bluuebunny/crossref_metadata_2025_split huggingface dataset:
Runoff and erosion from Australia's tropical semi‐arid rangelands: influence of ground cover for differing space and time scales
Authors: Bartley Rebecca , Roth Christian H. , Ludwig John , McJannet David , Liedloff Adam , Corfield Jeff , Hawdon Aaron , Abbott Brett 
Published: September 2006

AbstractThis paper highlights the relevant issues influencing the amount and arrangement of ground cover in savanna rangelands in Australia, and presents field measurements from hillslope scale flumes, which demonstrate how runoff and sediment loss vary with spatial patterns in ground cover. Hillslopes with relatively high mean cover, but with small patches bare of vegetation, are shown to have between 6 and 9 times more runoff, and up to 60 times more sediment loss than similar hillslopes that do not contain bare patches. The majority of sediment lost from the hillslopes is composed of fine (suspended) rather than coarse (bedload) material, although the absolute sediment loads are comparatively low. These low loads are considered to be the result of lower than average rainfall during the measurement period (2002–2005) and the high and prolonged rates of historical hillslope erosion that have exhausted the erodible material from the A‐horizon. The collected data also demonstrate that a large proportion of soil is lost during the initial ‘flushing’ period of runoff events.The results presented have important implications for the management of savanna grazing systems by highlighting (i) the significance of bare patches in contributing to runoff and soil loss from hillslopes; (ii) the importance of having medium to high cover patches at the bottom of hillslopes for trapping and storing sediment and therefore reducing its entry into the stream network; and (iii) how maintenance of ground cover during the dry season reduces sediment concentrations in runoff occurring early in the wet season. Copyright © 2006 John Wiley & Sons, Ltd.
One step synthesis of silver nanorods by autoreduction of aqueous silver ions with hydroxyapatite: An inorganic–inorganic hybrid nanocomposite
Authors: Arumugam Sujatha K. , Sastry Thotapalli Parvathaleswara , Sreedhar B. , Mandal Asit Baran 
Published: September 2006

AbstractIn this report, a novel method for the synthesis of silver nanoparticles on the surface of hydroxyapatite is described. Hydroxyapatite crystals are synthesized from acid mineralized solution, a byproduct of bone glue industries, by a simple chemical precipitation method, which results in the formation of hydroxyapatite nanocrystals. The reduction of silver ions occurs by the electron transfer from the hydroxyl groups on the surface of hydroxyapatite. This results in the formation of silver nanorods and needle shaped nanoparticles that are bound on the surface of hydroxyapatite, and the observed silver nanocrystals show anisotropic structure. Thus, hydroxyapatite crystals can be used as a new class of inorganic scaffolds for the synthesis of nanomaterials with implications in designing inorganic–inorganic hybrid nanocomposites for different applications. © 2006 Wiley Periodicals, Inc. J Biomed Mater Res, 2007
Retinoid receptors, transporters, and metabolizers as therapeutic targets in late onset Alzheimer disease
Authors: Goodman Ann B. 
Published: September 2006

AbstractVitamin A (retinoid) is required in the adult brain to enable cognition, learning, and memory. While brain levels of retinoid diminish over the course of normal ageing, retinoid deficit is greater in late onset Alzheimer disease (LOAD) brains than in normal‐aged controls. This paper reviews recent evidence supporting these statements and further suggests that genes necessary for the synthesis, transport and function of retinoid to and within the ageing brain are appropriate targets for treatment of LOAD. These genes tend to be clustered with genes that have been proposed as candidates in LOAD, are found at chromosomal regions linked to LOAD, and suggest the possibility of an overall coordinated regulation. This phenomenon is termed Chromeron and is analogous to the operon mechanism observed in prokaryotes. Suggested treatment targets are the retinoic‐acid inactivating enzymes (CYP26)s, the retinol binding and transport proteins, retinol‐binding protein (RBP)4 and transthyretin (TTR), and the retinoid receptors. TTR as a LOAD target is the subject of active investigation. The retinoid receptors and the retinoid‐inactivating enzymes have previously been proposed as targets. This is the first report to suggest that RBP4 is an amenable treatment target in LOAD. RBP4 is elevated in type‐2 diabetes and obesity, conditions associated with increased risk for LOAD. Fenretinide, a novel synthetic retinoic acid (RA) analog lowers RBP4 in glucose intolerant obese mice. The feasibility of using fenretinide either as an adjunct to present LOAD therapies, or on its own as an early prevention strategy should be determined. J. Cell. Physiol. 209: 598–603, 2006. © 2006 Wiley‐Liss, Inc.
A role of novel serpin maspin in tumor progression: The divergence revealed through efforts to converge
Authors: Sheng Shijie 
Published: September 2006

