bluuebunny/crossref_metadata_2025_split huggingface dataset:
Identification of sediment source and sink areas in a Himalayan watershed using GIS and remote sensing
Authors: Jain M. K. , Mishra S. K. , Shah R. B. 
Published: November 2009

AbstractErosion is a natural geomorphic process occurring continually over the Earth's surface and it largely depends on topography, vegetation, soil and climatic variables, and therefore, exhibits pronounced spatial variability due to catchment heterogeneity and climatic variation. This problem can be circumvented by discretizing the catchment into approximately homogeneous sub‐areas using GIS. In this study, the remote sensing and GIS techniques (through Imagine®8.6 and ArcGIS®9.1 software) were used for derivation of spatial information, catchment discretization, data processing etc. for the Himalayan Chaukhutia watershed (India). Various thematic layers for different factors of USLE were generated and overlaid to compute spatially distributed gross soil erosion maps for the watershed using 18‐year rainfall data. The concept of transport limited accumulation was formulated and used in ArcGIS® for generating the transport capacity maps. Using these maps, the gross soil erosion was routed to the catchment outlet using hydrological drainage paths, for derivation of transport capacity limited sediment outflow maps. These maps depict the amount of sediment rate from a particular grid in spatial domain and the pixel value of the outlet grid indicates the sediment yield at the outlet of the watershed. Up on testing, the proposed method simulated the annual sediment yield with less than ±40% error. Copyright © 2009 John Wiley & Sons, Ltd.
Cytochrome P450 1B1 mRNA untranslated regions interact to inhibit protein translation
Authors: Devlin Andrea H. , Thompson Paul , Robson Tracy , McKeown Stephanie R. 
Published: November 2009

AbstractCYP1B1 mRNA is expressed constitutively in all normal extrahepatic human tissues, though the protein is usually undetectable. In contrast, CYP1B1 protein is expressed at high levels in tumors. In this study CYP1B1 mRNA and protein expression was measured in a panel of cell lines indicating that CYP1B1 regulation is altered in tumor cell lines in vitro. Interrogation of ONCOMINE revealed that CYP1B1 mRNA is not significantly overexpressed in tumors compared to normal tissues, suggesting CYP1B1 is subject to posttranscriptional control. Analysis of the CYP1B1 mRNA revealed a complex 5′ untranslated region (UTR) containing a small upstream open‐reading frame (uORF). These features are present in mRNAs subject to translational control so the effect of the 5′UTR was tested using in vitro translation in CHO‐K1 cells. The 5′UTR significantly inhibited luciferase reporter gene translation, and mutation of the uORF start codon abolished the inhibitory effect. The 5′UTR also interacted with the microRNA‐27b recognition element in the CYP1B1 mRNA 3′UTR to almost completely inhibit translation. CYP1B1 is subject to a high degree of translational control, which may explain the absence of protein expression in normal cells. Alterations in translational control during malignant transformation may help to explain the tumor‐specific expression of CYP1B1 protein. © 2009 Wiley‐Liss, Inc.
The tumor suppressor parafibromin is required for posttranscriptional processing of histone mRNA
Authors: Farber Leslie J. , Kort Eric J. , Wang PengFei , Chen Jindong , Teh Bin T. 
Published: November 2009

AbstractParafibromin, encoded by the geneHRPT2, is a tumor suppressor protein associated with the RNA polymerase II‐associated complex, Paf1 complex.HRPT2mutations were first identified in patients with the multiple endocrine neoplasia syndrome, hyperparathyroidism‐jaw tumor (HPT‐JT) syndrome, and have also been found in sporadic parathyroid and renal tumors. However, the mechanisms by which parafibromin suppresses tumor formation remain unknown. In this study, we identify a novel role of parafibromin in the regulation of replication‐dependent histones. Both in vitro and in vivo analyses reveal a posttranscriptional role of parafibromin in histone mRNA processing. Downregulation of parafibromin through RNA interference or in vivo mutations lead to uncleaved histone mRNA with polyadenylated tails. These results indicate that parafibromin regulates the 3′ processing of histone RNA, an essential component of the cell cycle. © 2009 Wiley‐Liss, Inc.
The synergistic anticancer effect of troglitazone combined with aspirin causes cell cycle arrest and apoptosis in human lung cancer cells
Authors: Yan Kun‐Huang , Yao Chih‐Jung , Chang Hwan‐You , Lai Gi‐Ming , Cheng Ann‐Lii , Chuang Shuang‐En 
Published: November 2009

