bluuebunny/crossref_metadata_2025_split huggingface dataset:
Conduction block and glial injury induced in developing central white matter by glycine, GABA, noradrenalin, or nicotine, studied in isolated neonatal rat optic nerve
Authors: Constantinou Stavros , Fern Robert 
Published: January 2009

AbstractThe damaging effects of excessive glutamate receptor activation have been highlighted recently during injury in developing central white matter. We have examined the effects of acute exposure to four other neurotransmitters that have known actions on white matter. Eighty minutes of Glycine or GABA‐A receptor activation produced a significant fall in the compound action potential recorded from isolated post‐natal day 10 rat optic nerve. This effect was largely reversed upon washout. Nicotinic acetylcholine receptor (nAChR) or adrenoreceptor activation with noradrenalin resulted in an ∼35% block of the action potential that did not reverse during a 30‐min washout period. While the effect of nAChR activation was blocked by a nAChR antagonist, the effect of noradrenalin was not ablated by α‐ or β‐adrenoreceptor blockers applied alone or in combination. In the absence of noradrenalin, co‐perfusion with α‐ and β‐adrenoreceptor blockers resulted in nonreversible nerve failure indicating that tonic adrenoreceptor activation is required for nerve viability, while overactivation of these receptors is also damaging. Nerves exposed to nAChR + adrenoreceptor activation showed no axon pathology but had extensive glial injury revealed by ultrastructural analysis. Oligodendroglia exhibited regions of membrane vacuolization while profound changes were evident in astrocytes and included the presence of swollen and expanded mitochondria, vacuolization, cell processes disintegration, and membrane breakdown. Blinded assessment revealed higher levels of astrocyte injury than oligodendroglial injury. The findings show that overactivation of neurotransmitter receptors other than those for glutamate can produce extensive injury to developing white matter, a phenomenon that may be clinically significant. © 2009 Wiley‐Liss, Inc.
GDNF‐enhanced axonal regeneration and myelination following spinal cord injury is mediated by primary effects on neurons
Authors: Zhang Liqun , Ma Zhengwen , Smith George M. , Wen Xuejun , Pressman Yelena , Wood Patrick M. , Xu Xiao‐Ming 
Published: January 2009

AbstractWe previously demonstrated that coadministration of glial cell line‐derived neurotrophic factor (GDNF) with grafts of Schwann cells (SCs) enhanced axonal regeneration and remyelination following spinal cord injury (SCI). However, the cellular target through which GDNF mediates such actions was unclear. Here, we report that GDNF enhanced both the number and caliber of regenerated axons in vivo and increased neurite outgrowth of dorsal root ganglion neurons (DRGN) in vitro, suggesting that GDNF has a direct effect on neurons. In SC‐DRGN coculture, GDNF significantly increased the number of myelin sheaths produced by SCs. GDNF treatment had no effect on the proliferation of isolated SCs but enhanced the proliferation of SCs already in contact with axons. GDNF increased the expression of the 140 kDa neural cell adhesion molecule (NCAM) in isolated SCs but not their expression of the adhesion molecule L1 or the secretion of the neurotrophins NGF, NT3, or BDNF. Overall, these results support the hypothesis that GDNF‐enhanced axonal regeneration and SC myelination is mediated mainly through a direct effect of GDNF on neurons. They also suggest that the combination of GDNF administration and SC transplantation may represent an effective strategy to promote axonal regeneration and myelin formation after injury in the spinal cord. © 2009 Wiley‐Liss, Inc.
Tripchlorolide protects neuronal cells from microglia‐mediated β‐amyloid neurotoxicity through inhibiting NF‐κB and JNK signaling
Authors: Pan Xiao‐Dong , Chen Xiao‐Chun , Zhu Yuan‐Gui , Chen Li‐Min , Zhang Jing , Huang Tian‐Wen , Ye Qin‐Yong , Huang Hua‐Pin 
Published: January 2009

