bluuebunny/crossref_metadata_2025_split huggingface dataset:
Late‐Holocene buried forests on the Oregon Coast
Authors: Hart Roger , Peterson Curt 
Published: September 2006

AbstractDeposits of late‐Holocene beach sand buried conifer forests episodically emerge on beaches of the Oregon coast. Simultaneously, sand dunes buried late‐Holocene forests growing on marine terraces landward of the beaches. Dune ramps, up to 60 m in elevation, connected the beach and dune deposits. The average age of wood samples from stumps rooted on the shore platforms is 3·07 ± 1·45 ka. The average age of wood and charcoal samples embedded in forest soil on the marine terraces is 3·27 ± 1·46 ka.Between 1994 and 2006, winter storm waves exposed more than 4·5 km2 of late‐Holocene forest soil on shore platforms at 19 localities. Rooted stumps without soil were uncovered at an additional 14 localities. Once exposed, wave action eroded the soil rapidly (one to two years). The intact forest soil and roots on the shore platforms must have been nearly continuously buried, protected and preserved prior to recent exposure.The late‐Holocene buried forest provides the basis for a conceptual model of coastal evolution. A three stage reversal of erosion and sand supply must have occurred: (1) wave erosion switched to seaward advancement of forests, (2) forest growth and soil development switched to burial beneath beach and dune sand and (3) burial and preservation switched to wave erosion, truncation of dune ramps and landward retreat of sea cliffs. Copyright © 2006 John Wiley & Sons, Ltd.
Setup for EDFA stages based on pump power splitting yielding improved noise figure
Authors: Rapp Lutz 
Published: September 2006

AbstractPump power splitting is an effective means to save cost of erbium‐doped fibre amplifiers (EDFAs) by providing the power emitted by a single pump laser diode to several fibre coils. However, a major drawback of this approach is the increase of the noise figure with decreasing input power. In this paper, a modification of the standard setup yielding improved noise figure without impact on the achievable output power is presented. Deterioration of the dynamical behaviour is avoided by using a modified feedforward control technique. Copyright © 2006 AEIT
Gaussian inputs: performance limits over non‐coherent SISO and MIMO channels
Authors: Perera Rasika R. , Abhayapala Thushara D. , Pollock Tony S. 
Published: September 2006

AbstractPerformance limits of information transfer over a discrete time memoryless Rayleigh fading channel with neither the receiver nor the transmitter knowing the fading coefficients except its statistics is an important problem in information theory. We derive closed form expressions for the mutual information of single input single output (SISO) and multiple input multiple output (MIMO) Rayleigh fading channels for any antenna number at any signal to noise ratio (SNR). Using these expressions, we show that the maximum mutual information of non‐coherent Rayleigh fading MIMO channels is achieved with a single transmitter and multiple receivers when the input distribution is Gaussian. We show that the addition of transmit antennas for a fixed number of receivers result in a reduction of mutual information. Furthermore, we argue that the mutual information is bounded by the SNR in both SISO and MIMO systems showing the sub‐optimality of Gaussian signalling in non‐coherent Rayleigh fading channels. Copyright © 2006 AEIT
On the performance optimization in multiuser MIMO systems
Authors: Boche Holger , Jorswieck Eduard A. 
Published: September 2006

AbstractWe maximize the performance of multiple‐input multiple‐output (MIMO) multiple access channels (MAC) and broadcast channels (BC) under individual and sum power constraints. We observe that the performance metrics sum capacity and sum mean‐square error (MSE) belong to a general class of functions which are the trace of a matrix‐monotone function. The sum capacity if successive interference cancellation (SIC) is applied in the uplink or if Costa Precoding is applied in the downlink, or the normalised sum MSE if a multi‐user minimum mean‐square error (MMSE) receiver is applied at the base, belong to that class of performance functions. We use Löwner's representation of matrix monotone functions in order to characterise the optimum transmission strategies. Using the Karush‐Kuhn‐Tucker optimality conditions, we show that the mutual covariance matrix optimisation can be decomposed into power allocation and covariance matrix optimisation under individual power constraints. The covariance matrix optimisation under individual power constraints in turn can be decomposed into a kind of modified single‐user covariance matrix optimisation treating the other users as noise. The concrete structure of the single‐user program depends on the performance metric used. The proposed algorithms efficiently solve the multi‐user MIMO performance optimisation problem. These results generalise the results regarding the performance capacity optimisation recently reported for sum capacity optimisation and the results regarding the sum MSE optimisation. The optimal transmit strategy deconstructs into two independent parts: the coding and the signal processing part. The second part is adapted to the channel and performs multi‐user power control and transmit covariance matrix optimisation. Copyright © 2006 AEIT
Dynamic zone topology routing protocol for MANETs
Authors: Abolhasan Mehran , Wysocki Tadeusz A. 
Published: September 2006

