bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of hyperthermia in combination with TRAIL on the JNK‐Bim signal transduction pathway and growth of xenograft tumors
Authors: Alcala Marco A. , Park Kyungsoo , Yoo Jinsang , Lee Dae‐Hee , Park Bae‐hang , Lee Byeong‐Chel , Bartlett David L. , Lee Yong J. 
Published: June 2010

AbstractApproximately 25% of patients with colorectal cancer develop metastases to the liver, and surgery is currently the best treatment available. But there are several patients who are unresectable, and isolated hepatic perfusion (IHP) offers a different approach in helping to treat these patients. IHP is a method used for isolating the liver and delivering high doses of chemotherapeutic agents. The efficacy of IHP has been improved by combining hyperthermia not only with chemotherapeutics but with other deliverable agents such as tumor necrosis factor‐related apoptosis‐inducing ligand (TRAIL). In this study, we used human colorectal cancer CX‐1 cells and treated them with hyperthermia and TRAIL, causing cytotoxicity. We were able to demonstrate that the numbers of live cells were significantly reduced with hyperthermia and 10 ng/ml of TRAIL combined. We also showed that the effect of hyperthermia on TRAIL in our studies was enhancement of the apoptotic pathway by the promotion of JNK and BimELactivity as well as PARP cleavage. We have also used our CX‐1 cells to generate tumors in Balb/c nude mice. With intratumoral injections of TRAIL combined with hyperthermia at 42°C, we were able to show a delayed onset of tumor growth in our xenograft model. J. Cell. Biochem. 110: 1073–1081, 2010. Published 2010 Wiley‐Liss, Inc.
α4 phosphoprotein interacts with EDD E3 ubiquitin ligase and poly(A)‐binding protein
Authors: McDonald William J. , Sangster Shirley M. , Moffat Lori D. , Henderson Michelle J. , Too Catherine K.L. 
Published: June 2010

AbstractMammalian α4 phosphoprotein, the homolog of yeast Tap42, is a component of the mammalian target‐of‐rapamycin (mTOR) pathway that regulates ribogenesis, the initiation of translation, and cell‐cycle progression. α4 is known to interact with the catalytic subunit of protein phosphatase 2A (PP2Ac) and to regulate PP2A activity. Using α4 as bait in yeast two‐hybrid screening of a human K562 erythroleukemia cDNA library, EDD (E3 isolated by differential display) E3 ubiquitin ligase was identified as a new protein partner of α4. EDD is the mammalian ortholog of Drosophila hyperplastic discs gene (hyd) that controls cell proliferation during development. The EDD protein contains a PABC domain that is present in poly(A)‐binding protein (PABP), suggesting that PABP may also interact with α4. PABP recruits translation factors to the poly(A)‐tails of mRNAs. In the present study, immunoprecipitation/immunoblotting (IP/IB) analyses showed a physical interaction between α4 and EDD in rat Nb2 T‐lymphoma and human MCF‐7 breast cancer cell lines. α4 also interacted with PABP in Nb2, MCF‐7 and the human Jurkat T‐leukemic and K562 myeloma cell lines. COS‐1 cells, transfected with Flag‐tagged‐pSG5‐EDD, gave a (Flag)‐EDD–α4 immunocomplex. Furthermore, deletion mutants of α4 were constructed to determine the binding site for EDD. IP/IB analysis showed that EDD bound to the C‐terminal region of α4, independent of the α4‐PP2Ac binding site. Therefore, in addition to PP2Ac, α4 interacts with EDD and PABP, suggesting its involvement in multiple steps in the mTOR pathway that leads to translation initiation and cell‐cycle progression. J. Cell. Biochem. 110: 1123–1129, 2010. Published 2010 Wiley‐Liss, Inc.
Spatial and functional relationships between air conduits and blood capillaries in the pulmonary gas exchange tissue of adult and developing chickens
Authors: Makanya Andrew N. , El‐Darawish Yosif , Kavoi Boniface M. , Djonov Valentin 
Published: June 2010

