bluuebunny/crossref_metadata_2025_split huggingface dataset:
Assessing Body Composition With DXA and Bioimpedance: Effects of Obesity, Physical Activity, and Age
Authors: Völgyi Eszter , Tylavsky Frances A. , Lyytikäinen Arja , Suominen Harri , Alén Markku , Cheng Sulin 
Published: January 2008

Objective: This study evaluated to what extent dual‐energy X‐ray absorptiometry (DXA) and two types of bioimpedance analysis (BIA) yield similar results for body fat mass (FM) in men and women with different levels of obesity and physical activity (PA).Methods and Procedures: The study population consisted of 37–81‐year‐old Finnish people (82 men and 86 women). FM% was estimated using DXA (GE Lunar Prodigy) and two BIA devices (InBody (720) and Tanita BC 418 MA). Subjects were divided into normal, overweight, and obese groups on the basis of clinical cutoff points of BMI, and into low PA (LPA) and high PA (HPA) groups. Agreement between the devices was calculated by using the Bland–Altman analysis.Results: Compared to DXA, both BIA devices provided on average 2–6% lower values for FM% in normal BMI men, in women in all BMI categories, and in both genders in both HPA and LPA groups. In obese men, the differences were smaller. The two BIA devices provided similar means for groups. Differences between the two BIA devices with increasing FM% were a result of the InBody (720) not including age in their algorithm for estimating body composition.Discussion: BIA methods provided systematically lower values for FM than DXA. However, the differences depend on gender and body weight status pointing out the importance of considering these when identifying people with excess FM.
SIK2 Can be Activated by Deprivation of Nutrition and It Inhibits Expression of Lipogenic Genes in Adipocytes
Authors: Du Jing , Chen Qiu , Takemori Hiroshi , Xu Haiyan 
Published: January 2008

Objective: Determine the biological function of SIK2 in 3T3‐L1 adipocytes.Methods and Procedures: 3T3‐L1 adipocytes were treated with serum‐free, serum/glucose‐free, or complete Dulbecco's Modified Eagle's Medium (DMEM) for 15 min, or 10 µg/ml oligomycin in serum‐free DMEM for 15 min, or different doses of 5‐amino‐4‐imidazolecarboxamide (AICAR) for different periods of time in serum‐free DMEM. After treatment, SIK2 kinase activity was measured by examining phosphorylation of a peptide substrate. SIK2 was overexpressed and knocked down in 3T3‐L1 CAR adipocytes using adenovirus‐mediated gene transfer for the assessment of lipogenic gene expression and triglyceride content. Electroporation was used to transiently transfect 3T3‐L1 adipocytes with fatty acid synthase (FAS) promoter‐driven luciferase construct to evaluate the effect of SIK2 on FAS transcription.Results: In 3T3‐L1 adipocytes, SIK2 can be activated by nutrient deprivation, inhibition of ATP synthesis, and treatment of AICAR. Overexpression of SIK2 repressed the expression of lipogenic genes, including FAS, acetyl CoA carboxylase 2 (ACC2), and stearoyl CoA desaturase 1 (SCD1), and reduced triglyceride content. Reduction of endogenous SIK2 expression through RNA interference increased the expression of FAS, ACC2, and SCD1. This effect is independent of adenosine monophosphate–activated protein kinase (AMPK) since neither phosphorylation state nor protein level of AMPKα1 and AMPKα2 was affected by SIK2 overexpression. SIK2 inhibits the expression of FAS‐promoter driven luciferase reporter gene, and this effect can be reversed by overexpression of constitutively active sterol regulatory element binding protein–1 (SREBP‐1). Furthermore, SIK2 also reduces the nuclear translocation of endogenous SREBP‐1.Discussion: Our results support a role for SIK2 in adipocyte energy metabolism. SIK2 may function similarly to AMPK for turning off lipogenesis in low‐energy state.
Differential expression and regulation of myristoylated alanine‐rich C kinase substrate (MARCKS) in the hippocampus of C57/BL6J and DBA/2J mice
Authors: McNamara Robert K. , Vasquez Patricia A. , Mathe Aleksander A. , Lenox Robert H. 
Published: February 2008

