Academic literature on the topic 'ADNFLE'
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Journal articles on the topic "ADNFLE"
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Mathews, Gregory C. "Is Too Much Inhibition to Blame in Autosomal Dominant Nocturnal Frontal Lobe Epilepsy?" Epilepsy Currents 7, no. 4 (July 2007): 114–16. http://dx.doi.org/10.1111/j.1535-7511.2007.00193.x.
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Seizures and Enhanced Cortical GABAergic Inhibition in Two Mouse Models of Human Autosomal Dominant Nocturnal Frontal Lobe Epilepsy. Klaassen A, Glykys J, Maguire J, Labarca C, Mody I, Boulter J. Proc Natl Acad Sci USA 2006;103(50):19152–19157. Selected mutations in the human α4 or β2 neuronal nicotinic acetylcholine receptor subunit genes cosegregate with a partial epilepsy syndrome known as autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE). To examine possible mechanisms underlying this inherited epilepsy, we engineered two ADNFLE mutations ( Chrna4S252F and Chrna4+L264) in mice. Heterozygous ADNFLE mutant mice show persistent, abnormal cortical electroencephalograms with prominent delta and theta frequencies, exhibit frequent spontaneous seizures, and show an increased sensitivity to the proconvulsant action of nicotine. Relative to WT, electrophysiological recordings from ADNFLE mouse layer II/III cortical pyramidal cells reveal a >20-fold increase in nicotine-evoked inhibitory postsynaptic currents with no effect on excitatory postsynaptic currents. i.p. injection of a subthreshold dose of picrotoxin, a use-dependent γ-aminobutyric acid receptor antagonist, reduces cortical electroencephalogram delta power and transiently inhibits spontaneous seizure activity in ADNFLE mutant mice. Our studies suggest that the mechanism underlying ADNFLE seizures may involve inhibitory synchronization of cortical networks via activation of mutant α4-containing nicotinic acetylcholine receptors located on the presynaptic terminals and somatodendritic compartments of cortical GABAergic interneurons.
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Combi, Romina, Luigi Ferini-Strambi, Arianna Montruccoli, Vera Bianchi, Massimo Malcovati, Marco Zucconi, Leda Dalprà, and Maria Luisa Tenchini. "Two new putative susceptibility loci for ADNFLE." Brain Research Bulletin 67, no. 4 (October 2005): 257–63. http://dx.doi.org/10.1016/j.brainresbull.2005.06.032.
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Bertrand, D., F. Picard, S. Le Hellard, S. Weiland, I. Favre, H. Phillips, S. Bertrand, S. F. Berkovic, A. Malafosse, and J. Mulley. "How Mutations in the nAChRs Can Cause ADNFLE Epilepsy." Epilepsia 43 (July 24, 2002): 112–22. http://dx.doi.org/10.1046/j.1528-1157.43.s.5.16.x.
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Mody, Istvan. "Calcium and Autosomal Dominant Nocturnal Frontal Lobe Epilepsy (ADNFLE)." Epilepsy Currents 3, no. 6 (November 2003): 221–22. http://dx.doi.org/10.1046/j.1535-7597.2003.03603.x.
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Mullen, Saul A., Patrick W. Carney, Annie Roten, Michael Ching, Paul A. Lightfoot, Leonid Churilov, Umesh Nair, et al. "Precision therapy for epilepsy due to KCNT1 mutations." Neurology 90, no. 1 (December 1, 2017): e67-e72. http://dx.doi.org/10.1212/wnl.0000000000004769.
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ObjectiveTo evaluate quinidine as a precision therapy for severe epilepsy due to gain of function mutations in the potassium channel gene KCNT1.MethodsA single-center, inpatient, order-randomized, blinded, placebo-controlled, crossover trial of oral quinidine included 6 patients with severe autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) due to KCNT1 mutation. Order was block randomized and blinded. Four-day treatment blocks were used with a 2-day washout between. Dose started at 900 mg over 3 divided doses then, in subsequent participants, was reduced to 600 mg, then 300 mg. Primary outcome was seizure frequency measured on continuous video-EEG in those completing the trial.ResultsProlonged QT interval occurred in the first 2 patients at doses of 900 and 600 mg quinidine per day, respectively, despite serum quinidine levels well below the therapeutic range (0.61 and 0.51 μg/mL, reference range 1.3–5.0 μg/mL). Four patients completed treatment with 300 mg/d without adverse events. Patients completing the trial had very frequent seizures (mean 14 per day, SD 7, median 13, interquartile range 10–18). Seizures per day were nonsignificantly increased by quinidine (median 2, 95% confidence interval −1.5 to +5, p = 0.15) and no patient had a 50% seizure reduction.ConclusionQuinidine did not show efficacy in adults and teenagers with ADNFLE. Dose-limiting cardiac side effects were observed even in the presence of low measured serum quinidine levels. Although small, this trial suggests use of quinidine in ADNFLE is likely to be ineffective coupled with considerable cardiac risks.Clinical trials registrationAustralian Therapeutic Goods Administration Clinical Trial Registry (trial number 2015/0151).Classification of evidenceThis study provides Class II evidence that for persons with severe epilepsy due to gain of function mutations in the potassium channel gene KCNT1, quinidine does not significantly reduce seizure frequency.
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Becchetti, Andrea. "Neuronal Nicotinic Receptors in Sleep-Related Epilepsy: Studies in Integrative Biology." ISRN Biochemistry 2012 (December 9, 2012): 1–25. http://dx.doi.org/10.5402/2012/262941.
