bluuebunny/crossref_metadata_2025_split huggingface dataset:
Sonography of chronic Achilles tendinopathy: A case–control study
Authors: Leung John L.Y. , Griffith James F. 
Published: August 2007

AbstractPurposeTo describe the sonographic appearance of Achilles tendon in normal subjects and patients with chronic Achilles tendinopathy with the aim of establishing diagnostic sonographic criteria for Achilles tendinopathy.MethodsA prospective, cross‐sectional, case–control sonographic study of the Achilles tendon was undertaken. Thirty tendons in 21 patients and 100 tendons in 50 control subjects were selected. Sonographic assessment included tendon thickness, echogenicity, fibrillar pattern, and presence of calcifications. Power Doppler imaging was used to assess tendon vascularity. Paratendinous structures and plantar fascia were also examined.ResultsTendinopathic tendons were larger than normal tendons in both cross‐sectional area and antero‐posterior diameter. Hypoechoic areas within the tendon were more commonly seen in patients. Disruption of fibrillar pattern, increase in tendon vascularity, increased Kager's fat pad echogenicity, and paratenon thickening were solely seen in patients. Fluid in the retrocalcaneal bursa and calcaneal bony abnormalities were seen in both groups without a significant difference.ConclusionAchilles tendinopathy results in enlargement, particularly of the mid‐ and distal portions of the tendon, disruption of fibrillar pattern, and increase in tendon vascularity. Additional signs are increased Kager's fat pad echogenicity and paratenon thickening. Tendon calcification, changes in retrocalcaneal bursae, and calcaneal contour are not specific for Achilles tendinopathy. © 2007 Wiley Periodicals, Inc. J Clin Ultrasound, 2008
Ultrastructural modifications of cell membranes induced by “electroporation” on melanoma xenografts
Authors: Spugnini Enrico P. , Arancia Giuseppe , Porrello Alessandro , Colone Marisa , Formisano Giuseppe , Stringaro Annarita , Citro Gennaro , Molinari Agnese 
Published: August 2007

AbstractElectroporation (EP) has been widely employed in the past years as a safe and effective technique to drive drugs and DNA plasmids into target cells both for experimental and therapeutic purposes. Despite the large bulk of literature on this topic, often describing successful outcomes, there is a lack of knowledge about the intimate mechanism(s) controlling this phenomenon. In this paper, we describe a number of ultrastructural alterations in the cellular membranes following the exposure of orthotopic melanomas and red blood cells to trains of biphasic pulses. Specifically, melanoma xenografts grown in nude mice were subject to trains of eight biphasic pulses using an electric field of 1250 or 2450 V/cm, excised after 5 min and processed for electron microscopy. The freeze‐fracturing analysis of both cell types evidenced defects in the dynamic assembly of lipids and proteins, which generate “areas with rough structure” and intensive clustering of intramembrane proteins. Such modifications could be the hallmarks of lipid and protein alterations, of protein cohesion reduction, and of changes in lipid orientation inside cell membranes, as postulated in several mathematical models applied to electroporation, and warrant further investigations. Microsc. Res. Tech., 2007. © 2007 Wiley‐Liss, Inc.
Imaging FRET standards by steady‐state fluorescence and lifetime methods
Authors: Domingo Beatriz , Sabariegos Rosario , Picazo Fernando , Llopis Juan 
Published: August 2007

AbstractImaging fluorescence resonance energy transfer (FRET) between molecules labeled with fluorescent proteins is emerging as a powerful tool to study changes in ions, ligands, and molecular interactions in their physiological cellular environment. Different methods use either steady‐state fluorescence properties or lifetime to quantify the FRET rate. In addition, some provide the absolute FRET efficiency whereas others are simply a relative index very much influenced by the actual settings and instrumentation used, which makes the interpretation of a given FRET rate very difficult. The use and exchange of FRET standards in laboratories using these techniques would help to overcome this drawback. We report here the construction and systematic evaluation of FRET standard probes of varying FRET efficiencies. The standards for intramolecular FRET were protein fusions of the cyan and yellow variants of A. victoria green fluorescent protein (ECFP and citrine) joined by short linkers or larger protein spacers, or ECFP tagged with a tetracysteine motif and labeled with the biarsenical fluorochrome, FlAsH. Negative and positive controls of intermolecular FRET were also used. We compared these FRET standards with up to four FRET quantification methods: ratioing of acceptor to donor emission, donor intensity recovery upon acceptor photobleach, sensitized emission after spectral unmixing of raw images, and fluorescence lifetime imaging (FLIM). The latter was obtained with a frequency‐domain setup able to provide high quality lifetime images in less than a second, and is thus very well suited for live cell studies. The FRET rates or indexes of the standards were in good agreement regardless of the method used. For the CFP‐tetraCys/FlAsH pair, the rate calculated from CFP quenching was faster than that obtained by FLIM. Microsc. Res. Tech., 2007. © 2007 Wiley‐Liss, Inc.
Age‐related changes of NADPH‐diaphorase‐positive neurons in the rat inferior colliculus and auditory cortex
Authors: Sánchez‐Zuriaga Daniel , Martí‐Gutiérrez Nuria , De La Cruz Maria Ángeles Pérez , Peris‐Sanchis Maria Rosa 
Published: August 2007

