bluuebunny/crossref_metadata_2025_split huggingface dataset:
Single subject task‐related BOLD signal artifact in a real‐time fMRI feedback paradigm
Authors: Zhang Xiaochu , Ross Thomas J. , Jo Salmeron Betty , Yang Shaolin , Yang Yihong , Stein Elliot A. 
Published: May 2010

AbstractReal‐time functional magnetic resonance imaging (rtfMRI) has been proposed as a method of providing feedback to develop a participant's ability to control his or her own neuronal activity. However, this BOLD signal is vulnerable to contamination from nonneuronal sources that can also be shaped by the feedback provided. Here we illustrate an artifact found while training participants to control signal from an ROI in the insula. As the artifact was directly behind the eye and the experiment used an echo‐planar imaging (EPI) sequence with phase encoding direction that included the orbits and the insula in the same line, we hypothesized that the artifact was due to eye motion. We demonstrate a reduced training effect when eyeball signal is regressed out of the data and reproduce the artifact with block design voluntary eye movement. Further, using independent components analysis on historical data, we find the artifact is common in BOLD data, but typically not task‐correlated, even in tasks where one might expect differing amounts of eye movement in the active task blocks. The artifact, thus, does not significantly impact group results in typical fMRI experiments. Finally, we demonstrate this particular artifact can be avoided in rtfMRI experiments by ensuring that the phase encoding direction does not project any eye movement related artifact onto the ROI being used for feedback training. Our findings underscore the importance of taking great care in designing rtfMRI feedback procedures to avoid contamination with nonneuronal sources of BOLD signal alteration. Hum Brain Mapp, 2011. © 2010 Wiley‐Liss, Inc.
Disorder‐specific dysfunctions in patients with attention‐deficit/hyperactivity disorder compared to patients with obsessive‐compulsive disorder during interference inhibition and attention allocation
Authors: Rubia Katya , Cubillo Ana , Woolley James , Brammer Michael J. , Smith Anna 
Published: May 2010

AbstractBackground: Abnormalities in inhibitory control and underlying fronto‐striatal networks is common to both attention deficit hyperactivity disorder (ADHD) and obsessive‐compulsive‐disorder (OCD). The aim of this study was to investigate disorder‐specific abnormalities in neural networks mediating interference inhibition and selective attention. Method: Event‐related functional magnetic resonance imaging (fMRI) was used to compare brain activation of boys with ADHD (18), with OCD (10), and healthy boys during (20) during a Simon task that measures interference inhibition and controls for and therefore comeasures attention allocation. Results: During interference inhibition, both patient groups shared mesial frontal dysfunction compared to controls. Disorder‐specific dysfunctions were observed in OCD patients in dorsolateral prefrontal cortex during the oddball condition and in ADHD patients in inferior parietal lobe during interference inhibition and in caudate and posterior cingulate during the simpler oddball condition. The decreased activation in caudate and cingulate in ADHD was furthermore negatively correlated with ADHD symptoms and positively with OCD behavioral traits. Conclusions: The study shows that ADHD and OCD patients have shared but also disorder‐specific brain dysfunctions during interference inhibition and attention allocation. Both disorders shared dysfunction in mesial frontal cortex. Disorder‐specific dysfunctions, however, were observed in dorsolateral prefrontal cortex in OCD patients and in caudate, cingulate, and parietal brain regions in ADHD patients. The disorder‐specific dissociation of striato‐cingulate activation that was increased in OCD compared to ADHD patients, was furthermore inversely related to the symptomatology of the two disorders, and may potentially reflect differential dopamine modulation of striatal brain regions. Hum Brain Mapp, 2011. © 2010 Wiley‐Liss, Inc.
Embodied visual perception of distorted finger postures
Authors: Schürmann Martin , Hlushchuk Yevhen , Hari Riitta 
Published: May 2010