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Although Mendelian diseases are rare, when considered one by one, overall they constitute a significant social burden. Besides the medical aspects, they propose us one of the most general biological problems. Given the simplest physiological perturbation of an organism, that is, a single gene mutation, how do its effects percolate through the hierarchical biological levels to determine the pathogenesis? And how robust is the physiological system to this perturbation? To solve these problems, the study of genetic epilepsies caused by mutant ion channels presents special advantages, as it can exploit the full range of modern experimental methods. These allow to extend the functional analysis from single channels to whole brains. An instructive example is autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE), which can be caused by mutations in neuronal nicotinic acetylcholine receptors. In vitro, such mutations often produce hyperfunctional receptors, at least in heterozygous condition. However, understanding how this leads to sleep-related frontal epilepsy is all but straightforward. Several available animal models are helping us to determine the effects of ADNFLE mutations on the mammalian brain. Because of the complexity of the cholinergic regulation in both developing and mature brains, several pathogenic mechanisms are possible, which also present different therapeutic implications.
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Xie, Na, Weiwei Qin, Jianzhong Deng, Jinxing Qi, Dewang Niu, Guifeng Lu, and Qun Wang. "A novel KCNT1 mutation in a Chinese family with severe autosomal-dominant nocturnal frontal lobe epilepsy." Translational Neuroscience 12, no. 1 (January 1, 2021): 330–34. http://dx.doi.org/10.1515/tnsci-2020-0182.
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Abstract We describe a Chinese family with severe autosomal-dominant nocturnal frontal lobe epilepsy (ADNFLE) and psychiatric problems in whom whole-exome family trio sequencing identified a heterozygous mutation in the potassium channel subfamily T, member 1 (KCNT1), a sodium-gated potassium channel gene, which was a novel missense mutation c.2153A>T (p. Asp718Val). The typical characteristics of the three patients in the family were refractory epilepsy, acquired cognitive impairment, and psychiatric problems, which include hallucinations and suicidal thoughts and behaviors. The age at onset was found to be earlier in son and daughter of the proband than that of the proband, as proven by the proband’s history of an epileptic seizure at the age of 16 years and her son’s and daughter’s history of seizures at the age of 8 years. Magnetic resonance imaging findings were negative for any abnormalities. Because of psychiatric symptoms, these three patients were administered risperidone at different times during their illness. The protestor’s son had tried fenofibrate treatment, but clinical remission was unclear. In summary, our findings broadened the mutation database in relation to KCNT1 and implicated the sodium-gated potassium channel complex in ADNFLE, more broadly, in the pathogenesis of focal epilepsies.
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Willoughby, John O., Kenneth J. Pope, and Vaughn Eaton. "Nicotine as an Antiepileptic Agent in ADNFLE: An N-of-One Study." Epilepsia 44, no. 10 (August 12, 2003): 1363. http://dx.doi.org/10.1046/j.1528-1157.2003.11903.x.
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Willoughby, John O., Kenneth J. Pope, and Vaughn Eaton. "Nicotine as an Antiepileptic Agent in ADNFLE: An N-of-One Study." Epilepsia 44, no. 9 (August 12, 2003): 1238–40. http://dx.doi.org/10.1046/j.1528-1157.2003.58102.x-i1.
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Sansoni, Veronica, Matilde Forcella, Alessandra Mozzi, Paola Fusi, Roberto Ambrosini, Luigi Ferini-Strambi, and Romina Combi. "Functional Characterization of a CRH Missense Mutation Identified in an ADNFLE Family." PLoS ONE 8, no. 4 (April 11, 2013): e61306. http://dx.doi.org/10.1371/journal.pone.0061306.
Full textDissertations / Theses on the topic "ADNFLE"
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BRUSCO, SIMONE. "Mutant heteromeric nicotinic receptors in brain development and sleep-related epilepsy." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2017. http://hdl.handle.net/10281/153196.