AbstractNitric oxide (NO) has been implied in age‐related changes of the central nervous system (CNS) and the central auditory pathway. The present study was conducted to investigate whether the number of NO‐producing cells and their morphometric characteristics in the inferior colliculus (IC) and the auditory cortex (AC) are changed with the increasing age of the subjects. IC and AC sections of adult and senile Wistar rats were studied using the histochemical detection of NADPH‐diaphorase activity (NADPH‐d), a marker for neurons containing nitric oxide synthase (NOS). Our results showed a decreased area of the somas of NADPH‐d‐positive neurons in the dorsal cortex (DC) of the IC and a diffuse loss of NADPH‐d‐positive neurons in the senile IC and primary cortical auditory area (Te1). However, an increased number of NO‐producing cells have been shown by other authors in different parts of the ageing auditory pathway and CNS. It seems that age‐related changes in NADPH‐d‐positive cells may follow a region‐specific route. These changes may be related to hearing impairments with increasing age. Microsc. Res. Tech., 2007. © 2007 Wiley‐Liss, Inc.
An improved confocal FRAP technique for the measurement of long‐term actin dynamics in individual stress fibers
Authors: Campbell J.J. , Knight M.M. 
Published: August 2007

AbstractThe present study describes an improved fluorescent recovery after photobleaching (FRAP) technique, which has been successfully used to quantify actin dynamics within individual fibers. Chondrocytes were transfected with an eGFP‐actin plasmid and cultured on glass coverslips. In cells expressing eGFP‐actin, confocal microscopy was used to bleach 3 × 1 μm regions accurately positioned along individual stress fibers. The subsequent fluorescent recovery over a 10‐min imaging period was assessed from a series of intensity profiles, positioned along the length of the stress fibers and spanning the bleach region. From these profiles, the normalized fluorescent intensity values were plotted against time. In this way, the technique provided sufficient spatial precision to describe the long‐term behavior within individual stress fibers while accounting for the inherent movement. An identical procedure was used to examine FRAP for eGFP‐actin within the interfiber region. The FRAP curves for stress fibers were accurately modeled by two phase exponentials which indicated only partial recovery with a mobile fraction of 46%. This suggests that some of the F‐actin molecules were in a tightly bound configuration with negligible turnover. The interfiber region exhibited similar two phase exponential FRAP with a mobile fraction of 68%. This partial recovery may be due to the presence, within the interfiber region, of both G‐actin and fine F‐actin fibers beneath the resolution of the confocal microscope. In conclusion, the present FRAP methodology overcomes many of the limitations of previous studies in order to provide new data describing long‐term actin dynamics within individual stress fibers. Microsc. Res. Tech., 2007. © 2007 Wiley‐Liss, Inc.
Evaluation of top, angle, and side cleaned FIB samples for TEM analysis
Authors: Montoya Eduardo , Bals Sara , Rossell Marta D. , Schryvers Dominique , Van Tendeloo Gustaaf 
Published: August 2007

AbstractTEM specimens of a LaAlO3/SrTiO3 multilayer are prepared by FIB with internal lift out. Using a Ga+1 beam of 5 kV, a final cleaning step yielding top, top‐angle, side, and bottom‐angle cleaning is performed. Different cleaning procedures, which can be easily implemented in a dual beam FIB system, are described and compared; all cleaning types produce thin lamellae, useful for HRTEM and HAADF‐STEM work up to atomic resolution. However, the top cleaned lamellae are strongly affected by the curtain effect. Top‐angle cleaned specimens show an amorphous layer of around 5 nm at the specimen surfaces, due to damage and redeposition. Furthermore, it is observed that the LaAlO3 layers are preferentially destroyed and transformed into amorphous material, during the thinning process. Microsc. Res. Tech., 2007. © 2007 Wiley‐Liss, Inc.
Tradeoffs between somatic and gonadal investments during development in the African clawed frog (Xenopus laevis)
Authors: McCoy Krista A. , McCoy Michael W. , Amick Alison , Guillette Louis J. , St. Mary Colette M. 
Published: August 2007