AbstractRecent research has focused on soluble oligomeric assemblies of β‐amyloid peptides (Aβ) as the proximate cause of neuroinflammation, synaptic loss, and the eventual dementia associated with Alzheimer's disease (AD). In this study, tripchlorolide (T4), an extract of Tripterygium wilfordii Hook. F (TWHF), was studied as a novel agent to suppress neuroinflammatory process in microglial cells and to protect neuronal cells against microglia‐mediated oligomeric Aβ toxicity. T4 significantly attenuated oligomeric Aβ(1‐42)‐induced release of inflammatory productions such as tumor necrosis factor‐α, interleukin‐1β, nitric oxide (NO), and prostaglandin E2. It also downregulated the protein levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase‐2 (COX‐2) in microglial cells. Further molecular mechanism study demonstrated that T4 inhibited the nuclear translocation of nuclear factor‐κB (NF‐κB) without affecting I‐κBα phosphorylation. It repressed Aβ‐induced JNK phosphorylation but not ERK or p38 MAPK. The inhibition of NF‐κB and JNK by T4 is correlated with the suppression of inflammatory mediators in Aβ‐stimulated microglial cells. These results suggest that T4 protects neuronal cells by blocking inflammatory responses of microglial cells to oligomeric Aβ(1‐42) and that T4 acts on the signaling of NF‐κB and JNK, which are involved in the modulation of inflammatory response. Therefore, T4 may be an effective agent in modulating neuroinflammatory process in AD. © 2009 Wiley‐Liss, Inc.
Fatty liver is associated with insulin resistance, risk of coronary heart disease, and early atherosclerosis in a large European population #
Authors: Gastaldelli Amalia , Kozakova Michaela , Hφjlund Kurt , Flyvbjerg Allan , Favuzzi Angela , Mitrakou Asimina , Balkau Beverley 
Published: January 2009

Abstract
Patients with fatty liver (FL) disease have a high risk of developing diabetes and cardiovascular diseases. The aim was to evaluate the association between FL, insulin resistance (IR), coronary heart disease (CHD) risk, and early atherosclerosis in a large European population (RISC Study). In 1,307 nondiabetic subjects (age 30-60 years) recruited at 19 centers, we evaluated liver enzymes, lipids, insulin sensitivity (by euglycemic-hyperinsulinemic clamp), glucose tolerance (by 75 g oral glucose tolerance test), carotid atherosclerosis as intima media thickness (IMT), CHD risk by the Framingham Heart study prediction score, and physical activity (by accelerometer). The presence of FL was estimated using the fatty liver index (FLI; >60, likelihood >78% presence FL; FLI <20 likelihood >91% absence of FL). Subjects were divided into three groups: G1: FLI <20 (n = 608); G3: FLI >60 (n = 234), G2: intermediate group (n = 465). Compared to G1, G3 included more men (70% versus 24%) and people with impaired glucose tolerance (23% versus 5%). IMT increased with FLI (G3 = 0.64 ± 0.08 versus G1 = 0.58 ± 0.08 mm, P < 0.0001). FLI was associated with increased CHD risk (r = 0.48), low-density lipoprotein cholesterol (r = 0.33), alanine aminotransferase (r = 0.48), aspartate aminotransferase (r = 0.25), systolic blood pressure (r = 0.39) and IMT (r = 0.30), and reduced insulin sensitivity (r = −0.43), high-density lipoprotein cholesterol (r = −0.50), adiponectin (r = −0.42), and physical activity (r = −0.16, all P < 0.0001). The correlations hold also in multivariate analysis after adjusting for age, gender, and recruiting center. Conclusion: In middle-age nondiabetic subjects, increased IMT, CHD risk, and reduced insulin sensitivity are associated with high values of FLI. (Hepatology 2009.)
Parenting and child behaviour problems: a longitudinal analysis of non‐shared environment
Authors: Mullineaux Paula Y. , Deater‐Deckard Kirby , Petrill Stephen A. , Thompson Lee A. 
Published: January 2009

AbstractThis study examined potential non‐shared environmental processes in middle childhood by estimating statistical associations between monozygotic (MZ) twin differences in externalizing and internalizing problems and positive social engagement, and differential maternal positivity and negativity, over 1 year. Seventy‐seven pairs of identical twins participated (M=6.08‐years old, 65% male) in two annual home visits. Observers' ratings and maternal reports were gathered. At both assessments, the twin who showed more conduct problems (maternal report and observers' ratings) and less positive social engagement (positive affect, responsiveness) received more maternal negativity and less maternal warmth (self‐reports and observers' ratings), relative to his or her genetically identical co‐twin. The same patterns held over time, for the associations between change in differential MZ twin conduct problems and social engagement and change in differential maternal behaviour. Effects for child internalizing problems were not consistent within or across raters. Overall, these results indicated that differential maternal warmth and negativity—self‐perceived and observed by others—are important aspects of sibling differentiation for both problematic and adaptive behaviours during middle childhood. Copyright © 2009 John Wiley & Sons, Ltd.
Changes in cry acoustics and distress ratings while the infant is crying
Authors: Wood Rebecca M. 
Published: January 2009