AbstractTroglitazone (TGZ) is a synthetic thiazolidinedione drug belonging to a group of potent peroxisome proliferator‐activated receptor γ (PPARγ) agonists known to inhibit proliferation, alter cell cycle regulation, and induce apoptosis in various cancer cell types. TGZ is an oral anti‐type II diabetes drug that can reverse insulin resistance. For more then 100 yr, aspirin, a nonselective cyclooxygenase (COX) inhibitor, has been successfully used as an anti‐inflammatory drug. Recently, Aspirin (ASA) and some other nonsteroidal anti‐inflammatory drugs (NSAIDs) have drawn much attention for their protective effects against colon cancer and cardiovascular disease; it has been observed that ASA's anti‐tumor effect can be attributed to inhibition of cell cycle progression, induction of apoptosis, and inhibition of angiogenesis. In this report we demonstrate for the first time that, when administered in combination, TGZ and ASA can produce a strong synergistic effect in growth inhibition and G1 arrest in lung cancer CL1‐0 and A549 cells. Examination by colony formation assay revealed an even more profound synergy. In Western blot, combined TGZ and ASA also could downregulate Cdk2, E2F‐1, cyclin B1, cyclin D3 protein, and the ratio of phospho‐Rb/Rb. Importantly, apoptosis was synergistically induced by the combination treatment, as evidenced by caspase‐3 activation and PARP cleavage. The involvement of PI3K/Akt inhibition and p27 upregulation, as well as hypophosphorylation of Rac1 at ser71, were demonstrated. Taken together, these results suggest that clinically achievable concentrations of TGZ and ASA used in combination may produce a strong anticancer synergy that warrants further investigation for its clinical applications. © 2009 Wiley‐Liss, Inc.
Fem1b, a proapoptotic protein, mediates proteasome inhibitor‐induced apoptosis of human colon cancer cells
Authors: Subauste M. Cecilia , Sansom Owen J. , Porecha Nehal , Raich Natacha , Du Liqin , Maher Joseph F. 
Published: November 2009

AbstractIn the treatment of colon cancer, the development of resistance to apoptosis is a major factor in resistance to therapy. New molecular approaches to overcome apoptosis resistance, such as selectively upregulating proapoptotic proteins, are needed in colon cancer therapy. In a mouse model with inactivation of the adenomatous polyposis coli (Apc) tumor suppressor gene, reflecting the pathogenesis of most human colon cancers, the gene encoding feminization‐1 homolog b (Fem1b) is upregulated in intestinal epithelium following Apc inactivation. Fem1b is a proapoptotic protein that interacts with apoptosis‐inducing proteins Fas, tumor necrosis factor receptor‐1 (TNFR1), and apoptotic protease activating factor‐1 (Apaf‐1). Increasing Fem1b expression induces apoptosis of cancer cells, but effects on colon cancer cells have not been reported. Fem1b is a homolog of feminization‐1 (FEM‐1), a protein in Caenorhabditis elegans that is regulated by proteasomal degradation, but whether Fem1b is likewise regulated by proteasomal degradation is unknown. Herein, we found that Fem1b protein is expressed in primary human colon cancer specimens, and in malignant SW620, HCT‐116, and DLD‐1 colon cancer cells. Increasing Fem1b expression, by transfection of a Fem1b expression construct, induced apoptosis of these cells. We found that proteasome inhibitor treatment of SW620, HCT‐116, and DLD‐1 cells caused upregulation of Fem1b protein levels, associated with induction of apoptosis. Blockade of Fem1b upregulation with morpholino antisense oligonucleotide suppressed the proteasome inhibitor‐induced apoptosis of these cells. In conclusion, the proapoptotic protein Fem1b is downregulated by the proteasome in malignant colon cancer cells and mediates proteasome inhibitor‐induced apoptosis of these cells. Therefore, Fem1b could represent a novel molecular target to overcome apoptosis resistance in therapy of colon cancer. © 2009 Wiley‐Liss, Inc.
Silibinin inhibits human nonsmall cell lung cancer cell growth through cell‐cycle arrest by modulating expression and function of key cell‐cycle regulators
Authors: Mateen Samiha , Tyagi Alpna , Agarwal Chapla , Singh Rana P. , Agarwal Rajesh 
Published: November 2009

