bluuebunny/crossref_metadata_2025_split huggingface dataset:
3D comparison of low, intermediate, and advanced hippocampal atrophy in MCI
Authors: Apostolova Liana G. , Thompson Paul M. , Green Amity E. , Hwang Kristy S. , Zoumalan Charleen , Jack Clifford R. , Harvey Danielle J. , Petersen Ronald C. , Thal Leon J. , Aisen Paul S. , Toga Arthur W. , Cummings Jeffrey L. , DeCarli Charles S. 
Published: February 2010

AbstractWe applied the hippocampal radial atrophy mapping technique to the baseline and follow‐up magnetic resonance image data of 169 amnestic mild cognitive impairment (MCI) participants in the imaging arm of the Alzheimer's Disease Cooperative Study MCI Donepezil/Vitamin E trial. Sixty percent of the subjects with none to mild hippocampal atrophy rated with the visual medial temporal atrophy rating scale (MTA score < 2) and 33.8% of the subjects with moderate to severe (MTA ≥ 2) hippocampal atrophy converted to Alzheimer's disease (AD) during 3‐year follow‐up. MTA ≥ 2 showed a trend for greater left sided hippocampal atrophy versus MTA < 2 groups at baseline (Pcorrected = 0.08). Higher MTA scores were associated with progressive atrophy of the subiculum and the CA1‐3 subregions. The MTA < 2 group demonstrated significant bilateral atrophy progression at follow‐up (left Pcorrected = 0.008; right Pcorrected = 0.05). Relative to MTA < 2 nonconverters, MTA < 2 converters showed further involvement of the subiculum and CA1 and additional involvement of CA2‐3 at follow‐up. Right CA1 atrophy was significantly associated with conversion to dementia (for 1 mm greater right CA1 radial distance subjects had 50% reduced hazard for conversion). Greater CA1 and subicular atrophy can be demonstrated early and is predictive of future conversion to AD, whereas CA2‐3 involvement becomes more evident as the disease progresses. Hum Brain Mapp, 2010. © 2010 Wiley‐Liss, Inc.
Left cytoarchitectonic BA 44 processes syntactic gender violations in determiner phrases
Authors: Heim Stefan , van Ermingen Muna , Huber Walter , Amunts Katrin 
Published: February 2010

AbstractRecent neuroimaging studies make contradictory predictions about the involvement of left Brodmann's area (BA) 44 in processing local syntactic violations in determiner phrases (DPs). Some studies suggest a role for BA 44 in detecting local syntactic violations, whereas others attribute this function to the left premotor cortex. Therefore, the present event‐related functional magnetic resonance imaging (fMRI) study investigated whether left‐cytoarchitectonic BA 44 was activated when German DPs involving syntactic gender violations were compared with correct DPs (correct: ‘der Baum’—the[masculine] tree[masculine]; violated: ‘das Baum’—the[neuter] tree[masculine]). Grammaticality judgements were made for both visual and auditory DPs to be able to generalize the results across modalities. Grammaticality judgements involved, among others, left BA 44 and left BA 6 in the premotor cortex for visual and auditory stimuli. Most importantly, activation in left BA 44 was consistently higher for violated than for correct DPs. This finding was behaviourally corroborated by longer reaction times for violated versus correct DPs. Additional brain regions, showing the same effect, included left premotor cortex, supplementary motor area, right middle and superior frontal cortex, and left cerebellum. Based on earlier findings from the literature, the results indicate the involvement of left BA 44 in processing local syntactic violations when these include morphological features, whereas left premotor cortex seems crucial for the detection of local word category violations. Hum Brain Mapp, 2010. © 2010 Wiley‐Liss, Inc.
Cortical responses to consciousness of schematic emotional facial expressions: A high‐resolution EEG study
Authors: Babiloni Claudio , Vecchio Fabrizio , Buffo Paola , Buttiglione Maura , Cibelli Giuseppe , Rossini Paolo Maria 
Published: February 2010