AbstractBodily abnormalities in other persons often evoke an uneasy feeling, even disgust. Here, we studied the brain basis of such perceptual salience by presenting static pictures of distorted hand postures to healthy subjects during functional magnetic resonance imaging. Cortical activation sensitive to distorted (vs. natural) finger postures was found—with right‐hemispheric dominance—in the primary motor cortex, postcentral somatosensory areas, amygdala, and insula, and bilaterally in the putamen. This activation pattern suggests that the instantaneous “gut feelings” during the observation of bodily distortions in others are related to embodied percepts that also involve affect‐related brain areas. Hum Brain Mapp, 2011. © 2010 Wiley‐Liss, Inc.
Reduced somatosensory activations in swallowing with age
Authors: Malandraki Georgia A. , Perlman Adrienne L. , Karampinos Dimitrios C. , Sutton Bradley P. 
Published: May 2010

AbstractUnderstanding the neural functional organization of swallowing in healthy elders is essential in diagnosing and treating older adults with swallowing difficulties. The primary aims of this investigation were to identify the neural activation sites of different components of deglutition in healthy elders using functional Magnetic Resonance Imaging (fMRI) and to investigate age differences in the neural control of swallowing. Ten young (age range 19–25 years of age) and nine older (age range 66–77 years of age) right‐handed healthy individuals were scanned in a 3‐Tesla MRI scanner. Subjects were visually cued for both a “Swallow” task and for component/control tasks (“Prepare to swallow,” “Tap your tongue,” and “Clear your throat”). Behavioral interleaved gradient (BIG) methodology was used to address movement related artifacts. Between‐group comparisons revealed statistically stronger activations in the primary somatosensory cortex of young adults during the motor tasks examined. Both groups showed activations in the major motor areas involved in the initiation and execution of movement; however, areas involved in sensory processing, sensorimotor integration and/or motor coordination and control, showed reduced or limited activity in the elderly. Potential implications of these findings for clinical practice are discussed. Hum Brain Mapp, 2011. © 2010 Wiley‐Liss, Inc.
Evaluating the impact of community‐based health interventions: evidence from Brazil's Family Health Program
Authors: Rocha Romero , Soares Rodrigo R. 
Published: May 2010

AbstractThis paper analyzes the direct and indirect impacts of Brazil's Family Health Program, using municipality level mortality data from the Brazilian Ministry of Health, and individual level data from the Brazilian household survey. We estimate the effects of the program on mortality and on household behavior related to child labor and schooling, employment of adults, and fertility. We find consistent effects of the program on reductions in mortality throughout the age distribution, but mainly at earlier ages. Municipalities in the poorest regions of the country benefit particularly from the program. For these regions, implementation of the program is also robustly associated with increased labor supply of adults, reduced fertility, and increased school enrollment. Evidence suggests that the Family Health Program is a highly cost‐effective tool for improving health in poor areas. Copyright © 2010 John Wiley & Sons, Ltd.
Novel Mechanism of Antibodies to Hepatitis B Virus in Blocking Viral Particle Release from Cells†
Authors: Neumann Avidan U. , Phillips Sandra , Levine Idit , Ijaz Samreen , Dahari Harel , Eren Rachel , Dagan Shlomo , Naoumov Nikolai V. 
Published: May 2010

Abstract

Antibodies are thought to exert antiviral activities by blocking viral entry into cells and/or accelerating viral clearance from circulation. In particular, antibodies to hepatitis B virus (HBV) surface antigen (HBsAg) confer protection, by binding circulating virus. Here, we used mathematical modeling to gain information about viral dynamics during and after single or multiple infusions of a combination of two human monoclonal anti-HBs (HepeX-B) antibodies in patients with chronic hepatitis B. The antibody HBV-17 recognizes a conformational epitope, whereas antibody HBV-19 recognizes a linear epitope on the HBsAg. The kinetic profiles of the decline of serum HBV DNA and HBsAg revealed partial blocking of virion release from infected cells as a new antiviral mechanism, in addition to acceleration of HBV clearance from the circulation. We then replicated this approach

in vitro

, using cells secreting HBsAg, and compared the prediction of the mathematical modeling obtained from the

in vivo

kinetics.