AbstractRecent studies show that silibinin possesses a strong antineoplastic potential against many cancers; however, its efficacy and underlying molecular mechanisms in nonsmall cell lung cancer (NSCLC) are not well defined. Herein, we assessed silibinin activity on prime endpoints and key molecular targets such as cell number, cell‐cycle progression, and cell‐cycle regulatory molecules in three cell lines representing different NSCLC subtypes, namely large cell carcinoma cells (H1299 and H460) and a bronchioalveolar carcinoma cell line (H322). Silibinin treatment (10–75 µM) inhibited cell growth and targeted cell‐cycle progressing causing a prominent G1 arrest in dose‐ and time‐dependent manner. In mechanistic studies, silibinin (50–75 µM) modulated the protein levels of cyclin‐dependent kinases (CDKs) (4, 6, and 2), cyclins (D1, D3, and E), CDKIs (p18/INK4C, p21/Cip1, and p27/Kip1) in a differential manner in these three cell lines. Consistent with these observations, silibinin caused a reduction in kinase activity of CDK4 and 2 in all cell lines except no effect on CDK4 kinase activity in H460 cells, and concomitantly reduced Rb phosphorylation. Together, for the first time, these results identify potential molecular targets and anticancer effects of silibinin in NSCLC cells representing different NSCLC subtypes. © 2009 Wiley‐Liss, Inc.
Up regulation of GW112 Gene by NFκB promotes an antiapoptotic property in gastric cancer cells
Authors: Kim Kee K. , Park Key S. , Song Seok B. , Kim Kyoon E. 
Published: November 2009

AbstractTo clarify the regulatory mechanism of GW112 gene expression, 5′‐flanking region of the human GW112 gene was isolated and characterized in the present study. 5′‐RACE analysis showed a single transcription start site, which is located 142 nucleotides upstream of the translation initiation site. Transient transfection studies with serial deletion constructs and close examination of the sequences identified a putative NFκB binding sequence between −442 and −430, which could be responsible for efficient expression of the GW112 gene. Indeed, GW112 gene was found to be regulated by NFκB signals including overexpressed p65 and IκBα, IKK inhibitor, and proteasome inhibitor. Binding of NFκB to its putative site was confirmed by EMSA and ChIP assays. These results suggest that NFκB is an essential regulatory factor for GW112 transcription. Based on this finding, we next confirmed that inhibition of GW112 expression could induce apoptosis in the presence of cytotoxic agent in gastric cancer cells. Furthermore, knocking‐down or overexpression of GW112 gene in gastric cancer cells demonstrated that GW112 has an antiapoptotic property against the cytotoxic agents‐induced apoptosis. Taken together, these results suggest that GW112 could be an important mediator in NFκB‐dependent tumorigenesis of digestive tract tissues. © 2009 Wiley‐Liss, Inc.
Levodopa response in early Parkinson's disease
Authors: Hauser Robert A. , Auinger Peggy , Oakes David ,   on behalf of the Parkinson Study Group
Published: November 2009

AbstractTo further characterize the short‐term levodopa response in early PD, we performed a retrospective analysis of the ELLDOPA study which randomized 361 early PD subjects to placebo, levodopa 150, 300, or 600 mg/day. We evaluated change in UPDRS motor scores (UPDRSm) from baseline to weeks 9 and 24, and identified changes in UPDRSm that best discriminated treatment with levodopa from placebo. Linear regressions were used to determine associations between baseline characteristics and changes in UPDRSm. Mean percent improvement in UPDRSm in levodopa‐treated subjects was greater than that for placebo‐treated subjects (27.4% vs. 5.8% at 9 weeks, P < 0.001 and 26.2% vs. 4.0% at 24 weeks, P < 0.001). UPDRSm change at 9 weeks ranged from –92.9% (improvement) to 85.7% (worsening) for levodopa and –86.7% to 160% for placebo, and at 24 weeks ranged from –100.0% to 242.9% for levodopa and –87.5% to 112.5% for placebo. UPDRSm improvements of 22.0% at 9 weeks and 23.8% at 24 weeks best discriminated treatment with levodopa 300 mg/day (a common initial maintenance dosage in clinical practice) from placebo. Significant associations were not observed between baseline subject characteristics and magnitude of response from baseline to week 24. We conclude that although levodopa treatment significantly improved PD signs when compared with placebo, there was a wide range and considerable overlap in clinical responses to levodopa and placebo. A substantial proportion of subjects with early PD did not experience a robust response to levodopa. An improvement in UPDRSm of ∼22% best discriminated levodopa treatment from placebo. © 2009 Movement Disorder Society
Role of LINGO1 polymorphisms in Parkinson's disease
Authors: Haubenberger Dietrich , Hotzy Christoph , Pirker Walter , Katzenschlager Regina , Brücke Thomas , Zimprich Fritz , Auff Eduard , Zimprich Alexander 
Published: November 2009