AbstractMaspin, a 42 kDa protein, belongs to the serine protease inhibitor (serpin) superfamily and is more closely related to the ovalbumin‐like serpin subfamily (ov‐serpins). More than a decade after the discovery of the maspin gene, our pursuit of the molecular mechanisms of maspin revealed a significant divergence of maspin from other serpins. This review article summarizes recent advances in the identification of maspin‐binding proteins and the potential underlying molecular mechanisms of maspin in tumor progression. Specifically, the molecular interactions of maspin with the cell surface‐associated pro‐urokinase‐type plasminogen activator (pro‐uPA) and intracellular histone deacetylase 1 (HDAC1) are highlighted. Our new evidence suggests a new paradigm that maspin acts as a serpin‐like molecule to inhibit serine protease‐like targets. From an evolution point of view, the uniquely important function of maspin in development and tumor progression is likely due to its ancestral sequence code, and accordingly, its novel “meta”‐serpin structure. It is reasonable to hypothesize that the conservation of a serine protease‐like catalytic center in many molecules requires the co‐existence of endogenous antagonists. The unique inhibitory interaction of maspin with both HDAC1 and pro‐uPA might not be substituted by other serpins that have evolved to acquire higher target specificities. Thus, tumor suppressive maspin offers a unique therapeutic opportunity. J. Cell. Physiol. 209: 631–635, 2006. © 2006 Wiley‐Liss, Inc.
Truncated RAR beta isoform enhances proliferation and retinoid resistance
Authors: Swift Mari E. , Wallden Brett , Wayner Elizabeth A. , Swisshelm Karen 
Published: September 2006

AbstractWe previously reported the existence of a truncated isoform of the retinoic acid receptor beta, termed beta prime. Beta prime lacks the N‐terminal domains of beta 2 and beta 4, including the DNA‐binding domain. However, beta prime is able to heterodimerize and interact with transcription cofactors. To determine the effects of different retinoic acid receptor isoforms on cell proliferation and apoptosis, we transduced retinoid sensitive (MCF7) and retinoid‐resistant (MDA‐MB‐231) cells with retinoic acid receptor beta 2, beta 4, or beta prime. Expression of the truncated beta prime isoform induces resistance to retinoic acid treatment in retinoid sensitive MCF7 cells. In both retinoid sensitive and resistant cells, expression of full‐length beta 2 and beta 4 isoforms results in elevated sensitivity to retinoic acid treatment and caspase‐independent cell death. Cell death in beta 4 transduced MDA‐MB‐231 cells was accompanied by metaphase chromosome decondensation and breakage suggestive of mitotic catastrophe. Our results provide evidence that: (a) the truncated form of the retinoic acid receptor beta induces retinoid resistance rather than sensitivity; and (b) alternative pathways of cell death are mediated by different isoforms in breast cancer cells. J. Cell. Physiol. 209: 718–725, 2006. © 2006 Wiley‐Liss, Inc.
Emerging targets and novel strategies in the treatment of AIDS‐related Kaposi's sarcoma: Bidirectional translational science
Authors: Dezube Bruce J. , Sullivan Ryan , Koon Henry B. 
Published: September 2006

AbstractThrough the mentorship process, Dr. Arthur Pardee emphasized the critical importance of bidirectional translational research—not only advancing drug development from bench to bedside, but also bringing back precious clinical material to the laboratory to assess the biologic effects of therapeutic agents on their targets. This mini‐review focuses on the signal transduction pathways of Kaposi's sarcoma (KS) and on how the knowledge of such pathways has led to the rational development of molecularly targeted pathogenesis‐driven therapies. Acquired immune deficiency syndrome (AIDS) related‐KS results from co‐infection with human immunodeficiency virus and KS herpesvirus/human herpesvirus‐8 (KSHV/HHV8), which leads to the development of an angiogenic‐inflammatory state that is critical in the pathogenesis of KS. KS is driven by KSHV/HHV8‐specific pathways, which include viral G protein‐coupled receptor (vGPCR), viral interleukin‐6 (vIL‐6), and viral chemokine homologues. In addition, cellular growth/angiogenic pathways, such as vascular endothelial growth factor (VEGF), insulin‐like growth factor, platelet‐derived growth factor (PDGF), angiopoietin and matrix metalloproteinases (MMPs) are “pirated” by KSHV/HHV8. As a very tangible example of how translational research has led to a marked improvement in patient outcome, the signal transduction inhibitor imatinib (a tyrosine kinase inhibitor of c‐kit and PDGF) was administered to patients with KS whose tumors were serially biopsied. Not only did the patients' tumors regress, but also the regression was correlated with the inhibition of PDGF receptor (PDGFR) in the biopsy samples. Recent and future clinical trials of molecularly targeted therapy for the treatment of KS are a prelude to a shift in the paradigm of how KS is managed. J. Cell. Physiol. 209: 659–662, 2006. © 2006 Wiley‐Liss, Inc.
Up‐regulation of bone morphogenetic protein receptor IB by growth factors enhances BMP‐2‐induced human bone cell functions
Authors: Singhatanadgit Weerachai , Salih Vehid , Olsen Irwin 
Published: September 2006

