates. Stress–life curves were generated under constant amplitude loading at three stress ratios: R=−1, 0 and 0.5. In the bare materials, failure always occurred in the adhesive itself leaving the substrates intact. At fatigue lives below about 100 000 cycles, the clad alloy specimens also failed in this manner. However, at lower stress levels, the clad alloys failed by cracks initiating in the cladding layer along the end of the lap and subsequently propagating through the substrate. The fatigue strength of the substrate, due to the adhesive patch on the clad materials, was reduced by an order of magnitude compared to the Military Handbook values.
Fatigue life calculation by means of the cycle counting and spectral methods under multiaxial random loading
Authors: ŁAGODA T. , MACHA E. , NIESŁONY A. 
Published: March 2005

ABSTRACTThe paper contains a new algorithm for estimation of fatigue life in HCF regime under multiaxial random loading using spectral methods. Loading of Gaussian distribution and narrow‐ and broad‐band frequency spectra were assumed. Various characteristic states of multiaxial loading were considered. The equivalent stress history was determined with use of the failure criteria of multiaxial fatigue based on the critical plane. For determination of the critical plane position, the method of variance was applied. During simulation, the authors compared the results obtained by a spectral method in the frequency domain with those from the rain‐flow algorithm in the time domain. The paper also contains the results of fatigue tests for 18G2A structural steel subjected to bending and combined bending with torsion. The tests were performed in order to verify the proposed algorithms for determination of fatigue life. It has been shown that under multiaxial random loading results of fatigue life calculated according to the considered algorithms in frequency and time domains are well correlated with the results of experiments.
Electoral Politics, Ideology and American Social Policy
Authors: Peele Gillian 
Published: March 2005

Abstract This article addresses the politics of social policy in the context of the 2004 American presidential election. It examines the divisions in American society and their distinctive agendas. It also explores the record of the Bush administration on key social policy issues and shows how it relates to the broader conservative tradition as well as to the Clinton administration's reform of welfare. Finally, it examines the election results. The article argues that the Bush administration has a distinctive agenda on social policy issues and that its approach is likely to reduce further the role of the social government in the provision of social policy, by emphasizing market forces and philanthropy as well as cutting taxes. It also notes, however, that the Bush administration has taken a strong stance on traditional moral values and that its opposition to abortion and homosexuality is an important part of its political strategy.
The 48‐week efficacy of once‐daily saquinavir/ritonavir in patients with undetectable viral load after 3 years of antiretroviral therapy
Authors: Cardiello P , Srasuebkul P , Hassink E , Mahanontharit A , Samor T , Ruxrungtham K , Lange J , Cooper D , Phanuphak P 
Published: March 2005

ObjectivesTo evaluate the efficacy and safety of once‐daily saquinavir‐soft‐gel‐capsules/ritonavir (SQV‐SGC/RTV) 1600 mg/100 mg plus dual nucleoside reverse transcriptase inhibitors (NRTIs) in HIV‐infected patients with plasma viral load (pVL) <50 HIV‐1 RNA copies/mL following 3 years of antiretroviral therapy.MethodsA total of 69 patients with pVL <50 copies/mL after 162 weeks of antiretroviral treatment started SQV‐SGC/RTV 1600 mg/100 mg once‐daily while continuing dual NRTIs. Previous treatment consisted of 66 weeks of treatment with a half/full dose of zidovudine (ZDV)/zalcitabine (ddC), followed by 2 years of SQV‐SGC twice a day (bid) plus ZDV/lamivudine (3TC) or didanosine (ddI)/stavudine (d4T). Efficacy (pVL), safety and immunological changes (CD4 cell counts) were evaluated after 48 weeks in this open‐label, single‐arm prospective study.ResultsSQV‐SGC/RTV once‐daily was well tolerated. No patient changed regimens or was lost to follow‐up. After 48 weeks, 63 of 69 patients (91%) had pVL <50 copies/mL (five of the six remaining patients had pVL <400 copies/mL, and one patient had an unexplained rise to 39 500 copies/mL, which decreased to <50 copies/mL 12 weeks later). Median CD4 count increased from 534 cells/μL at the start of the SQV‐SGC/RTV once‐daily treatment to 664 cells/μL (P<0.001). Compared to the preceding 48 weeks on bid SQV‐SGC, the CD4 cell count improved significantly on once‐daily SQV‐SGC/RTV (P<0.001).ConclusionsThese data support the use of SQV‐SGC/RTV 1600 mg/100 mg once‐daily with two NRTIs as a convenient, safe and cost‐saving regimen to maintain viral suppression and CD4 counts for 48 weeks in this preselected cohort on highly active antiretroviral therapy (HAART) with pVL <50 copies/mL. The CD4 count rise may be a result of continued immune reconstitution in patients with well‐controlled infection.
Are maternal smoking and stress during pregnancy related to ADHD symptoms in children?
Authors: Rodriguez Alina , Bohlin Gunilla 
Published: March 2005

