bluuebunny/crossref_metadata_2025_split huggingface dataset:
Identification and association of the single nucleotide polymorphisms in calpain3 (CAPN3) gene with carcass traits in chickens
Authors: Zhang Zeng-Rong , Liu Yi-Ping , Yao Yong-Gang , Jiang Xiao-Song , Du Hua-Rui , Zhu Qing 
Published: March 2009

Abstract

Background
The aim of this study is to screen single nucleotide polymorphisms (SNP) of chicken Calpain3 (CAPN3) gene and to analyze the potential association between CAPN3 gene polymorphisms and carcass traits in chickens. We screened CAPN3 single nucleotide polymorphisms (SNP) in 307 meat-type quality chicken from 5 commercial pure lines (S01, S02, S03, S05, and D99) and 4 native breeds from Guangdong Province (Huiyang Huxu chicken and Qingyuan Ma chicken) and Sichuan Province (Caoke chicken and Shandi Black-bone chicken), China.

Results
Two SNPs (11818T>A and 12814T>G) were detected by single strand conformation polymorphism (SSCP) method and were verified by DNA sequencing. Association analysis showed that the 12814T>G genotypes were significantly associated with body weight (BW), carcass weight (CW), breast muscle weight (BMW), and leg muscle weight (LMW). Haplotypes constructed on the two SNPs (H1, TG; H2, TT; H3, AG; and H4, AT) were associated with BW, CW (P < 0.05), eviscerated percentage (EP), semi-eviscerated percentage (SEP), breast muscle percentage (BMP), and leg muscle percentage (LMP) (P < 0.01). Diplotype H1H2 was dominant for BW, CW, and LMP, and H2H2 was dominant for EP, SEP, and BMP.

Conclusion
We speculated that the CAPN3 gene was a major gene affecting chicken muscle growth and carcass traits or it was linked with the major gene(s). Diplotypes H1H2 and H2H2 might be advantageous for carcass traits.
Identification of candidate genes for human pituitary development by EST analysis
Authors: Ma Yueyun , Qi Xiaofei , Du Jianjun , Song Shaojun , Feng Dongyun , Qi Jia , Zhu Zhidong , Zhang Xin , Xiao Huasheng , Han Zeguang , Hao Xiaoke 
Published: March 2009

Abstract

Background
The pituitary is a critical neuroendocrine gland that is comprised of five hormone-secreting cell types, which develops in tandem during the embryonic stage. Some essential genes have been identified in the early stage of adenohypophysial development, such as PITX1, FGF8, BMP4 and SF-1. However, it is likely that a large number of signaling molecules and transcription factors essential for determination and terminal differentiation of specific cell types remain unidentified. High-throughput methods such as microarray analysis may facilitate the measurement of gene transcriptional levels, while Expressed sequence tag (EST) sequencing, an efficient method for gene discovery and expression level analysis, may no-redundantly help to understand gene expression patterns during development.

Results
A total of 9,271 ESTs were generated from both fetal and adult pituitaries, and assigned into 961 gene/EST clusters in fetal and 2,747 in adult pituitary by homology analysis. The transcription maps derived from these data indicated that developmentally relevant genes, such as Sox4, ST13 and ZNF185, were dominant in the cDNA library of fetal pituitary, while hormones and hormone-associated genes, such as GH1, GH2, POMC, LHβ, CHGA and CHGB, were dominant in adult pituitary. Furthermore, by using RT-PCR and in situ hybridization, Sox4 was found to be one of the main transcription factors expressed in fetal pituitary for the first time. It was expressed at least at E12.5, but decreased after E17.5. In addition, 40 novel ESTs were identified specifically in this tissue.

Conclusion
The significant changes in gene expression in both tissues suggest a distinct and dynamic switch between embryonic and adult pituitaries. All these data along with Sox4 should be confirmed to further understand the community of multiple signaling pathways that act as a cooperative network that regulates maturation of the pituitary. It was also suggested that EST sequencing is an efficient means of gene discovery.
Functional and genetic analysis in type 2 diabetes of Liver X receptor alleles – a cohort study
Authors: Dahlman Ingrid , Nilsson Maria , Gu Harvest F , Lecoeur Cecile , Efendic Suad , Östenson Claes G , Brismar Kerstin , Gustafsson Jan-Åke , Froguel Philippe , Vaxillaire Martine , Dahlman-Wright Karin , Steffensen Knut R 
Published: March 2009

Abstract

Background
Liver X receptor alpha (LXRA) and beta (LXRB) regulate glucose and lipid homeostasis in model systems but their importance in human physiology is poorly understood. This project aimed to determine whether common genetic variations in LXRA and LXRB associate with type 2 diabetes (T2D) and quantitative measures of glucose homeostasis, and, if so, reveal the underlying mechanisms.