AbstractBone morphogenetic proteins (BMP) stimulate osteoblast differentiation by signal transduction via three BMP receptors (BMPR‐IA, ‐IB, and ‐II). Several growth factors, including transforming growth factor‐β1 (TGF‐β1), fibroblast growth factor‐2 (FGF‐2) and platelet‐derived growth factor‐AB (PDGF‐AB), have also been shown to play an important part in osteogenesis. The mechanism underlying these activities is unclear, but these growth factors could modulate the BMP/BMPR pathway by up‐regulating BMPR expression, thereby enhancing the osteogenic responses of bone cells to the BMP. In this study we have therefore examined the effects of TGF‐β1, FGF‐2, and PDGF‐AB on BMPR expression and BMP‐2‐mediated osteoblast functions in primary human bone cells. The results showed that although the ligand BMP‐2 and growth factors had little effect on BMPR‐IA and ‐II transcript expression, they significantly up‐regulated BMPR‐IB mRNA specifically. However, only the growth factors, but not the ligand BMP‐2, increased the surface expression of the BMPR‐IB antigen, which was found to be due to a differential effect of BMP‐2 and the growth factors on the Smurf1/Smad6‐induced breakdown process. Pre‐incubation of the cells with the growth factors significantly augmented BMP‐2‐induced Smad1/5/8 phosphorylation, and Dlx5 expression ALP activity, compared with that of cells treated with BMP‐2 alone. When cells were transfected with siRNA targeting BMPR‐IB, the growth factors neither up‐regulated BMPR‐IB transcript expression nor enhanced BMP‐2‐induced Smad1/5/8 phosphorylation, Dlx5 expression and ALP activity. The results indicate that increased BMPR‐IB by TGF‐β1, FGF‐2, and PDGF‐AB significantly enhances BMP‐2‐induced osteogenic functions in vitro, suggesting that they might positively modulate bone formation by up‐regulating BMPR‐IB in vivo. J. Cell. Physiol. 209: 912–922, 2006. © 2006 Wiley‐Liss, Inc.
The discovery of mRNA interferases: Implication in bacterial physiology and application to biotechnology
Authors: Inouye Masayori 
Published: September 2006

AbstractEscherichia coli contains a large number of suicide or toxin genes, whose expression leads to cell growth arrest and eventual cell death. This raises intriguing questions as to why E. coli contains so many toxin genes and what are their roles in bacterial physiology. Among these, MazF has been shown to be a sequence‐specific endoribonuclease, which cleaves mRNAs at ACA sequences to completely inhibit protein synthesis. MazF is therefore called mRNA interferase. A number of other mRNA interferases with different cleavage specificities have been discovered not only in E. coli, but also in other bacteria including Mycobacterium tuberculosis. Induction of MazF in the cell leads to cellular dormancy termed quasi‐dormancy. In spite of complete cell growth inhibition, cells in the quasi‐dormant state are fully capable of energy metabolism, amino acids and nucleic acids biosynthesis and RNA and protein synthesis. The quasi‐dormancy may be implicated in cell survival under stress conditions and may play a major role in pathogenicity of M. tuberculosis. The quasi‐dormant cells provide an intriguing novel biotechnological system producing only a protein of interest in a high yield. MazF causing Bak‐dependent programmed cell death in mammalian cells may be used as a tool for gene therapy against cancer and AIDS. The discovery of a novel way to interfere with mRNA function by mRNA interferases opens a wide variety of avenues in basic as well as applied and clinical sciences. J. Cell. Physiol. 209: 670–676, 2006. © 2006 Wiley‐Liss, Inc.
The deuterostome ancestor
Authors: Gerhart John 
Published: September 2006