AbstractTradeoffs between time to and size at metamorphosis occur in many organisms with complex life histories. The ability to accelerate metamorphosis can increase survival to the next life stage, but the resulting smaller size at metamorphosis is often associated with lower post‐metamorphic survival or reduced fecundity of adults. Reduced fecundity is thought to be because of reduced energy reserves, longer time to maturity, or reduced capacity to carry eggs or compete for mates. This pattern could also be explained by a shift in allocation to somatic growth that further retards the growth or development of reproductive tissues. The main goal of this study was to determine if the relationship between growth and development of somatic and gonadal tissues depends on environmental conditions. We address this question through two experiments in which we quantify the development and growth of the body and gonads of Xenopus laevis reared in different resource environments. First, tadpoles were reared communally and development and growth were evaluated over time. Restricted food reduced somatic and gonadal growth rate, but did not affect the developmental rate of either tissue type. Second, tadpoles were reared individually and evaluated at metamorphosis. Restricted food reduced somatic development and growth, but only influenced size, and not developmental stage of testes at metamorphosis. This work demonstrates that environmental conditions influence tradeoffs between growth and development of somatic and gonadal tissues, apparently in a sex‐specific manner. These tradeoffs may contribute to phenotypic correlations between small size and reduced fitness J. Exp. Zool. 307A:637–646, 2007. © 2007 Wiley‐Liss, Inc.
Tfap2 transcription factors in zebrafish neural crest development and ectodermal evolution
Authors: Hoffman Trevor L. , Javier Anna L. , Campeau Shelley A. , Knight Robert D. , Schilling Thomas F. 
Published: August 2007

AbstractTranscription factor AP2 (Tfap2) genes play essential roles in development of the epidermis and migratory cells of the neural crest (NC) in vertebrate embryos. These transcriptional activators are among the earliest genes expressed in the ectoderm and specify fates within the epidermis/crest through both direct and indirect mechanisms. The Tfap2 family arose from a single ancestral gene in a chordate ancestor that underwent gene duplication to give up to five family members in living vertebrates. This coincided with the acquisition of important roles in NC development by Tfap2 genes suggesting that this gene family was important in ectodermal evolution and possibly in the origin of NC. Here, we show that a zebrafish tfap2c is expressed in the nonneural ectoderm during early development and functions redundantly with tfap2a in NC specification. In zebrafish embryos depleted of both tfap2a and tfap2c, NC cells are virtually eliminated. Cell transplantation experiments indicate that tfap2c functions cell‐autonomously in NC specification. Cells of the enveloping layer, which forms a temporary skin layer surrounding the ectoderm, also fail to differentiate or to express appropriate keratins in tfap2c deficient embryos. The role of Tfap2 genes in epidermal and NC development is considered here in the broader context of ectodermal evolution. Distinct, tissue‐specific functions for Tfap2 genes in different vertebrates may reflect subfunctionalisation of an ancestral gene that consequently led to the gain of novel roles for different subfamily members in patterning the epidermis and NC. J. Exp. Zool. (Mol. Dev. Evol.) 308B:679–691, 2007. © 2007 Wiley‐Liss, Inc.
On the search for glycated lipoprotein ApoA‐I in the plasma of diabetic and nephropathic patients
Authors: Lapolla Annunziata , Brioschi Maura , Banfi Cristina , Tremoli Elena , Bonfante Luciana , Cristoni Simone , Seraglia Roberta , Traldi Pietro 
Published: August 2007

AbstractThe analysis of plasma samples from healthy, diabetic and nephropathic subjects was carried out by 2D gel electrophoresis. This approach shows clear differences among the three classes of subjects. In the case of diabetic and nephropathic patients intense spots appear. Their enzymatic digestion followed by matrix assisted laser desorption ionization/mass spectrometry (MALDI/MS) analysis shows that an overexpression of unglycated and glycated ApoA‐I is present in both pathological states. Interestingly, this trend is also observed for the retinol‐binding protein (RBP). The data obtained can be relevant to assess possible risks associated either with the glycation level of ApoA‐I or with the overexpression of RBP. In fact, in the former case possibly a different functionality of the glycated protein is to be expected, reflecting a different efficiency in cholesterol transport. In the latter case, the increase of RBP level can be related to the overweight of the diabetic subjects under investigation: it is known that obesity leads to RBP overexpression. In the case of nephropathic patients, the RBP level increases in parallel with serum creatinin. Copyright © 2007 John Wiley & Sons, Ltd.
The myelin‐associated glycoprotein inhibitor BENZ induces outgrowth and survival of rat dorsal root ganglion cell cultures
Authors: Nowicki Marcin , Kosacka Joanna , Brossmer Reinhard , Spanel‐Borowski Katharina , Borlak Jürgen 
Published: August 2007