Methods
Eight common single nucleotide polymorphisms in LXRA and LXRB were analyzed for association with T2D in one French cohort (N = 988 cases and 941 controls), and for association with quantitative measures reflecting glucose homeostasis in two non-diabetic population-based samples comprising N = 697 and N = 1344 adults. Investigated quantitative phenotypes included fasting plasma glucose, serum insulin, and HOMAIR as measure of overall insulin resistance. An oral glucose tolerance test was performed in N = 1344 of adults. The two alleles of the proximal LXRB promoter, differing only at the SNP rs17373080, were cloned into reporter vectors and transiently transfected, whereupon allele-specific luciferase activity was measured. rs17373080 overlapped, according to in silico analysis, with a binding site for Nuclear factor 1 (NF1). Promoter alleles were tested for interaction with NF1 using direct DNA binding and transactivation assays.

Results
Genotypes at two LXRB promoter SNPs, rs35463555 and rs17373080, associated nominally with T2D (P values 0.047 and 0.026). No LXRA or LXRB SNP associated with quantitative measures reflecting glucose homeostasis. The rs17373080 C allele displayed higher basal transcription activity (P value < 0.05). The DNA-mobility shift assay indicated that oligonucleotides corresponding to either rs17373080 allele bound NF1 transcription factors in whole cell extracts to the same extent. Different NF1 family members showed different capacity to transactivate the LXRB gene promoter, but there was no difference between promoter alleles in NF1 induced transactivation activity.

Conclusion
Variations in the LXRB gene promoter may be part of the aetiology of T2D. However, the association between LXRB rs35463555 and rs17373080, and T2D are preliminary and needs to be investigated in additional larger cohorts. Common genetic variation in LXRA is unlikely to affect the risk of developing T2D or quantitative phenotypes related to glucose homeostasis.
Enhanced antitumor efficacy of cisplatin in combination with HemoHIM in tumor-bearing mice
Authors: Park Hae-Ran , Ju Eun-Jin , Jo Sung-Kee , Jung Uhee , Kim Sung-Ho , Yee Sung-Tae 
Published: March 2009

AbstractBackgroundAlthough cisplatin is one of the most effective chemotherapeutic agents, cisplatin alone does not achieve a satisfactory therapeutic outcome. Also cisplatin accumulation shows toxicity to normal tissues. In this study, we examined the possibility of HemoHIM both to enhance anticancer effect with cisplatin and to reduce the side effects of cisplatin in melanoma-bearing mice.MethodsHemoHIM was prepared by adding the ethanol-insoluble fraction to the total water extract of a mixture of 3 edible herbs, Angelica Radix, Cnidium Rhizoma and Paeonia Radix. Anticancer effects of HemoHIM with cisplatin were evaluated in melanoma-bearing mice. We used a Cr51-release assay to measure the activity of NK/Tc cell and ELISA to evaluate the production of cytokines.ResultsIn melanoma-bearing mice, cisplatin (4 mg/kg B.W.) reduced the size and weight of the solid tumors, and HemoHIM supplementation with cisplatin enhanced the decrease of both the tumor size (p < 0.1) and weight (p < 0.1). HemoHIM itself did not inhibit melanoma cell growthin vitro, and did not disturb the effects of cisplatinin vitro. However HemoHIM administration enhanced both NK cell and Tc cell activity in mice. Interestingly, HemoHIM increased the proportion of NK cells in the spleen. In melanoma-bearing mice treated with cisplatin, HemoHIM administration also increased the activity of NK cells and Tc cells and the IL-2 and IFN-γ secretion from splenocytes, which seemed to contribute to the enhanced efficacy of cisplatin by HemoHIM. Also, HemoHIM reduced nephrotoxicity as seen by tubular cell of kidney destruction.ConclusionHemoHIM may be a beneficial supplement during cisplatin chemotherapy for enhancing the anti-tumor efficacy and reducing the toxicity of cisplatin.
Chromato-panning: an efficient new mode of identifying suitable ligands from phage display libraries
Authors: Noppe Wim , Plieva Fatima , Galaev Igor Yu , Pottel Hans , Deckmyn Hans , Mattiasson Bo 
Published: March 2009

Abstract

Background
Phage Display technology is a well established technique for high throughput screening of affinity ligands. Here we describe a new compact chromato-panning procedure for selection of suitable binders from a phage peptide display library.