AbstractHemichordates, the phylum of bilateral animals closest to chordates, can illuminate the evolutionary origins of various chordate traits to determine whether these were already present in a shared ancestor (the deuterostome ancestor) or were evolved within the chordate line. We find that an anteroposterior map of gene expression domains, representing 42 genes of neural patterning, is closely similar in hemichordates and chordates, though it is restricted to the neural ectoderm in chordates whereas in hemichordates, which have a diffuse nervous system, it encircles the whole body. This map allows an accurate alignment of the anterioposterior axes of members of the two groups. We propose that this map dates back at least to the deuterostome ancestor. The map of dorsoventral expression domains, organized along a Bmp–Chordin developmental axis, is also similar in the two groups in terms of many gene expression domains and for the placement of the gill slits, heart, and post‐anal tail. The two groups, however, differ in two major respects along this axis. The nervous system and epidermis are not segregated into distinct territories in hemichordates, as they are in chordates, and furthermore, the mouth is on the Chordin side in hemichordates but the Bmp side in chordates. The dorsoventral dimension has undergone extensive modification in the chordate line, including centralization of the nervous system, segregation of epidermis, derivation of the notochord, perhaps from the gut midline, and relocation of the mouth. Based on the shared domain maps, speculations can be made for the remodeling of the body axis in the chordate line. J. Cell. Physiol. 209: 677–685, 2006. © 2006 Wiley‐Liss, Inc.
Deregulation of cyclin E meets dysfunction in p53: Closing the escape hatch on breast cancer
Authors: Barton Michelle Craig , Akli Said , Keyomarsi Khandan 
Published: September 2006

AbstractIn this review, we focus on pathways intersecting through p53 and cyclin E, highlighting how oncogenic effects of cyclin E deregulation, especially overexpression of shortened or low molecular weight (LMW) forms of cyclin E protein, are amplified by loss of regulatory control through p53 to promote tumor development. Expression of cyclin E protein promotes progression into S‐phase, an activity opposed by p53‐regulated activation of checkpoint controls or apoptosis. Loss of p53 function is an escape hatch by which tumor cells, initiated by a number of means including cyclin E deregulation, can avoid cell cycle arrest or cell death and progress through further stages of unchecked deregulation and growth. To determine how this escape hatch is opened and, ultimately, how to close it, we must understand the networks of normal signaling and processing in a cell and where they intersect. J. Cell. Physiol. 209: 686–694, 2006. © 2006 Wiley‐Liss, Inc.
Galactosemia: The good, the bad, and the unknown
Authors: Fridovich‐Keil Judith L. 
Published: September 2006

Abstractα‐D‐Galactose is metabolized in species ranging from E. coli to mammals predominantly via a series of sequential reactions collectively known as the Leloir pathway. Deficiency of any one of these enzymes in humans results in a form of the inherited metabolic disorder, galactosemia, although the symptoms and severity depend upon the enzyme impaired, and the degree of functional deficiency (Tyfield and Walter, 2002, The Metabolic and Molecular Bases of Inherited Disease. New York: McGraw Hill.). Studies of these enzymes, and the disorders associated with their loss, have led to a much deeper appreciation of the intricate and interwoven levels of regulation that govern their normal function. These insights have further identified likely mediators of outcome severity in patients, and have enabled a rational approach to the development of novel strategies of intervention. J. Cell. Physiol. 209: 701–705, 2006. © 2006 Wiley‐Liss, Inc.
An architectural perspective of cell‐cycle control at the G1/S phase cell‐cycle transition
Authors: Stein Gary S. , van Wijnen André J. , Stein Janet L. , Lian Jane B. , Montecino Martin , Zaidi Sayyed K. , Braastad Corey 
Published: September 2006

AbstractA prominent role for the execution of cell cycle and growth regulatory mechanisms within the three‐dimensional context of nuclear architecture is becoming increasingly evident. Signaling pathways and regulatory networks that govern activation and suppression of genes controlling proliferation are functionally integrated for the organization and assembly of transcriptional machinery in nuclear microenvironments. The transcriptional activation of histone genes at the G1/S phase transition (S‐point) is temporarily, functionally, and spatially distinct from transcriptional mechanisms at the restriction point (R‐point). The spatial distinction in R‐point versus S‐point control is the localization of clustered histone gene loci at cajal bodies, which is modulated during the cell cycle. Histone nuclear factor P (HiNF‐P), the principal factor mediating H4 histone gene transcription, is the final link in the signaling cascade that is initiated with growth factor dependent induction of cyclin E/CDK2 kinase activity at the R‐point and culminates in the NPAT‐mediated activation of histone H4 genes through HiNF‐P at the G1/S phase cell‐cycle transition. J. Cell. Physiol. 209: 706–710, 2006. © 2006 Wiley‐Liss, Inc.
Is it going to be SIN?
Authors: Buchholz Christian J. , Cichutek Klaus 
Published: September 2006

