bluuebunny/crossref_metadata_2025_split huggingface dataset:
Enzymatic assay of marine bacterial phosphatases by capillary electrophoresis with laser‐induced fluorescence detection
Authors: Chichester Kimberly D. , Sebastian Marta , Ammerman James W. , Colyer Christa L. 
Published: August 2008

AbstractMicrobial ectoenzyme activities in aquatic environments are important determinants of polymer hydrolysis and indicators of the state of microbial carbon, nitrogen, and phosphorus nutrition. Marine ectoenzymes are found on the cell surface or in the periplasmic space of gram‐negative heterotrophic bacteria. Phosphatases, which remove phosphate groups from substrates, are one example of an ectoenzyme. Enzyme assays based on‐capillary electrophoresis (CE) take advantage of CE's high‐efficiency separation, extremely low sample volume requirements, and its ability to electrophoretically mix and separate zones of enzymes, substrates, and products all in one experimental run. CE has better resolving power and, when utilized with laser‐induced fluorescence (LIF) detection, it is more sensitive than chromatography. CE‐LIF is a promising tool for determining different phosphatases within a single microbial strain as well as the functional diversity between strains. In this study, four bacterial strains were studied (Shewanella sp., TW7, BB2AT2, and Vibrio alginolyticus) with each yielding at least one phosphatase that was kinetically characterized. Km values were calculated and found to be in the range of 0.0725–3.35 µM, whereas Vmax values ranged from 1.02×10−3 to 1.05×10−2 µM/min. The large range of values demonstrates differences among the phosphatases, suggesting different roles for each phosphatase not only between the species but also within a single bacterial species. This can have the important implications for organic matter processing in the sea.
Social influences on foraging behavior in young nonhuman primates: Learning what, where, and how to eat
Authors: Rapaport Lisa G. , Brown Gillian R. 
Published: August 2008

AbstractHuman infants rely on social interactions to acquire food‐related information.1, 2 Adults actively teach children about food through culturally diverse feeding practices. Characteristics we share with the other primates, such as complex diets, highly social lives, and extended juvenile periods, suggest that social learning may be important during ontogeny throughout the order. Although all young primates typically pay attention to feeding adults, great apes and callitrichids, in particular, acquire new foraging techniques through abilities unknown in other nonhuman primates; that is, they learn by imitation. However, ape social learning is almost exclusively infant‐initiated, while adult callitrichids actively teach their young. It is unlikely that the same selective forces have acted to favor sophisticated social‐learning mechanisms in both taxa.3, 4 Equipped with an ape brain, complex foraging methods, and a cooperative infant‐care system, early hominins were uniquely poised to take social learning about food and foraging techniques to a new level.
Effects of pre or posttraining dorsal hippocampus D‐AP5 injection on fear conditioning to tone, background, and foreground context
Authors: Schenberg Eduardo Ekman , Oliveira Maria Gabriela Menezes 
Published: August 2008

AbstractNMDA receptor antagonist D‐AP5 was injected into the dorsal hippocampus of Wistar rats before or immediately after the training session in fear conditioning. Training was conducted both with signaled (background context) or unsignaled (foreground context) footshocks. Contextual fear conditioning was assessed 24 h later and tone fear conditioning 48 h after training (only in the signaled footshock condition). Pretraining injections impaired conditioned fear to contextual features, both in background and foreground configurations, whereas tone fear conditioning was left intact. Posttraining injections were ineffective in all cases. We conclude that dorsal hippocampal NMDA receptors are required for contextual fear acquisition independently of context saliency and that they are not required to early consolidation processes. © 2008 Wiley‐Liss, Inc.
Hippocampal levels of phosphorylated protein kinase a (phosphor‐S96) are linked to spatial memory enhancement by SGS742
Authors: Sunyer Berta , Shim Ki‐Shuk , An Gunyong , Höger Harald , Lubec Gert 
Published: August 2008