AbstractThe myristoylated alanine‐rich C kinase substrate (MARCKS) is a major protein kinase C (PKC) substrate in brain that binds the inner surface of the plasma membrane, calmodulin, and cross‐links filamentous actin, all in a PKC phosphorylation‐reversible manner. MARCKS has been implicated in hippocampal‐dependent learning and long‐term potentiation (LTP). Previous studies have shown DBA/2 mice to exhibit poor spatial/contextual learning, impaired hippocampal LTP, and hippocampal mossy fiber hypoplasia, as well as reduced hippocampal PKC activity and expression relative to C57BL/6 mice. In the present study, we assessed the expression (mRNA and protein) and subcellular distribution (membrane and cytolsol) of MARCKS in the hippocampus and frontal cortex of C57BL/6 and DBA/2 mice using quantitative western blotting. In the hippocampus, total MARCKS mRNA and protein levels in C57BL/6J mice were significantly lower (∼45%) compared with DBA/2J mice, and MARCKS protein was observed predominantly in the cytosolic fraction. MARCKS expression in frontal cortex did not differ significantly between strains. To examine the dynamic regulation of MARCKS subcellular distribution, mice from each strain were subjected to 60 min restraint stress and MARCKS subcellular distribution was determined 24 h later. Restraint stress resulted in a significant reduction in membrane MARCKS expression in C57BL/6J hippocampus but not in the DBA/2J hippocampus despite similar stress‐induced increases in serum corticosterone. Restraint stress did not affect cytosolic or total MARCKS levels in either strain. Similarly, restraint stress (30 min) in rats also induced a significant reduction in membrane MARCKS, but not total or cytosolic MARCKS, in the hippocampus but not in frontal cortex. In rats, chronic lithium treatment prior to stress exposure reduced hippocampal MARCKS expression but did not affect the stress‐induced reduction in membrane MARCKS. Collectively these data demonstrate higher resting levels of MARCKS in the hippocampus of DBA/2J mice compared to C57BL/6J mice, and that acute stress leads to a long‐term reduction in membrane MARCKS expression in C57BL/6J mice and rats but not in DBA/2J mice. These strain differences in hippocampal MARCKS expression and subcellular translocation following stress may contribute to the differences in behaviors requiring hippocampal plasticity observed between these strains.
3D numerical simulations of energy transport in the stochastic boundary of TEXTOR-DED with a finite difference method
Authors: Zagórski R. , Jakubowski M.W. , Kalentev A. , Schmitz O. , Schneider R. , Stepniewski W. 
Published: January 2008

The effect of magnetic field line ergodization that eliminates magnetic surfaces (either by a resonant magnetic perturbation like in TEXTOR-DED or by intrinsic plasma effects like in W7-X) imposes the need for plasma transport models being able to describe this properly. To handle the ergodicity the concept of local magnetic coordinates allowing a correct discretization of the transport equations with minimized numerical errors is used. For the simulation of plasma transport in perturbed volume, a numerical method based on the finite difference concept has been developed, using a custom-tailored unstructured grid in local magnetic coordinates. This grid is generated by field line tracing to guarantee complete separation of the large parallel transport along B and that perpendicular to B and the ergodicity of the magnetic field does not limit applicability of the method in contrast to the methods based on finite volume ansatz. Perpendicular and parallel fluxes can be effectively separated in our approach and treated independently in the numerical method which has been implemented in the FINDIF code.The finite difference code FINDIF is used to investigate the energy transport in the complex 3D TEXTOR-DED tokamak geometry, where the plasma structures and transport are closely related to the structure of the magnetic field lines. Numerical grids have been prepared in order to simulate 12/4 and 6/2 modes of the DED operation, respectively. In particular, the question, what is the role of long and short magnetic field lines in the heat transfer from the core plasma to divertor surface, is addressed. Simulation results are compared with experimentally determined temperature profiles and heat fluxes at the target.
The Transcription Factor MtSERF1 of the ERF Subfamily Identified by Transcriptional Profiling Is Required for Somatic Embryogenesis Induced by Auxin Plus Cytokinin in Medicago truncatula
Authors: Mantiri Feky R. , Kurdyukov Sergey , Lohar Dasharath P. , Sharopova Natalya , Saeed Nasir A. , Wang Xin-Ding , VandenBosch Kathryn A. , Rose Ray J. 
Published: January 2008