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Il termine epilessia notturna del lobo frontale (NFLE) descrive un ampio gruppo di epilessie parziali presentanti origine eterogenea. Gli attacchi originano a livello del lobo frontale, solitamente durante la fase 2 del sonno, e sono caratterizzati da complessi cluster ipercinetici stereotipati. Circa il 12% dei soggetti affetti dalla forma autosomica dominante di questa patologia (ADNFLE) presentano mutazioni nei geni codificanti le subunità dei recettori nicotinici neuronali (nAChRs) eteromerici. Oltre a promuovere direttamente l’eccitabilità neuronale in un network neuronale maturo, nAChRs mutanti possono contribuire alla patogenesi di questo disturbo durante lo sviluppo del SNC, influenzando il rimodellamento sinaptico. Un’alterata trasmissione colinergica potrebbe perciò condurre ad uno sbilancio tra input eccitatori ed inibitori a livello della corteccia prefrontale (PFC) facilitando così l’insorgenza di accessi epilettici. Abbiamo preso in considerazione gli effetti di una mutazione della subunità β2 associata a un fenotipo ADNFLE (β2-V287L) in fasi precoci dello sviluppo cerebrale. L’espressione della mutazione durante le prime due settimane di vita postnatale risulta necessaria per l’instaurarsi del fenotipo epilettico. Sfruttando un modello murino condizionale abbiamo analizzato come nAChRs mutanti contribuiscano a alterare il bilancio tra eccitazione ed inibizione nel cervello. Abbiamo dapprima analizzato come la mutazione β2-V287L influenzi lo sviluppo del sistema GABAergico. Registrazioni di patch-clamp evidenziano che la mutazione non influenza lo switch eccitatorio/inibitorio della trasmissione GABAergica (il quale presenta un ruolo chiave nel remodelling sinaptico), né influenza l’espressione dei recettori GABAA. Abbiamo quindi considerato il contributo della mutazione a carico del sistema glutamatergico. I risultati evidenziano che i nAChRs eteromerici iniziano ad esercitare il loro effetto verso la fine della prima settimana di vita postnatale in topo. Non sono state osservate correnti somatiche nicotiniche in questo stadio né in fasi più avanzate in neuroni piramidali: tale dato suggerisce che i nAChRs eteromerici sono siti principalmente a livello presinaptico, dove la loro attivazione promuove il rilascio di neurotrasmettitore. L’analisi dei mutanti mutazione mette in luce una più alta frequenza delle EPSCs sia in condizioni di controllo che in seguito a somministrazione di nicotina, rispetto al gruppo di controllo. L’analisi della distribuzione delle ampiezze delle EPSC mette in luce un incremento delle stesse tra P7-9 e P10-12 più pronunciato nei topi transgenici. Il nostro lavoro ha inoltre messo in luce come anche mutazioni loss-of-function possono condurre ad un fenotipo NFLE: abbiamo considerato l’effetto patogenico di una mutazione a carico della subunità α2 (Ile297Phe) identificato in una coorte di pazienti affetti da ADNFLE e NFLE. nAChRs ipofunzionali potrebbero limitare la capacità degli interneuroni inibitori di contenere la propagazione degli accessi epilettici, favorendo perciò l’insorgenza degli attacchi. Risulta quindi chiaro che mutazioni in geni codificanti per nAChRs eteromerici possono contribuire ad un fenotipo epilettico a diversi livelli, promuovendo l’eccitabilità in una rete neuronale adulta (che è ancora suscettibile al rimodellamento) o influenzando lo sviluppo di una rete neuronale funzionale, o entrambi. L’ADNFLE risulta perciò non classificabile semplicemente come una canalopatia, ma come un disturbo più complesso dello sviluppo. Il nostro obiettivo è comprendere meglio il ruolo dei nAChRs nello sviluppo del SNC ed il loro contributo nella nella epileptogenesi, oltre che il loro ruolo nella corteccia prefrontale matura. Speriamo così di identificare una finestra temporale precoce per approntare una terapia farmacologica che impedisca l’insorgenza della ADNFLE.The nocturnal frontal lobe epilepsy (NFLE) comprises a large group of partial epilepsies with heterogeneous origin. Approximately 12% of the families affected by the autosomal dominant form of NFLE (ADNFLE) carry mutations on genes coding for subunits of the heteromeric neuronal nicotinic receptors (nAChRs). Attacks arise in the frontal lobe, usually during stage 2 of sleep, and are characterized by clusters of complex and stereotyped hyperkinetic seizures.This is consistent with the widespread expression of nAChRs, and particularly α4β2, in the mammalian brain.Besides directly promoting hyperexcitability in mature networks through cell depolarization and/or altered neurotransmitter release, mutant nAChRs could determine the pathogenetic process during early developmental phases, by affecting synaptic remodeling. Cholinergic signaling has been recently found to affect the development of both GABAergic and glutamatergic systems. . Aberrant cholinergic transmission can lead to an unbalance between excitatory and inhibitory transmission in prefrontal cortex (PFC), therefore facilitating the epileptic fits.We investigated the effect of β2-V287L, a mutant nAChR subunit linked to ADNFLE, in early developmental stages, during which its expression is crucial for the epileptic phenotype to manifest. By using a murine strain which conditionally expresses β2-V287L, we analyzed how the mutant nAChR modifies the balance between excitation and inhibition in the adult brain, leading to the formation of a neuronal network susceptible to seizures. We first considered how β2-V287L (a gain-of-function mutation) affects the development of GABAergic system. By patch-clamp recordings, we observed that mutant nAChRs did not interphere with the GABAergic excitatory/inhibitory transition during early developmental stages (which is known to play a role in synaptic remodelling) nor influenced GABAA receptors’ expression.We then considered the contribute of the mutation to the development of glutamatergic signaling. Our findings revealed that heteromeric nAChRs start to exert their effect on glutamatergic transmission at the end of the first postnatal week in mice. No somatic nicotinic currents have been detected at this as well as at later developmental stages in pyramidal neurons, suggesting that heteromeric nAChRs are mainly located at synaptic level where they stimulate neurotransmitter release. Analysis of transgenic mice highlighted an increase in EPSC frequency both in control condition and following nicotine exposure, compared to control littermates. Cumulative distribution of the EPSC amplitudes showed a larger increase in EPSC amplitude between P7-9 and P10-12 in transgenic mice compared to controls.In our work we also showed how loss of function mutations can lead to a NFLE-like phenotype: in particular, we considered the pathogenic effect of an α2 subunit mutation (Ile297Phe) identified in a cohort including ADNFLE and NFLE patients. A hypofunctional nAChR could hinder the ability of inhibitory interneurons to contain seizure propagation, therefore contributing to seizures.It appears clear that mutations in genes coding for heteromeric nAChRs can contribute to an epileptic phenotype at different levels, promoting excitability in adult neuronal networks (which are still susceptible to remodelling), or affecting the development of a functional cortical circuitry, or both. ADNFLE appears therefore not only to be a channelopaty but a more complex developmental disease.Our aim is to shed new light on the nAChR contribution to brain development and its role in the establishment of an epileptic phenotype, besides its direct effect on excitability in mature prefrontal networks. In this way, we should be able to identify a temporal window for early pharmacological treatment during the pathogenetic process in order to prevent the establishment of ADNFLE
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MENEGHINI, SIMONE. "Cholinergic transmission in the cerebral cortex of a conditional murine model of ADNFLE." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2016. http://hdl.handle.net/10281/116649.
