bluuebunny/crossref_metadata_2025_split huggingface dataset:
Multiple cellular and molecular mechanisms Are involved in human Aβ clearance by transplanted adult astrocytes
Authors: Pihlaja Rea , Koistinaho Jari , Kauppinen Riitta , Sandholm Jouko , Tanila Heikki , Koistinaho Milla 
Published: August 2011

AbstractAstrocytes and microglia are able to degrade potentially neurotoxic β‐amyloid (Aβ) deposits typical for Alzheimer's disease (AD) pathology. Contrary to microglia, astrocytes degrade human Aβ from tissue sections in vitro without any additional stimulation, but it has remained unclear whether transplanted astrocytes are able to clear deposited human Aβ in vivo. We transplanted adult mouse astrocytes into the hippocampi of transgenic mice mimicking AD and observed their fate, effects on microglial responses, and Aβ clearance. After 2‐months follow‐up time, we discovered a significant reduction in Aβ burden compared with AD mice infused with PBS only. The remaining Aβ deposits were fragmented and most of the Aβ immunoreactivity was seen within the transplanted astrocytes. Concomitant to Aβ reduction, both CD68 and CD45 immunoreactivities were significantly upregulated but phagocytic microglia were often surrounding and engulfing Aβ burdened, TUNEL‐positive astrocytes rather than co‐localizing with Aβ alone. Astrocytes are known to degrade Aβ also by secreting proteases involved in Aβ catabolism. To study the contribution of neprilysin (NEP), angiotensin‐converting enzyme‐1 (ACE‐1), and endothelin‐converting enzyme‐2 (ECE‐2) in human Aβ clearance, we utilized an ex vivo assay to demonstrate that adult astrocytes respond to human Aβ by upregulating NEP expression. Further, incubation of adult astrocytes with known inhibitors of NEP, ACE‐1, or ECE‐2 significantly inhibited the removal of human Aβ from the tissue suggesting an important role for these proteases in Aβ clearance by adult astrocytes ex vivo. © 2011 Wiley‐Liss, Inc.
Decreased frontostriatal microstructural organization in attention deficit/hyperactivity disorder
Authors: de Zeeuw Patrick , Mandl René C.W. , Hulshoff Pol Hilleke E. , van Engeland Herman , Durston Sarah 
Published: August 2011

AbstractFrontostriatal brain areas have been implicated in the neurobiology of attention deficit/hyperactivity disorder (ADHD), but little work has directly addressed the white matter connections between these regions. The present study investigates the microstructural organization and myelination of frontostriatal white matter in children with ADHD and controls. Diffusion tensor imaging and magnetization transfer imaging scans were acquired in 30 children with ADHD and 34 controls. A study specific volume of interest (VOI) of frontostriatal white matter was created using a tractography based statistical group map. Fractional anisotropy (FA, indexing microstructural organization) and magnetization transfer ratio (MTR, indexing macromolecular content, myelin in particular) were computed for the frontostriatal VOI and for total cerebral white matter. Exploratory analyses were conducted investigating the effect of stimulant use on these measures. Frontostriatal FA but not MTR was decreased in ADHD compared with controls. There were no differences in FA or MTR for total cerebral white matter. Frontostriatal FA correlated negatively with teacher‐rated attention problems in controls but not children with ADHD. The duration of stimulant use did not affect the main results. Changes in frontostriatal connectivity in ADHD appear to be related to changes in microstructural organization rather than myelination per se. A correlation with attention problems for controls suggests that frontostriatal organization is relevant to ADHD‐related behaviors. Hum Brain Mapp, 2012. © 2011 Wiley Periodicals, Inc
Event‐related potential activity in the basal ganglia differentiates rewards from nonrewards: Temporospatial principal components analysis and source localization of the feedback negativity: Commentary
Authors: Cohen Michael X , Cavanagh James F. , Slagter Heleen A. 
Published: August 2011

AbstractFoti et al. propose that a reward‐related brain potential component recorded from scalp EEG is generated by deep brain basal ganglia structures. Previous work, cited in their original article, provides only speculative and theoretical support for this interpretation. Based on empirical and anatomical evidence, we argue that this scalp‐recorded ERP component is highly unlikely to be generated by the basal ganglia. Hum Brain Mapp, 2011. © 2011 Wiley Periodicals, Inc.
Response inhibition and reward anticipation in medication‐naïve adults with attention‐deficit/hyperactivity disorder: A within‐subject case‐control neuroimaging study
Authors: Carmona Susana , Hoekzema Elseline , Ramos‐Quiroga J. Antoni , Richarte Vanesa , Canals Clara , Bosch Rosa , Rovira Mariana , Carlos Soliva Juan , Bulbena Antonio , Tobeña Adolf , Casas Miguel , Vilarroya Oscar 
Published: August 2011