Abstract
Transcriptional profiling of embryogenic callus produced from Medicago truncatula mesophyll protoplasts indicated up-regulation of ethylene biosynthesis and ethylene response genes. Using inhibitors of ethylene biosynthesis and perception, it was shown that ethylene was necessary for somatic embryogenesis (SE) in this model legume. We chose several genes involved in ethylene biosynthesis and response for subsequent molecular analyses. One of these genes is a gene encoding a transcription factor that belongs to the AP2/ERF superfamily and ERF subfamily of transcription factors. We demonstrate that this gene, designated M. truncatula SOMATIC EMBRYO RELATED FACTOR1 (MtSERF1), is induced by ethylene and is expressed in embryogenic calli. MtSERF1 is strongly expressed in the globular somatic embryo and there is high expression in a small group of cells in the developing shoot meristem of the heart-stage embryo. RNA interference knockdown of this gene causes strong inhibition of SE. We also provide evidence that MtSERF1 is expressed in zygotic embryos. MtSERF1 appears to be essential for SE and may enable a connection between stress and development.
Identification and verification of QTL associated with growth traits in two genetic backgrounds of Barramundi (Lates calcarifer)
Authors: Wang C. M. , Lo L. C. , Feng F. , Zhu Z. Y. , Yue G. H. 
Published: January 2008

SummaryQuantitative trait loci (QTL) affecting growth traits have previously been mapped in linkage groups (LG) 2, 3 and 23 of Barramundi (Lates carcalifer), but these QTL have not been verified in different genetic backgrounds and environments. Here, we report the identification and verification of QTL for growth traits on LG2, 3, 10 and 23 in F1 families constructed using brooders from the Singapore Marine Aquaculture Center (MAC) and from wild stocks collected in Thailand (THAI). The previously detected QTL for body weight and length linked to marker Lca371 on LG2 were confirmed in both the MAC and THAI families, whereas other QTL previously mapped to LG3 and 23 were only detected in one of the two families. QTL for body weight and length were identified in the MAC family, but not in the THAI family, in a region where the insulin‐like growth factor 2 (IGF2) and tyrosine hydroxylase 1 (TH1) genes are located on LG10. Significant epistatic interactions were identified between markers Lca287 on LG2 and IGF2 on LG10 for growth trait QTL in the MAC family, but not in the THAI family. Effects of the IGF2, TH1 and parvalbumin 1 candidate genes were family‐specific. Our results indicate that some but not all QTL are family‐specific in Barramundi.
The effect of a c.‐8G>T polymorphism on the expression of cytochrome b5A and boar taint in pigs
Authors: Peacock J. , Lou Y. , Lundström K. , Squires E. J. 
Published: January 2008

SummaryThe level of cytochrome b5A (CYB5A) in pig testis is correlated with boar taint from androstenone and an AF016388:c.‐8G>T polymorphism in CYB5A has been linked with low androstenone levels in the fat of pigs. In this study, we developed a polymerase chain reaction‐based assay to genotype 1242 boars from eight lines for the c.‐8G>T SNP. The c.‐8T allele was found in all eight lines at a frequency ranging from 1.8% to 20.3% with an overall frequency of 8.6%. Significant deviations from Hardy–Weinberg equilibrium were found in the Hampshire, Landrace and Yorkshire breeds. The homozygous mutant c.‐8TT occurred infrequently and was not found in some lines, but was consistently associated with low androstenone levels in fat. Both CYB5A mRNA and CYB5A protein levels were decreased in the c.‐8TT genotype in a subset of Yorkshire boars, suggesting that low levels of CYB5A protein in the c.‐8TT mutant were not due to inefficient translation of CYB5A mRNA. There were significant but modest marker effects on fat androstenone levels in Landrace, Yorkshire and a Large White/Duroc cross and fat skatole in Duroc and Sire Line breeds. There was no effect of CYB5A genotype on bulbourethral gland length, suggesting that this SNP will not affect reproductive traits. We conclude that the c.‐8G>T SNP in the CYB5A gene has a significant but modest effect on boar taint in male pigs and could be useful in some breeds as part of a panel of SNP markers in a marker‐assisted selection programme to produce low boar taint pigs.
Linkage mapping of the locus responsible for forelimb‐girdle muscular anomaly of Japanese black cattle on bovine chromosome 26
Authors: Masoudi A. A. , Uchida K. , Yokouchi K. , Ohwada K. , Abbasi A. R. , Tsuji T. , Watanabe T. , Hirano T. , Sugimoto Y. , Kunieda T. 
Published: January 2008