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In recent years, several mutations have been identified in the CHRNA4 and CHRNB2 gene, coding for the α4 and β2 subunits of nAChRs, respectively. These mutations are resposible for the onset of around 12% of the cases of an idiopathic form of epilepsy, the nocturnal frontal lobe epilepsy (NFLE). Autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) is a partial epilepsy characterized by short nocturnal seizure episodes, occurring during stage II of sleep. The attacks originate in the frontal lobe and may lead to cognitive and psycological impairment. The mutations identified to date show a common gain of receptor function often caused by hypersensitivity to ligand binding and retarded desensitization. Recently, Manfredi and colleagues generated, in a FVB background, a mouse model carrying an identified human β2 nAChR subunit mutation (β2-V287L) in a tetracycline-controlled expression system (Tet-Off system). This model is interesting not only for its similarities to human ADNFLE symptoms, but also for its contribution to study the developmental effect of the mutation. During our investigations, we performed whole-cell patch-clamp recordings on layer V neurons in the Fr2 region of PFC brain slices obtained from mature FVB mice. In the first part of our work, we focused on the regulation of fast-spiking (FS) interneurons by heteromeric nAChRs in wild-type animals. The Fr2 region constitutes the main output channel to subcortical structures and is crucial for spread of synchronized activity. Pyramidal neurons in layer V are tightly controlled by a dense network of GABAergic cells and, in particular, FS cells are the main responsible of feed-forward inhibition in the neocortex. Taken toghether, our results show that α4β2* nAChRs regulate GABA release onto FS cells in layer V, which reveals a potentially potent mechanism to stimulate physiological excitability as well as cause pathological hyperexcitability in prefrontal areas. In the second part of our study, we investigated the excitatory/inhibitory balance in mature PFC circuits of mice expressing β2-V287L nAChR subunits. In particular, we studied the nAChR-dependent glutamate and GABA release on PFC layer V pyramidal neurons, by measuring spontaneous excitatory and inhibitory post-synaptic currents (EPSCs, IPSCs) in the presence or in the absence of nicotine. In the absence of nicotine, neither excitatory nor inhibitory transmission showed major differences between β2-V287L and control mice, indicating that the expression of mutant nicotinic receptors doesn’t affect the basal excitatory/inhibitory ratio. In mature (older than P28) mice expressing β2-V287L subunits, we observed a potentiation of both EPSCs and IPSCs stimulation in response to 10 μM nicotine, compared to the control littermates. Then, we focused on the reciprocal inhibition sensed by the two major types of GABAergic neurons, the Fast Spiking interneurons and the Regular Spiking Non Pyramidal neurons. In transgenic animals, we observed different levels of basal inhibitory tone and opposite reactions after nicotine administration. Taken toghether, these data suggest the presence of altered connection ratios among interneurons that can lead to hyperexcitability during periods of intense PFC stimulation, as in stage II of sleep. For these reasons, ADNFLE has to be treated as a developmental disease and not as a channelopathy.
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MODENA, DEBORA. "NEURONAL NICOTINIC RECEPTORS AND EPILEPSY: A MORPHO-FUNCTIONAL STUDY ON A CONDITIONAL MURINE MODEL." Doctoral thesis, Università degli Studi di Milano, 2020. http://hdl.handle.net/2434/699808.