In vitro

, HepeX-B treatment of HBsAg-producing cells showed cellular uptake of antibodies, resulting in intracellular accumulation of viral particles. Blocking of HBsAg secretion also continued after HepeX-B was removed from the cell culture supernatants.

Conclusion:

These results identify a novel antiviral mechanism of antibodies to HBsAg (anti-HBs) involving prolonged blocking of the HBV and HBsAg subviral particles release from infected cells. This may have implications in designing new therapies for patients with chronic HBV infection and may also be relevant in other viral infections.
Beneficial Paracrine Effects of Cannabinoid Receptor 2 on Liver Injury and Regeneration†
Authors: Teixeira-Clerc Fatima , Belot Marie-Pierre , Manin Sylvie , Deveaux Vanessa , Cadoudal Thomas , Chobert Marie-Noele , Louvet Alexandre , Zimmer Andreas , Tordjmann Thierry , Mallat Ariane , Lotersztajn Sophie 
Published: May 2010

Abstract

The cannabinoid receptor 2 (CB2) plays a pleiotropic role in innate immunity and is a crucial mediator of liver disease. In this study, we investigated the impact of CB2 receptors on the regenerative process associated with liver injury. Following acute hepatitis induced by carbon tetrachloride (CCl4), CB2 was induced in the nonparenchymal cell fraction and remained undetectable in hepatocytes. Administration of CCl4 to CB2−/− mice accelerated liver injury, as shown by increased alanine/aspartate aminotransferase levels and hepatocyte apoptosis, and delayed liver regeneration, as reflected by a retarded induction of hepatocyte proliferating cell nuclear antigen expression; proliferating cell nuclear antigen induction was also delayed in CB2−/− mice undergoing partial hepatectomy. Conversely, following treatment with the CB2 agonist JWH-133, CCl4-treated WT mice displayed reduced liver injury and accelerated liver regeneration. The CCl4-treated CB2−/− mice showed a decrease in inducible nitric oxide synthase and tumor necrosis factor-α expression, and administration of the nitric oxide donor moldomine (SIN-1) to these animals reduced hepatocyte apoptosis, without affecting liver regeneration. Impaired liver regeneration was consecutive to an interleukin-6 (IL-6)-mediated decrease in matrix metalloproteinase 2 (MMP-2) activity. Indeed, CCl4-treated CB2−/− mice displayed lower levels of hepatic IL-6 messenger RNA and increased MMP-2 activity. Administration of IL-6 to these mice decreased MMP-2 activity and improved liver regeneration, without affecting hepatocyte apoptosis. Accordingly, administration of the MMP inhibitor CTTHWGFTLC to CCl4-treated CB2−/− mice improved liver regeneration. Finally,

in vitro

studies demonstrated that incubation of hepatic myofibroblasts with JWH-133 increased tumor necrosis factor-α and IL-6 and decreased MMP-2 expressions.

Conclusion:

CB2 receptors reduce liver injury and promote liver regeneration following acute insult, via distinct paracrine mechanisms involving hepatic myofibroblasts. These results suggest that CB2 agonists display potent hepatoprotective properties, in addition to their antifibrogenic effects.
HB‐EGF orchestrates the complex signals involved in triple‐negative and trastuzumab‐resistant breast cancer
Authors: Yotsumoto Fusanori , Oki Eiji , Tokunaga Eriko , Maehara Yoshihiko , Kuroki Masahide , Miyamoto Shingo 
Published: May 2010