Results
Both phages and E. coli cells pass non-hindered through the interconnected pores of macroporous gel, so called cryogel. After coupling a ligand to a monolithic cryogel column, the phage library was applied on the column and non-bound phages were washed out. The selection of strong phage-binders was achieved already after the first panning cycle due to the efficient separation of phage-binders from phage-non-binders in chromatographic mode rather than in batch mode as in traditional biopanning procedures. E. coli cells were applied on the column for infection with the specifically bound phages.

Conclusion
Chromato-panning allows combining several steps of the panning procedure resulting in 4–8 fold decrease of total time needed for phage selection.
The C-terminal sequence of the large hepatitis delta antigen is variable but retains the ability to bind clathrin
Authors: Wang Yu-Cheng , Huang Chi-Ruei , Chao Mei , Lo Szecheng J 
Published: March 2009

Abstract

Background
Hepatitis delta virus (HDV) is a defected RNA virus and requires its encoded large antigen (LDAg) to interact with helper viral proteins (HBsAgs) during assembly. Recently, a study demonstrated a direct binding of the LDAg C-terminus from genotype I HDV to the clathrin heavy chain (CHC), which suggests that this interaction might facilitate HDV assembly. If LDAg binding to clathrin is essential to HDV life cycle, a clathrin box sequence at the C-terminus of LDAg should be conserved across all HDV. However, the C-terminal sequence of LDAg is variable among 43 HDV isolates.

Results
Based on the presence and location of clathrin box at the C-terminus of LDAg from 43 isolates of HDV, we classified them into three groups. Group 1 (13 isolates) and 2 (26 isolates) contain a clathrin box located at amino acids 199–203 and 206–210, respectively, as found in genotype I and genotype II. Group 3 (4 isolates) contains no clathrin box as found in genotype III. CHC binding by three different LDAg (genotype I to III) was then tested by in vivo and in vitro experiments. Transfection of plasmids which encode fusion proteins of EGFP and full-length of LDAg from three genotypes into HuH-7 cells, a human heptoma cell line, was performed. GFP-pull down assays showed that a full-length of CHC was co-precipitated by EGFP-LDI, -LDII and -LDIII but not by EGFP. Further in vitro studies showed a full-length or fragment (amino acids 1 to 107) of CHC can be pull-down by 13-amino-acid peptides of LDAg from three genotypes of HDV.

Conclusion
Both in vivo and in vitro studies showed that CHC can bind to various sequences of LDAg from the three major genotypes of HDV. We therefore suggest that the clathrin-LDAg interaction is essential to the HDV life-cycle and that sequences binding to clathrin are evolutionarily selected, but nonetheless show the diversity across different HDV genotypes.
Stereotactic radiosurgery for glioblastoma: retrospective analysis
Authors: Biswas Tithi , Okunieff Paul , Schell Michael C , Smudzin Therese , Pilcher Webster H , Bakos Robert S , Vates G Edward , Walter Kevin A , Wensel Andrew , Korones David N , Milano Michael T 
Published: March 2009

Abstract

Purpose
This retrospective study was done to better understand the conditions for which stereotactic radiosurgery (SRS) for glioblastoma may be efficacious.

Methods
Between 2000 and 2007, 33 patients with a pathological diagnosis of glioblastoma received SRS with the Novalis® Shaped Beam Radiosurgery system. Eighteen patients (54%) underwent salvage SRS for recurrence while 15 (45%) patients received upfront SRS following standard fractionated RT for newly diagnosed glioblastoma.

Results
There were no RTOG grade >2 acute side effects. The median survival after SRS was 6.7 months (range 1.4 – 74.7). There was no significant difference in overall survival (from the time of initial diagnosis) with respect to the timing of SRS (p = 0.2). There was significantly better progression free survival in patients treated with SRS as consolidation versus at the time of recurrence (p = 0.04). The majority of patients failed within or at the margin of the SRS treatment volume (21/26 evaluable for recurrence).

Conclusion
SRS is well tolerated in the treatment of glioblastoma. As there was no difference in survival whether SRS is delivered upfront or at recurrence, the treatment for each patient should be individualized. Future studies are needed to identify patients most likely to respond to SRS.
Elevated P75NTR expression causes death of engrailed-deficient midbrain dopaminergic neurons by Erk1/2 suppression
Authors: Alavian Kambiz N , Sgadò Paola , Alberi Lavinia , Subramaniam Srinivasa , Simon Horst H 
Published: March 2009