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Autosomal Dominant Nocturnal Frontal Lobe Epilepsy (ADNFLE) is a focal epilepsy characterized by hyperkinetic seizures frequently arising in the frontal lobe during sleep. The ADNFLE families often bear mutations on genes coding for subunits of the nicotinic cerebral acetylcholine receptors (nAChRs), that regulate excitability and neurotransmitter release. By regulating arousal, the cholinergic system modulates the sleep-waking cycle and is implicated in cognitive processes, besides exerting a crucial role during synaptogenesis. A widespread cerebral nAChR subtype is α4β2, and the first ADNFLE-linked mutation found on the β2 subunit was β2-V287L. In this study, we applied immunohistochemical and electrophysiological methods to a murine model of ADNFLE conditionally expressing β2-V287L, which develops spontaneous seizures during slow-wave sleep, only when the transgene is expressed during brain development (Manfredi et al., 2009). First, we studied whether the expression of β2-V287L could alter the maturation of the GABAergic system, which is known to regulate synaptogenesis during early postnatal stages. We focused on the most important Cl- cotransporter, the K+/Cl- cotransporter-2 (KCC2), that sets the transmembrane Cl- gradient in the brain. The balance of abundance and activity of KCC2 is implicated in epileptogenesis as well as in the compensatory responses observed in hyperexcitable networks. Hence, we studied the postnatal distribution of this protein in wild-type (WT) and β2-V287L mice by means of immunohistochemical staining and densitometric analysis. In β2-V287L mice, the KCC2 amount in layer V of prefrontal cortex (PFC) was lower than in the control littermates at postnatal day 8 (P8). Consistently, electrophysiological recordings on pyramidal neurons showed that the GABAergic excitatory to inhibitory switch was delayed in PFC layer V of mice carrying the transgene. At later stages, however (P60), the amount of KCC2 in PFC layer V was instead higher in transgenic mice, accompanied by a decreased KCC2 expression in the reticular thalamic nucleus (RT). These data suggest that β2-V287L could produce stable alterations of the PFC synaptic network, by delaying the GABAergic switch, whereas the late reversal of KCC2 expression in β2-V287L could be a compensatory response to hyperexcitability or a direct contribution to seizure facilitation in the adult thalamocortical network (Chapter 2). In PFC, layer V is the most prone to develop seizures. In normal conditions, layer V pyramidal cell activity is tightly controlled by parvalbumin-positive (PV+) fast-spiking (FS) cells and somatostatin-positive (SOM+) regular-spiking non-pyramidal (RSNP) cells, the two most abundant GABAergic interneuron populations in this region. We thus studied the spontaneous excitatory (EPSC) and inhibitory (IPSC) postsynaptic currents by applying patch-clamp methods to pyramidal, FS and RSNP neurons in murine brain slices. In mice expressing β2-V287L, the ratio between the basal frequencies of EPSCs and IPSCs increased in pyramidal neurons, whereas an opposite effect was observed in FS (but not in RSNP) cells. This suggests that i) a higher basal excitatory input is present in mice carrying the transgene, and ii) this effect could be due to an impairment of the normal inhibitory feedback produced by FS interneurons on pyramidal cells. To better determine the cellular basis of these observations, we estimated the number of both PV+ and SOM+ neurons and of the GABAergic and glutamatergic synaptic terminals contacting these neurons. To this purpose, we used immunohistochemical staining and 3D reconstruction of neurons and terminals. We found no significant changes in the GABAergic cell populations, nor in the GABAergic terminals. However, PV+ cells displayed a significant increase of glutamatergic terminals, suggesting that the functional decrease of glutamatergic input onto FS cells was not caused by a decreased synaptic density, but by a decreased efficacy of glutamatergic transmission onto FS cells (Chapter 3). A parallel analysis was focused on the main cerebral cholinergic nuclei and thalamic RT showing no significant differences in mice bearing the transgene (Chapter 4). Our chronic model of hyperexcitability opens the way to future studies on the role of β2-V287L on synapse formation and how it can be pharmacologically modulated to attempt preventive therapeutic approaches in epilepsy. In the secondary project of my work, we carried out a preliminary study of the protein α-synuclein in both WT and β2-V287L mice. The physiological role of α-synuclein and the reason of its accumulation in neurodegenerative pathologies, such as Parkinson’s disease (PD) and dementia with Lewy bodies (DLB), is unknown. Both PD and DLB also show non-motor manifestations, such as sleep dysfunction and EEG alterations, which in DLB became frequently epileptic seizures. We thus hypothesize a functional link between α-synuclein and the cholinergic system. We quantified α-synuclein in CTRL and β2-V287L mice, using immunofluorescence methods on the corpus striatum (CS) and the somatosensory cortex. Moreover, a colocalization analysis was done for GABA and glutamate vesicular transporters with α-synuclein, to check if the colocalization index was altered in epileptic mice. We found a significant decrease of α-synuclein expression in the dorsolateral CS of the epileptic mice, and an increase of the colocalization ratio in GABAergic synapses of the dorsomedial CS. These preliminary results suggest the existence of a functional relationship between α-synuclein and nAChRs (Chapter 5).
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Zeller, Caterina Barbara [Verfasser], and Leonard [Akademischer Betreuer] Holbach. "Klinisch-pathologische Korrelationen bei Patienten mit lymphoproliferativen Erkrankungen der okulären Adnexe / Caterina Barbara Zeller. Betreuer: Leonard Holbach." Erlangen : Universitätsbibliothek der Universität Erlangen-Nürnberg, 2012. http://d-nb.info/1021570982/34.
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Randrianjatovo-Gbalou, Irina. "Substances exopolymériques de biofilms bactériens : quantification in situ et étude de leur rôle dans la cohésion de la matrice extracellulaire." Thesis, Toulouse 3, 2016. http://www.theses.fr/2016TOU30010/document.