AbstractA number of therapeutic strategies targeting epidermal growth factor receptor (EGFR) have not always led to success in the present state of breast cancer therapy. Notably, there is currently no way to treat trastuzumab‐resistant and triple‐negative breast cancer (TNBC). Here, we found that heparin‐binding epidermal growth factor‐like growth factor (HB‐EGF), a member of the EGFR ligands, was predominantly expressed in breast cancer and that treatment with crossreacting material 197 (CRM197), a specific inhibitor of HB‐EGF, blocked ERK as well as AKT activation via complexes of EGFR and unknown growth factor receptors in TNBC or through complexes of EGFR and human epidermal growth factor receptor‐2 in trastuzumab‐resistant breast cancer, caused significant cell apoptosis and inhibited tumor growth. Accordingly, we can provide a novel concept that a certain EGFR ligand is recognized as a rational target against breast cancer. In addition, it is plausible that CRM197 could be an effective anticancer agent for molecularly targeted therapies.
Immortalization of oral keratinocytes by functional inactivation of the p53 and pRb pathways
Authors: Smeets Serge J. , van der Plas Marlon , Schaaij‐Visser Tieneke B.M. , van Veen Eva A.M. , van Meerloo Johan , Braakhuis Boudewijn J.M. , Steenbergen Renske D.M. , Brakenhoff Ruud H. 
Published: May 2010

AbstractA subgroup of head and neck squamous cell carcinomas (HNSCCs) contains high‐risk human papillomavirus‐type 16 (HPV16). The viral E6 and E7 oncoproteins inactivate the p53 and pRb proteins, respectively. We examined the causative effect of HPV16 E6 and E7 expression on the immortalization of normal oral keratinocytes (OKCs) and compared the resulting phenotype with alternative ways of p53‐ and pRb‐pathway abrogation frequently found in HNSCCs without HPV. Primary OKCs were conditionally immortalized with temperature‐sensitive SV40 large T‐antigen and human telomerase, allowing these cells to return to their senescent primary state after temperature shift. HPV16 E6 and E7 were introduced to overcome senescence, determined with population doubling (PD) as read‐out. For comparison, we downregulated p53 and p16 by short hairpin RNA genes and expressed mutant p53R(175)H and cyclinD1. Expression of HPV16 E6 caused an extended life span similar to expression of mutant p53R(175)H or p53 knockdown. Expression of mutant p53R(175)H seemed to cause additional activation of the hypoxia and WNT signaling pathways. HPV16 E7 expression had no direct effect on lifespan, similar to p16 knockdown or cyclinD1 expression. In combination with HPV16 E6 or other functional inactivations of p53, abrogation of the pRb‐pathway by either HPV16 E7 or other manipulations caused an immortal phenotype. Our data show the causative role of HPV16 E6/E7 in early squamous carcinogenesis. Activity of each gene could be mimicked by other genetic events frequently found in HNSCC without HPV. This data provides the experimental proof of causal association of HPV in HNSCC carcinogenesis and further support the crucial role of the p53‐ and pRb‐pathways.
Does a helicase activity help mismatch repair in eukaryotes?
Authors: Song Limin , Yuan Fenghua , Zhang Yanbin 
Published: May 2010

AbstractMismatch repair (MMR) corrects innate DNA replication infidelities. Many components of eukaryotic MMR have been identified, the molecular mechanism of MMR has been largely demonstrated, and furthermore the nick‐directed MMR reactions have been reconstituted with purified human proteins in vitro. However, some fundamental questions still remain to be answered. One such question is whether a DNA helicase activity is required for MMR in eukaryotes. This short review presents an overview of the interactions between eukaryotic DNA helicases and MMR factors, and suggests a possible mechanism for how DNA helicases may be involved in repair of DNA mismatches. © 2010 IUBMB IUBMB Life 62(7): 548–553, 2010
Validation of the intact rat weanling uterotrophic assay with notes on the formulation and analysis of the positive control chemical in vehicle
Authors: Tyl Rochelle W. , Marr Melissa C. , Brown Sherri S. , Dolbow Emily A. , Myers Christina B. 
Published: May 2010