AbstractIs conscious perception of emotional face expression related to enhanced cortical responses? Electroencephalographic data (112 channels) were recorded in 15 normal adults during the presentation of cue stimuli with neutral, happy or sad schematic faces (duration: “threshold time” inducing about 50% of correct recognitions), masking stimuli (2 s), and go stimuli with happy or sad schematic faces (0.5 s). The subjects clicked left (right) mouse button in response to go stimuli with happy (sad) faces. After the response, they said “seen” or “not seen” with reference to previous cue stimulus. Electroencephalographic data formed visual event‐related potentials (ERPs). Cortical sources of ERPs were estimated by LORETA software. Reaction time to go stimuli was generally shorter during “seen” than “not seen” trials, possibly due to covert attention and awareness. The cue stimuli evoked four ERP components (posterior N100, N170, P200, and P300), which had similar peak latency in the “not seen” and “seen” ERPs. Only N170 amplitude showed differences in amplitude in the “seen” versus “not seen” ERPs. Compared to the “not seen” ERPs, the “seen” ones showed prefrontal, premotor, and posterior parietal sources of N170 higher in amplitude with the sad cue stimuli and lower in amplitude with the neutral and happy cue stimuli. These results suggest that nonconscious and conscious processing of schematic emotional facial expressions shares a similar temporal evolution of cortical activity, and conscious processing induces an early enhancement of bilateral cortical activity for the schematic sad facial expressions (N170). Hum Brain Mapp, 2010. © 2010 Wiley‐Liss, Inc.
Music interferes with learning from television during infancy
Authors: Barr Rachel , Shuck Lauren , Salerno Katherine , Atkinson Emily , Linebarger Deborah L. 
Published: February 2010

AbstractInfants are frequently exposed to music during daily activities, including free play, and while viewing infant‐directed videotapes that contain instrumental music soundtracks. In Experiment 1, an instrumental music soundtrack was played during a live or televised demonstration to examine its effects on deferred imitation by 6‐, 12‐, and 18‐month‐old infants. Transfer of information was indexed via deferred imitation of the target actions following a 24‐h delay. For half the infants, the music context was also reinstated at the time of test. Performance by experimental groups was compared to that of a baseline control group that participated in the test session without prior exposure to the demonstration. Imitation performance was above baseline for the live groups but not for the video groups regardless of age or the music context at test. In Experiment 2, we added matched sound effects to the video demonstration and infants performed above baseline. We conclude that the music track creates additional cognitive load, disrupts selective attention to the target actions and inhibits transfer of learning from television of the imitation task. Music may impair an infant's ability to translate information from a two‐dimensional to three‐dimensional world even if the auditory context remains the same. Copyright © 2010 John Wiley & Sons, Ltd.
In vivo tumor suppression activity by T cell‐specific T‐bet restoration
Authors: Lee Kihyun , Min Hyun Jung , Jang Eun Jung , Hong Jeong‐Ho , Hwang Eun Sook 
Published: February 2010

AbstractT‐box‐containing protein expressed in T cells (T‐bet) is a master transcription factor for the development of interferon (IFN) γ‐producing T helper 1 (Th1) cells and also functions in other immune cells including natural killer (NK), cytotoxic T lymphocytes and dendritic cells. T‐bet‐deficient mice increased susceptibility to viral infection and tumor development due to the defective functions of immune cells. T‐bet is known to play a key role in NK‐mediated antimetastatic response; however, it remains to be characterized whether T‐bet is essential for in vivo tumor suppression mediated by T cells. Here, we have investigated in vivo tumor suppression effect of T‐bet‐restored T cells using T cell‐specific and inducible T‐bet transgenic mice generated in a T‐bet‐deficient background. T‐bet‐null mice increased susceptibility to tumor development, whereas induction of T cell‐specific T‐bet expression upon melanoma cell injection substantially suppressed tumor development by inducing IFNγ production in T cells and tumor cell apoptosis. Late induction of T‐bet expression in tumor‐bearing mice produced comparable amounts of IFNγ with control and significantly decreased tumor volume. In addition, increased melanoma lung metastasis in T‐bet‐deficient mice was strikingly inhibited by T‐bet restoration in T cells. Intravenous injection of activated Th1 cells, not T‐bet‐null Th1 cells, attenuated metastatic melanoma progression, in addition, restoration of T‐bet in T‐bet‐null Th1 cells certainly retrieved antimetastatic activity. These results suggest that T‐bet expression in T cells is crucial for the control of tumor development and antimetastatic activity.
The marine compound spongistatin 1 targets pancreatic tumor progression and metastasis
Authors: Rothmeier Andrea S. , Schneiders Uta M. , Wiedmann Romina M. , Ischenko Ivan , Bruns Christiane J. , Rudy Anita , Zahler Stefan , Vollmar Angelika M. 
Published: February 2010

