Association between IDH3B Genotypes and Economic Traits in a Crossbred F2 Population between Duroc and Jeju Native Black Pigs
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제주재래흑돼지와 듀록의 교배 Keywords:
Isocitrate dehydrogenase
Longissimus dorsi
Isocitrate dehydrogenase 1 gene mutations are found in most World Health Organization grade II and III gliomas and secondary glioblastomas. Isocitrate dehydrogenase 1 mutations are known to have prognostic value in high-grade gliomas. However, their prognostic significance in low-grade gliomas remains controversial. We determined the predictive and prognostic value of isocitrate dehydrogenase 1 status in low-grade gliomas. The association of isocitrate dehydrogenase 1 status with clinicopathological and genetic factors was also evaluated. Clinical information and genetic data including isocitrate dehydrogenase 1 mutation, O 6-methylguanine DNA methyltransferase promoter methylation, 1p/19q chromosome loss, and TP53 mutation of 417 low-grade gliomas were collected from the Chinese Glioma Genome Atlas database. Kaplan–Meier and Cox proportional hazards regression analyses were performed to evaluate the prognostic effect of clinical characteristics and molecular biomarkers. Isocitrate dehydrogenase 1 mutation was identified as an independent prognostic factor for overall, but not progression-free, survival. Notably, isocitrate dehydrogenase 1 mutation was found to be a significant prognostic factor in patients with oligodendrogliomas, but not in patients with astrocytomas. Furthermore, O 6-methylguanine DNA methyltransferase promoter methylation (p = 0.017) and TP53 mutation (p < 0.001), but not 1p/19q loss (p = 0.834), occurred at a higher frequency in isocitrate dehydrogenase 1-mutated tumors than in isocitrate dehydrogenase 1 wild-type tumors. Younger patient age (p = 0.041) and frontal lobe location (p = 0.010) were significantly correlated with isocitrate dehydrogenase 1 mutation. Chemotherapy did not provide a survival benefit in patients with isocitrate dehydrogenase 1-mutated tumors. Isocitrate dehydrogenase 1 mutation was an independent prognostic factor in low-grade gliomas, whereas it showed no predictive value for chemotherapy response. Isocitrate dehydrogenase 1 mutation was highly associated with O 6-methylguanine DNA methyltransferase promoter methylation and TP53 mutation.
Isocitrate dehydrogenase
IDH2
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Isocitrate dehydrogenase 1 (IDH1), a key rate-limiting enzyme in tricarboxylic acid cycle, is found within the cytoplasm and peroxisomes. In recent years, IDH1 mutation is discovered in most glioma and its large scale metabolites, 2-hydroxyglutarate, may be involved in tumor as potential carcinogens, and is shown to be closely related to better patients′ survival as well. IDH1 mutation is anticipated to be a novel genetic biomarker which will guide the treatments of clinical glioma.
Key words:
Isocitrate dehydrogenase 1; Mutation; Glioma; Tumor markers, biological; Prognosis
Isocitrate dehydrogenase
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Ultrasound technology provides a oportunity to quickly and economically estimate carcass atributes on the live animal (Brethour, 2000). In general, this technology has been used to detect variation for fat depth and ribeye area ( longissimus dorsi muscle) in performance tested yearling bulls at several countries. In the present study, real time ultrasonography was used to predict the ribeye area (RA) and the subcutaneous fat thickness (FT) in Nellore crossbred.
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Longissimus dorsi
Subcutaneous fat
Beef Cattle
Longissimus muscle
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To highlight recent researches which may show promise for histomolecular classification and new treatments for gliomas.All articles cited in this review were mainly searched from PubMed, which were published in English from 1996 to 2010.Original articles and critical reviews selected were relevant to the isocitrate dehydrogenase-1/2 mutation in gliomas and other tumors.Extraordinary high rates of somatic mutations in isocitrate dehydrogenase-1/2 occur in the majority of World Health Organization grade II and grade III gliomas as well as grade IV secondary glioblastomas. Isocitrate dehydrogenase-1/2 mutations are associated with younger age at diagnosis and a better prognosis in patients with mutated tumors. The functional role of isocitrate dehydrogenase-1/2 mutations in the pathogenesis of gliomas is still unclear.Isocitrate dehydrogenase-1/2 mutations define a specific subtype of gliomas and may have great significance in the diagnosis, prognosis, and treatment of patients with these tumors.
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Isocitrate dehydrogenase
IDH2
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Two hundred sixty-two rotational and F1 sows were mated to Duroc, Yorkshire, or Landrace boars to study performance differences between equivalent three-breed rotational and three-breed terminal crossbreeding systems. Matings were made to maximize heterosis. The sows were fed either 1.8 or 2.7 kg/d (2.25 and 3.15 kg/d in winter months) during gestation. These matings produced 934 litters to determine the effect of crossbreeding system, breed composition within crossbreeding system, and gestation feeding level on litter sizes and weights, sow weight and backfat thickness at weaning, daily feed intake of the sow during lactation, interval from weaning to estrus, and farrowing rate. Feeding level during gestation was not an important source of variation for any of the traits except litter birth weight and daily feed intake of the sow during lactation. Litter size marketed was .37 pigsAitter greater (P < .05) for the terminal-cross sows than those sows from the rotational crossbreeding system. Litter weights at birth and 56 d were .8 and 6.5 kg heavier (P < .02, .03), respectively, for the terminal crossbreeding system than for the rotational crossbreeding system. Sow weight and backfat thickness at weaning, daily feed intake during lactation, and farrowing rate were not affected (P > .10) by crossbreeding system. Weaning-to-estrus interval was 1.3 d shorter (P < .03) for sows in the terminal crossbreeding system than for those in the rotational system.(ABSTRACT TRUNCATED AT 250 WORDS)
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Isocitrate dehydrogenase 1 (IDH1) mutations have been discovered to be frequent and highly conserved in secondary glioblastoma multiforme and lower-grade gliomas. Although IDH1 mutations confer a unique genotype that has been associated with a favorable prognosis, the role of the mutated IDH1 enzyme and its metabolites in tumor initiation and maintenance remains unresolved. However, given that IDH1 mutations are homogeneously expressed and are limited solely to tumor tissue, targeting this mutation could potentially yield novel treatment strategies for patients with glioblastoma multiforme.