AbstractThe documented data regarding the three‐dimensional structure of the air capillaries (ACs), the ultimate sites of gas exchange in the avian lung is contradictory. Further, the mode of gas exchange, described as cross‐current has not been clearly elucidated. We studied the temporal and spatial arrangement of the terminal air conduits of the chicken lung and their relationship with the blood capillaries (BCs) in embryos as well as the definitive architecture in adults. Several visualization techniques that included corrosion casting, light microscopy as well as scanning and transmission electron microscopy were used. Two to six infundibulae extend from each atrium and give rise to numerous ACs that spread centrifugally. Majority of the ACs are tubular structures that give off branches, which anastomose with their neighboring cognates. Some ACs have globular shapes and a few are blind‐ending tapering tubes. During inauguration, the luminal aspects of the ACs are characterized by numerous microvillus‐like microplicae, which are formed during the complex processes of cell attenuation and canalization of the ACs. The parabronchial exchange BCs, initially inaugurated as disorganized meshworks, are reoriented via pillar formation to lie predominantly orthogonal to the long axes of the ACs. The remodeling of the retiform meshworks by intussusceptive angiogenesis essentially accomplishes a cross‐current system at the gas exchange interface in the adults, where BCs form ring‐like patterns around the ACs, thus establishing a cross‐current system. Our findings clarify the mode of gas exchange in the parabronchial mantle and illuminate the basis for the functional efficiency of the avian lung. Microsc. Res. Tech. 74:159–169, 2011. © 2010 Wiley‐Liss, Inc.
Formation of cyclic acylphosphoramidates in mass spectra of N‐monoalkyloxyphosphoryl amino acids using electrospray ionization tandem mass spectrometry
Authors: Gao Xiang , Ni Feng , Bao Jian , Liu Yan , Zhang Zhen , Xu Pengxiang , Zhao Yufen 
Published: June 2010

AbstractThe fragmentation reactions of N‐monoalkyloxyphosphoryl amino acids (N‐MAP‐AAs) were studied by electrospray ionization tandem mass spectrometry (ESI‐MS). The sodiated cyclic acylphosphoramidates (CAPAs) were formed through a characteristic pentacoordinate phosphate participated rearrangement reaction in the positive‐ion ESI‐MS/MS and HR‐MS/MS of N‐MAP‐AAs, in which the fragmentation patterns were clearly different from those observed in the corresponding ESI‐MS/MS of N‐dialkyloxyphosphoryl amino acids/peptides and N‐phosphono amino acids. The formation of CAPAs depended on the chemical structures of N‐terminal phosphoryl groups, such as alkyloxy group, negative charge and alkali metal ion. A possible integrated rearrangement mechanism for both P‐N to P‐O phosphoryl group migration and formation of CAPAs was proposed. The fragmentation patterns of CAPAs as novel intermediates in gas phase were also investigated. In addition, it was found that the formation of α‐amino acid CAPAs was more favorable than β‐ or γ‐CAPAs in gas phase, which was consistent with previous solution‐phase experiments. Copyright © 2010 John Wiley & Sons, Ltd.
Melatonin's protective action against ischemic neuronal damage is associated with up‐regulation of the MT2 melatonin receptor
Authors: Lee Choong Hyun , Yoo Ki‐Yeon , Choi Jung Hoon , Park Ok Kyu , Hwang In Koo , Kwon Young‐Guen , Kim Young‐Myeong , Won Moo‐Ho 
Published: June 2010