AbstractBackground: Previous research suggests that ADHD patients are characterized by both reduced activity in the inferior frontal gyrus (IFG) during response inhibition tasks (such as the Go‐NoGo task), and reduced activity in the ventral striatum during reward anticipation tasks (such as the Monetary‐Incentive‐Delay [MID] task). However, no prior research has applied either of these paradigms in medication‐naïve adults with ADHD, nor have these been implemented in an intrasubject manner. Methods: The sample consisted of 19 medication‐naïve adults with ADHD and 19 control subjects. Main group analyses were based on individually defined regions of interest: the IFG and the VStr for the Go‐NoGo and the MID task respectively. In addition, we analyzed the correlation between the two measures, as well as between these measures and the clinical symptoms of ADHD. Results: We observed reduced bilateral VStr activity in adults with ADHD during reward anticipation. No differences were detected in IFG activation on the Go‐NoGo paradigm. Correlation analyses suggest that the two tasks are independent at a neural level, but are related behaviorally in terms of the variability of the performance reaction time. Activity in the bilateral VStr but not in the IFG was associated negatively with symptoms of hyperactivity/impulsivity. Conclusions: Results underline the implication of the reward system in ADHD adult pathophysiology and suggest that frontal abnormalities during response inhibition performance may not be such a pivotal aspect of the phenotype in adulthood. In addition, our findings point toward response variability as a core feature of the disorder. Hum Brain Mapp 33:2350–2361, 2012. © 2011 Wiley Periodicals, Inc.
Ultrasound‐guided fine needle aspiration diagnosis of supraglottic laryngeal cancer
Authors: Lopchinsky Richard A. , Amog‐Jones Glenda F. , Pathi Renuka 
Published: August 2011

AbstractBackground.Although intraoperative laryngoscopic examination and biopsy of patients who present with locally advanced supraglottic carcinomas remains the standard of care, there are occasions when a more expedited biopsy can be helpful.Methods and Results.We describe a quick diagnostic technique of ultrasound‐guided fine needle aspiration of endolaryngeal advanced supraglottic carcinomas, which can be performed in the clinic without any preparation. Ultrasound scanning is performed through the thyrohyoid membrane. The tumor is visualized as an irregular hypoechoic mass. While continuing to visualize the mass, a 21‐gange needle attached to a syringe is passed through the contralateral thyrohyoid membrane into the mass. Suction is applied, and the aspirate is sent for cytologic study.Conclusions.When formal intraoperative laryngoscopy and biopsy is not feasible or timely, ultrasound‐guided fine‐needle aspiration biopsy enables a rapid diagnosis and eliminates the cost, side effects, and risks of a direct laryngoscopy. © 2011 Wiley Periodicals, Inc.† Head Neck, 2013
Genetic interactions in the adrenergic system genes: analysis of antipsychotic‐induced weight gain
Authors: Luca Vincenzo De , Souza Renan P. , Viggiano Emanuela , Sickert Laertes , Teo Celine , Zai Clement , Tiwari Arun K. , Müller Daniel J , Lieberman Jeffery A. , Volavka Jan , Meltzer Herbert Y. , Kennedy James L. 
Published: August 2011

Atypical antipsychotics (AP) have high affinity for many neurotransmitter receptors. Among these receptors, APs are antagonist at α‐adrenergic and β‐adrenergic receptors, and this pharmacological property has been postulated to be involved in the mechanism of action of these drugs with respect to both clinical response and adverse effects.ObjectiveWe tested the hypotheses that AP‐induced weight gain is associated with genetic variation in adrenergic receptors and pathway enzymes. We analyzed nine genetic polymorphisms across seven adrenergic genes (ADRA1A, ADRA2A, ADRA2C, ADRB3, DBH, MAOA and COMT).MethodsOne hundred thirty‐nine patients with schizophrenia were prospectively assessed for AP‐induced weight gain. The HelixTree software (Golden Helix, Bozeman, MT, USA) was employed to detect differences in genotypic distribution between weight gainer and non‐weight gainer groups. Furthermore, for the dopamine β‐hydroxylase haplotype, we were able to obtain both the molecular and the statistical phases, analyzing the phenotype considering both phases.ResultsWeight gain was not associated with any adrenergic gene.ConclusionsOur results suggest that genetic polymorphisms in the adrenergic system may not play a major role in AP‐induced weight gain; however, adrenergic 2A receptor gene that produced previously the most consistent associations with this phenotype showed a significant interaction with the monoamine oxidase A in weight gainers. Copyright © 2011 John Wiley & Sons, Ltd.
The prevalence and clinical‐demographic correlates of diabetes mellitus in chronic schizophrenic patients receiving clozapine
Authors: Zhang Ruiling , Hao Wei , Pan Miao , Wang Chuansheng , Zhang Xiuli , Chen Da Chun , Xiu Mei Hong , De Yang Fu , Kosten Thomas R. , Zhang Xiang Yang 
Published: August 2011