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Les biofilms représentent une contrainte technologique dans le secteur industriel et sont à l'origine de nombreux cas d'infections chroniques dans le domaine médical. De ce fait, la compréhension des processus biologiques qui s'opèrent au sein de ces communautés microbiennes est un défi permanent. Des méthodes spécifiques, sensibles et diversifiées s'avèrent essentielles pour apporter une connaissance approfondie de l'organisation des biofilms en réponse à des facteurs environnementaux. La matrice extracellulaire qui englobe les microorganismes constitue un réseau complexe, et la description de sa composition et de sa structure constitue un enjeu majeur. Des outils de caractérisation in situ et non-destructifs des Substances ExoPolymériques (SEP) ont pu être proposés lors de ce travail de thèse : des méthodes de quantification ciblant spécifiquement chaque composant majeur de la matrice extracellulaire ont ainsi été développées et validées sur des biofilms modèles. Ces biofilms, choisis pour leur diversité en terme de matrice extracellulaire sont formés par les souches Pseudomonas aeruginosa ATCC 15442, Bacillus licheniformis CIP 110824 et Weissella confusa LBAE-UPS C39-2. Des critères communs ont été retenus pour guider le choix des marqueurs retenus pour développer les dosages : spécificité pour la détection de toutes les formes moléculaires d'une même famille biochimique, sensibilité pour la détection de faibles quantités de polymères dans des biofilms en microplaque, et possibilité d'observation en microscopie basée sur la détection de fluorescence. Une stratégie commune a été adoptée pour la quantification des exoprotéines (ePN), exopolysaccharides (ePS) et fibres amyloïdes (FA) de la matrice et a consisté à : (i) définir une molécule standard pour calibrer le test ; (ii) analyser d'éventuelles interférences en solution ; (iii) valider la faisabilité et la fiabilité du test in situ par la méthode des ajouts dosées réalisée sur chacun des biofilms modèles. Un composé naturel pro-fluorescent, l'épicocconone, a été retenu pour la quantification des exoprotéines. Le test a montré une limite de détection de 0,2 µg par puits, sans aucune interférence significative des autres composants majeurs du biofilms (ePS, ADNe, cellules). D'autre part, les protéines sous forme amyloïdes ont pu être détectées avec la même sensibilité que les non amyloïdes par ce marqueur. Par la suite, les exopolysaccharides ont été dosés en exploitant la réaction de Schiff, et la méthode a permis d'obtenir une limite de détection de 0,3 µg par puits. Les protéines amyloïdes bactériennes (FA) ont également été quantifiées au moyen du marqueur Thioflavine T. La k-caséine a été utilisée comme étalon, après fibrillation de la protéine native in vitroBiofilms are detrimental in many industrial and medical areas and understanding of biofilms processes has been a challenge for decades. Specific, sensitive and rapid methods for monitoring biofilm formation are essential for a deep knowledge of biofilm organization and response to environmental factors. In such complex network that constitutes the biofilm matrix, it has become a major issue to succeed in describing its composition and local structure to determine the interactions that govern the biofilm formation. Non-destructive and in situ methods for Exopolymeric Substances (EPS) characterization were proposed along this PhD work. The first aim of the study was to propose some quantitative tools that would specifically target each major compound of the biofilm matrix. Some performance criteria were commonly established to guide the choice of each dye and to validate each step of the analytical development. These requirements can be displayed in terms of biochemical specificity, sensitivity and applicability on fluorescence-based microscopy. A common experimental strategy was carried out to quantify the exoproteins (ePN), exopolysaccharides (ePS) and amyloid fibrils (AF) and aimed at (i) choosing a calibration standard; (ii) analyzing in vitro interferences; (iii) validating the practicability and the reliability of each proposed method for an in situ implementation on biofilms. This last criteria was verified by implementing the Standard Addition Method (SAM). For that purpose, a first method was developed to take advantage of a natural pro-fluorescent dye, called epicocconone, to quantify the ePN of three model bacterial biofilms formed by the strains Bacillus licheniformis CIP 110824, Pseudomonas aeruginosa ATCC 15442 and Weissella confusa LBAE-UPS C39.2. The three bacterial models were chosen because of their contrasted EPS matrix composition. This method showed a detection limit of about 0.2µg per well and no significant interference were revealed. Moreover the epicocconone assay was able to quantify the AF with the same sensitivity as the other proteins. Subsequently, exopolysaccharides from the same strains were assayed by applying the Periodic acid-Schiff reaction in a microplate format. This chemical reaction targets the majority of the hydroxyl groups of carbohydrate and allows to give an exhaustive estimation of the sugar content of the matrix with a detection limit of 0.3µg per well. Bacterial amyloids were also specifically quantified by the using of the benzothiazole dye Thioflavine T (ThT). An amyloidogenic protein, the ?-casein, was used as standard after an in vitro fibrillation of the native form
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Marques, Virginie. "Nécessité, potentiel et limitations de l’approche en unités taxonomiques moléculaires pour analyser la biodiversité de l’ADN environnemental des poissons." Thesis, Montpellier, 2020. http://www.theses.fr/2020MONTG039.