AbstractMelatonin is a potent free radical scavenger and antioxidant and has protective effects against ischemic damage. In the present study, we examined the relationship between the neuroprotective effects of melatonin and the activation of MT2 melatonin receptor in the hippocampal CA1 region (CA1) after transient cerebral ischemia. MT2 immunoreactivity and protein levels were increased in the CA1 after ischemic damage. Most of MT2‐immunoreactive cells were colocalized with astrocytes, not microglia, in the ischemic CA1. In the melatonin‐sham group, MT2 immunoreaction and protein levels were increased compared with the sham group, and MT2 immunoreactivity and its protein levels in the melatonin‐ischemia group were similar to those in the melatonin‐sham group. In addition, melatonin treatment attenuated the activation of astrocytes and microglia. These results indicate that MT2 are increased and expressed in astrocytes in the ischemic region after an ischemic insult. The activation of MT2 melatonin receptor in the CA1 after melatonin treatment may be involved in the neuroprotective effect associated with melatonin after ischemic injury. © 2010 Wiley‐Liss, Inc.
3R tau expression modifies behavior in transgenic mice
Authors: Shiryaev Natalia , Jouroukhin Yan , Gozes Illana 
Published: June 2010

AbstractTauopathy is a group of disorders characterized by the accumulation of hyperphosphorylated tau protein in the brain, resulting in dementia. Here, tau‐related behavior was evaluated in a mouse model with brain overexpression of the shortest human tau isoform (0N3R). Two groups of animals [tau‐transgenic (tau‐tg) and control littermates] were tested for learning and memory at 1 and 7 months. In the Morris water maze, all mice learned the task at 1 month of age and did not learn at 7 months. In contrast, at 7 months, the tau‐tg animals demonstrated better retention of the passive avoidance response compared with their control littermates, which did not learn. In the open field test, no differences were measured between transgenic and nontransgenic young mice, but significantly higher locomotion was observed in the 7‐month‐old tau‐tg mice compared with controls. Behavior during the elevated plus maze test was the same at 1 month, but at 7 months increased entrance to the different arms was observed in the tau‐tg group. Tau expression and phosphorylation levels were analyzed at 8 months. In the subcortical brain region associated with passive avoidance behavior, the tau‐tg mice demonstrated increased brain tau expression coupled with reduced relative phosphorylation. In contrast, increased tau expression and phosphorylation were measured in the cerebral cortex of the tau‐tg mice. In conclusion, 7‐8‐month‐old tau‐tg mice overexpressing nonmutated 0N3R human tau isoform demonstrated enhanced behavior in the passive avoidance test, paralleled by relative tau hypophosphorylation in the subcortical brain region. © 2010 Wiley‐Liss, Inc.
Glial cell line‐derived neurotrophic factor–secreting genetically modified human bone marrow‐derived mesenchymal stem cells promote recovery in a rat model of Parkinson's disease
Authors: Glavaski‐Joksimovic Aleksandra , Virag Tamas , Mangatu Thomas A. , McGrogan Michael , Wang Xue Song , Bohn Martha C. 
Published: June 2010

AbstractParkinson's disease (PD) is a neurodegenerative disease characterized by progressive degeneration of nigrostriatal dopaminergic (DA) neurons. The therapeutic potential of glial cell line‐derived neurotrophic factor (GDNF), the most potent neurotrophic factor for DA neurons, has been demonstrated in many experimental models of PD. However, chronic delivery of GDNF to DA neurons in the brain remains an unmet challenge. Here, we report the effects of GDNF‐releasing Notch‐induced human bone marrow‐derived mesenchymal stem cells (MSC) grafted into striatum of the 6‐hydroxydopamine (6‐OHDA) progressively lesioned rat model of PD. Human MSC, obtained from bone marrow aspirates of young, healthy adult volunteers, were transiently transfected with the intracellular domain of the Notch1 gene (NICD) to generate SB623 cells. SB623 cells expressing GDNF and/or humanized Renilla green fluorescent protein (hrGFP) following lentiviral transduction or nontransduced cells were stereotaxically placed into rat striatum 1 week after a unilateral partial 6‐OHDA striatal lesion. At 4 weeks, rats that had received GDNF‐transduced SB623 cells had significantly decreased amphetamine‐induced rotation compared with control rats, although this effect was not observed in rats that received GFP‐transduced or nontransduced SB623 cells. At 5 weeks, rejuvenated tyrosine hydroxylase‐immunoreactive (TH‐IR) fibers that appeared to be host DA axons were observed in and around grafts. This effect was more prominent in rats that received GDNF‐secreting cells and was not observed in controls. These observations suggest that human bone‐marrow derived MSC, genetically modified to secrete GDNF, hold potential as an allogeneic or autologous stem cell therapy for PD. © 2010 Wiley‐Liss, Inc.
Hypothyroid state does not protect but delays neuronal death in the hippocampal CA1 region following transient cerebral ischemia: Focus on oxidative stress and gliosis
Authors: Lee Choong Hyun , Yoo Ki‐Yeon , Hwang In Koo , Choi Jung Hoon , Park Ok Kyu , Li Hua , Kang Il‐Jun , Kwon Young‐Guen , Kim Young‐Myeong , Won Moo Ho 
Published: June 2010