AbstractAcoustics and distress ratings were examined during four minutes of naturally occurring crying from 20 healthy, 1‐month‐old infants. Two listeners made continuous judgements of infant distress during every 10‐s segment of each cry sample. Dysphonation, number of wails, and pause duration were related to distress ratings across the 4 min of crying. Means and variances of ratings and acoustics, and the predictive value of each acoustic variable to ratings, differed in the first and second halves of the samples. Differences in the pattern of results occurred for individual infants. The results highlight the importance of studying the cry as a dynamic acoustic signal that may provide unique information about an individual infant's level of distress. Copyright © 2009 John Wiley & Sons, Ltd.
Is prior performance priced through closed‐end fund discounts?
Authors: Bleaney Michael , Todd Smith R. 
Published: January 2009

AbstractIn open‐end mutual funds (unit trusts), there is a strong positive cross‐sectional relationship between net inflows to individual funds and past performance, as if investors attributed performance to managerial skill. Performance shows only very weak persistence, however, so at first sight investors do not appear to gain anything by responding to past performance information. This behaviour can be explained by the fact that past performance is effectively unpriced in the unit trust market, since management fees are unresponsive to demand. If investors believe that there is a non‐zero probability that future performance will turn out to be positively correlated with past performance (i.e. that there is an element of managerial skill in performance), but a zero probability that this correlation will be negative, it is rational to prefer funds with better past performance when performance is not priced. In other words, it costs nothing to insure against the possibility of some managerial skill effect.If this explanation of the flow–performance relationship in unit trusts is correct, one would expect the relationship between investor demand and past fund performance to be much weaker if past performance were to be priced. We test this hypothesis in the market for closed‐end funds (investment trusts). Because closed‐end funds do not trade at net asset value, but at a price determined in the market, strong demand will raise the ratio of price to net asset value (known as the premium). Since it is well established that premiums are mean‐reverting, future shareholder returns on funds currently on high premiums tend to be depressed by the reversion of the premium to the mean. In the closed‐end fund market, as for open‐end funds, there is little evidence of performance persistence, and therefore, to the extent that funds with good past performance are pushed to higher premiums, the expected return on them is less than on the average fund. This implicit pricing mechanism should mean that demand is a declining function of the premium, so that, even if demand is an increasing function of past performance for a given premium, any effect on the premium itself will be muted.We test this hypothesis for closed‐end funds traded in the US and the UK. We find that there is a statistically significant effect of past performance on the premium in both countries. However, consistent with the hypothesis, it has limited economic significance, since it represents only a small component of premium variability. Copyright © 2008 John Wiley & Sons, Ltd.
Application of Raman spectroscopy for cervical dysplasia diagnosis
Authors: Kanter Elizabeth M. , Vargis Elizabeth , Majumder Shovan , Keller Matthew D. , Woeste Emily , Rao Gautam G. , Mahadevan‐Jansen Anita 
Published: January 2009

AbstractCervical cancer is the second most common malignancy among women worldwide, with over 490 000 cases diagnosed and 274 000 deaths each year. Although current screening methods have dramatically reduced cervical cancer incidence and mortality in developed countries, a “See and Treat” method would be preferred, especially in developing countries. Results from our previous work have suggested that Raman spectroscopy can be used to detect cervical precancers; however, with a classification accuracy of 88%, it was not clinically applicable. In this paper, we describe how incorporating a woman's hormonal status, particularly the point in menstrual cycle and menopausal state, into our previously developed classification algorithm improves the accuracy of our method to 94%. The results of this paper bring Raman spectroscopy one step closer to being utilized in a clinical setting to diagnose cervical dysplasia. (© 2009 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim)
Large‐volume‐apheresis facilitates autologous transplantation of hematopoietic progenitors in poor mobilizer patients
Authors: Majado Maria Juliana , Minguela Alfredo , González‐García Consuelo , Salido Eduardo , Blanquer Miguel , Funes Consuelo , Insausti Carmen Luisa , García‐Hernández Ana María , Moraleda José María , Morales Alfonso 
Published: January 2009