SummaryForelimb‐girdle muscular anomaly is an autosomal recessive disorder of Japanese black cattle characterized by tremor, astasia and abnormal shape of the shoulders. Pathological examination of affected animals reveals hypoplasia of forelimb‐girdle muscles with reduced diameter of muscle fibres. To identify the gene responsible for this disorder, we performed linkage mapping of the disorder locus using an inbred pedigree including a great‐grand sire, a grand sire, a sire and 26 affected calves obtained from a herd of Japanese black cattle. Two hundred and fifty‐eight microsatellite markers distributed across the genome were genotyped across the pedigree. Four markers on the middle region of bovine chromosome 26 showed significant linkage with the disorder locus. Haplotype analysis using additional markers in this region refined the critical region of the disorder locus to a 3.5‐Mb interval on BTA26 betweenBM4505andMOK2602. Comparative mapping data revealed several potential candidate genes for the disorder, includingNRAP,PDZD8andHSPA12A, which are associated with muscular function.
‘Real‐life’ reduction in cholesterol with statins, 1993 to 2002
Authors: Murphy Michael J. , Wei Li , Watson Alexander D. , MacDonald Thomas M. 
Published: January 2008

WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT • Statins reduce cholesterol concentrations and cardiovascular events in randomized clinical trials.• Much less is known about their impact in the setting of normal care. WHAT THIS STUDY ADDS • This is the first study to assess the effectiveness of lipid‐lowering treatment in the general population.• We have also estimated the resultant impact on major vascular events.• We have examined the actual and potential impact of lipid‐lowering treatment.AIMSTo evaluate the impact of lipid‐lowering treatment on cholesterol concentrations in the setting of normal care.METHODSThis was a retrospective review of all cholesterol measurements made in Tayside, Scotland, between 1993 and 2002, linked to dispensed prescribing data for lipid‐lowering drugs. It was conducted in the setting of normal care and included all patients who underwent cholesterol measurement. The main outcome measure was cholesterol concentration.RESULTSA total of 401 489 cholesterol measurements were made on 128 240 patients over the study period. Measurements were categorized as treated and untreated according to whether patients were exposed to lipid‐lowering treatment at the time the total cholesterol concentration was measured. Those categorized as untreated fell by 0.86 mmol l−1 (13.9%) and those categorized as treated by 1.45 mmol l−1 (23.5%). The difference between baseline and follow‐up cholesterol concentrations in intention‐to‐treat patients was 1.53 mmol l−1 (24%) in 2002. In the same year, mean cholesterol concentration was 4.71 mmol l−1 (a fall of 1.65 mmol l−1 or 25.9%) in patients judged to be taking their lipid‐lowering medication, compared with 5.20 mmol l−1 (a fall of 1.16 mmol l−1 or 18.2%) in those judged not to be taking treatment. Cholesterol fell by 0.38 mmol l−1 (6.3%) in a cohort of never treated patients (n = 33 679) between 1993 and 2002.CONCLUSIONSThe impact of lipid‐lowering drugs on population cholesterol concentrations in the setting of normal care was significant and comparable with the cholesterol reductions seen in the setting of major statin trials, despite a significant proportion of the population receiving low dose treatment. In those subjects judged to be taking their medication, the benefits achieved were substantial. The impact of nondrug factors is indicated by the fall in population cholesterol seen in the absence of lipid‐lowering treatment.
CD49d expression is an independent predictor of overall survival in patients with chronic lymphocytic leukaemia: a prognostic parameter with therapeutic potential
Authors: Shanafelt Tait D. , Geyer Susan M. , Bone Nancy D. , Tschumper Renee C. , Witzig Tom E. , Nowakowski Greg S. , Zent Clive S. , Call Tim G. , LaPlant Betsy , Dewald Gordon W. , Jelinek Diane F. , Kay Neil E. 
Published: February 2008

