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  • 1
    Language: English
    In: Leukemia, 2017-01, Vol.31 (1), p.18-25
    Description: Recurrent molecular markers have been routinely used in acute myeloid leukemia (AML) for risk assessment at diagnosis, whereas their post-induction monitoring still represents a debated issue. We evaluated the prognostic value and biological impact of minimal residual disease (MRD) and of the allelic ratio (AR) of FLT3-internal-tandem duplication (ITD) in childhood AML. We retrospectively screened 494 children with de novo AML for FLT3-ITD mutation, identifying 54 harboring the mutation; 51% of them presented high ITD-AR at diagnosis and had worse event-free survival (EFS, 19.2 versus 63.5% for low ITD-AR, 〈0.05). Forty-one percent of children with high levels of MRD after the 1st induction course, measured by a patient-specific real-time-PCR, had worse EFS (22.2 versus 59.4% in low-MRD patients, P〈0.05). Next, we correlated these parameters with gene expression, showing that patients with high ITD-AR or persistent MRD had characteristic expression profiles with deregulated genes involved in methylation and acetylation. Moreover, patients with high CyclinA1 expression presented an unfavorable EFS (20.3 versus 51.2% in low CyclinA1 group, P〈0.01). Our results suggest that ITD-AR levels and molecular MRD should be considered in planning clinical management of FLT3-ITD patients. Different transcriptional activation of epigenetic and oncogenic profiles may explain variability in outcome among these patients, for whom novel therapeutic approaches are desirable.
    Subject(s): fms-Like Tyrosine Kinase 3 - genetics ; Disease-Free Survival ; Leukemia, Myeloid, Acute - diagnosis ; Prognosis ; Epigenesis, Genetic - genetics ; Humans ; Child, Preschool ; Retrospective Studies ; Gene Expression Regulation, Leukemic ; Child ; Neoplasm, Residual - genetics ; Leukemia, Myeloid, Acute - genetics ; Molecular targeted therapy ; Gene mutations ; Gene expression ; Health aspects ; Innovations ; Index Medicus
    ISSN: 0887-6924
    E-ISSN: 1476-5551
    Source: Nature Open Access
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 2
    Language: English
    In: Ultrasound in obstetrics & gynecology, 2008-12, Vol.32 (7), p.951-954
    Description: We report a rare case of polymicrogyria diagnosed at 27 weeks' gestation on ultrasound examination and associated with cytomegalovirus (CMV) infection. The ultrasound finding suggesting this diagnosis was the direct visibility of the overfolded cortical ribbon. The cerebral surface was clearly visible because of a markedly enlarged pericerebral space associated with micrencephaly secondary to CMV infection. Bilateral opercular dysplasia was also present. Very few sonographic markers of infectious fetopathy were observed other than periventricular cysts located behind both ventricular horns. Magnetic resonance imaging (MRI) of the fetal brain confirmed the ultrasound findings and also showed the presence of marked micrencephaly, whereas cephalic measurements acquired on ultrasound examination (biparietal diameter and head circumference) were within the normal range. This case emphasizes the complementary roles of sonography and MRI in the prenatal diagnosis of cerebral abnormalities. Moreover, it illustrates the fact that polymicrogyria is easier to diagnose on ultrasound examination during the second trimester, before the development of secondary sulci. Copyright © 2008 ISUOG. Published by John Wiley & Sons, Ltd.
    Subject(s): polymicrogyria ; magnetic resonance imaging ; cytomegalovirus ; prenatal diagnosis ; ultrasonography ; CMV ; Gynecology. Andrology. Obstetrics ; Biological and medical sciences ; Infectious diseases ; Medical sciences ; Viral diseases ; Cytomegalovirus Infections - diagnostic imaging ; Humans ; Brain Diseases - diagnostic imaging ; Microcephaly - diagnostic imaging ; Pregnancy Trimester, Third ; Abortion, Induced ; Pregnancy ; Cysts - diagnostic imaging ; Ultrasonography, Prenatal ; Malformations of Cortical Development - diagnostic imaging ; Malformations of Cortical Development - virology ; Adult ; Female ; Cytomegalovirus Infections - pathology ; Index Medicus
    ISSN: 0960-7692
    E-ISSN: 1469-0705
    Source: Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 3
    Language: English
    In: Cell death & disease, 2017-06-22, Vol.8 (6), p.e2896-e2896
    Description: The 18 kDa translocator protein TSPO localizes on the outer mitochondrial membrane (OMM). Systematically overexpressed at sites of neuroinflammation it is adopted as a biomarker of brain conditions. TSPO inhibits the autophagic removal of mitochondria by limiting PARK2-mediated mitochondrial ubiquitination via a peri-organelle accumulation of reactive oxygen species (ROS). Here we describe that TSPO deregulates mitochondrial Ca2+ signaling leading to a parallel increase in the cytosolic Ca2+ pools that activate the Ca2+ -dependent NADPH oxidase (NOX) thereby increasing ROS. The inhibition of mitochondrial Ca2+ uptake by TSPO is a consequence of the phosphorylation of the voltage-dependent anion channel (VDAC1) by the protein kinase A (PKA), which is recruited to the mitochondria, in complex with the Acyl-CoA binding domain containing 3 (ACBD3). Notably, the neurotransmitter glutamate, which contributes neuronal toxicity in age-dependent conditions, triggers this TSPO-dependent mechanism of cell signaling leading to cellular demise. TSPO is therefore proposed as a novel OMM-based pathway to control intracellular Ca2+ dynamics and redox transients in neuronal cytotoxicity.