AbstractThe novel myelin‐associated glycoprotein (MAG) inhibitor BENZ binds to the N‐acetylneuraminic acid (Neu5Ac) portion of the N‐terminal Ig‐like domain of MAG. Treatment of rat dorsal root ganglion (DRG) cell cultures with BENZ‐induced outgrowth of neurofilament 200–positive neurites improved survival of neurons and increased the number of GFAP‐positive cells, as determined by fluorescence and confocal laser microscopy and by Western immunoblotting. Furthermore, treatment of DRG cell cultures with BENZ repressed gene and protein expression of the small GTPase RhoA but induced expression of Rho GTP–activating proteins 5 and 24, likely to counteract protein kinase A activity. Specifically, expression of inhibitors of neurite outgrowth, for example, Rock2 and PAK4, was repressed, but cofilin 1, a promoter of axonal growth, was induced. We propose that the MAG inhibitor BENZ abrogates the RhoA–ROCK–cofilin pathway to promote neurite outgrowth. Our findings require confirmation by in vivo animal studies. © 2007 Wiley‐Liss, Inc.
Structure, properties, and functions of the human small heat‐shock protein HSP22 (HspB8, H11, E2IG1): A critical review
Authors: Shemetov Anton A. , Seit‐Nebi Alim S. , Gusev Nikolai B. 
Published: August 2007

AbstractThe recently described human HSP22 belongs to the superfamily of small heat‐shock proteins containing a conservative α‐crystallin domain. HSP22 seems to be involved in regulation of cell proliferation, cardiac hypertrophy, apoptosis, and carcinogenesis, and expression of point mutants of HSP22 correlates with development of different neuromuscular diseases. Therefore, an investigation of the structure and properties of HSP22 is desirable for understanding its multiple functions. HSP22 seems to belong to the group of so‐called intrinsically disordered proteins and possesses a highly flexible structure. HSP22 tends to form small‐molecular‐mass oligomers and interacts with biological membranes and many different proteins, among them glycolytic enzymes and different protein kinases. HSP22 possesses chaperonelike activity and prevents aggregation of denatured proteins both in vitro and in vivo. Depending on the cell type and its expression, HSP22 might have either pro‐ or anti‐apoptotic effects. Chaperonelike activity seems to be important for antiapoptotic effects, whereas interaction with and regulation of certain protein kinases might be important for the proapoptotic effects of HSP22. Expression of K141N or K141E mutants of HSP22 correlates with development of distal hereditary motor neuropathy and/or Charcot‐Marie‐Tooth disease. These mutations destabilize the structure of HSP22, affect its interaction with other small heat‐shock proteins, and decrease its chaperonelike activity. HSP22 decreases or prevents aggregation of Huntingtin fragments and amyloid‐β peptide 1–40 of the Dutch type. Thus, HSP22 seems to play an important role in the nervous system, and further investigations are needed to understand the molecular mechanisms of its functioning. © 2007 Wiley‐Liss, Inc.
Nuclear magnetic resonance studies of energy metabolism and glutamine shunt in hepatic encephalopathy and hyperammonemia
Authors: Zwingmann Claudia 
Published: August 2007

AbstractHepatic encephalopathy (HE) in both acute and chronic liver failure is more likely a reversible functional disease rather than an irreversible pathological lesion of brain cells. Metabolic alterations underlie many of the mechanisms leading to HE. This paper summarizes in vivo and ex vivo 1H‐, 13C‐, and 15N‐nuclear magnetic resonance (NMR) spectroscopy data on patients and experimental models of HE. In vivo NMR spectroscopy provides a unique opportunity to study metabolic changes noninvasively in the brain in vivo, and to quantify various metabolites in localized brain areas, and ex vivo NMR permits the high‐resolution measurement of metabolites and the identification of different metabolic pathways. In vivo and ex vivo 1H‐NMR investigations consistently reveal severalfold increases in brain glutamine and concomitant decreases in myo‐inositol, an important osmolyte in astrocytes. An osmotic disturbance in these cells has long been suggested to be responsible for astrocyte swelling and brain edema. However, ex vivo 13C‐NMR studies have challenged the convention that glutamine accumulation is the major cause of brain edema in acute HE. They rather indicate a limited anaplerotic flux and capacity of astrocytes to detoxify ammonia by glutamine synthesis and emphasize distortions of energy and neurotransmitter metabolism. However, recent 15N‐NMR investigations have demonstrated that glutamine fluxes between neurons and astrocytes are affected by ammonia. Further NMR studies may provide novel insights into the relationship between brain edema and/or astrocyte pathology and changes in inter‐ and intracellular glutamine homeostasis, which may secondarily alter brain energy metabolism. © 2007 Wiley‐Liss, Inc.
Expression of an acyl‐CoA synthetase, lipidosin, in astrocytes of the murine brain and its up‐regulation during remyelination following cuprizone‐induced demyelination
Authors: Song Si‐Young , Kato Chieko , Adachi Eijiro , Moriya‐Sato Ayako , Inagawa‐Ogashiwa Masayo , Umeda Rieko , Hashimoto Naohiro 
Published: August 2007