AbstractCognitive enhancement by the GABA (B) receptor antagonist SGS742 has been well‐documented, but mechanisms of action are not fully elucidated. Previous work has proposed involvement of somatostatin‐14 and protein kinase C in cognitive enhancement; phospho‐protein kinase A (p‐PKA), fyn, and phospho‐fyn are known signaling systems for spatial memory. It was the aim of the study to determine hippocampal levels of these proteins following SGS742‐treatment and to correlate them with the outcome from the Morris water maze (MWM), represented by the parameter “time spent in the target quadrant” during the probe trial. OF1 mice were used for the experiments and divided into four groups: intraperitoneal SGS742 and saline solution treatment, both, tested in the MWM, and two yoked controls. Six hours following the probe trial, hippocampal protein levels were determined by immunoblotting. In the MWM, time spent in the target quadrant was significantly enhanced by SGS742 treatment. p‐PKA levels were significantly increased only in the SGS742‐treated group tested in the MWM as compared to saline treatment. In yoked controls, no significant differences in p‐PKA levels between SGS742 and saline treatment were observed. Somatostatin‐14 levels were significantly increased in both SGS742‐treated groups. No statistically significant changes of other protein levels were observed. We propose that GABA (B) antagonism represented by SGS742 treatment led to cognitive enhancement involving p‐PKA, because yoked controls treated with SGS742 were comparable to yoked saline‐treated controls. The finding that somatostatin‐14 was also induced in the SGS742‐treated yoked controls points to a drug side effect, and therefore the role of somatostatin‐14 for cognitive enhancement remains open. © 2008 Wiley‐Liss, Inc.
The protein kinase C phosphorylation site on GAP‐43 differentially regulates information storage
Authors: Holahan Matthew , Routtenberg Aryeh 
Published: August 2008

AbstractProtein kinase C (PKC) is known to regulate phosphorylation of substrates such as MARCKS, GAP‐43, and the NMDA receptor, all of which have been linked to synaptic plasticity underlying information storage processes. Here we report on three transgenic mice isoforms differentiated both by mutation of the PKC site on GAP‐43 as well as by their performance in three learning situations: (1) a radial arm maze task, which evaluates spatial memory and its retention, (2) fear conditioning which assesses contextual memory, and (3) the water maze which also evaluates spatial memory and its retention. The present results show, for the first time to our knowledge, that the phosphorylation state of a single site on an identified brain growth‐ and plasticity‐associated protein differentially regulates performance of three different memory‐associated tasks. © 2008 Wiley‐Liss, Inc.
The human hippocampus at 7 T—In vivo MRI
Authors: Theysohn Jens M. , Kraff O. , Maderwald S. , Schlamann M.U. , de Greiff A. , Forsting M. , Ladd S.C. , Ladd M.E. , Gizewski E.R. 
Published: August 2008

AbstractThe human hippocampus plays a central role in various neuropsychiatric disorders, such as temporal lobe epilepsy (TLE), Alzheimer's dementia, mild cognitive impairment, and schizophrenia. Its volume, morphology, inner structure, and function are of scientific and clinical interest. Magnetic resonance (MR) imaging is a widely employed tool in neuroradiological workup regarding changes in brain anatomy, (sub‐) volumes, and cerebral function including the hippocampus. Gain in intrinsic MR signal provided by higher field strength scanners and concomitant improvements in spatial resolution seem highly valuable. An examination protocol permitting complete, high‐resolution imaging of the human hippocampus at 7 T was implemented. Coronal proton density, T2, T2*, and fluid‐attenuated inversion recovery contrasts were acquired as well as an isotropic 3D magnetization‐prepared rapid acquisition gradient‐echo (500 μm isotropic voxel dimension, noninterpolated). Observance of energy deposition restrictions within acceptable scan times remained challenging in the acquisition of thin, spin‐echo‐based sections. At the higher resolution enabled by 7 T, demarcation of the hippocampus and some internal features including gray/white matter differentiation and depiction of the hippocampal mantle becomes much more viable when compared with 1.5 T; thus, in the future, this imaging technology might help in the diagnosis of subtle hippocampal changes. © 2008 Wiley‐Liss, Inc.
Modulation of AMPA receptor‐mediated ion current by pituitary adenylate cyclase‐activating polypeptide (PACAP) in CA1 pyramidal neurons from rat hippocampus
Authors: Costa L. , Santangelo F. , Li Volsi G. , Ciranna L. 
Published: August 2008