AbstractBackgroundThe homeodomain transcription factorsEngrailed-1andEngrailed-2are required for the survival of mesencephalic dopaminergic (mesDA) neurons in a cell-autonomous and gene-dose-dependent manner. Homozygote mutant mice, deficient of both genes (En1-/-;En2-/-), die at birth and exhibit a loss of all mesDA neurons by mid-gestation. In heterozygote animals (En1+/-;En2-/-), which are viable and fertile, postnatal maintenance of the nigrostriatal dopaminergic system is afflicted, leading to a progressive degeneration specific to this subpopulation and Parkinson's disease-like molecular and behavioral deficits.ResultsIn this work, we show that the dose ofEngrailedis inversely correlated to the expression level of the pan-neurotrophin receptor geneP75NTR(Ngfr). Loss of mesDA neurons in theEngrailed-null mutant embryos is caused by elevated expression of this neurotrophin receptor: Unusually, in this case, the cell death signal of P75NTRis mediated by suppression of Erk1/2 (extracellular-signal-regulated kinase 1/2) activity. The reduction in expression ofEngrailed, possibly related to the higher levels of P75NTR, also decreases mitochondrial stability. In particular, the dose ofEngraileddetermines the sensitivity to cell death induced by the classic Parkinson-model toxin MPTP and to inhibition of the anti-apoptotic members of the Bcl-2 family of proteins.ConclusionOur study links the survival function of theEngrailedgenes in developing mesDA neurons to the regulation ofP75NTRand the sensitivity of these neurons to mitochondrial insult. The similarities to the disease etiology in combination with the nigral phenotype ofEn1+/-;En2-/-mice suggests that haplotype variations in theEngrailedgenes and/orP75NTRthat alter their expression levels could, in part, determine susceptibility to Parkinson's disease.
Loop-mediated isothermal amplification applied to filarial parasites detection in the mosquito vectors: Dirofilaria immitis as a study model
Authors: Aonuma Hiroka , Yoshimura Aya , Perera Namal , Shinzawa Naoaki , Bando Hironori , Oshiro Sugao , Nelson Bryce , Fukumoto Shinya , Kanuka Hirotaka 
Published: March 2009

Abstract

Background
Despite recent advances in our understanding of the basic biology behind transmission of zoonotic infectious diseases harbored by arthropod vectors these diseases remain threatening public health concerns. For effective control of vector and treatment, precise sampling indicating the prevalence of such diseases is essential. With an aim to develop a quick and simple method to survey zoonotic pathogen-transmitting vectors, LAMP (loop-mediated isothermal amplification) was applied to the detection of filarial parasites using a filarial parasite-transmitting experimental model that included one of the mosquito vectors, Aedes aegypti, and the canine heartworm, Dirofilaria immitis.

Results
LAMP reactions amplifying the cytochrome oxidase subunit I gene demonstrated high sensitivity when a single purified D. immitis microfilaria was detected. Importantly, the robustness of the LAMP reaction was revealed upon identification of an infected mosquito carrying just a single parasite, a level easily overlooked using conventional microscopic analysis. Furthermore, successful detection of D. immitis in wild-caught mosquitoes demonstrated its applicability to field surveys.

Conclusion
Due to its simplicity, sensitivity, and reliability, LAMP is suggested as an appropriate diagnostic method for routine diagnosis of mosquito vectors carrying filarial parasites. This method can be applied to the survey of not only canine filariasis but also lymphatic filariasis, another major public health problem. Therefore, this method offers great promise as a useful diagnostic method for filarial parasite detection in endemic filariasis regions.
Maturation of gastric electrical activity, gastric emptying and intestinal permeability in preterm newborns during the first month of life
Authors: Riezzo Giuseppe , Indrio Flavia , Raimondi Francesco , Montagna Osvaldo , Salvia Gennaro , Massimo Bisceglia , Polimeno Lorenzo , Cavallo Luciano , Francavilla Ruggiero 
Published: March 2009

Abstract

Introduction
Immaturity of motility, intestinal epithelial barrier function and absorptive capacity may play a role in the pathophysiology of intestinal diseases in preterms. We determined the gastric electrical activity and emptying, and intestinal permeability, in preterm newborns to verify if a maturation pattern exists in preterm newborns during the first month of life.

Patients and methods
Eighteen preterm newborns (median 34 wks, range 2 wks) completed the study. They underwent the recording of gastric electrical activity by means of cutaneous electrogastrography, the ultrasound examination of gastric emptying, and the lactulose-to-mannitol ratio from permeability-absorption test on days 3, 7, 15, and 30 after birth.

Results
Gastric electrical activity and emptying showed only slight changes between day 3 and day 7. On the contrary, an evident maturation in permeability, expressed as L/Mratio, was evident over time (Friedman Repeated Measures Analysis, p = 0.004).