ObjectiveTo examine the prevalence and correlates of diabetes in a large sample of Chinese patients with schizophrenia on long‐term clozapine treatment, because this population previously has received little systematic study.MethodsTwo hundred and six inpatients meeting Diagnostic and Statistical Manual of Mental Disorders, 4th Edition schizophrenia criteria were recruited in a cross‐sectional naturalistic study, and compared with 615 healthy control subjects matched for age, sex, education, and body mass index (BMI). The patient's psychopathology was assessed using the Positive and Negative Syndrome Scale (PANSS). Diagnoses of diabetes were established through review of medical records and fasting blood glucose testing, or an oral glucose tolerance test.ResultsDiabetes mellitus was more common in patients than in the normal controls (22.3% vs 6.2%) (odds ratio = 4.37, confidence interval (CI) 2.76–6.92, p < 0.001). The prevalence of diabetes increased with age across five age‐groups as compared with normal controls (X2 = 18.0, df = 4, p = 0.001). The PANSS total score and sub‐scores showed no differences between the diabetic and non‐diabetic groups. Logistic regression in the patients revealed significant associations between diabetes and a family history of diabetes (p < 0.001), age (p < 0.01), and BMI (p < 0.05).ConclusionLong‐term clozapine treatment was associated with an increased and clinically important risk of diabetes mellitus in Chinese chronic schizophrenic patients, which is consistent with previous reports in Western populations. Copyright © 2011 John Wiley & Sons, Ltd.
Detection of mitochondrial deoxyribonucleic acid alterations in urine from urothelial cell carcinoma patients
Authors: Dasgupta Santanu , Shao Chunbo , Keane Thomas E. , Duberow David P. , Mathies Richard A. , Fisher Paul B. , Kiemeney Lambertus A. , Sidransky David 
Published: August 2011

AbstractOur study aims at understanding the timing and nature of mitochondrial deoxyribonucleic acid (mtDNA) alterations in urothelial cell carcinoma (UCC) and their detection in urine sediments. The entire 16.5 kb mitochondrial genome was sequenced in matched normal lymphocytes, tumor and urine sediments from 31 UCC patients and compared to different clinical stages and histological grades. The mtDNA content index was examined in all the specimens. Sixty‐five percent (20/31) of the patients harbored at least 1 somatic mtDNA mutation. A total of 25 somatic mtDNA mutations were detected, which were more frequent in the respiratory complex coding regions (Complex I, III, IV and V) of the mtDNA and significantly affected respiratory Complex III compared to the other complexes (p = 0.021–0.039). Compared to Stage Ta, mtDNA mutation was higher in Stage T1 and significantly higher in Stage T2 (p = 0.01) patients. MtDNA mutation was also significantly higher (p = 0.04) in Stage T2 compared to Stage T1 patients. Ninety percent (18/20) of the patients harboring mtDNA mutation in the tumor also had mutation in their urine sediments. Eighty percent (20/25) of the tumor‐associated mtDNA mutations was detectable in the urine sediments. Compared to the normal lymphocytes, the mtDNA content increased significantly in the tumor (p = 0.0013) and corresponding urine sediments (p = 0.0025) in 19/25 (76%) patients analyzed. Our results indicate that mtDNA alterations occur frequently in progressive stages of UCC patients and are readily detectable in the urine sediments. MtDNA mutations appear to provide a promising tool for developing early detection and monitoring strategies for UCC patients.
Host‐derived osteopontin maintains an acute inflammatory response to suppress early progression of extrinsic cancer cells
Authors: Hsieh Yu‐Hua , Margaret Juliana M. , Ho Kang‐Jey , Kuo Hui‐Chien , van der Heyde Henri , Elmets Craig , Chang Pi‐Ling 
Published: August 2011