AbstractPituitary adenylate cyclase‐activating polypeptide (PACAP), a neurotrophic and neuromodulatory peptide, was recently shown to enhance NMDA receptor‐mediated currents in the hippocampus (Macdonald, et al. 2005. J Neurosci 25:11374–11384). To check if PACAP might also modulate AMPA receptor function, we tested its effects on AMPA receptor‐mediated synaptic currents on CA1 pyramidal neurons, using the patch clamp technique on hippocampal slices. In the presence of the NMDA antagonist D‐AP5, PACAP (10 nM) reduced the amplitude of excitatory postsynaptic currents (EPSCs) evoked in CA1 pyramidal neurons by stimulation of Schaffer collaterals. Following a paired‐pulse stimulation protocol, the paired‐pulse ratio was unaffected in most neurons, suggesting that the AMPA‐mediated EPSC was modulated by PACAP mainly at a postsynaptic level. PACAP also modulated the currents induced on CA1 pyramidal neurons by applications of either glutamate or AMPA. The effects of PACAP were dose‐dependent: at a 0.5 nM dose, PACAP increased AMPA‐mediated current; such effect was blocked by PACAP 6–38, a selective antagonist of PAC1 receptors. The enhancement of AMPA‐mediated current by PACAP 0.5 nM was abolished when cAMPS‐Rp, a PKA inhibitor, was added to the intracellular solution. At a 10 nM concentration, PACAP reduced AMPA‐mediated current; such effect was not blocked by PACAP 6–38. The inhibitory effect of 10 nM PACAP was mimicked by Bay 55–9837 (a selective agonist of VPAC2 receptors), persisted in the presence of intracellular BAPTA and was abolished by intracellular cAMPS‐Rp. Stimulation‐evoked EPSCs in CA1 neurons were significantly reduced following application of the PAC1 antagonist PACAP 6–38; this result indicates that PAC1 receptors in the CA1 region are tonically activated by endogenous PACAP and enhance CA3‐CA1 synaptic transmission. Our results show that PACAP differentially modulates AMPA receptor‐mediated current in CA1 pyramidal neurons by activation of PAC1 and VPAC2 receptors, both involving the cAMP/PKA pathway; the functional significance will be discussed in light of the multiple effects exerted by PACAP on the CA3‐CA1 synapse at different levels. © 2008 Wiley‐Liss, Inc.
Acidosis induces multi‐drug resistance in rat prostate cancer cells (AT1) in vitro and in vivo by increasing the activity of the p‐glycoprotein via activation of p38
Authors: Sauvant Christoph , Nowak Martin , Wirth Claudia , Schneider Bettina , Riemann Anne , Gekle Michael , Thews Oliver 
Published: August 2008

AbstractBecause solid growing tumors often show hypoxia and pronounced extracellular acidosis, the aim of this study was to analyze the impact of an acidotic environment on the activity of the p‐glycoprotein (pGP) and on the cellular content and cytotoxicity of the chemotherapeutic drug daunorubicin in the AT1 R‐3327 Dunning prostate carcinoma cell line cultured in vitro and in vivo. In vitro, extracellular acidosis (pH 6.6) activated p38 and ERK1/2 and thereby induced daunorubicin resistance via a pronounced activation of pGP. De‐novo protein synthesis was not necessary and analysis of transport kinetics indicated a fast and persistent pGP activation at pH 6.6 (when compared with 7.4). Intracellular acidification also induced daunorubicin resistance via activation of pGP, which was mediated by activation of p38 alone. In vivo, tumors were implanted subcutaneously, and the tumor pH was artificially lowered by forcing anaerobic metabolism. In vivo, the reduced extracellular pH of 6.6 was also able to induce daunorubicin resistance, which was abolished by inhibition of p38. These results suggest that pGP activity is dependent on extracellular pH in vitro and in vivo. Moreover, there is strong indication that this effect is mediated via activation of p38 in vivo. Activation of ERK is also suitable to induce pGP activity. Therefore, inhibition of p38 (and ERK) may be used to prevent acidosis induced increase in pGP activity and thereby attenuate multidrug resistance. In addition, supportive treatments reducing tumor acidosis may improve the cytotoxic effect of chemotherapeutic drugs. © 2008 Wiley‐Liss, Inc.
Activating transcription factor 4 is critical for proliferation and survival in primary bone marrow stromal cells and calvarial osteoblasts
Authors: Zhang Xiaoyan , Yu Shibing , Galson Deborah L. , Luo Min , Fan Jie , Zhang Jian , Guan Youfei , Xiao Guozhi 
Published: August 2008

AbstractActivating transcription factor 4 (ATF4) is essential for bone formation. However, the mechanism of its actions in bone is poorly understood. The present study examined the role for ATF4 in the regulation of proliferation and survival of primary mouse bone marrow stromal cells (BMSCs) and osteoblasts. Results showed that Atf4−/− cells display a severe proliferative defect as measured by multiple cell proliferation assays. Cell cycle progression of Atf4−/− BMSCs was largely delayed with significant G1 arrest. Expression of cyclin D1 was decreased both at the mRNA and protein level. A similar proliferation defect was observed in Atf4−/− calvarial periosteal osteoblasts when compared with wt control. Knocking down Atf4 mRNA by small interfering RNA in MC3T3‐E1 subclone 4 preosteoblasts markedly reduced expression of cyclin D1 and cell proliferation. In contrast, overexpression of ATF4 increased cyclin D1 expression as well as cell proliferation in Atf4−/− BMSCs. In addition, apoptosis was significantly increased in Atf4−/− BMSCs and calvarial periosteal osteoblasts relative to wt controls. Taken together, these results for the first time demonstrate that ATF4 is a critical regulator of proliferation and survival in BMSCs and osteoblasts in vitro and in vivo. J. Cell. Biochem. 105: 885–895, 2008. © 2008 Wiley‐Liss, Inc.
Gaussian basis set of double zeta quality for atoms K through Kr: Application in DFT calculations of molecular properties
Authors: Camiletti G. G. , Machado S. F. , Jorge F. E. 
Published: August 2008