    Subject(s): Protein kinase A ; Glutamic acid ; Phosphorylation ; Reactive oxygen species ; Calcium (intracellular) ; Calcium ; Toxicity ; Homeostasis ; Cytotoxicity ; Inflammation ; Kinases ; Calcium (mitochondrial) ; Autophagy ; NAD(P)H oxidase ; Calcium influx ; Calcium signalling ; Signal transduction ; Ubiquitination ; Mitochondria ; Neurotoxicity ; Protein kinase ; Protein expression ; Age ; Calcium homeostasis ; Index Medicus ; Original
    ISSN: 2041-4889
    E-ISSN: 2041-4889
    Source: Nature Open Access
    Source: PubMed Central
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 4
    Language: English
    In: Swarm intelligence, 2011-12, Vol.5 (3), p.283-304
    Description: Task partitioning is the decomposition of a task into two or more sub-tasks that can be tackled separately. Task partitioning can be observed in many species of social insects, as it is often an advantageous way of organizing the work of a group of individuals. Potential advantages of task partitioning are, among others: reduction of interference between workers, exploitation of individuals’ skills and specializations, energy efficiency, and higher parallelism. Even though swarms of robots can benefit from task partitioning in the same way as social insects do, only few works in swarm robotics are dedicated to this subject. In this paper, we study the case in which a swarm of robots has to tackle a task that can be partitioned into a sequence of two sub-tasks. We propose a method that allows the individual robots in the swarm to decide whether to partition the given task or not. The method is self-organized, relies on the experience of each individual, and does not require explicit communication between robots. We evaluate the method in simulation experiments, using foraging as testbed. We study cases in which task partitioning is preferable and cases in which it is not. We show that the proposed method leads to good performance of the swarm in both cases, by employing task partitioning only when it is advantageous. We also show that the swarm is able to react to changes in the environmental conditions by adapting the behavior on-line. Scalability experiments show that the proposed method performs well across all the tested group sizes.
    Subject(s): Computer Systems Organization and Communication Networks ; Foraging ; Swarm robotics ; Computer Science ; Appl.Mathematics/Computational Methods of Engineering ; Artificial Intelligence (incl. Robotics) ; Communications Engineering, Networks ; Task partitioning ; Computer Communication Networks ; Self-organization ; Robotics industry ; Peace movements ; Analysis ; Energy efficiency ; Robotics ; Methods ; Robots
    ISSN: 1935-3812
    E-ISSN: 1935-3820
    Source: Alma/SFX Local Collection
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  • 5
    Language: English
    In: British journal of cancer, 2001-12-14, Vol.85 (12), p.1831-1837
    Description: Familial papillary thyroid carcinoma (PTC) is a well recognized disease. However, genetic predisposition to familial PTC is rare and the molecular alterations at the origin of the pathology are unknown. The association between PTC and lymphocytic thyroiditis (LT) has been reported recently. We communicate here 6 cases of PTC associated with LT in 2 unrelated families. PTC was diagnosed on classical nuclear and architectural criteria. It was bilateral in 5 cases. Architecture was equally distributed between typical PTC and its follicular variant. LT was present in variable degrees, including in 4 cases, oncocytic metaplasia. Using the RT-PCR technique, we observed a RET/PTC rearrangement in the carcinomatous areas of patients of both families: PTC1 in family 1 and PTC3 in family 2 and a RET/PTC rearrangement in non-malignant thyroid tissue with LT in family 2. The RET/PTC band was weaker or absent in pure LT areas. Furthermore, using a polyclonal ret antibody, an apical or a diffuse cytoplasmic ret onc protein immunolabelling was observed in the three patients with RET/PTC1 rearrangement and in the three patients with RET/PTC3 rearrangement. In conclusion our data: (1) show the presence of a RET/PTC 1 or 3 rearrangement (depending on the family) together with a variable expression of ret protein in all the PTCs; (2) suggest that the molecular event at the origin of the PTCs seems to be particular to each one of the studied families; and (3) confirm that the ret proto-oncogene activating rearrangement(s) is an early event in the thyroid tumorigenic process and that it can be observed in association with LT.