AbstractWe investigated protective effects of hypothyroidism on delayed neuronal death, gliosis, lipid peroxidation and Cu,Zn‐superoxide dismutase (SOD1) in the gerbil hippocampal CA1 region (CA1) after 5 min of transient cerebral ischemia. The hypothyroidism was induced by 0.025% methimazole treatment. Free triiodothyronine and thyroxine levels were markedly decreased in the hypothyroid group. Four days after ischemia/reperfusion, only a few NeuN‐immunoreactive (+) neurons were detected in the CA1 of euthyroid‐ischemia (eu‐ischemia) group; however, at this time point, the number of NeuN+ neurons was significantly higher in the hypothyroid‐ischemia (hypo‐ischemia) group than in the eu‐ischemia group. At 5 days postischemia, NeuN+ neurons were significantly decreased in the hypo‐ischemia group: The number of NeuN+ neurons in this group was similar to that in the eu‐ischemia group. Activations of GFAP+ astrocytes and Iba‐1+ microglia in the CA1 were higher in the eu‐ischemia group 3 and 4 days after ischemia/reperfusion. At 5 days postischemia, the activations of both the glial cells in the CA1 were similar between the two groups. 4‐Hydroxy‐2‐nonenal (HNE), a marker for lipid peroxidation, immunoreactivity in the eu‐ischemia group was higher than in the hypo‐ischemia group; at 5 days postischemia, the immunoreactivity was similar between the two groups. In contrast, SOD1 level was lower in the CA1 of the eu‐ischemia group. These results suggest that hypothyroid state does not protect against delayed neuronal death but only delays the neuronal death in the hippocampal CA1 region after transient cerebral ischemia by reducing lipid peroxidation and increasing SOD1. © 2010 Wiley‐Liss, Inc.
Deletion of aquaporin‐4 renders retinal glial cells more susceptible to osmotic stress
Authors: Pannicke Thomas , Wurm Antje , Iandiev Ianors , Hollborn Margrit , Linnertz Regina , Binder Devin K. , Kohen Leon , Wiedemann Peter , Steinhäuser Christian , Reichenbach Andreas , Bringmann Andreas 
Published: June 2010

AbstractThe glial water channel aquaporin‐4 (AQP4) is implicated in the control of ion and osmohomeostasis in the sensory retina. Using retinal slices from AQP4‐deficient and wild‐type mice, we investigated whether AQP4 is involved in the regulation of glial cell volume under altered osmotic conditions. Superfusion of retinal slices with a hypoosmolar solution induced a rapid swelling of glial somata in tissues from AQP4 null mice but not from wild‐type mice. The swelling was mediated by oxidative stress, inflammatory lipid mediators, and sodium influx into the cells and was prevented by activation of glutamatergic and purinergic receptors. Distinct inflammatory proteins, including interleukin‐1β, interleukin‐6, and inducible nitric oxide synthase, were up‐regulated in the retina of AQP4 null mice compared with control, whereas cyclooxygenase‐2 was down‐regulated. The data suggest that water flux through AQP4 is involved in the rapid volume regulation of retinal glial (Müller) cells in response to osmotic stress and that deletion of AQP4 results in an inflammatory response of the retinal tissue. Possible implications of the data for understanding the pathophysiology of neuromyelitis optica, a human disease that has been suggested to involve serum antibodies to AQP4, are discussed. © 2010 Wiley‐Liss, Inc.
The decade of the dendritic NMDA spike
Authors: Antic Srdjan D. , Zhou Wen‐Liang , Moore Anna R. , Short Shaina M. , Ikonomu Katerina D. 
Published: June 2010