Background: There are some indications that maternal lifestyle during pregnancy (smoking and stress) contributes to symptoms of ADHD in children. We prospectively studied whether prenatal exposure to maternal smoking and/or stress is associated with ADHD symptoms and diagnostic criteria (according to DSM‐IV) in 7‐year‐olds.Methods: Nulliparous Scandinavian women were consecutively recruited at their first prenatal health care visit and assessments of smoking and stress were collected at gestational weeks 10, 12, 20, 28, 32, and 36. Children were followed up at 7 years old. We obtained full data for 72% of the sample: ADHD symptoms were rated by 74% of mothers (n = 290) and 96% of eligible teachers (n = 208). Attrition analyses showed no differences on key variables between participants and non‐participants at follow‐up.Results: Results of multiple regression analyses showed prenatal exposure to smoking (β = .16,p < .01) and stress (β = .18,p < .01) were independently associated with later symptoms of ADHD. Results of logistic regression analyses showed that fulfillment of the diagnostic criteria for ADHD was related to exposure to prenatal stress (β = .68,p < .01) especially in boys. The results were not confounded by sociodemographic factors or birth outcomes.Conclusions: This study provides evidence that prenatal exposure to stress and smoking is independently associated with later symptoms of ADHD in human children, particularly for boys. Because stress and smoking are relatively common during pregnancy, and yet preventable, these results are of public health significance.
Heterodimerization of opioid receptor‐like 1 and µ‐opioid receptors impairs the potency of µ receptor agonist
Authors: Wang Hung‐Li , Hsu Chia‐Yu , Huang Pei‐Chen , Kuo Yo‐Li , Li Allen H. , Yeh Tu‐Hsueh , Tso An‐Swe , Chen Ying‐Ling 
Published: March 2005

AbstractNociceptin activation of ORL1 (opioid receptor‐like 1 receptor) has been shown to antagonize µ receptor‐mediated analgesia at the supraspinal level. ORL1 and µ‐opioid receptor (µR) are co‐expressed in several subpopulations of CNS neurons involved in regulating pain transmission. The amino acid sequence of ORL1 also shares a high degree of homology with that of µ receptor. Thus, it is hypothesized that ORL1 and µR interact to form the heterodimer and that ORL1/µR heterodimerization may be one molecular basis for ORL1‐mediated antiopioid effects in the brain. To test this hypothesis, myc‐tagged ORL1 and HA‐tagged µR are co‐expressed in human embryonic kidney (HEK) 293 cells. Co‐immunoprecipitation experiments demonstrate that ORL1 dimerizes with µR and that intracellular C‐terminal tails of ORL1 and µR are required for the formation of ORL1/µR heterodimer. Second messenger assays further indicate that formation of ORL1/µR heterodimer selectively induces cross‐desensitization of µR and impairs the potency by which [d‐Ala2,N‐methyl‐Phe4,Gly‐ol5]enkephalin (DAMGO) inhibits adenylate cyclase and stimulates p42/p44 mitogen‐activated protein kinase (MAPK) phosphorylation. These results provide the evidence that ORL1/µR heterodimerization and the resulting impairment of µ receptor‐activated signaling pathways may contribute to ORL1‐mediated antiopioid effects in the brain.
Phosphorylation state of postsynaptic density proteins
Authors: Trinidad J. C. , Thalhammer A. , Specht C. G. , Schoepfer R. , Burlingame A. L. 
Published: March 2005

AbstractThe postsynaptic density (PSD) is an electron‐dense structure located at the synaptic contacts between neurons. Its considerable complexity includes cytoskeletal and scaffold proteins, receptors, ion channels and signaling molecules, in line with the role of PSDs in signal transduction and processing. The phosphorylation state of components of the PSD is central to synaptic transmission and is known to play a role in synaptic plasticity, learning and memory. The presence of a range of kinases and phosphatases in the PSD defines potential key players in this context. However, the substrates that these enzymes target have not been fully identified to date. We analyzed the protein composition of purified PSD samples from adult mouse brains by strong cation exchange chromatography fractionation of a tryptic digest followed by nano‐reverse phase liquid chromatography coupled with electrospray ionization–quadrupole time of flight tandem mass spectrometry. This led to the identification of 244 proteins. To gain an insight into the phosphoproteome of the PSD we then purified phosphorylated tryptic peptides by immobilized metal ion affinity chromatography. This approach for the specific enrichment of phosphopeptides resulted in the identification of 42 phosphoproteins in the PSD preparation, 39 of which are known PSD components. Here we present a total of 83 in vivo phosphorylation sites.
Hypoxia sensitizes human malignant glioma cells towards CD95L‐induced cell death
Authors: Steinbach Joachim P. , Wolburg Hartwig , Klumpp Andrea , Weller Michael 
Published: March 2005