AbstractA clinical overlap between Parkinson's disease (PD) and essential tremor (ET) has prompted a discussion whether these conditions share common genetic susceptibility factors. Recently, the first genome‐wide association study in ET revealed a significant association with a variant in the LINGO1 gene. LINGO1 has also been demonstrated to play a role in the survival of dopaminergic neurons in an animal model of PD, and therefore constitutes a potential candidate gene for PD. In this study, SNPs rs9652490, rs11856808, and rs7177008 of LINGO1 were genotyped in a total of 694 Austrian subjects (349 PD, 345 controls). No association could be found between genotype or allele counts and PD. Neither did a subgroup analysis in tremor‐dominant patients with PD reveal a significant association. This study on LINGO1‐variants in PD argues against a major role of LINGO1 gene variations for PD. © 2009 Movement Disorder Society
Idiopathic spinal myoclonus: A clinical and neurophysiological assessment of a movement disorder of uncertain origin
Authors: Esposito Marcello , Edwards Mark J. , Bhatia Kailash P. , Brown Peter , Cordivari Carla 
Published: November 2009

AbstractSpinal Myoclonus (SM) is characterized by brief and sudden movements caused by the activation of muscles belonging to adjacent spinal myotomes. Recent reports have indicated that “typical” clinical and electrophysiological features of SM can be mimicked voluntarily. A useful tool that can distinguish between organic and psychogenic jerks is the detection of a Bereitschaftspotential (BP). In this study, we looked for evidence of a BP in a cohort of patients with idiopathic SM. A clinical and neurophysiological assessment of 20 patients affected by idiopathic SM was performed. A video EEG‐EMG multichannel recording was performed in each patient to detect BP. An expert neurophysiologist (PB) reviewed the BP recordings and divided them into those showing a definite, possible, and no BP. A clinical assessment of the videoed movements was performed by two neurologists expert in movement disorders (KB and MJE) who indicated if the movements were compatible with organic or psychogenic myoclonus. A definite or possible BP was recorded in 15 out of 20 patients. Clinical raters agreed in their clinical opinion on 15 patients (75%). All patients where both raters agreed the movements appeared to be organic had definite or possible BP. BP are commonly seen in patients with idiopathic SM. There is discordance between clinicians in their clinical rating of SM as organic or psychogenic, but even in those patients where movements appear clinically to be organic, a BP is commonly detected, indicating that the aetiology is psychogenic. This suggests that BP recordings are a useful adjunct to clinical assessment in the accurate diagnosis of patients with idiopathic SM. © 2009 Movement Disorder Society
Theory of mind in Parkinson's disease and related basal ganglia disorders: A systematic review
Authors: Bodden Maren Elisabeth , Dodel Richard , Kalbe Elke 
Published: November 2009

AbstractTheory of mind (ToM), defined as the ability to infer other people's mental states, is a crucial prerequisite of human social interaction and a major topic of interest in the recent neuroscientific research. It has been proposed that ToM is mediated by a complex neuroanatomical network that includes the medial prefrontal cortex, the anterior gyrus cinguli, the sulcus temporalis superior, the temporal poles, and the amygdala. Various neurological and psychiatric diseases are accompanied by aspects of dysfunctional ToM processing. In this review, the association between basal ganglia, involved in the organization of complex cognitive and emotional behavior, and ToM processing is discussed. The purpose of this review is to provide an overview of research on ToM abilities in basal ganglia disorders, especially Parkinson's Disease and related disorders. © 2009 Movement Disorder Society
Interruption of deep brain stimulation of the globus pallidus in primary generalized dystonia
Authors: Grabli David , Ewenczyk Claire , Coelho‐Braga Maria‐Clara , Lagrange Christelle , Fraix Valerie , Cornu Philippe , Benabid Alim‐Louis , Vidailhet Marie , Pollak Pierre 
Published: November 2009