AbstractThe matricellular protein osteopontin (OPN), expressed in various cancer types and elevated in the blood of cancer patients, is thought to have different functions when derived from host versus cancer cells. To assess the effect of host‐derived OPN on growth of cancers of epithelial origin, we established a line of cutaneous squamous cell carcinoma (SCC) cells, named ONSC, which lacks the OPN gene and develops SCC in syngeneic wild‐type (WT) and OPN‐null mice. At 8 and/or 10 week after subcutaneous injection of ONSC cells in mice, however, there was a lower tumor incidence in WT mice, suggesting that host‐derived OPN is associated with suppression of early growth of extrinsic cancer cells. Histological, immunohistochemical, biochemical and hematological analyses were performed on the tumor microenvironment and blood from tumor‐bearing mice during the first week after implantation. Host‐derived OPN suppression of extrinsic ONSC cell progression is likely mediated through elicitation of an early innate inflammatory response, through its function as a chemoattractant and/or by enhancing survival of inflammatory cells. Further, consistent with a previous report, the serum levels of host‐derived OPN, which are elevated during the early phase of tumor growth in mice implanted with ONSC, appear to reflect an anti‐tumor progression effect.
Raman spectroscopy: a potential tool for early objective diagnosis of neoplasia in the oesophagus
Authors: Almond L. Max , Hutchings Joanne , Shepherd Neil , Barr Hugh , Stone Nick , Kendall Catherine 
Published: August 2011

AbstractThere is a profound clinical need for a diagnostic tool that will enable clinicians to identify early neoplastic change in the oesophagus. Raman Spectroscopy (RS) has demonstrated the potential to provide non‐invasive, rapid, objective diagnosis of endoscopically invisible precancerous oesophageal dysplasia in vitro. RS analyses biological material to identify highly specific biochemical information that can be used to influence clinical care. Raman spectroscopic mapping could provide automated assessment of tissue biopsies to aid histopathological diagnosis in vitro. Furthermore, the recent development of fibre‐optic Raman probes has enabled endoscopic assessment of oesophageal mucosa in vivo. Accurate identification of dysplasia will enable targeted endoscopic resection of early lesions preventing the development of oesophageal cancer. This review summarises the development of Raman systems for use as laboratory based analytical adjuncts and endoscopic diagnostic tools in the distal oesophagus. (© 2011 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim)
Shear stress regulates expression of death‐associated protein kinase in suppressing TNFα‐induced endothelial apoptosis
Authors: Rennier Keith , Ji Julie Y. 
Published: August 2011

AbstractDeath associated protein kinase (DAPK) is a positive regulator in tumor necrosis factor α (TNFα)‐induced apoptotic pathway, and DAPK expression is lost in cancer cells. In the vasculature, misdirected apoptosis in endothelial cells leads to pathological conditions such as inflammation and physiological shear stress is protective against apoptosis. Using bovine aortic endothelial cells, we found that DAPK expression increased, while the auto‐inhibitory phosphorylation of serine 308 decreased with shear stress at 12 dynes/cm2 for 6 h. Quantitative RT‐PCR revealed a corresponding increase in DAPK mRNA [P < 0.01]. We found that after 18‐h TNFα induction, shearing cells for another 6 h significantly reduced apoptosis based on TUNEL staining [P < 0.05], although cell necrosis was not affected. Under the same conditions, we observed significantly decreased overall DAPK, as well as phospho‐serine 308 DAPK [P < 0.05] compared to TNFα treatment alone. Caspase‐3 and ‐7 activities downstream of DAPK were also attenuated. Shearing cells alone resulted in enhanced apoptosis, likely due to increased DAPK activity. Our findings were further supported by DAPK siRNA, which yielded contrary results. We present conclusive evidence for the first time that shear stress of up to 6 h up‐regulates DAPK expression and activation. However, in the presence of apoptotic stimuli such as TNFα, shear stress caused decrease in DAPK activity. In fact, long‐term shear stress of 24 h significantly reduced overall DAPK expression. Our findings strongly support a novel role for DAPK in mediating effects of shear stress in suppressing cytokine‐activated apoptosis. J. Cell. Physiol. 227: 2398–2411, 2012. © 2011 Wiley Periodicals, Inc.
CREB coactivator CRTC2/TORC2 and its regulator calcineurin crucially mediate follicle‐stimulating hormone and transforming growth factor β1 upregulation of steroidogenesis
Authors: Fang Wei‐Ling , Lee Ming‐Ting , Wu Leang‐Shin , Chen Yun‐Ju , Mason Jian , Ke Ferng‐Chun , Hwang Jiuan‐Jiuan 
Published: August 2011