    Subject(s): Thyroid. Thyroid axis (diseases) ; Biological and medical sciences ; Endocrinopathies ; Medical sciences ; Malignant tumors ; Oncogene Proteins - genetics ; Carcinoma, Papillary - genetics ; Follow-Up Studies ; Adenoma - genetics ; Humans ; Middle Aged ; Thyroid Neoplasms - complications ; Male ; Thyroiditis, Autoimmune - complications ; Carcinoma, Papillary - complications ; Proto-Oncogenes ; Immunoenzyme Techniques ; Cell Transformation, Neoplastic - genetics ; Adult ; Female ; Proto-Oncogene Proteins c-ret ; Neoplastic Syndromes, Hereditary - genetics ; Nuclear Receptor Coactivators ; Cytoplasm - chemistry ; Genetic Predisposition to Disease ; RNA, Messenger - genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Thyroiditis, Autoimmune - genetics ; Thyroid Neoplasms - genetics ; Receptor Protein-Tyrosine Kinases - genetics ; Oncogene Proteins, Fusion - genetics ; Pedigree ; Chromosomes, Human, Pair 10 - ultrastructure ; RNA, Neoplasm - genetics ; Aged ; Transcription Factors ; Chromosomes, Human, Pair 10 - genetics ; DNA, Neoplasm - genetics ; Protein-Tyrosine Kinases ; Index Medicus ; ret oncogene activation ; lymphocytic thyroiditis ; familial PTC ; Regular
    ISSN: 0007-0920
    E-ISSN: 1532-1827
    Source: Nature Open Access
    Source: Academic Search Ultimate
    Source: Nature Journals Online
    Source: PubMed Central
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 6
    Article
    Article
    1996
    ISSN: 0003-2999 
    Language: English
    In: Anesthesia and analgesia, 1996-03, Vol.82 (3), p.666-668
    Subject(s): Biological and medical sciences ; Anesthesia ; Medical sciences ; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Local anesthesia. Pain (treatment) ; Epilepsy, Tonic-Clonic - drug therapy ; Humans ; Anticonvulsants - therapeutic use ; Magnesium Sulfate - therapeutic use ; Epilepsy, Tonic-Clonic - etiology ; Blood Patch, Epidural - adverse effects ; Eclampsia - etiology ; Pregnancy ; Puerperal Disorders - drug therapy ; Puerperal Disorders - etiology ; Adult ; Female ; Eclampsia - drug therapy
    ISSN: 0003-2999
    E-ISSN: 1526-7598
    Source: Hellenic Academic Libraries Link
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  • 7
    Language: English
    In: Journal of medical genetics, 2011-07, Vol.48 (7), p.497-504
    Description: BackgroundThe RET/GDNF signalling pathway plays a crucial role during development of the kidneys and the enteric nervous system. In humans, RET activating mutations cause multiple endocrine neoplasia, whereas inactivating mutations are responsible for Hirschsprung disease. RET mutations have also been reported in fetuses with renal agenesis, based on analysis of a small series of samples.Objective and methodsTo characterise better the involvement of RET and GDNF in kidney development defects, a series of 105 fetuses with bilateral defects, including renal agenesis, severe hypodysplasia or multicystic dysplastic kidney, was studied. RET and GDNF coding sequences, evolutionary conserved non-coding regions (ECRs) in promoters, 3′UTRs, and RET intron 1 were analysed. Copy number variations at these loci were also investigated.ResultsThe study identified: (1) a low frequency (〈7%) of potential mutations in the RET coding sequence, with inheritance from the healthy father for four of them; (2) no GDNF mutation; (3) similar allele frequencies in patients and controls for most single nucleotide polymorphism variants, except for RET intron 1 variant rs2506012 that was significantly more frequent in affected fetuses than in controls (6% vs 2%, p=0.01); (4) distribution of the few rare RET variants unidentified in controls into the various 5′-ECRs; (5) absence of copy number variations.ConclusionThese results suggest that genomic alteration of RET or GDNF is not a major mechanism leading to renal agenesis and other severe kidney development defects. Analysis of a larger series of patients will be necessary to validate the association of the RET intron 1 variant rs2506012 with renal development defects.