AbstractGiven that pre‐apheresis CD34+ cell count (PA‐CD34) predicts the apheresis' yield, a minimum of 5 to 20 PA‐CD34/μl is required in many institutions to initiate cell collection. The aim of this study was to clarify whether large‐volume‐apheresis (LVA) could facilitate progenitor cell transplantation in patients with low PA‐CD34. Apheresis was initiated in 226 patients, disregarding PA‐CD34, at days: +5 in G‐CSF, +10 in cyclophosphamide+G‐CSF, and +15 to +20 in other chemotherapy+G‐CSF mobilization, when leucocytes >2.5 × 109/L. Four times the blood volume was processed. Patients were grouped according to their PA‐CD34: ≥10/μl (group‐A, n = 143); <10/μl but ≥5/μl (group‐B, n = 40) and <5/μl (group‐C, n = 43). No differences were found in diagnoses, gender, age, previous treatments or mobilization regimen between groups. Enough CD34+ cells (>1.9 × 106/kg) were obtained in 31 patients (72%) from group‐C, although in this group two mobilizations were needed in 20 patients (46.5%), compared to 5 (3.5%) and 1 (2.5%) in groups A and B, respectively (P < 0.01). Evenly three apheresis or more were required in 28 patients (65.1%) from group‐C, compared to 8 (5.6%) and 6 (15.0%) in groups A and B, respectively (P < 0.01). In conclusion LVA can facilitate autologous transplantation in poor‐mobilizer‐patients, low PA‐CD34 should not be an inflexible exclusion factor. J. Clin. Apheresis, 2009. © 2009 Wiley‐Liss, Inc.
Prostate cancer promotes CD11b positive cells to differentiate into osteoclasts
Authors: Mizutani Kosuke , Sud Sudha , Pienta Kenneth J 
Published: January 2009

AbstractBone is the preferred site of prostate cancer metastasis, contributing to the morbidity and mortality of this disease. A key step in the successful establishment of prostate cancer bone metastases is activation of osteoclasts with subsequent bone resorption causing the release of several growth factors from the bone matrix. CD11b+ cells in bone marrow are enriched for osteoclast precursors. Conditioned media from prostate cancer PC‐3 cells induces CD11b+ cells from human peripheral blood to differentiate into functional osteoclasts with subsequent bone resorption. Analysis of PC‐3 conditioned media revealed high amounts of IL‐6 and IL‐8. CD11b+ cells were cultured with M‐CSF and RANKL, IL‐6, IL‐8, and CCL2, alone or in combination. All of these conditions induced osteoclast fusion, but cells cultured with M‐CSF, IL‐6, IL‐8, and CCL2 were capable of limited bone resorption. Co‐incubation with IL‐6 and IL‐8 and the RANK inhibitor, RANK‐Fc, failed to inhibit osteoclast fusion and bone resorption, suggesting a potential RANKL‐independent mechanism of functional osteoclast formation. This study demonstrates that functional osteoclasts can be derived from CD11b+ cells derived from human PBMCs. Prostate cancer cells secrete factors, including IL‐6 and IL‐8, that play an important role in osteoclast fusion by a RANKL‐independent mechanism. J. Cell. Biochem. 106: 563–569, 2009. © 2009 Wiley‐Liss, Inc.
Lack of lymphatic vessel phenotype in LYVE‐1/CD44 double knockout mice
Authors: Luong Mai X. , Tam Joshua , Lin Qingcong , Hagendoorn Jeroen , Moore Kathryn J. , Padera Timothy P. , Seed Brian , Fukumura Dai , Kucherlapati Raju , Jain Rakesh K. 
Published: January 2009

AbstractLymphatic vessels play a key role in maintaining tissue‐fluid homeostasis, immune surveillance and metastasis. The hyaluronan receptor, LYVE‐1, is widely used as a molecular marker for adult and embryonic lymphatic endothelium, but its physiological functions have not yet been established in vivo. In agreement with a recent report, LYVE‐1−/− mice, which are healthy and fertile, do not display any defects related to congenital abnormalities of the lymphatic system. One hypothesis for the absence of a phenotype in LYVE‐1 null mice is that other hyaluronan receptors, such as CD44, may compensate for LYVE‐1. To test this hypothesis, we created LYVE‐1/CD44 double knockout mice with appropriate littermate controls. Lymphatic vessel structure and function, as determined by histological methods and intravital microscopy, show that LYVE‐1−/−, CD44−/− and LYVE‐1−/−/CD44−/− mice are indistinguishable from wild‐type mice under normal conditions. Furthermore, resolution of carrageenan‐induced paw edema is comparable in all genotypes. However, LYVE‐1−/−/CD44−/− mice exhibit increased edema formation in a carrageenan‐induced paw inflammation model compared to wild‐type mice, but not to LYVE−/− or CD44−/− mice. These data suggest that LYVE‐1 and CD44 are not required for the formation or function of lymphatics, but do not rule out a role for LYVE‐1 in inflammation. J. Cell. Physiol. 219: 430–437, 2009. © 2009 Wiley‐Liss, Inc.
Phytoestrogens regulate mRNA and protein levels of guanine nucleotide‐binding protein, beta‐1 subunit (GNB1) in MCF‐7 cells
Authors: Naragoni Srivatcha , Sankella Shireesha , Harris Kinesha , Gray Wesley G. 
Published: January 2009