Full textAbstract:
La vitesse et l’intensité des changements globaux nécessitent de nouveaux moyens d’observations de la biodiversité qui soient rapides, non-destructifs, standardisés, déployables à large échelle et dans les écosystèmes les plus reculés (océan profond). Les méthodes de recensement classiques reposent sur l’identification morphologique ou sonore des espèces, mais celles-ci sont coûteuses en temps et en expertise. Au-delà de ces signaux, les animaux laissent aussi des traces d’ADN dans leur environnement sous la forme de cellules dermiques, de mucus ou de fèces. Le metabarcoding de cet ADN environnemental (ADNe) consiste à le collecter, l’amplifier et le séquencer pour identifier les espèces présentes grâce à des bases de séquences génétiques de référence. Or, ces bases de référence sont incomplètes, ce qui limite fortement le potentiel de l’ADNe pour révéler la biodiversité présente. Cette thèse a pour but de développer une approche alternative basée sur des unités taxonomiques moléculaires (MOTUs) pour analyser la biodiversité des macroorganismes aquatiques, et plus particulièrement celle des poissons osseux. J’ai tout d’abord réalisé une synthèse globale et spatialisée de la couverture taxonomique des bases de référence de séquences génétiques pour tous les poissons osseux, qui montre une sous-représentation des espèces de la zone tropicale ainsi que des lacunes concernant les espèces menacées et non-indigènes. Seules 13% des espèces de poisson sont séquencées pour le marqueur le plus commun, ce qui exclut toute ambition d’analyse exhaustive de la biodiversité par assignation aux espèces à court et moyen terme. En conséquence, j’ai développé un pipeline bio-informatique pour générer des estimations de la diversité en unités taxonomiques moléculaires (MOTUs) par famille de poissons. Les résultats démontrent que cette diversité en MOTUs représente un excellent proxy de la diversité en espèces à différentes échelles spatiales. Ensuite une application du metabarcoding de l’ADNe et de l’approche en MOTUs a permis d’estimer la diversité fonctionnelle, basée sur les traits des espèces, et la diversité phylogénétique, basée sur l’histoire évolutive des espèces, des poissons tropicaux de manière plus exhaustive que des méthodes traditionnelles (vidéos, plongées). Enfin, dans une première analyse globale de la diversité des récifs coralliens en ADNe, qui rassemble 251 échantillons récoltés depuis l’Océan Indien jusque dans les Caraïbes, l’approche en MOTUs permet de reconstruire les gradients biogéographiques des poissons mais aussi de révéler une hétérogénéité spatiale locale jusqu’alors sous-estimée. Alors qu’il est aujourd’hui crucial de mettre en place des méthodes de suivi efficaces, non dépendantes de spécialistes et à haute fréquence temporelle pour mieux comprendre les effets des changements globaux sur la biodiversité, ces travaux démontrent tout le potentiel de l’ADNe avec approche en MOTUs pour construire des indicateurs robustes de plusieurs facettes de la biodiversité à plusieurs échelles, mais aussi tester les hypothèses théoriques sous-jacentes à la distribution de cette biodiversitéThe speed and intensity of global change requires new means of observing biodiversity that are rapid, non-destructive, standardized, widely deployable and in remote ecosystems (deep sea). Conventional inventory methods are based on morphological or acoustic identification of species, which are costly in terms of time and expertise. Beyond these signals, animals also leave traces of DNA in their environment in the form of dermal cells, mucus or feces. The metabarcoding of this environmental DNA (eDNA) consists in collecting this DNA, amplifying and sequencing it to identify the species present using a genetic reference database. However, these reference databases are incomplete, which severely limits the potential of eDNA. The aim of this thesis is to develop an alternative approach based on molecular taxonomic units (MOTUs) to analyze the biodiversity of aquatic macroorganisms, and more particularly that of bony fish. I first performed a global and spatialized synthesis of the taxonomic coverage of the genetic reference database for all bony fishes, which shows an under-representation of species in the tropical zone as well as taxonomic gaps for endangered and non-indigenous species. Only 13% of fish species are sequenced for the most common marker, which excludes any ambition for an exhaustive analysis of biodiversity using only species-level assignments in the short or medium term. Consequently, I have developed a bioinformatics pipeline to generate estimates of diversity using molecular taxonomic units (MOTUs) by fish family. It shows how this MOTU diversity represents an excellent proxy for species diversity at different spatial scales. Then an application of eDNA metabarcoding and the MOTUs approach allowed to estimate the functional diversity, based on species traits, and the phylogenetic diversity, based on the evolutionary history of the species, of tropical fishes in a more exhaustive way than traditional methods (videos, dives). Finally, in a first global analysis of coral reef diversity in eDNA, which brings together 251 samples collected from the Indian Ocean to the Caribbean, the MOTUs approach allows the reconstruction of major trends in fish biogeography but also reveals local spatial heterogeneity hitherto underestimated. While it is now crucial to set up efficient, non-specialist dependent and high temporal frequency monitoring methods to better understand the effects of global changes on biodiversity, this work demonstrates the full potential of eDNA using a MOTUs approach to build robust indicators of several facets of biodiversity at several scales, but also to test theoretical hypotheses underlying the distribution of this biodiversity
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Brun, Stéphanie. "Techniques d'exploration chromosomique en prénatal : mises au point et applications." Thesis, Bordeaux, 2019. http://www.theses.fr/2019BORD0184/document.