AbstractIn the field of cortical cellular physiology, much effort has been invested in understanding thick apical dendrites of pyramidal neurons and the regenerative sodium and calcium spikes that take place in the apical trunk. Here we focus on thin dendrites of pyramidal cells (basal, oblique, and tuft dendrites), and we discuss one relatively novel form of an electrical signal (“NMDA spike”) that is specific for these branches. Basal, oblique, and apical tuft dendrites receive a high density of glutamatergic synaptic contacts. Synchronous activation of 10–50 neighboring glutamatergic synapses triggers a local dendritic regenerative potential, NMDA spike/plateau, which is characterized by significant local amplitude (40–50 mV) and an extraordinary duration (up to several hundred milliseconds). The NMDA plateau potential, when it is initiated in an apical tuft dendrite, is able to maintain a good portion of that tuft in a sustained depolarized state. However, if NMDA‐dominated plateau potentials originate in proximal segments of basal dendrites, they regularly bring the neuronal cell body into a sustained depolarized state, which resembles a cortical Up state. At each dendritic initiation site (basal, oblique, and tuft) an NMDA spike creates favorable conditions for causal interactions of active synaptic inputs, including the spatial or temporal binding of information, as well as processes of short‐term and long‐term synaptic modifications (e.g., long‐term potentiation or long‐term depression). Because of their strong amplitudes and durations, local dendritic NMDA spikes make up the cellular substrate for multisite independent subunit computations that enrich the computational power and repertoire of cortical pyramidal cells. We propose that NMDA spikes are likely to play significant roles in cortical information processing in awake animals (spatiotemporal binding, working memory) and during slow‐wave sleep (neuronal Up states, consolidation of memories). © 2010 Wiley‐Liss, Inc.
Mechanical stiffness of liver tissues in relation to integrin β1 expression may influence the development of hepatic cirrhosis and hepatocellular carcinoma
Authors: Zhao Gang , Cui Jing , Qin Qi , Zhang Jungang , Liu Lin , Deng Shichang , Wu Chenlin , Yang Ming , Li Shaoshan , Wang Chunyou 
Published: June 2010

AbstractBackground and ObjectivesIncreased rigidity of the extracellular matrix (ECM) is commonly associated with hepatocellular carcinoma (HCC). The purpose of this study was to quantitate the mechanical stiffness of various hepatic tissues, evaluate integrin β1 expression, and investigate the correlation between these two factors in the development of HCC.MethodsTwenty‐three normal specimens, 152 cases of cirrhosis, and 105 cases of HCC were included in this study. The mechanical stiffness of the ECM of each specimen was detected using atomic force microscopy to calculate elastic modulus (E) values. Integrin β1 expression was also evaluated using semi‐quantitative RT‐PCR, western blot, and immunohistochemistry. Expression of integrin β1 in HepG2 cells plated on substrates with different mechanical stiffnesses was also evaluated.ResultsA positive correlation between ECM mechanical stiffness and integrin β1 expression was detected. Expression of integrin β1 also correlated with Edmondson pathologic grade, encapsulation, metastasis, and HBV infection (P < 0.01). In vitro, expression of integrin β1 by HepG2 cells was also significantly higher when the cells were plated on stiffer substrates.ConclusionsExpression of integrin β1 is regulated by the mechanical stiffness of the ECM, and correlates with the invasion and metastasis events of HCC in patients with cirrhosis. J. Surg. Oncol. 2010;102:482–489. © 2010 Wiley‐Liss, Inc.
Effect of surface roughness of mechanical seals under blood sealing
Authors: Tomioka Jun , Miyanaga Norifumi 
Published: June 2010