AbstractInsertional mutagenesis resulting in a leukaemia‐like lymphoproliferative disease, as observed in the X‐SCID (severe combined immunodeficiency) clinical trial using a γ‐retroviral vector that transferred a functional copy of the defective gene into hematopoietic precursor cells of affected children, sparked a debate about a ban on conventional γ‐retroviral vectors. This commentary summarizes the relevant data on this topic and concludes that there is no preclinical or clinical evidence as yet that SIN vectors, which self‐inactivate the retroviral long terminal repeats (LTRs), will indeed show an improved safety profile. Conventional murine leukaemia virus (MLV) vectors can thus be used further in clinical gene therapy trials but require a thorough case‐by‐case risk‐benefit analysis. Copyright © 2006 John Wiley & Sons, Ltd.
Synthesis and PET evaluation of (R)‐[S‐methyl‐11C]thionisoxetine, a candidate radioligand for imaging brain norepinephrine transporters
Authors: Schou Magnus , Pike Victor W. , Varrone Andrea , Gulyás Balázs , Farde Lars , Halldin Christer 
Published: September 2006

AbstractIntroduction: (R)‐3‐(2‐(methylthio)phenoxy)‐N‐methyl‐3‐phenylpropan‐1‐amine [(R)–thionisoxetine; 1] is a potent inhibitor of the norepinephrine transporter (NET). We aimed to label 1 with carbon‐11 (t1/2 = 20.4 min) for evaluation as a radioligand for imaging NET in living brain with positron emission tomography (PET).Methods: Methyl 3‐(2‐((R)‐3‐(methylamino)‐1‐phenylpropoxy)phenylthio)‐propanoate (MPPP) and 1 were each prepared from o‐hydroxythiophenol in three steps. Treatment of MPPP with potassium t‐butoxide and [11C]methyl iodide in tetrahydrofuran gave [S‐methyl‐11C]thionisoxetine ([11C]1), which was purified with HPLC. The distribution of radioactivity in brain after intravenous injection of [11C]1 into cynomolgus monkey was followed with PET and the appearance of radiometabolites in plasma monitored with radio‐HPLC.Results: [11C]1 was obtained in high yield from [11C]methyl iodide. Of the radioactivity injected into monkey, 2.4% entered brain. Ratios of radioactivity in thalamus, mesencephalon, occipital cortex and caudate to that in cerebellum at 93 min were 1.3, 1.2, 1.2 and 1.1, respectively. The radioactivity in plasma corresponding to unchanged radioligand decreased to 53% at 45 min, with the remainder represented by hydrophilic radiometabolites.Conclusions: MPPP is an effective precursor for 11C‐methylation to [11C]1, suggesting that the S‐γ‐propionic acid methyl ester protecting group may have wider value in the 11C‐labeling of aryl methyl sulfides. However, the relatively low ratios of radioactivity to the cerebellum together with an unexpected accumulation of radioactivity in the caudate, makes [11C]1 an unpromising NET radioligand. Copyright © 2006 John Wiley & Sons, Ltd.
The impact of subordinate–supervisor similarity in growth‐need strength on work outcomes: the mediating role of perceived similarity
Authors: Huang Xu , Iun Joyce 
Published: September 2006

AbstractBased on data collected from 205 vertical dyads, we found that subordinate–supervisor similarity in their self‐reported growth‐need strength (GNS) had a positive effect on subordinate‐perceived and supervisor‐perceived global similarity. The findings also suggested that subordinate‐perceived global similarity mediates the link between similarity in GNS and subordinate's trust in and loyalty to supervisor; whereas supervisor‐perceived global similarity mediates the link between similarity in GNS and supervisor‐rated in‐role/extra‐role performances. In addition, we found that subordinate–supervisor similarity in self‐reported GNS and perceived global similarity had independent effects on work outcomes for both subordinates and supervisors. Copyright © 2006 John Wiley & Sons, Ltd.