AbstractContracted basis sets of double zeta (DZ) quality for the atoms from K to Kr are presented. They were determined from fully optimized basis sets of primitive Gaussian‐type functions generated in atomic Hartree‐Fock calculations. Sets of Gaussian polarization functions optimized at the Möller‐Plesset second‐order level were added to the DZ basis set. This extends earlier work on segmented contracted DZ basis set for atoms H‐Ar. From this set, using the BP86 nonhybrid and B3LYP hybrid functionals, dissociation energy, geometric parameters, harmonic vibrational frequency, and electric dipole moment of a set of molecules were calculated and compared with results obtained with other basis sets and with experimental data reported in the literature. In addition, 57Fe and 77Se nuclear magnetic resonance chemical shifts in Fe(C5H5)2, H2Se, and CSe2 were calculated using density functional theory and gauge‐including atomic orbitals and, then, compared with theoretical and experimental values previously published in the literature. Except for chemical shift, one verifies that our results give the best agreement with experimental and benchmark values. © 2008 Wiley Periodicals, Inc. J Comput Chem, 2008
Molecular cloning and characterization of a new gene, Oocyte‐G1
Authors: Zhang Yong , Wu Ji 
Published: August 2008

AbstractOocytes are recognized as a source of regulatory molecules that influence follicular development through an array of actions on granulosa cells. Recently, more and more hormones and signaling molecules were identified during follicular developmental processes; however, the details about their functions are still unclear. During efforts to clone follicular development‐related genes, we isolated a cDNA fragment by DDRT‐PCR. To obtain cDNA 5′‐ and 3′‐end sequences, we screened a mouse ovarian cDNA library. After screening the library, an open reading frame of 2,994 bp for the new gene (Oocyte‐G1), which encodes a 997‐residue protein, was cloned. Northern blot analysis revealed the presence of ∼3.6 kb Oocyte‐G1 mRNA in ovary, lung, kidney, testis and brain. Northern analysis of RNA from ovaries in vivo showed that Oocyte‐G1 was weakly expressed on day 5 and at a moderate level on day 10. Thereafter, on day 15 or in adults (day 40), there was an increase in expression, followed by a decline in ovaries on day 20 or older (day 120). Furthermore, we studied the Ooctye‐G1 protein by using the antiserum against a peptide sequence unique to this gene in Western blotting and immunolocalization. The antiserum recognized a prominent band of ∼110 kDa in immunoblots and signals were dispersed in oocytes and some cumulus granulosa cells. Our results suggest the potential role of Oocyte‐G1 in ovarian follicular development. J. Cell. Physiol. 218: 75–83, 2009. © 2008 Wiley‐Liss, Inc.
Thrombospondin‐1‐induced apoptosis of brain microvascular endothelial cells can be mediated by TNF‐R1
Authors: Rege Tanya A. , Stewart Jerry , Dranka Brian , Benveniste Etty N. , Silverstein Roy L. , Gladson Candece L. 
Published: August 2008

AbstractThrombospondin‐1 (TSP‐1) treatment of dermal microvascular endothelial cells (MvEC) has been shown to upregulate Fas ligand (FasL) and to induce apoptosis by a mechanism that requires caspase‐8 activity. We have examined the potential anti‐angiogenic effects of TSP‐1 on primary human brain MvEC. The addition of TSP‐1 to primary human brain MvEC cultured as monolayers on type 1 collagen, induced cell death and apoptosis (evidenced by caspase‐3 cleavage) in a dose‐ (5–30 nM) and time‐dependent (maximal at 17 h) manner. TSP‐1 treatment for 17 h induced caspase‐3 cleavage that required caspase‐8 activity and the tumor necrosis factor receptor 1 (TNF‐R1). We did not find a requirement for Fas, or the tumor necrosis‐related apoptosis‐inducing ligand receptors (TRAIL‐R) 1 and 2. We confirmed the findings using caspase inhibitors, blocking antibodies and small interfering RNA (siRNA). Further analysis indicated that the TSP‐1 induction of caspase‐3 cleavage of primary human brain MvEC adherent to collagen required the synthesis of new message and protein, and that TSP‐1 induced the expression of TNFα mRNA and protein. Consistent with these findings, when the primary human brain MvEC were propagated on collagen gels mAb anti‐TNF‐R1 reversed the inhibitory effect, in part, of TSP‐1 on tube formation and branching. These data identify a novel mechanism whereby TSP‐1 can inhibit angiogenesis‐through induction of apoptosis in a process mediated by TNF‐R1. J. Cell. Physiol. 218: 94–103, 2009. © 2008 Wiley‐Liss, Inc.
Inhibition of myogenesis by Notch: Evidence for multiple pathways
Authors: Buas Matthew F. , Kabak Shara , Kadesch Tom 
Published: August 2008