AbstractThe limited scalability of the proactive and reactive routing protocols have resulted in the introduction of new generation of routing in mobile ad hoc networks, called hybrid routing. These protocols aim to extend the scalability of such networks beyond several hundred to thousand of nodes by defining a virtual infrastructure in the network. However, many of the hybrid routing protocols proposed to date are designed to function using a common pre‐programmed static zone map. Other hybrid protocols reduce flooding by grouping nodes into clusters, governed by a cluster‐head, which may create performance bottlenecks or a single point of failures at each cluster‐head node. We propose a new routing strategy in which zones are created dynamically, using a dynamic zone creation algorithm. Therefore, nodes are not restricted to a specific region. Additionally, nodes perform routing and data forwarding in a cooperative manner, which means that in the case failure, route recalculation is minimised. Routing overheads are also further reduced by introducing a number of GPS‐based location tracking mechanisms, which reduces the route discovery area and the number of nodes queried to find the required destination. Copyright © 2006 AEIT
A novel multi‐access scheme for UWB‐PPM communication systems
Authors: Khani Hassan , Azmi Paeiz 
Published: September 2006

AbstractIn this paper, it is shown that some spikes exist in power spectral density (PSD) of ultra‐wideband‐time‐hopping‐pulse‐position‐modulation (UWB‐TH‐PPM) transmitted signal. Analytical and numerical simulation results show that these spikes severely degrade UWB‐TH‐PPM system bit‐error‐rate performance and must be properly removed. This paper proposes a novel multi‐access scheme that uses both direct‐sequence (DS) and time‐hopping (TH) multi‐access schemes to remove these harmful spikes. Analytical and numerical simulation results show that the proposed scheme removes the spikes from the PSD of the UWB‐TH‐PPM transmitted signal and yields better performance. In this paper, the performance of the proposed multi‐access scheme is examined with numerical simulations in the presence of additive white Gaussian noise (AWGN), multipath interference (MPI), narrow‐band interference (NBI), and multi‐access interference (MAI); and furthermore closed form representations for the probability of error of both proposed and conventional multi‐access UWB‐PPM schemes are given. Copyright © 2006 AEIT
Homocysteine‐induced myofibroblast differentiation in mouse aortic endothelial cells
Authors: Sen Utpal , Moshal Karni S. , Tyagi Neetu , Kartha Ganesh K. , Tyagi Suresh C. 
Published: September 2006

AbstractDifferentiation of myofibroblast, as evidenced by α‐smooth muscle actin (α‐SMA) expression, is largely mediated by transforming growth factor‐β1 (TGF‐β1). This mechanism often follows inflammatory events such as endothelial damage due to oxidative stress, which can further leads to vascular thickening, stiffness, and fibrosis. We hypothesized that hyperhomocysteinemia (HHcy)‐induced oxidative stress lead to vascular stiffness, in part due to endothelial–myofibroblast differentiation and alteration of collagen homeostasis in the extracellular matrix (ECM). We tested our hypothesis in vitro using mouse aortic endothelial cells (MAEC). Our result shows that Hcy induces α‐SMA and collagen type‐1 expression in MAEC as evidenced by immunoblot and confocal imaging. RT‐PCR shows robust increase of α‐SMA and collagen type‐1 mRNA level in Hcy‐induced condition. We demonstrated that Hcy induces autophosphorylation of focal adhesion kinase (FAK) (a member of the protein tyrosine kinase (PTK) family) at Tyr‐397. PP2 (general PTK inhibitor) as well as FAK siRNA abrogates Hcy‐mediated α‐SMA formation. In addition to that, Hcy‐mediated TGF‐β1 induction was inhibited by TGF‐β R1 kinase inhibitor II (ALK5 inhibitor II) and attenuated FAK phosphorylation and α‐SMA expression. Furthermore, we showed that Hcy activates ERK‐44/42 (extracellular signal‐regulated kinase) pathway and augments collagen type‐1 deposition. Studies with pharmacological ERK blocker, PD98059 and ERK siRNA attenuated ERK‐44/42 phosphorylation and collagen type‐1 synthesis. Taken together our results demonstrate that Hcy‐mediated TGF‐β1 upregulation triggers endothelial–myofibroblast differentiation secondary to FAK phosphorylation and that Hcy‐induced ERK activation is involved in ECM remodeling by altering collagen type‐1 homeostasis. J. Cell. Physiol. 209: 767–774, 2006. © 2006 Wiley‐Liss, Inc.
Ultraviolet B‐induced matrix metalloproteinase‐1 and ‐3 secretions are mediated via PTEN/Akt pathway in human dermal fibroblasts
Authors: Oh Jang‐Hee , Kim Aeyung , Park Jong‐Min , Kim Shin‐Hyoung , Chung An‐Sik 
Published: September 2006