AbstractStimulation (DBS) of the globus pallidus (GP) is effective to treat generalized dystonia. Little is known about the evolution of dystonia in case of arrest after a long period of stimulation. This study describes the course of dystonia during a 48 hours period without stimulation followed by a 24 hours period after turning ON the stimulator. 14 patients with generalized dystonia treated with bilateral GP DBS for 3 years or more were recruited. Blinded video‐based analysis was performed using Burke‐Fahn‐Marsden scale at (1) baseline (ON stimulation), (2) up to 48 hours after the stimulator was turned OFF, and (3) 24 hours after the stimulator was turned ON. 13 patients completed the 48 hours OFF‐stimulation period. The dystonia movement score progressively worsened from 24.3 ± 13.9 at baseline to 48.9 ± 19.8 after 48 hours (P < 0.00001). The disability score also worsened from 4.4 ± 1.2 at baseline to 5.7 ± 1.5 after 48 hours without stimulation (P < 0.001). When the neurostimulator was turned ON, the dystonia scores returned to baseline level after 10 hours. The interruption of GP DBS in dystonia results in a progressive worsening which is rapidly reversible once the neurostimulator is turned ON. © 2009 Movement Disorder Society
A comparison of treatment thresholds in two large Parkinson's disease clinical trial cohorts
Authors: Marras Connie , Lang Anthony E. , Eberly Shirley W. , Oakes David , Fahn Stanley , Schwid Steven R. , Hyson Christopher , Shoulson Ira ,   of the Parkinson Study Group DATATOP and PRECEPT investigators
Published: November 2009

AbstractDeprenyl and Tocopherol Antioxidative Therapy of Parkinsonism (DATATOP) and Parkinson Research Examination of CEP‐1347 Trial (PRECEPT) were two clinical trials of potential disease‐modifying agents for Parkinson's disease that used the time to reaching disability sufficient to require dopaminergic therapy as the primary endpoint. To compare the thresholds for initiating dopaminergic treatment for Parkinson's disease between the two studies, conducted fifteen years apart. Baseline and 12‐month endpoint characteristics for subjects in the placebo arms of the two studies were compared. DATATOP placebo subjects had slightly higher total Unified Parkinson's Disease Rating Scale (UPDRS) scores at baseline than PRECEPT placebo subjects (26.1 vs. 23.6, P = 0.03). Time to endpoint was not significantly different. Mean total UPDRS scores at endpoint among those subjects reaching endpoint by 12 months were 48.4 in DATATOP and 37.5 in PRECEPT (P < 0.0001). Baseline disease severity and time to disability requiring dopaminergic therapy were similar in the DATATOP and PRECEPT trials. The threshold for starting dopaminergic treatment was lower in PRECEPT than in the earlier DATATOP study. This may relate to changes in philosophies with respect to starting treatment for Parkinson's disease, but the factors underlying this change remain to be elucidated. © 2009 Movement Disorder Society
Cognitive impulsivity in Parkinson's disease patients: Assessment and pathophysiology
Authors: Robert Gabriel , Drapier Dominique , Verin Marc , Millet Bruno , Azulay Jean‐Philippe , Blin Olivier 
Published: November 2009

AbstractImpulsivity may be induced by therapeutic interventions (dopamine replacement therapies and sub‐thalamic nucleus (STN) stimulation) in patients with Parkinson's disease (PD). The present review has two goals. First, to describe the most frequently encountered facets of cognitive impulsivity and to stress the links between cognitive impulsivity and aspects such as reward‐related decision making, risk‐taking, and time‐processing in healthy population. The most widely used related cognitive impulsivity paradigms are presented. Second, to review the results of studies on cognitive impulsivity in healthy volunteers and in patients with PD, the latter support the applicability and clinical relevance of this construct in PD population. Data show that PD treatments may favor impulsivity via different mechanisms. Suggestions on the roles of dopamine and STN in the pathophysiology of cognitive impulsivity are proposed. © 2009 Movement Disorder Society
Validation of self‐report depression rating scales in Huntington's disease
Authors: De Souza Jennifer , Jones Lisa A. , Rickards Hugh 
Published: November 2009

AbstractThe aim of this study was to assess the criterion validity of three self‐report measures of depression in a sample of patients with Huntington's disease (HD). Fifty patients with HD completed the Beck Depression Inventory‐II (BDI‐II), the Hospital Anxiety and Depression Scale (HADS), and the Depression Intensity Scale Circles (DISCs). Current psychiatric status was assessed using the schedules for clinical assessment in neuropsychiatry (SCAN), and ICD‐10 diagnosis was used as the gold standard. Receiver operating characteristics (ROC) curves were obtained and the sensitivity, specificity, positive, and negative predictive values were calculated for different cut‐off scores on each rating scale. Twelve patients (24%) met ICD‐10 criteria for depressive disorder. The depression sub‐scale of the HADS (HADS‐D) at an optimal cut‐off of 6/7 was found to discriminate maximally between depressed and nondepressed patients in this population. The DISCs at a cut‐off of 1/2 also performed well at detecting possible “cases” of depression, whereas the BDI‐II performed the least satisfactorily of all scales. The HADS‐D and DISCs are good screening measures for depression in the HD population and the DISCs may be particularly useful in those patients with more severe communicative and cognitive deficits. © 2009 Movement Disorder Society