AbstractThe intact female weanling version in the Organization for Economic Cooperation and Development (OECD) uterotrophic assay Test Guideline (TG) 440 is proposed as an alternative to the adult ovariectomized female version, because it does not involve surgical intervention (vs the ovariectomized version) and detects direct/indirect‐acting estrogenic/anti‐estrogenic substances (vs the ovariectomized version which detects only direct‐acting estrogenic/anti‐estrogenic substances binding to the estrogen receptor). This validation study followed OECD TG 440, with six female weanling rats (postnatal day 21) per dose group and six treatment groups. Females were weighed and dosed once daily by oral gavage for three consecutive days, with one of six doses of 17α‐ethinyl estradiol in corn oil at 5 ml kg−1at 0 and 0.1–10 µg kg−1per day. On postnatal day 24, the juvenile females were euthanized by CO2asphyxiation, weighed, livers weighed and uteri weighed wet and blotted. The presence or absence of vaginal patency was recorded. Absolute and relative (to terminal body weight) uterine wet and blotted weights and uterine luminal fluid weights were significantly increased at 3.0 and 10.0 (bothP< 0.01) µg kg−1per day, and increased to ∼140% of control values at 1.0 µg kg−1per day (not statistically significantly).In vivobody weights, weight changes, feed consumption, liver weights and terminal body weights were unaffected. Vaginal patency was not acquired in any female at any dose, although vaginal puckering was observed in one female at 10.0 µg kg−1per day. Therefore, this intact weanling uterotrophic assay is validated in our laboratory for use under US and European endocrine toxicity testing programs/legislation. Copyright © 2010 John Wiley & Sons, Ltd.
The use of FTIR spectroscopy to assess quantitative changes in the biochemical composition of microalgae
Authors: Wagner Heiko , Liu Zhixin , Langner Uwe , Stehfest Katja , Wilhelm Christian 
Published: May 2010

AbstractA mid‐infrared spectroscopic method was developed for the simultaneous and quantitative determination of total protein, carbohydrate and lipid contents of microalgal cells. Based on a chemometric approach, measured FTIR (Fourier transform infrared) spectra from algal cells were reconstructed by a partial least square algorithm, using the spectra of the reference substances to determine their relative contribution to the overall cell spectrum. From this specific absorption, absolute macromolecular cell composition [pg cell–1] can be calculated using calibration curves, which have been validated by independent biochemical methods. The future potential of this method for photosynthesis research is shown by its application to follow time‐resolved changes in the cellular composition of microalgae during an illumination period of several hours. We show how the macromolecular composition can be investigated by FTIR spectroscopy methods. This can substantially increase the efficiency of screening processes like bioreactor monitoring and may be beneficial in metabolic engineering of algal cells. (© 2010 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim)
Chloride intracellular channel 5 modulates adipocyte accumulation in skeletal muscle by inhibiting preadipocyte differentiation
Authors: Li Feng‐Na , Yin Jing‐Dong , Ni Jian‐Jun , Liu Ling , Zhang Hai‐Yan , Du Min 
Published: May 2010

AbstractIntramuscular fat, the total lipid deposited within skeletal muscle, has been regarded as a potential factor responsible for meat quality in animal production and insulin resistance in humans. The objective of present study was to identify candidate genes which control intramuscular fat accumulation through using animal models. PIC pigs (lean‐type) and Rongchang pigs (obese‐type) were used. By scanning the mRNA samples of longissimus dorsi muscle with Affymetrix Gene‐Chip microarray technology, sus scrofa chloride intracellular channel 5 (CLIC5) was isolated, and its mRNA abundance and protein expression level were reversely related with the intramuscular fat content of pigs. Furthermore, over‐expression of CLIC5 dramatically increased the proliferation of 3T3‐L1 preadipocytes, while inhibited adipocytic differentiation accompanied by the down‐regulation of c/EBPα, LPL, and PPARγ protein. Our results suggest that CLIC5 might be a crucial regulator of adipose accumulation in skeletal muscle of pigs. J. Cell. Biochem. 110: 1013–1021, 2010. © 2010 Wiley‐Liss, Inc.
Regulation of AP‐1 Activity in Glucose‐Stimulated Insulinoma Cells
Authors: Müller Isabelle , Endo Takeshi , Thiel Gerald 
Published: May 2010