AbstractMatrix Metalloproteinases (MMPs) are crucial enzymes for ultraviolet irradiation‐induced photoaging in human skin. Ultraviolet B (UVB) stimulates dermal fibroblasts to increase MMP‐1 and ‐3 expression and extracellular matrix (ECM) degradation in photoaging. We investigated whether phosphatase and tensin homolog (PTEN)/Akt pathway is involved in secretions of MMP‐1 and ‐3 in human dermal fibroblasts. The increase in MMP‐1 and ‐3 expression and secretion occurred along with the increase in PTEN and Akt phosphorylation by UVB irradiation in a dose‐ and time‐dependent manner. However, treatment with a casein kinase 2 inhibitor, 5,6‐dichloro‐1‐β‐D‐ribofuranosyl‐benzimidazole, inhibited their phosphorylations and MMP‐1 and ‐3 secretions. Transfection of wild‐type PTEN (Wt‐PTEN) decreased basal and UVB‐induced MMP‐1 and ‐3 secretions, as well as activator protein‐1 (AP‐1) activity, while transfection of small interference RNA of PTEN (siRNA‐PTEN), phosphatase‐inactive PTEN (C124S‐PTEN), or lipid phosphatase‐inactive PTEN (G129E‐PTEN) increased basal or UVB‐induced MMP‐1 and ‐3 secretions and AP‐1 activity. Transfection of constitutively active Akt (Myr‐Akt) also increased basal or UVB‐induced MMP‐1 and ‐3 secretions, as well as AP‐1 activity. However, transfection of kinase‐inactive Akt (K179M‐Akt) decreased their secretions, but showed no significant change of AP‐1 activity without UVB irradiation, and a significant increase of AP‐1 activity with UVB irradiation. Treatment with the phosphatidylinositol 3‐kinase inhibitors, LY294002 or wortmannin, downregulated basal and UVB‐induced MMP‐1 and ‐3 secretions. In conclusion, UVB irradiation increases PTEN and Akt phosphorylation in human dermal fibroblasts, and these inhibition of PTEN and activation of Akt by phosphorylation are involved in UVB‐induced MMP‐1 and ‐3 secretions partly through upregulation of AP‐1 activity. J. Cell. Physiol. 209: 775–785, 2006. © 2006 Wiley‐Liss, Inc.
Sulfated glycosaminoglycans mediate the effects of FGF2 on the osteogenic potential of rat calvarial osteoprogenitor cells
Authors: Ling Ling , Murali Sadasivam , Dombrowski Christian , Haupt Larisa M. , Stein Gary S. , van Wijnen Andre J. , Nurcombe Victor , Cool Simon M. 
Published: September 2006

AbstractFibroblast growth factor‐2 (FGF2) is a powerful promoter of bone growth. We demonstrate here that brief exposure to FGF2 enhances mineralized nodule formation in cultured rat osteoprogenitor cells due to an expansion of cells that subsequently mineralize. This mitogenic effect is mediated via sulfated glycosaminoglycans (GAGs), FGFR1, and the extracellular signal‐regulated kinase (ERK) pathway. The GAGs involved in this stimulation are chondroitin sulfates (CS) rather than heparan sulfates (HS). However, continuous FGF2 treatment reduces alkaline phosphatase (ALP) activity, downregulates collagen Iα1 (ColIα1) and FGFR3 expression, upregulates the expression and secretion of osteopontin (OPN) and inhibits mineralization. The inhibitory effects of FGF2 on FGFR3 expression and ALP activity are also mediated by the ERK pathway, although the effects of FGF2 on ColIα1 and OPN expression are mediated by GAGs and PKC activity. Thus short‐term activation of FGF2/FGFR1 promotes osteoprogenitor proliferation and subsequent differentiation, while long‐term activation of FGF2 signaling disrupts mineralization by modulating osteogenic marker expression. This study thus establishes the central role of sulfated GAGs in the osteogenic progression of osteoprogenitors. J. Cell. Physiol. 209: 811–825, 2006. © 2006 Wiley‐Liss, Inc.
Prolonged absence of myostatin reduces sarcopenia
Authors: Siriett Victoria , Platt Leanne , Salerno Mônica Senna , Ling Nicholas , Kambadur Ravi , Sharma Mridula 
Published: September 2006