Conclusion
In preterm healthy newborns of 34 weeks gestational age, electrical and motor activity are completely developed at birth whilst the intestinal epithelial barrier clearly improves during the first week of life.
Randomized Phase II Study of Gefitinib Compared With Placebo in Chemotherapy-Naive Patients With Advanced Non–Small-Cell Lung Cancer and Poor Performance Status
Authors: Goss Glenwood , Ferry David , Wierzbicki Rafal , Laurie Scott A. , Thompson Joyce , Biesma Bonne , Hirsch Fred R. , Varella-Garcia Marileila , Duffield Emma , Ataman Ozlem U. , Zarenda Marc , Armour Alison A. 
Published: March 2009

Purpose To compare gefitinib with placebo in chemotherapy naïve patients with advanced non–small-cell lung cancer (NSCLC) and poor performance status. Patients and Methods NSCLC patients (chemotherapy naïve, WHO performance status 2 or 3; unfit for chemotherapy; stage IIIB/IV) were randomly assigned to gefitinib (250 mg/d) plus best supportive care (BSC; n = 100) or placebo plus BSC (n = 101). The primary end point was progression-free survival (PFS). Secondary end points included overall survival (OS), objective response rate (ORR), quality of life (QOL), pulmonary symptom improvement (PSI), and safety. Correlation of gefitinib efficacy with EGFR gene copy number (fluorescent in situ hybridization [FISH]) was explored. Results Hazard ratios (HRs; gefitinib:placebo) were 0.82 (95% CI, 0.60 to 1.12; P = .217) for PFS and 0.84 (95% CI, 0.62 to 1.15; P = .272) for OS. As expected for this patient population, OS for both arms was poor, at about 3 months. ORRs were 6.0% (gefitinib) and 1.0% (placebo). QOL and PSI rates were 21.1% and 28.3% (gefitinib) and 20.0% and 28.3% (placebo), respectively. In EGFR FISH-positive patients (n = 32), HRs were 0.29 (95% CI, 0.11 to 0.73) for PFS and 0.44 (95% CI, 0.17 to 1.12) for OS. No unexpected adverse events occurred. Conclusion There was no statistically significant difference in PFS, OS, and ORRs after treatment with gefitinib or placebo, in the overall population; improvements in QOL and symptoms were similar in both groups. Tolerability profile of gefitinib was consistent with previous studies. PFS was statistically significantly improved for gefitinib-treated patients with EGFR FISH-positive tumors.
Microsatellite Instability, Mismatch Repair Deficiency, and BRAF Mutation in Treatment-Resistant Germ Cell Tumors
Authors: Honecker Friedemann , Wermann Hendrik , Mayer Frank , Gillis Ad J.M. , Stoop Hans , van Gurp Ruud J.L.M. , Oechsle Karin , Steyerberg Ewout , Hartmann Jörg Th. , Dinjens Winand N.M. , Oosterhuis J. Wolter , Bokemeyer Carsten , Looijenga Leendert H.J. 
Published: March 2009

Purpose Mismatch repair (MMR) deficiency and microsatellite instability (MSI) are associated with cisplatin resistance in human germ cell tumors (GCTs). BRAF mutation (V600E) is found in MSI colorectal cancers. The role of RAS/RAF pathway mutations in GCT treatment response is unknown. Patients and Methods Two patient cohorts were investigated: 100 control GCTs (50 seminomas and 50 nonseminomas) and 35 cisplatin-based chemotherapy-resistant GCTs. MMR proteins were analyzed by immunohistochemistry, and eight microsatellite loci were examined for MSI. Tumors were assessed for specific BRAF and KRAS mutations. Results Resistant tumors showed a higher incidence of MSI than controls: 26% versus 0% in two or more loci (P < .0001). All resistant tumors were wild-type KRAS, and two controls (2%) contained a KRAS mutation. There was a significantly higher incidence of BRAF V600E mutation in resistant tumors compared with controls: 26% versus 1% (P < .0001). BRAF mutations were highly correlated with MSI (P = .006), and MSI and mutated BRAF were correlated with weak or absent staining for hMLH1 (P = .017 and P = .008). Low or absent staining of hMLH1 was correlated with promoter hypermethylation (P < .001). Tumors lacking expression of hMLH1 or MSH6 were significantly more frequent in resistant GCTs than in controls (P = .001 and 0.0036, respectively). Within the subgroup of resistant tumors, patients with MSI showed a trend to longer progression-free survival (P = .068). Conclusion We report for the first time a correlation between a gene mutation—BRAF V600E—and cisplatin resistance in nonseminomatous GCTs. Furthermore, a correlation between MMR deficiency, MSI, and treatment failure is confirmed.