AbstractTreatment of pancreatic cancer remains a major challenge and new anticancer drugs are urgently required. Our study presents the marine natural compound spongistatin 1 as a promising experimental drug. Spongistatin 1 was applied in an orthotopicin vivomodel of human pancreatic cancer. Spongistatin 1 significantly reduced tumor growth, which correlates with a strong apoptosis induction (DNA‐fragmentation) and long‐term effects on clonogenic survival of pancreatic tumor cells (L3.6pl)in vitro. In addition, the formation of metastasis was reduced in spongistatin 1‐treated mice, which is in line with a diminished MMP‐9 activity in tumor tissue determined by zymography. Based on the pronounced efficacy of spongistatin 1, the underlying mechanisms were studied in more detail.In vitroadhesion, as well as migration, and invasion assays showed spongistatin 1 to influence these critical steps in the metastatic cascade. Furthermore, spongistatin 1 induced anoikis in L3.6pl cells. Exposure to spongistatin 1 leads to phosphorylation, and thus inactivation of the antiapoptotic protein Bcl‐2 in pancreatic tumor cells. siRNA experiments silencing Bcl‐2 suggest a role of Bcl‐2 in anoikis and cell migration. Taken together, spongistatin 1 not only proved to be a potent experimental drug but also served as a chemical tool to examine the role of the antiapoptotic protein Bcl‐2 in pancreas carcinoma, thereby supporting the hypothesis of a link between apoptosis signaling and metastasis.
Estimating the attributable fraction for melanoma: A meta‐analysis of pigmentary characteristics and freckling
Authors: Olsen Catherine M. , Carroll Heidi J. , Whiteman David C. 
Published: February 2010

AbstractEpidemiologic research has demonstrated convincingly that certain pigmentary characteristics are associated with increased relative risks of melanoma; however there has been no comprehensive review to rank these characteristics in order of their importance on a population level. We conducted a systematic review of the literature and meta‐analysis to quantify the contribution of pigmentary characteristics to melanoma, estimated by the population‐attributable fraction (PAF). Eligible studies were those that permitted quantitative assessment of the association between histologically confirmed melanoma and hair colour, eye colour, skin phototype and presence of freckling; we identified 66 such studies using citation databases, followed by manual review of retrieved references. We calculated summary relative risks using weighted averages of the log RR, taking into account random effects, and used these to estimate the PAF. The pooled RRs for pigmentary characteristics were: 2.64 for red/red‐blond, 2.0 for blond and 1.46 for light brown hair colour (vs. dark); 1.57 for blue/blue‐grey and 1.51 for green/grey/hazel eye colour (vs. dark); 2.27, 1.99 and 1.35 for skin phototypes I, II and III respectively (vs. IV); and 1.99 for presence of freckling. The highest PAFs were observed for skin phototypes 1/II (0.27), presence of freckling (0.23), and blond hair colour (0.23). For eye colour, the PAF for blue/blue‐grey eye colour was higher than for green/grey/hazel eye colour (0.18 vs. 0.13). The PAF of melanoma associated with red hair colour was 0.10. These estimates of melanoma burden attributable to pigmentary characteristics provide a basis for designing prevention strategies for melanoma.
TNF-α mediates diabetes-enhanced chondrocyte apoptosis during fracture healing and stimulates chondrocyte apoptosis Through FOXO1
Authors: Kayal Rayyan A , Siqueira Michelle , Alblowi Jazia , McLean Jody , Krothapalli Nanarao , Faibish Dan , Einhorn Thomas A , Gerstenfeld Louis C , Graves Dana T 
Published: February 2010