AbstractSarcopenia is a progressive age‐related loss of skeletal muscle mass and strength. Parabiotic experiments show that circulating factors positively influence the proliferation and regenerative capacity of satellite cells in aged mice. In addition, we believe that negative regulators of muscle mass also serve to balance the signals that influence satellite cell activation and regeneration capacity with ageing. Myostatin, a negative regulator of pre‐ and postnatal myogenesis, inhibits satellite cell activation and muscle regeneration postnatally. To investigate the role of myostatin during age‐related sarcopenia, we examined muscle mass and regeneration in young and old myostatin‐null mice. Young myostatin‐null muscle fibers were characterized by massive hypertrophy and hyperplasia and an increase in type IIB fibers, resulting in a more glycolytic muscle. With ageing, wild‐type muscle became increasingly oxidative and fiber atrophy was prominent. In contrast no fiber type switching was observed and atrophy was minimal in aged myostatin‐null muscle. The effect of ageing on satellite cell numbers appeared minimal, however, satellite cell activation declined significantly in both wild‐type and myostatin‐null muscles. In young mice, lack of myostatin resulted in increased satellite cell number and activation compared to wild‐type, suggesting a greater propensity to undergo myogenesis, a difference maintained in the aged mice. In addition, muscle regeneration of myostatin‐null muscle following notexin injury was accelerated and fiber hypertrophy and type were recovered with regeneration, unlike in wild‐type muscle. In conclusion, a lack of myostatin appears to reduce age‐related sarcopenia and loss of muscle regenerative capacity. J. Cell. Physiol. 209: 866–873, 2006. © 2006 Wiley‐Liss, Inc.
Blood vessels and desmin control the positioning of nuclei in skeletal muscle fibers
Authors: Ralston E. , Lu Z. , Biscocho N. , Soumaka E. , Mavroidis M. , Prats C. , Lømo T. , Capetanaki Y. , Ploug T. 
Published: September 2006

AbstractSkeletal muscle fibers contain hundreds to thousands of nuclei which lie immediately under the plasmalemma and are spaced out along the fiber, except for a small cluster of specialized nuclei at the neuromuscular junction. How the nuclei attain their positions along the fiber is not understood. Here we show that the nuclei are preferentially localized near blood vessels (BV), particularly in slow‐twitch, oxidative fibers. Thus, in rat soleus muscle fibers, 81% of the nuclei appear next to BV. Lack of desmin markedly perturbs the distribution of nuclei along the fibers but does not prevent their close association with BV. Consistent with a role for desmin in the spacing of nuclei, we show that denervation affects the organization of desmin filaments as well as the distribution of nuclei. During chronic stimulation of denervated muscles, new BV form, along which muscle nuclei align themselves. We conclude that the positioning of nuclei along muscle fibers is plastic and that BV and desmin intermediate filaments each play a distinct role in the control of this positioning. J. Cell. Physiol. 209: 874–882, 2006. © 2006 Wiley‐Liss, Inc.
Corticotropin‐releasing factor (CRF) receptor type 2 in the human stomach: Protective biological role by inhibition of apoptosis
Authors: Chatzaki Ekaterini , Lambropoulou Maria , Constantinidis Theodoros C. , Papadopoulos Nikolaos , Taché Yvette , Minopoulos George , Grigoriadis Dimitri E. 
Published: September 2006

AbstractCorticotropin‐releasing factor agonists exert inhibitory effects in stomach functions possibly through peripheral routes. We have previously reported the expression of Urocortin (Ucn) I, an endogenous ligand of both CRF receptor types CRF1 and CRF2, in the human stomach. We examined CRF1 and CRF2 expression in the same tissue. Using RT‐PCR, CRF2 but not CRF1 transcripts were detected in RNA extracts from normal human stomach. In addition, immunohistochemical analysis revealed receptor protein in epithelial gastric cells. In order to investigate the biological role of CRF2 in these cells, an in vitro model was established, using the gastric cancer cell line AGS transiently transfected to express functional CRF2. The effect of the CRF2 endogenous ligands CRF, Ucns I and II on the growth parameters of the AGS/CRF2 was examined. After 1 day of exposure, all three ligands reduced the degree of apoptosis (16%–19%, n = 9, P < 0.05) compared to non‐treated controls and this effect was observed for 3 days of treatment. No such effect was detected in non‐transfected cells, suggesting mediation through CRF2 receptors. Administration of CRF, Ucns I and II had no effect on the proliferation rate of AGS/CRF2 cells or on the release of PGE2 by them. Our results demonstrate CRF2 expression in the human gastric mucosa and indicate a physiological role of this receptor type in regulating apoptosis, an important parameter of gastric cell regeneration. Paracrine effects exerted by locally expressed endogenous ligands, such as Ucn I, support a significant role of the peripheral CRF system in gastric physiology. J. Cell. Physiol. 209: 905–911, 2006. © 2006 Wiley‐Liss, Inc.
Inhibition of PPARγ prevents type I diabetic bone marrow adiposity but not bone loss
Authors: Botolin Sergiu , McCabe Laura R. 
Published: September 2006