Summary In vitro studies have demonstrated that surface expression of CD49d on chronic lymphocytic leukaemia (CLL) B cells facilitates leukaemic cell–stromal interactions by binding to fibronectin. This interaction reduces both spontaneous and drug‐induced apoptosis. The present study measured CD49d expression by flow cytometry in a cohort of untreated CLL patients previously accrued to a prospective observational study and evaluated the relationship with overall survival (OS). Among the 158 CLL patients tested, the percentage of leukaemic B cells expressing CD49d ranged from 0 to 100%. When all risk factors were treated as continuous variables, CD49d expression showed moderate correlation with expression of ZAP‐70 (r = 0·54; P < 0·0001) and CD38 (r = 0·58; P < 0·0001) but not %IGHV mutation. As a continuous variable, CD49d expression strongly correlated with OS (P < 0·0001). Recursive partitioning analysis suggested the 45% threshold of CD49d expression best predicted OS. Multivariate analysis, controlling for disease stage, ZAP‐70, IGHV status and fluorescent in situ hybridization defects identified CD49d as an independent predictor of OS and was a better predictor of clinical outcome than ZAP‐70, IGHV, or cytogenetics. This observational cohort study suggests that CLL B‐cell expression of CD49d is an easily measurable and independent predictor of OS and CD49d expression in CLL. Importantly, anti‐CD49d antibodies are already approved for treatment of other human diseases. Clinical testing of anti‐CD49d therapy in CLL appears warranted.
The Y606C RET mutation causes a receptor gain of function
Authors: Ercolino T. , Lombardi A. , Becherini L. , Piscitelli E. , Cantini G. , Gaglianò M. S. , Serio M. , Luconi M. , Mannelli M. 
Published: January 2008

SummaryContext  Medullary thyroid carcinoma (MTC) is the most common feature of multiple endocrine neoplasia type 2A (MEN2A) and occurs in almost all patients affected by germline RET mutations.Objective  We identified and characterized an activating germline RET point mutation (G>A substitution leading to the heterozygous missense mutation Y606C in exon 10), in a 58‐year‐old female affected by MTC.Design  The RET/Y606C and RET/C620Y, obtained by site‐directed mutagenesis, as well as the RET/wild‐type (wt) were cloned in an expression vector and transiently transfected in NIH3T3 fibroblasts. In vitro cell model was used to evaluate the effect of Y606C mutation on the RET downstream signalling pathways through Western blot analysis.Results  We found that the cysteine insertion, due to the Y606C mutation, results in increased receptor dimerization, which is accompanied by an increased tyrosine phosphorylation of the Y905 residue in the RET/Y606C, demonstrating that the Y606C mutation is associated with constitutive receptor activation. As RET activation results in an intracellular signalling cascade involving extracellular signal‐regulated kinases (ERKs), we investigated ERK activity in our transfected cells. Results demonstrated a significant increase in ERK2 phosphorylation in the RET/Y606C vs. the RET/wt and RET/C620Y transfected cells, suggesting an up‐regulation of RET signalling.Conclusions  All these findings demonstrate that the Y606C mutation is associated with RET constitutive activation and thus has to be considered of pathogenetic relevance in the development of MTC.
Visfatin, low‐grade inflammation and body mass index (BMI)
Authors: Samara Anastasia , Pfister Michèle , Marie Berangère , Visvikis‐Siest Sophie 
Published: January 2008

SummaryObjective  Visfatin is an adipokine with revealing roles in inflammatory mechanisms but its implication in inflammation related to excessive adiposity/obesity is not studied yet. Our aim was to investigate the relations of visfatin with inflammation markers and body mass index (BMI) in the peripheral blood mononuclear cells (PBMCs), a type of cells closely related to inflammatory mechanisms.Design  Cross‐sectional study, quantification of visfatin, TNF‐α, IL‐6 mRNA in PBMCs.Patients  Eighty‐three supposed healthy individuals from the STANISLAS cohort, belonging in three BMI categories: BMI < 25 kg/m2 (lean), 25 kg/m2 ≤ BMI < 30 kg/m2 (overweight) or BMI ≥ 30 kg/m2 (obese).Measurements  We measured visfatin gene expression (by real‐time quantitative PCR), in relation to gene expression of the pro‐inflammatory cytokines TNF‐α, IL‐6 in PBMCs and to anthropometric parameters (weight, BMI, waist : hip ratio), blood pressure, lipid profile, glucose and inflammatory markers (C‐reactive protein, lymphocyte count).Results  Visfatin expression in PBMCs was significantly associated with BMI in a negative way (r = –0·21, P = 0·05). Global anova analysis test for lean and over‐weight/obese individuals showed a negative significant association between visfatin expression in PBMCs and BMI both for men and women (P = 0·05 and P = 0·01, respectively) and these associations remained significant after separating subjects in three groups (lean, overweight, obese) for men and women (P = 0·02 and P = 0·05, respectively). Correlation analysis between levels of expression of visfatin and TNF‐α showed a significant positive linear association (r2 = 0·27, P < 0·0001).Conclusion  These findings reveal a probable new role of visfatin in inflammation reflected in PBMCs, in the context of obesity.