AbstractPhytoestrogens (PEs) are non‐steroidal ligands, which regulate the expression of number of estrogen receptor‐dependent genes responsible for a variety of biological processes. Deciphering the molecular mechanism of action of these compounds is of great importance because it would increase our understanding of the role(s) these bioactive chemicals play in prevention and treatment of estrogen‐based diseases. In this study, we applied suppression subtractive hybridization (SSH) to identify genes that are regulated by PEs through either the classic nuclear‐based estrogen receptor or membrane‐based estrogen receptor pathways. SSH, using mRNA from genistein (GE) treated MCF‐7 cells as testers, resulted in a significant increase in GNB1 mRNA expression levels as compared with 10 nM 17β estradiol or the no treatment control. GNB1 mRNA expression was up regulated two‐ to fivefold following exposure to 100.0 nM GE. Similarly, GNB1 protein expression was up regulated 12‐ to 14‐fold. GE regulation of GNB1 was estrogen receptor‐dependent, in the presence of the anti‐estrogen ICI‐182,780, both GNB1 mRNA and protein expression were inhibited. Analysis of the GNB1 promoter using ChIP assay showed a PE‐dependent association of estrogen receptor α (ERα) and β (ERβ) to the GNB1 promoter. This association was specific for ERα since association was not observed when the cells were co‐incubated with GE and the ERα antagonist, ICI. Our data demonstrate that the levels of G‐protein, beta‐1 subunit are regulated by PEs through an estrogen receptor pathway and further suggest that PEs may control the ratio of α‐subunit to β/γ‐subunits of the G‐protein complex in cells. J. Cell. Physiol. 219: 584–594, 2009. © 2009 Wiley‐Liss, Inc.
Secretome from mesenchymal stem cells induces angiogenesis via Cyr61
Authors: Estrada Rosendo , Li Na , Sarojini Harshini , AN Jin , Lee Menq‐Jer , Wang Eugenia 
Published: January 2009

AbstractIt is well known that bone marrow‐derived mesenchymal stem cells (MSCs) are involved in wound healing and regeneration responses. In this study, we globally profiled the proteome of MSCs to investigate critical factor(s) that may promote wound healing. Cysteine‐rich protein 61 (Cyr61) was found to be abundantly present in MSCs. The presence of Cyr61 was confirmed by immunofluorescence staining and immunoblot analysis. Moreover, we showed that Cyr61 is present in the culture medium (secretome) of MSCs. The secretome of MSCs stimulates angiogenic response in vitro, and neovascularization in vivo. Depletion of Cyr61 completely abrogates the angiogenic‐inducing capability of the MSC secretome. Importantly, addition of recombinant Cyr61 polypeptides restores the angiogenic activity of Cyr61‐depleted secretome. Collectively, these data demonstrate that Cyr61 polypeptide in MSC secretome contributes to the angiogenesis‐promoting activity, a key event needed for regeneration and repair of injured tissues. J. Cell. Physiol. 219: 563–571, 2009. © 2009 Wiley‐Liss, Inc.
Msx2 induces epithelial‐mesenchymal transition in mouse mammary epithelial cells through upregulation of Cripto‐1
Authors: di Bari M.G. , Ginsburg E. , Plant J. , Strizzi L. , Salomon D.S. , Vonderhaar B.K. 
Published: January 2009

AbstractEpithelial‐mesenchymal transition (EMT) is a process occurring during both embryogenesis and early stages of invasive cancer. Epithelial cells that undergo EMT become more migratory and invasive with a mesenchymal morphology. Herein we assess EMT induction in a mouse mammary epithelial cell line driven by Msx2, a homeobox‐containing transcription factor important during mammary gland development. NMuMG cells, a normal mouse mammary epithelial cell line, stably transfected with a Msx2 cDNA showed downregulation of an epithelial marker E‐cadherin and upregulation of the mesenchymal markers vimentin and N‐cadherin. Furthermore, overexpression of Cripto‐1, a member of the epidermal growth factor‐CFC protein family already known to be involved in EMT, was detected in Msx2‐transfected cells. The expression of Cripto‐1 was accompanied by activation of the tyrosine kinase c‐Src pathway and an increase in the invasive ability of the cells. Functional assays also demonstrated inhibition of the invasive behavior of the Msx2‐transfected cells by a c‐Src specific inhibitor. Moreover, immunohistochemistry of human infiltrating breast carcinomas showed positive staining for Msx2 only in the infiltrating tumor cells while the non‐infiltrating tumor cells were negative. These results suggest that Msx2 may play a significant role in promoting EMT in epithelial cells that acquire properties involved in tumor invasion. J. Cell. Physiol. 219: 659–666, 2009. Published 2009 Wiley‐Liss, Inc.