AbstractThe transcriptional activity of AP‐1 has been analyzed in glucose‐stimulated INS‐1 insulinoma cells using a chromosomally embedded AP‐1‐responsive reporter gene. We show that AP‐1 activity was significantly elevated in glucose‐treated INS‐1 cells. Preincubation of the cells with nifedipine or expression of the Ca2+ binding protein parvalbumin in the cytoplasm of INS‐1 cells reduced AP‐1 activity. Thus, activation of L‐type Ca2+ channels and an elevated cytoplasmic Ca2+ concentration are crucial to connecting glucose stimulation with enhanced AP‐1 activity. Expression of dominant negative forms of A‐Raf, MKK4 or MKK6 and pharmacological inhibition of MEK and p38 revealed that extracellular signal‐regulated protein kinase, p38 and c‐Jun NH2‐terminal protein kinase participate in the upregulation of AP‐1 activity. Expression of dominant‐negative mutants of c‐Jun and Elk‐1 reduced AP‐1 transcriptional activity in INS‐1 cells indicating that c‐Jun and ternary complex factors are involved in the regulation of AP‐1 activity in glucose‐stimulated insulinoma cells. J. Cell. Biochem. 110: 1481–1494, 2010. © 2010 Wiley‐Liss, Inc.
Sodium 5,6‐benzylidene‐L‐ascorbate induces oxidative stress, autophagy, and growth arrest in human colon cancer HT‐29 cells
Authors: Cheung F.W.K. , Che C.T. , Sakagami H. , Kochi M. , Liu W.K. 
Published: May 2010

AbstractOur previous studies have demonstrated the oxidative stress properties of sodium ascorbate (SAA) and its benzaldehyde derivative (SBA) on cancer cell lines, but the molecular mechanisms mediating their cytotoxicity remain unclear. In this study, we treated human colon cancer HT‐29 cells with SAA and SBA, and found a significant exposure time‐dependent increase of cytotoxicity in both treatments, with a higher cytotoxicity for 24 h with SAA (IC50 = 5 mM) than SBA (IC50 = 10 mM). A short‐term treatment of cells with 10 mM SAA for 2 h revealed a destabilization of the lysosomes and subsequent induction of cell death, whereas 10 mM SBA triggered a remarkable production of reactive oxidative species, phosphorylation of survival kinase AKT, expression of cyclin kinase‐dependent inhibitor p21, and induction of transient growth arrest. The crucial role of p21 mediating this cytotoxicity was confirmed by isogenic derivatives of the human colon carcinoma HCT116 cell lines (p21+/+ and p21−/−), and immunoprecipitation studies with p21 antibody. The SAA cytotoxicity was blocked by co‐incubation with catalase, whereas the SBA cytotoxicity and its subsequent growth arrest were abolished by N‐acetyl‐L‐cysteine (NAC), but was not affected by PI3K phosphorylation inhibitor LY294002, or catalase, suggesting two separated oxidative stress pathways were mediated by these two ascorbates. In addition, neither active caspase 3 nor apoptotic bodies but autophagic vacuoles associated with increased LC3‐II were found in SBA‐treated HT‐29 cells; implicating that SBA induced AKT phosphorylation‐autophagy and p21‐growth arrest in colon cancer HT‐29 cells through an NAC‐inhibitable oxidative stress pathway. J. Cell. Biochem. 111: 412–424, 2010. © 2010 Wiley‐Liss, Inc.