AbstractNotch signaling is critical for skeletal muscle development and regeneration, permitting the expansion of progenitor cells by preventing premature differentiation. We have interrogated the pathways through which ligand‐mediated signaling inhibits myogenesis by identifying Notch target genes and assessing their impact on differentiation in vitro. Notch activation led to the robust induction of the transcriptional repressors Hey1 and HeyL in myoblasts, but only constitutive expression of Hey1 blocked myogenesis. siRNA‐mediated knockdown of Hey1 had no effect on Notch's ability to inhibit differentiation, suggesting the existence of additional, possibly redundant pathways. We identified 82 genes whose expression was activated when C2C12 myoblasts were cultured in the presence of the Notch ligand Dll4. One of these, MyoR, is a novel Notch‐responsive gene, whose protein product is known to repress myogenesis in vitro. siRNA‐mediated knockdown of MyoR alone, or in combination with Hey1, was also ineffective at rescuing differentiation in the presence of Dll4. Our data support a model in which Notch signaling inhibits myogenesis through multiple pathways, two of which are defined by the Notch target genes Hey1 and MyoR. J. Cell. Physiol. 218: 84–93, 2009. © 2008 Wiley‐Liss, Inc.
The use of mesenchymal (skeletal) stem cells for treatment of degenerative diseases: Current status and future perspectives
Authors: Abdallah Basem M. , Kassem Moustapha 
Published: August 2008

AbstractHuman bone marrow derived‐mesenchymal (skeletal) stem (MSC) cells are a group of non‐hematopoietic stem cells residing in the perivascular niches in bone marrow. These cells have the capacity to differentiate mainly into mesoderm‐type cells such as osteoblasts, chondrocytes and adipocytes and possibly but not proven to non‐mesodermal cell types. Recently, there has been an increased interest in understanding the biology of MSC due to their potential use in cell‐based therapy for multiple degenerative diseases. Here, we will provide an update on the current status of these novel therapeutic opportunities. J. Cell. Physiol. 218: 9–12, 2009. © 2008 Wiley‐Liss, Inc.
Sonographic assessment of uterine and ovarian development in normal girls aged 1 to 12 years
Authors: Badouraki Maria , Christoforidis Athanasios , Economou Ippoliti , Dimitriadis Athanassios S. , Katzos George 
Published: August 2008

AbstractPurpose.To provide normal references of sonographic uterine and ovarian size in girls aged 1–12 years.Method.Ninety‐nine girls were enrolled in the study (mean age ± SD, 6.9 ± 2.4 years [range, 1–12 years]). Pubertal status was classified according to Tanner staging, whereas for height and weight assessment a standard stadiometer and weight scale were employed. All subjects underwent pelvic sonographic examination for the measurement of uterine length, volume, ratio of anteroposterior diameter at the fundus divided by the anteroposterior diameter at the cervix (fundal–cervical [F/C] ratio), and ovarian volume and morphology.Results.A gradual increase with age was observed in all uterine and ovarian measurements. Cubic model analysis provided the best curve estimation for uterine length, uterine volume, and ovarian volume in relation to age. Uterine length, uterine volume, ovarian volume and F/C ratio were significantly correlated to both age and height. With respect to ovarian morphology, there was a gradual decrease in frequency of the homogeneous and the paucicystic appearances with increasing age. The macrocystic appearance was observed after the age of 6 years, and its frequency increased gradually with age.Conclusion.There is a continuous increase in size of internal female genitalia from early childhood until the onset of puberty. We have provided reference percentile charts of normal uterine length, uterine volume, and ovarian volume in girls aged 1–12 years. © 2008 Wiley Periodicals, Inc. J Clin Ultrasound, 2008