AbstractDiabetes type I is associated with bone loss and increased bone adiposity. Osteoblasts and adipocytes are both derived from mesenchymal stem cells located in the bone marrow, therefore we hypothesized that if we could block adipocyte differentiation we might prevent bone loss in diabetic mice. Control and insulin‐deficient diabetic BALB/c mice were chronically treated with a peroxisomal proliferator‐activated receptor γ (PPARγ) antagonist, bisphenol‐A‐diglycidyl ether (BADGE), to block adipocyte differentiation. Effects on bone density, adiposity, and gene expression were measured. BADGE treatment did not prevent diabetes‐associated hyperglycemia or weight loss, but did prevent diabetes‐induced hyperlipidemia and effectively blocked diabetes type I‐induced bone adiposity. Despite this, BADGE treatment did not prevent diabetes type I suppression of osteoblast markers (runx2 and osteocalcin) and bone loss (as determined by micro‐computed tomography). BADGE did not suppress osteoblast gene expression or bone mineral density in control mice, however, chronic (but not acute) BADGE treatment did suppress osteocalcin expression in osteoblasts in vitro. Taken together, our findings suggest that BADGE treatment is an effective approach to reduce serum triglyceride and free fatty acid levels as well as bone adiposity associated with type I diabetes. The inability of BADGE treatment to prevent bone loss in diabetic mice suggests that marrow adiposity is not linked to bone density status in type I diabetes, but we cannot exclude the possibility of additional BADGE effects on osteoblasts or other bone cells, which could contribute to preventing the rescue of the bone phenotype. J. Cell. Physiol. 209: 967–976, 2006. © 2006 Wiley‐Liss, Inc.
Pharmacologic inhibitors of extracellular signal‐regulated kinase (ERKs) and c‐Jun NH2‐terminal kinase (JNK) decrease glutathione content and sensitize human promonocytic leukemia Cells to arsenic trioxide‐induced apoptosis
Authors: Ramos Adrian M. , Fernandez Carlos , Amrán Donna , Esteban Diego , de Blas Elena , Palacios María A. , Aller Patricio 
Published: September 2006

AbstractTreatment with 1–4 µM As2O3slightly induced apoptosis in U‐937 human promonocitic leukemia cells. This effect was potentiated by co‐treatment with MEK/ERK (PD98059, U0126) and JNK (SP600125, AS601245) inhibitors, but not with p38 (SB203580, SB220025) inhibitors. However, no potentiation was obtained using lonidamine, doxorubicin, or cisplatin instead of As2O3. Apoptosis potentiation by mitogen‐activated protein kinase (MAPK) inhibitors involved both the intrinsic and extrinsic executionary pathways, as demonstrated by Bax activation and cytochromecrelease from mitochondria, and by caspase‐8 activation and Bid cleavage, respectively; and the activation of both pathways was prevented by Bcl‐2 over‐expression. Treatment with MEK/ERK and JNK inhibitors, but not with p38 inhibitors, caused intracellular glutathione (GSH) depletion, which was differentially regulated. Thus, while it was prevented byN‐acetyl‐L‐cysteine (NAC) in the case of U0126, it behaved as a NAC‐insensitive process, regulated at the level of DL‐buthionine‐(S,R)‐sulfoximine (BSO)‐sensitive enzyme activity, in the case of SP600125. The MEK/ERK inhibitor also potentiated apoptosis and decreased GSH content in As2O3‐treated NB4 human acute promyelocytic leukemia (APL) cells, but none of these effects were produced by the JNK inhibitor. MEK/ERK and JNK inhibitors did not apparently affect As2O3transport activity, as measured by intracellular arsenic accumulation. SP600126 greatly induced reactive oxygen species (ROS) accumulation, while BSO and U0126 had little or null effects. These results, which indicate that glutathione is a target of MAP kinases in myeloid leukemia cells, might be exploited to improve the antitumor properties of As2O3, and provide a rationale for the use of kinase inhibitors as therapeutic agents. J. Cell. Physiol. 209: 1006–1015, 2006. © 2006 Wiley‐Liss, Inc.