    Subject(s): molecular genetics ; evolutionary conserved non-coding regions ; CNVs ; renal medicine ; variants ; Renal agenesis ; renal hypodysplasia ; Nephrology. Urinary tract diseases ; Biological and medical sciences ; Kidneys ; Medical sciences ; Malformations of the urinary system ; Fetus - abnormalities ; Kidney Diseases - congenital ; Humans ; Glial Cell Line-Derived Neurotrophic Factor - genetics ; Signal Transduction - genetics ; Mutation - genetics ; Open Reading Frames - genetics ; Kidney Diseases - genetics ; DNA Copy Number Variations ; Congenital Abnormalities - genetics ; Kidney - abnormalities ; Gene Expression Regulation, Developmental ; Alleles ; Polymorphism, Single Nucleotide - genetics ; Proto-Oncogene Proteins c-ret - genetics ; Fetus ; Genetic aspects ; Research ; Gene mutations ; Health aspects ; Index Medicus
    ISSN: 0022-2593
    E-ISSN: 1468-6244
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 8
    Language: English
    In: Towards Autonomous Robotic Systems, p.90-101
    Description: In this work, we study behavioral specialization in a swarm of autonomous robots. In the studied swarm, a robot working repeatedly on the same type of task improves in task performance due to learning. Robots may exploit this positive effect of learning by selecting with higher probability the tasks on which they have improved their performance. However, even though the exploitation of such performance-improving effects is clearly a benefit, specialization also entails certain costs. Using a task allocation strategy that allows the robots to behaviorally specialize, we study the trade-off between costs and benefits in simulation experiments. Additionally, we give a perspective on the impact of this trade-off in systems that use specialization.
    Subject(s): task allocation ; specialization ; division of labor ; self-organization ; swarm robotics ; swarm intelligence
    ISBN: 3642232310
    ISBN: 9783642232312
    ISSN: 0302-9743
    E-ISSN: 1611-3349
    Source: SpringerLINK Lecture Notes in Computer Science Contemporary (1997-present)
    Source: SpringerLINK Lecture Notes in Computer Science (2015)
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  • 9
    Language: English
    Description: Dysfunctional mitochondria characterise Parkinson's Disease (PD). Uncovering etiological molecules, which harm the homeostasis of mitochondria in response to pathological cues, is therefore pivotal to inform early diagnosis and therapy in the condition, especially in its idiopathic forms. This study proposes the 18 kDa Translocator Protein (TSPO) to be one of those. Both in vitro and in vivo data show that neurotoxins, which phenotypically mimic PD, increase TSPO to enhance cellular redox-stress, susceptibility to dopamine-induced cell death, and repression of ubiquitin-dependent mitophagy. TSPO amplifies the extracellular signal-regulated protein kinase 1 and 2 (ERK1/2) signalling, forming positive feedback, which represses the transcription factor EB (TFEB) and the controlled production of lysosomes. Finally, genetic variances in the transcriptome confirm that TSPO is required to alter the autophagy-lysosomal pathway during neurotoxicity.
    Source: UCL Discovery
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  • 10
    Language: English
    Description: Dysfunctional mitochondria characterise Parkinson’s Disease (PD). Uncovering etiological molecules, which harm the homeostasis of mitochondria in response to pathological cues, is therefore pivotal to inform early diagnosis and therapy in the condition, especially in its idiopathic forms. This study proposes the 18 kDa Translocator Protein (TSPO) to be one of those. Both in vitro and in vivo data show that neurotoxins, which phenotypically mimic PD, increase TSPO to enhance cellular redox-stress, susceptibility to dopamine-induced cell death, and repression of ubiquitin-dependent mitophagy. TSPO amplifies the extracellular signal-regulated protein kinase 1 and 2 (ERK1/2) signalling, forming positive feedback, which represses the transcription factor EB (TFEB) and the controlled production of lysosomes. Finally, genetic variances in the transcriptome confirm that TSPO is required to alter the autophagy–lysosomal pathway during neurotoxicity.
    Source: White Rose Research Repository
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