AbstractIn vitro and in vivo studies implicate that follicle‐stimulating hormone (FSH) and transforming growth factor β1 (TGFβ1) play crucial physiological roles in regulating ovarian granulosa cell function essential to fertility control in females. FSH induces cAMP and calcium signaling, thereby activating transcription factor CREB to upregulate steroidogenic gene expression, and TGFβ1 greatly enhances FSH‐stimulated steroidogenesis. A CREB coactivator CRTC2/TORC2 was identified to function as a cAMP and calcium‐sensitive coincidence sensor. This led us to explore the role of CRTC2 and its regulator calcineurin in FSH and TGFβ1‐stimulated steroidogenesis. Primary culture of granulosa cells from gonadotropin‐primed immature rats was used. Immunoblotting analysis shows that FSH rapidly and transiently induced dephosphorylation/activation of CRTC2, and FSH + TGFβ1 additionally induced late‐phase CRTC2 dephosphorylation. Immunofluorescence analysis further confirms FSH ± TGFβ1 promoted CRTC2 nuclear translocation. Using selective inhibitors, we demonstrate that FSH activated CRTC2 in a PKA‐ and calcineurin‐dependent manner, and TGFβ1 acting through its type I receptor (TGFβRI)‐modulated FSH action in a calcineurin‐mediated and PKA‐independent fashion. Next, we investigated the involvement of calcineurin and CRTC2 in FSH and TGFβ1‐stimulated steroidogenesis. Calcineurin and TGFβRI inhibitor dramatically reduced the FSH ± TGFβ1‐increased progesterone synthesis and protein levels of StAR, P450scc, and 3β‐HSD enzyme. Furthermore, chromatin‐immunoprecipitation and immunoprecipitation analyses demonstrate that FSH ± TGFβ1 differentially increased CRTC2, CREB, and CBP binding to these steroidogenic genes, and CREB nuclear association with CRTC2 and CBP. In all, this study reveals for the first time that CRTC2 and calcineurin are critical signaling mediators in FSH and TGFβ1‐stimulated steroidogenesis in ovarian granulosa cells. J. Cell. Physiol. 227: 2430–2440, 2012. © 2011 Wiley Periodicals, Inc.
Expression of a Musashi‐like gene in sexual and asexual development of the colonial chordate Botryllus schlosseri and phylogenetic analysis of the protein group
Authors: Gasparini Fabio , Shimeld Sebastian M. , Ruffoni Elena , Burighel Paolo , Manni Lucia 
Published: August 2011

AbstractTunicates are the unique chordates to possess species reproducing sexually and asexually. Among them, the colonial ascidian Botryllus schlosseri is a reference model for the study of similarities and differences in these two developmental pathways. We here illustrate the characterization and expression pattern during both pathways of a transcript for a gene orthologous to Dazap1. Dazap1 genes encode for RNA‐binding proteins and fall into the Musashi‐like (Msi‐like) group. Our phylogenetic analysis shows that these are related to other RNA‐binding proteins (Tardbp and several heterogeneous nuclear ribonucleoproteins types) that share the same modular domain structure of conserved tandem RNA Recognition Motifs (RRMs). We also classify the whole group as derived from a single ancient duplication of the RRM. Our results also show that Dazap1 is expressed with discrete spatiotemporal pattern during embryogenesis and blastogenesis of B. schlosseri. It is never expressed in wholly differentiated tissues, but it is located in all bud tissues and in different spatiotemporally defined territories of embryos and larva. These expression patterns could indicate different roles in the two processes, but an intriguing relationship appears if aspects of cell division dynamics are taken into account, suggesting that it is related to the proliferative phases in all tissues, and raising a similarity with known Dazap1 orthologs in other metazoans. Dev. Evol.) 316:562–573, 2011. © 2011 Wiley Periodicals, Inc.
Variations of frequency of landfalling typhoons in East China, 1450–1949
Authors: Chan Johnny C. L. , Liu Kin‐Sik , Xu Ming , Yang Qiuzhen 
Published: August 2011

AbstractOn the basis of Chinese government records, the number of tropical cyclones making landfall along the East China coast during the period 1450–1949 is examined. The annual number of typhoons making landfall in East China during this period is found to possess a positive and statistically significant trend, as well as oscillations on centennial to decadal timescales. By classifying the years using proxy records of the El Niño and Pacific Decadal Oscillation phenomena, the annual number of typhoon landfall is found to vary with the different phases of these two prominent oscillations, and such variations can be explained to a large extent physically based on modern‐day atmospheric data. These results, together with those from previous studies, suggest that variations in the number of landfalling tropical cyclones are largely governed by those in the planetary‐scale atmospheric circulations that go through oscillations on various timescales. Copyright © 2011 Royal Meteorological Society