AbstractA miniature mechanical seal with cooling water circulating system has been developed as a shaft seal for rotary blood pumps. The present paper describes the establishment of the experimental methods under blood sealing and the estimation of the effect of the surface roughness on the shaft seal problems, especially in the increase of the friction and the leakage. Micro‐leakage rates of the blood and the cooling water were measured by an ion chromatography. In this method, the ion concentration was converted into the leakage rate. The frictional loss torque was measured by a torque meter. Results are provided with three types of surface roughness, Ra = 0.009 µm, Ra = 0.088 µm and Ra = 0.170 µm. It is shown that as the surface roughness increases the leakage decreases while the frictional loss torque increases under blood sealing. The best surface roughness in the torque and the leakage characteristics were different. Copyright © 2010 John Wiley & Sons, Ltd.
Characteristic head drops and axial extension in advanced chorea‐acanthocytosis
Authors: Schneider Susanne A. , Lang Anthony E. , Moro Elena , Bader Benedikt , Danek Adrian , Bhatia Kailash P. 
Published: June 2010

AbstractChorea‐acanthocytosis is a rare autosomal recessive neurodegenerative disorder with a complex clinical presentation comprising of a mixed movement disorder (mostly chorea and dystonia), seizures, neuropathy and myopathy, autonomic features as well as dementia and psychiatric features. Because the differential diagnosis is wide, clinical clues and red flags are important. We report here our observation of characteristic neck and trunk flexion and extension spasms in four cases with advanced chorea‐acanthocytosis. © 2010 Movement Disorder Society
Standard guidelines for publication of deep brain stimulation studies in Parkinson's disease (Guide4DBS‐PD)
Authors: Vitek Jerrold L. , Lyons Kelly E. , Bakay Roy , Benabid Alim‐Louis , Deuschl Guenther , Hallett Mark , Kurlan Roger , Pancrazio Joseph J. , Rezai Ali , Walter Benjamin L. , Lang Anthony E. 
Published: June 2010

AbstractWhile the use of deep brain stimulation (DBS) for the treatment of neurological disorders has risen substantially over the last decade, it is often difficult to compare the results from different studies due to the lack of consistent reporting of key study parameters. We present guidelines to standardize the reporting of clinical studies of DBS for Parkinson's disease (PD). These guidelines provide a minimal set of required data elements to facilitate the interpretation and comparison of results across published clinical studies. The guidelines, summarized in the format of a checklist, may also have utility in the planning of clinical studies of DBS for PD as well as other neurological and psychiatric disorders. © 2010 Movement Disorder Society
Matrix‐assisted diffusion‐ordered spectroscopy: mixture resolution by NMR using SDS micelles
Authors: Tormena Claudio F. , Evans Robert , Haiber Stephan , Nilsson Mathias , Morris Gareth A. 
Published: June 2010

AbstractDiffusion‐ordered spectroscopy (DOSY) is a powerful technique for mixture analysis, but in its basic form it cannot separate the component spectra for species with very similar diffusion coefficients. It has been recently demonstrated that the component spectra of a mixture of isomers with nearly identical diffusion coefficients (the three dihydroxybenzenes) can be resolved using matrix‐assisted DOSY (MAD), in which diffusion is perturbed by the addition of a co‐solute such as a surfactant [R. Evans, S. Haiber, M. Nilsson, G. A. Morris, Anal. Chem. 2009, 81, 4548–4550]. However, little is known about the conditions required for such a separation, for example, the concentrations and concentration ratios of surfactant and solutes. The aim of this study was to explore the concentration range over which matrix‐assisted DOSY using the surfactant SDS can achieve diffusion resolution of a simple model set of isomers, the monomethoxyphenols. The results show that the separation is remarkably robust with respect to both the concentrations and the concentration ratios of surfactant and solutes, supporting the idea that MAD may become a valuable tool for mixture analysis. Copyright © 2010 John Wiley & Sons, Ltd.