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Isocitrate dehydrogenase mutational status defines distinct biologic behavior and clinical outcomes in low-grade gliomas. We sought to determine magnetic resonance imaging characteristics associated with isocitrate dehydrogenase mutational status to evaluate the predictive roles of magnetic resonance imaging features in isocitrate dehydrogenase mutational status and therefore their potential impact on the determination of clinical target volume in radiotherapy. Forty-eight isocitrate dehydrogenase-mutant and 28 isocitrate dehydrogenase–wild-type low-grade gliomas were studied. Isocitrate dehydrogenase mutation was related to more frequency of cortical involvement compared to isocitrate dehydrogenase–wild-type group (34/46 vs 6/24, P = .0001). Peritumoral edema was less frequent in isocitrate dehydrogenase–mutant tumors (32.6% vs 58.3% for isocitrate dehydrogenase–wild-type tumors, P = .0381). Isocitrate dehydrogenase–wild-type tumors were more likely to have a nondefinable border, while isocitrate dehydrogenase–mutant tumors had well-defined borders (66.7% vs 39.1%, P = .0287). Only 8 (17.4%) of 46 of the isocitrate dehydrogenase–mutant tumors demonstrated marked enhancement, while this was 66.7% in isocitrate–wild-type tumors ( P < .0001). Choline–creatinine ratio for isocitrate dehydrogenase–wild-type tumors was significantly higher than that for isocitrate dehydrogenase–mutant tumors. In conclusion, frontal location, well-defined border, cortical involvement, less peritumoral edema, lack of enhancement, and low choline–creatinine ratio were predictive for the definition of isocitrate dehydrogenase–mutant low-grade gliomas. Magnetic resonance imaging can provide an advantage in the detection of isocitrate dehydrogenase status indirectly and indicate the need to explore new design for treatment planning in gliomas. Choline–creatinine ratio in magnetic resonance spectroscopy could be a potential more reasonable reference for the new design of delineation of target volume in low-grade gliomas.
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The effects of breed of dam and level of winter supplement on subsequent postweaning feedlot performance of 213 steer and heifer calves from Hereford, Hereford × Holstein (Crossbred) and Holstein cows were determined. Calves fed in 2 succeeding years were sired by Angus (trials 1 and 2) and Charolais (trials 3 and 4) bulls. Each year calves that had been reared on range preweaning were group-fed (trials 1 and 3) and calves that had been reared in drylot preweaning were individually fed (trials 2 and 4). Very few of a large number of variables were influenced by level of supplement received by the dam. In breed of dam comparisons, Holstein progeny (calves from Holstein cows) was heavier initially (62 kg) and at slaughter (113 kg) than Hereford progeny (calves from Hereford cows). Crossbred progeny (calves from Crossbred cows) was intermediate for these traits. Holstein progeny was taller (9.5 cm) and longer (7.1 cm) initially, taller (10.4 cm) and longer (9.8 cm) at slaughter, required a longer feeding period (49 days) and was older at slaughter (49 days) than Hereford progeny; Crossbred progeny was intermediate in these traits but tended to respond more like Hereford than Holstein progency. Hereford and Crossbred progeny gained faster (.13 and .08 kg daily) than Holstein progeny. Crossbred and Holstein progeny consumed more daily feed (4 and 11%) and more total feed (14 and 43%), and required more feed per unit of gain (9 and 27%) than Hereford progeny.
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Isocitrate dehydrogenase 1 and 2 mutations are known to be early events in gliomagenesis and have a definite role in tumor progression.Isocitrate dehydrogenase1/2 mutation status is considered to be one of the most powerful independent positive predictor of outcome amongst all molecular markers described in association with gliomas. The inclusion of this parameter in the 2016 update of the World Health Organization Classification of Tumors of The Central Nervous System reinforced its importance in glioma classification and prognostication. As a result, now there is enough evidence to prove that Isocitrate dehydrogenase-mutant and Isocitrate dehydrogenase- wildtypegliomas are two biologically distinct categories of gliomas with likely different pathways of tumorigenesis, different clinical outcomes, and respond differently to similar treatment strategies. Increasing knowledge aboutthe role of IDH1/2 mutation in gliomagenesis has resulted in many novel targeting strategies being developed and evaluated forusefulness in the clinical setting. This literature review aims to highlight the diagnostic and prognostic importance of Isocitrate dehydrogenase1/2 gene mutations in adult gliomas.
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