Abstract
To gain insight into the effect of diabetes on fracture healing, experiments were carried out focusing on chondrocyte apoptosis during the transition from cartilage to bone. Type 1 diabetes was induced in mice by multiple low-dose streptozotocin injections, and simple transverse fractures of the tibia or femur was carried out. Large-scale transcriptional profiling and gene set enrichment analysis were performed to examine apoptotic pathways on total RNA isolated from fracture calluses on days 12, 16, and 22, a period of endochondral bone formation when cartilage is resorbed and chondrocyte numbers decrease. Tumor necrosis factor α (TNF-α) protein levels were assessed by ELISA and caspase-3 by bioactivity assay. The role of TNF was examined by treating mice with the TNF-specific inhibitor pegsunercept. In vitro studies investigated the proapoptotic transcription factor FOXO1 in regulating TNF-induced apoptosis of chondrogenic ATDC5 and C3H10T1/2 cells as representative of differentiated chondrocytes, which are important during endochondral ossification. mRNA profiling revealed an upregulation of gene sets related to apoptosis in the diabetic group on day 16 when cartilage resorption is active but not day 12 or day 22. This coincided with elevated TNF-α protein levels, chondrocyte apoptosis, enhanced caspase-3 activity, and increased FOXO1 nuclear translocation (p &lt; .05). Inhibition of TNF significantly reduced these parameters in the diabetic mice but not in normoglycemic control mice (p &lt; .05). Silencing FOXO1 using siRNA in vitro significantly reduced TNF-induced apoptosis and caspase activity in differentiated chondrocytes. The mRNA levels of the proapoptotic genes caspase-3, caspase-8, caspase-9, and TRAIL were significantly reduced with silencing of FOXO1 in chondrocytic cells. Inhibiting caspase-8 and caspase-9 significantly reduced TNF-induced apoptosis in chondrogenic cells. These results suggest that diabetes causes an upregulation of proapoptotic genes during the transition from cartilage to bone in fracture healing. Diabetes increased chondrocyte apoptosis through a mechanism that involved enhanced production of TNF-α, which stimulates chondrocyte apoptosis and upregulates mRNA levels of apoptotic genes through FOXO1 activation. © 2010 American Society for Bone and Mineral Research
Critical role for Y1 receptors in mesenchymal progenitor cell differentiation and osteoblast activity
Authors: Lee Nicola J , Doyle Kharen L , Sainsbury Amanda , Enriquez Ronaldo F , Hort Yvonne J , Riepler Sabrina J , Baldock Paul A , Herzog Herbert 
Published: February 2010

Abstract
The neuropeptide Y (NPY) system has been implicated in the regulation of bone homeostasis and osteoblast activity, but the mechanism behind this is unclear. Here we show that Y1 receptor signaling is directly involved in the differentiation of mesenchymal progenitor cells isolated from bone tissue, as well as the activity of mature osteoblasts. Importantly, the mRNA levels of two key osteogenic transcription factors, runx2 and osterix, as well as the adipogenic transcription factor PPAR-γ, were increased in long bones of Y1−/− mice compared with wild-type mice. In vitro, bone marrow stromal cells (BMSCs) isolated from Y1−/− mice formed a greater number of mineralized nodules under osteogenic conditions and a greater number of adipocytes under adipogenic conditions than controls. In addition, both the number and size of fibroblast colony-forming units formed in vitro by purified osteoprogenitor cells were increased in the absence of the Y1 receptors, suggestive of enhanced proliferation and osteogenesis. Furthermore, the ability of two specific populations of mesenchymal progenitor cells isolated from bone tissue, an immature mesenchymal stem cell population and a more committed osteoprogenitor cell population, to differentiate into osteoblasts and adipocytes in vitro was enhanced in the absence of Y1 receptor signaling. Finally, Y1 receptor deletion also enhanced the mineral-producing ability of mature osteoblasts, as shown by increased in vitro mineralization by BMSCs isolated from osteoblast-specific Y1−/− mice. Together these data demonstrate that the NPY system, via the Y1 receptor, directly inhibits the differentiation of mesenchymal progenitor cells as well as the activity of mature osteoblasts, constituting a likely mechanism for the high-bone-mass phenotype evident in Y1−/− mice. © 2010 American Society for Bone and Mineral Research
Replication of previous genome-wide association studies of bone mineral density in premenopausal American women
Authors: Ichikawa Shoji , Koller Daniel L , Padgett Leah R , Lai Dongbing , Hui Siu L , Peacock Munro , Foroud Tatiana , Econs Michael J 
Published: February 2010

Abstract
Bone mineral density (BMD) achieved during young adulthood (peak BMD) is one of the major determinants of osteoporotic fracture in later life. Genetic variants associated with BMD have been identified by three recent genome-wide association studies. The most significant single-nucleotide polymorphisms (SNPs) from these studies were genotyped to test whether they were associated with peak BMD in premenopausal American women. Femoral neck and lumbar spine BMD were determined by dual-energy X-ray absorptiometry in two groups of premenopausal women: 1524 white women and 512 black women. In premenopausal white women, two SNPs in the C6orf97/ESR1 region were significantly associated with BMD (p &lt; 4.8 × 10−4), with suggestive evidence for CTNNBL1 and LRP5 (p &lt; .01). Evidence of association with one of the two SNPs in the C6orf97/ESR1 region also was observed in premenopausal black women. Furthermore, SNPs in SP7 and a chromosome 4 intergenic region showed suggestive association with BMD in black women. Detailed analyses of additional SNPs in the C6orf97/ESR1 region revealed multiple genomic blocks independently associated with femoral neck and lumbar spine BMD. Findings in the three published genome-wide association studies were replicated in independent samples of premenopausal American women, suggesting that genetic variants in these genes or regions contribute to peak BMD in healthy women in various populations. © 2010 American Society for Bone and Mineral Research
Cross-sectional evidence of suppressed bone mineral accrual among female adolescent runners
Authors: Barrack Michelle T , Rauh Mitchell J , Nichols Jeanne F 
Published: February 2010