AbstractDeath ligands such as CD95 ligand (CD95L) have limited activity against glioma cells under normoxic conditions. Hypoxia is a critical aspect of the microenvironment of gliomas in vivo. We investigated the effect of co‐exposure to acute hypoxia and CD95 ligand in three human malignant glioma cell lines with different susceptibility to CD95L under normoxic conditions. Hypoxia sensitized all three cell lines towards CD95L‐induced cell death. Co‐exposure resulted in apoptotic changes in the early phase, with gradual conversion to secondary necrosis with increasing length of hypoxia. The mitochondrial injury induced by hypoxia was enhanced by co‐treatment, and caspase cleavage became prominent. Inhibition of the epidermal growth factor receptor (EGFR), although sensitizing glioma cells to CD95L under normoxia, protects glioma cells from hypoxia by reducing energy consumption. However, the opposing effects of EGFR signalling on death induced by CD95L or hypoxia were neutralized by co‐exposure to hypoxia and CD95L. Furthermore, inhibition of protein synthesis by cycloheximide also reduced glucose consumption and conferred protection from hypoxia, but did not modulate CD95L‐induced cell death under hypoxic conditions. These results suggest that death ligands may be useful to target hypoxic tumour cells resistant to conventional therapies or to complement strategies aiming at the induction of tumour hypoxia.
In vitro1H NMR spectroscopy shows an increase in N‐acetylaspartylglutamate and glutamine content in the hippocampus of amygdaloid‐kindled rats
Authors: Shirayama Yukihiko , Takahashi Seizo , Minabe Yoshio , Ogino Takashi 
Published: March 2005

AbstractWe examined energy metabolism and amino acid content in the hippocampus of amygdaloid‐kindled rats using 1H NMR spectroscopy. Three weeks after the last stage 5 seizure, kindled rats were killed by microwave irradiation. The hippocampus was dissected out and subjected to MeOH/CHCl3 extraction. All 1H spectra were analyzed to quantify absolute concentrations using a non‐linear least squares method, combined with a prior knowledge of chemical shifts. Saturation effects were compensated for by the T1 measurement of each component. Levels of energy metabolism‐related compounds, phosphocreatine, creatine, glucose and succinate were the same in both kindled rats and sham controls. Lactate concentration had a tendency to increase, although this was not statistically significant. When compared with sham controls, levels of aspartate, glutamate, glycine and glutamine, as well as GABA and inositol, were increased in the ipsilateral but not the contralateral hippocampus. In contrast, levels of taurine, alanine and threonine were unchanged. Finally, N‐acetylaspartylglutamate content was elevated, whereas N‐acetyl‐l‐aspartate content was unaltered in the ipsilateral hippocampus of kindled animals. Our results suggest that amygdala kindling may affects amino acid metabolism, but not energy metabolism.
Short‐ and long‐term enzymatic regulation secondary to metabolic insult in the rat retina
Authors: Acosta Monica L. , Kalloniatis Michael 
Published: March 2005

AbstractChanges in oxygen and/or glucose availability may result in altered levels of ATP production and amino acid levels, and alteration in lactic acid production. However, under certain metabolic insults, the retina demonstrates considerable resilience and maintains ATP production, and/or retinal function. We wanted to investigate whether this resilience would be reflected in alterations in the activity of key enzymes of retinal metabolism, or enzymes associated with amino acid production that may supply their carbon skeleton for energy production. Enzymatic assays were conducted to determine the activity of key retinal metabolic enzymes total ATPase and Na+/K+‐ATPase, aspartate aminotransferase and lactate dehydrogenase. In vitro anoxia led to an increase in retinal lactate dehydrogenase activity and to a decrease in retinal aspartate aminotransferase activity, without significant changes in Na+/K+‐ATPase activity. In vivo inhibition of glutamine synthetase resulted in a short‐term significant decrease in retinal aspartate aminotransferase activity. An increase in retinal aspartate aminotransferase and lactate dehydrogenase activities was accompanied by altered levels of amino acids in neurons and glia after partial inhibition of glial metabolism, implying that short‐ and long‐term up‐ and down‐regulation of key metabolic enzymes occurs to supply carbon skeletons for retinal metabolism. ATPase activity does not appear to fluctuate under the metabolic stresses employed in our experimental procedures.
ATP inhibits the hypoxia response in type I cells of rat carotid bodies
Authors: Xu Jianhua , Xu Fenglian , Tse Frederick W. , Tse Amy 
Published: March 2005