AbstractLipidosin is an 80‐kDa protein with long‐chain acyl‐CoA synthetase activity expressed in the brain, adrenal gland, testis, and ovary, which are selectively damaged in X‐linked adrenoleukodystrophy (X‐ALD). Western blot analysis of the cerebrum and cerebellum revealed a gradual increase in the expression of lipidosin postnatally. Light microscopic immunohistochemistry using a panel of specific monoclonal antibodies showed that the lipidosin‐immunopositive cells were ubiquitously distributed in the brain and were denser in the gray matter than in the white matter. Lipidosin immunoreactivity was colocalized with GFAP immunoreactivity but not with ubiquitin C‐terminal hydrolase 1 (= PGP9.5) immunoreactivity, a neuronal marker, and lipidosin‐producing cells detected by an antisense probe specific for lipidosin mRNA were also GFAP immunopositive. These data together with Western blot analysis of primary cultured astrocytes indicate that lipidosin is expressed in astrocytes. Immunoelectron microscopic analysis revealed that lipidosin immunoreactivity was widely distributed from perivascular endfeet to perisynaptic processes without being limited to peroxisomes. Lipidosin immunoreactivity was greatly increased in astrocytes in the area of remyelination following experimental demyelination induced by the administration of cuprizone to mice. These data suggest that lipidosin was involved in fatty acid metabolism during reconstruction of the myelin sheath. © 2007 Wiley‐Liss, Inc.
Bone morphogenetic proteins 4, 6, and 7 are up‐regulated in mouse spinal cord during experimental autoimmune encephalomyelitis
Authors: Ara Jahan , See Jill , Mamontov Polina , Hahn Ashleigh , Bannerman Peter , Pleasure David , Grinspan Judith B. 
Published: August 2007

AbstractAlthough spontaneous remyelination occurs in multiple sclerosis (MS), the extent of myelin repair is often inadequate to restore normal function. Oligodendrocyte precursors remaining in nonremyelinating MS plaques may be restricted by an inhibitory signal. Bone morphogenetic proteins (BMPs) have been implicated as repressors of oligodendrocyte development and inducers of astrogliogenesis. We hypothesized that BMPs are up‐regulated in MS lesions and play a role in demyelination and astrogliosis. We examined expression of BMPs in an animal model of MS, chronic experimental autoimmune encephalomyelitis (EAE) induced by the myelin oligodendrocyte glycoprotein (MOG) peptide in C57BL/6 mice. By 14 days postimmunization, compared to those of control mice, the lumbar spinal cords of MOG‐peptide EAE mice demonstrated prominent astrogliosis, infiltration of inflammatory cells, and disrupted expression of myelin proteins. Quantitative RT‐PCR showed that expression of BMP4, BMP6, and BMP7 mRNA increased 2‐ to 4‐fold in the lumbar spinal cords of animals with symptomatic EAE versus in vehicle‐treated and untreated controls on days 14, 21, and 42 postimmunization. BMP2 mRNA expression was not altered. BMP4 mRNA was much more abundant in the spinal cords of all animals than was mRNA encoding BMP2, BMP6, and BMP7. Immunoblot analysis confirmed the increased expression of BMP4 in the EAE animals. Immunohistochemistry revealed increased BMP4 immunoreactivity in areas of inflammation in MOG‐peptide EAE animals. BMP4 labeling was mostly limited to macrophages but was sometimes associated with astrocytes and oligodendrocytes. These results indicate that members of the BMP family are differentially expressed in adult spinal cord and are up‐regulated during EAE. © 2007 Wiley‐Liss, Inc.