Abstract
We aimed to evaluate patterns of bone mineral accrual among a cross-sectional sample of female adolescent runners and girls participating in a nonendurance running sport. One-hundred and eighty-three interscholastic competitive female athletes (age 16.0 ± 0.1 years), 93 endurance runners and 90 nonrunners, completed a menstrual and sports history questionnaire, had their height and weight measured, and underwent a dual-energy X-ray absorptiometry scan for the measurements of body composition and bone mass. For the majority of analyses, the girls were separated into four groups according to their age (13 to 14 years, 15 years, 16 years, and 17 to 18 years). Runners' height, weight, body mass index (BMI), percent body fat, lean tissue mass, number of menstrual cycles in the past year, and months of participation in a non-lean-build/variable-impact-loading sport were significantly lower than mean values for nonrunners. Although bone mass rose at all sites in the nonrunners between the ages of 13 to 14 years and 17 to 18 years, no such increase was noted in the runners. Runners compared with nonrunners exhibited significantly lower body weight and height-adjusted total body and lumbar spine bone mineral content (BMC) values and lower bone mineral density (BMD) Z-score values among the older (16 years and/or 17 to 18 years) but not younger (13 to 14 years and/or 15 years) age groups. These findings suggest that the runners, in contrast to the nonrunners, exhibited a suppressed bone mineral accrual pattern, which supports the notion that female adolescent endurance runners may be at risk for inadequate bone mass gains and thus a low peak BMD. © 2010 American Society for Bone and Mineral Research
Archaeological skeletons support a northwest European origin for Paget's disease of bone
Authors: Mays Simon 
Published: February 2010

Abstract
The strong genetic component in the etiology of Paget's disease of bone (PDB), together with marked geographic variation in its prevalence, with high frequencies in British populations, has led some to suggest that the disease originated in Britain and spread around the world in recent times by the migration and admixture of British populations. This study aims to investigate this hypothesis by studying the world geographic distribution of PDB cases identified in ancient skeletons excavated from archaeological sites. The methodology is a review of PDB cases described in the literature. There were 109 cases that met modern diagnostic criteria. All came from Western Europe, 94% from England. These data support the hypothesis that PDB originated in this geographic region. © 2010 American Society for Bone and Mineral Research
Evaluation of comparative effect of pre‐ and posttreatment of selenium on mercury‐induced oxidative stress, histological alterations, and metallothionein mRNA expression in rats
Authors: Agarwal Rakhi , Raisuddin S. , Tewari Shikha , Goel Sudhir K. , Raizada R. B. , Behari Jai Raj 
Published: February 2010

AbstractTo evaluate the effect of pre‐ or posttreatment of selenium (6 μmol/kg b.w., single intraperitoneal injection) in mercury intoxication, rats were exposed to mercury (12 μmol/kg b.w., single intraperitoneal injection). Exposure to mercury resulted in induced oxidative stress in liver, kidney, and brain tissues. Marked changes in serum biochemical parameters together with alterations in histopathology and an induction in metallothionein‐I and metallothionein‐II mRNA expression in the liver and kidney were observed. Pretreatment with selenium to mercury‐exposed animals had protective effect on the liver, whereas posttreatment had partial protection on restoration of altered oxidative stress parameters. In the kidney, pretreatment with selenium showed partial protection on restoration of altered biochemical parameters, whereas no protection was observed in posttreatment. The pretreatment with selenium resulted in restoration of mercury‐induced metallothionein‐I and metallothionein‐II mRNA expression, which was completely restored in the liver whereas partial restoration was observed in the kidney. Posttreatment with selenium resulted in further induction in metallothionein‐I and metallothionein‐II mRNA expression in the liver and kidney. In the brain, selenium showed partial protection on alerted biochemical parameters. Results indicate that pretreatment with selenium is beneficial in comparison to posttreatment in mercury intoxication. Thus, dietary intake of selenium within safe limit may, therefore, enable us in combating any foreseen effects due to mercury exposure. © 2010 Wiley Periodicals, Inc. J Biochem Mol Toxicol 24:123–135, 2010; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20320