SummaryDuring hypoxia, ATP was released from type I (glomus) cells in the carotid bodies. We studied the action of ATP on the intracellular Ca2+ concentration ([Ca2+]i) of type I cells dissociated from rat carotid bodies using a Ca2+ imaging technique. ATP did not affect the resting [Ca2+]i but strongly suppressed the hypoxia‐induced [Ca2+]i elevations in type I cells. The order of purinoreceptor agonist potency in inhibiting the hypoxia response was 2‐methylthioATP > ATP > ADP ≫ α, β‐methylene ATP > UTP, implicating the involvement of P2Y1 receptors. Simultaneous measurements of membrane potential and [Ca2+]i show that ATP inhibited the hypoxia‐induced Ca2+ signal by reversing the hypoxia‐triggered depolarization. However, ATP did not oppose the hypoxia‐mediated inhibition of the oxygen‐sensitive TASK‐like K+ background current. Neither the inhibition of the large‐conductance Ca2+‐activated K+ (maxi‐K) channels nor the removal of extracellular Na+ could affect the inhibitory action of ATP. Under normoxic condition, ATP caused hyperpolarization and increase in cell input resistance. These results suggest that the inhibitory action of ATP is mediated via the closure of background conductance(s) other than the TASK‐like K+, maxi‐K or Na+ channels. In summary, ATP exerts strong negative feedback regulation on hypoxia signaling in rat carotid type I cells.
Signal transduction pathways implicated in neural recognition molecule L1 triggered neuroprotection and neuritogenesis
Authors: Loers Gabriele , Chen Suzhen , Grumet Martin , Schachner Melitta 
Published: March 2005

AbstractThe signal transduction pathways involved in adhesion molecule L1‐triggered neuritogenesis and neuroprotection were investigated using the extracellular domain of mouse or human L1 in fusion with the Fc portion of human immunoglobulin G or L1 purified from mouse brain by affinity chromatography. Substrate L1‐triggered neuritogenesis and neuroprotection depended on distinct but also overlapping signal transduction pathways and on the expression of L1 at the neuronal cell surface. PI3 kinase inhibitors, Src family kinase inhibitors as well as mitogen‐activated protein kinase kinase inhibitors reduced both L1‐triggered neuritogenesis and neuroprotection. In contrast, fibroblast growth factor receptor inhibitors, a protein kinase A inhibitor, and an inhibitor of cAMP‐mediated signal transduction pathways, blocked neuritogenesis, but did not affect L1‐triggered neuroprotection. Proteolytic cleavage of L1 or its interaction partners is necessary for both L1‐mediated neuritogensis and neuroprotection. Furthermore, L1‐triggered neuroprotection was found to be associated with increased phosphorylation of extracellular signal‐regulated kinases 1/2, Akt and Bad, and inhibition of caspases. These observations suggest possibilities of differentially targeting signal transduction pathways for L1‐dependent neuritogenesis and neuroprotection.
PKC site mutations reveal differential modulation by insulin of NMDA receptors containing NR2A or NR2B subunits
Authors: Jones Michelle L. , Leonard John P. 
Published: March 2005

AbstractInsulin modulates N‐methyl‐d‐aspartate (NMDA) receptors in the CNS and potentiates currents of recombinant NMDA receptors in a subunit‐specific manner in Xenopus oocytes. Previously we identified two sites in the NR2B C‐terminus as targets for direct phosphorylation by C‐type protein kinases (PKCs). Mutating these sites reduced insulin potentiation of currents by one half, reflecting the PKC‐mediated portion of the NR2B insulin effect. The PKC‐proline rich tyrosine kinase (Pyk2)‐Src family kinase pathway may also mediate insulin potentiation. A dominant negative Pyk2 mutant significantly reduced insulin potentiation when co‐expressed with NR2B‐containing receptors, suggesting that Pyk2 and downstream Src‐family tyrosine kinases are involved, along with PKCs, in insulin potentiation of NR2B. The NR2A C‐terminus contains two residues homologous to the NR2B PKC targets. Mutating both these sites eliminated insulin potentiation of NR2A‐containing receptors, while co‐expression of dominant negative Pyk2 had no effect. Together, these data indicate that PKCs alone mediate the NR2A insulin effect. When tested individually for importance in insulin potentiation, the two PKC sites showed an additive effect in potentiation of NR2A‐containing receptors. Insulin modulation of NR2A‐containing receptors is mediated solely by PKCs, whereas insulin modulation of NR2B‐containing receptors is mediated by PKCs and tyrosine kinases (PTKs).