Full textAbstract:
ObjectifLe diagnostic prénatal (DPN) a pour but de détecter des pathologies foetales in utero. L’objectif de ce travail était de mettre au point et d’appliquer les techniques d’exploration chromosomique en prénatal. Nous avons, tout d’abord, validé et évalué une plateforme de séquençage basée sur la technologie des semi-conducteurs, Ion Proton®, pour le dépistage prénatal non-invasif (DPNI) des principales aneuploïdies en routine clinique, puis évalué l’intérêt de l’Analyse Chromosomique sur Puces à ADN (ACPA) dans le diagnostic prénatal des retards de croissance intra-utérin (RCIU) foetaux. Matériel et Méthodes Nous avons inclus prospectivement 2505 patientes enceintes analysées par huit laboratoires hospitalo-universitaires de génétique : 695 grossesses à haut risque pour la trisomie 21 (risque ≥1/250 ou avec anomalie échographique) dans une étude de validation de la technique du test ADN libre circulant (ADNlc), et 1810 grossesses à risque, sans anomalie échographique, en routine clinique. Les issues de grossesses étaient toutes disponibles dans l’étude de validation et pour 521 grossesses dans l’étude en routine clinique. L’ADNlc extrait d’échantillons plasmatiques était séquencé, puis les données étaient analysées à l’aide du logiciel WISECONDOR. Les résultats des tests ADNlc étaient comparés aux caryotypes foetaux ou 7 aux données à la naissance. Nous avons aussi évalué le taux d’échec et comparé trois méthodes d’évaluation de la fraction foetale (FF) (RASSF1A, DEFRAG et SANEFALCON). Nous avons rétrospectivement inclus tous les foetus référés pour un prélèvement invasif pour RCIU et étudié les résultats de technique d’hybridation in situ en fluorescence (FISH), caryotypes et ACPA. Résultats Les résultats des deux cohortes de l’étude sur l’ADNlc étaient cohérents et les âges gestationnels n’étaient pas significativement différents ; les données ont été combinées afin d’étoffer la cohorte à analyser. Respectivement, la sensibilité et la spécificité étaient de : 98.3% (95% IC, 93.5–99.7%) et 99.9% (95% IC, 99.4–100%) pour la trisomie 21; 96.7% (95% IC, 80.9–99.8%) et 100% (95% IC, 99.6–100%) pour la trisomie 18 ; et 94.1% (95% IC, 69.2–99.7%) et 100% (95% IC, 99.6–100%) pour la trisomie 13. Le taux de non rendus était de 1.2% initialement puis après réanalyse de 0.6%. L’estimation de la FF avec les méthodes RASSF1A et DEFRAG étaient comparables, toutes deux compatibles avec une utilisation en routine clinique. Parmi les 162 foetus RCIU (78 associés et 84 isolés) inclus dans l’étude ACPA, 15 avaient une FISH pathologique : 10 RCIU associés et cinq RCIU isolés. Parmi 143 foetus étudiés par ACPA, 10 (7%) présentaient un variant du nombre de copies (CNV), tous étaient des RCIUs associés (10/65 soit 15.4%; 95 IC: 8.4%‐26.2%), versus 0/78 dans le groupe RCIUs isolés (95% IC: 0%‐5.6%). Six foetus (4.2%) ont présenté des variants de signification inconnue (VSI) (trois RCIU associés et trois RCIU isolés). Conclusion : Notre étude évaluant le test ADNlc utilisant la technologie des semi-conducteurs est la première étude clinique à rapporter les issues de grossesses dans une population aussi large. La plateforme est performante pour le DPNI des principales aneuploïdies. Notre protocole robuste est facilement applicable en routine clinique. Notre étude souligne une augmentation de rendement diagnostique de l’ACPA de 6.1% (4/65) par rapport au caryotype pour le DPN des foetus présentant un RCIU associé. Aucun CNV pathogène n’a été mis en évidence dans le groupe RCIU isolé. L’ADNlc pourrait-il supplanter l’ACPA dans cette population de RCIU isolé ? Le développement du test ADNlc a permis de limiter le nombre de prélèvements invasifs et donc leurs complications [...]ObjectivePrenatal diagnosis allows to detect fetal pathologies in-utero. The goal of this work was both technical development and application of the chromosomal exploration technics in prenatal diagnosis. First, we aimed to validate and evaluate the performance metrics of the highthroughput semiconductor sequencing platform, Ion Proton®, in non-invasive prenatal genetic screening (NIPS) for common fetal aneuploidies in a clinical setting and, then to evaluate the diagnostic utility of prenatal diagnosis using the chromosomal microarray analysis (CMA) for fetuses presenting with isolated or associated intrauterine growth restriction (IUGR). Methods : First, regarding NIPS, a prospective cohort study including 2505 pregnant women from eight academic genetics laboratories (695 high risk pregnancies for trisomy 21 (risk ≥1/250 or with ultrasound anomalies) in a validation study, and 1810 such pregnancies, without ultrasound anomalies, in a real-life NIPS clinical setting) was conducted. An outcome was available for all cases in the validation cohort and for 521 in the clinical cohort. Cell-free DNA from plasma samples was sequenced using the Ion Proton sequencer, and sequencing data were analyzed using the open-access software, WISECONDOR. Performance metrics for detection 10 of trisomies 21, 18 and 13 were calculated based on either fetal karyotype result or clinical data collected at birth. We also evaluated the failure rate and compared three methods of fetal fraction quantification (RASSF1A assay, and DEFRAG and SANEFALCON software). Then, regarding the CMA study, we retrospectively included all fetuses with IUGR referred for prenatal testing and studied by rapid fluorescence in situ hybridization (FISH), karyotype, and CMA. Results :In the NIPS study, results from both cohorts were consistent and their gestational age was not significantly different, so their data were combined to increase the sample size for analysis. Sensitivities and specificities, respectively, were as follows: for trisomy 21, 98.3% (95% CI, 93.5–99.7%) and 99.9% (95% CI, 99.4–100%); for trisomy 18, 96.7% (95% CI, 80.9–99.8%) and 100% (95% CI, 99.6–100%); and for trisomy 13, 94.1% (95% CI, 69.2–99.7%) and 100% (95% CI, 99.6–100%). Our failure rate was 1.2% initially and as low as 0.6% after retesting some of the failed samples. Fetal fraction estimation by the RASSF1A assay was consistent with DEFRAG results, and both were adequate for routine diagnosis. Among the 162 IUGR fetuses (78 associated and 84 isolated IUGR) included in the CMA study, 15 had an abnormal FISH result: 10 associated and five isolated fetal IUGRs. Among the 143 fetuses studied by CMA, 10 (7%) presented pathogenic copy number variations (CNVs). All 10 were in the associated fetal IUGR group (10/65 or 15.4%; 95% confidence interval [CI]: 8.4%‐26.2%) versus 0/78 in the isolated fetal IUGR group (95% CI: 0%‐5.6%). Six fetuses (4.2%) carried variants of unknown significance (VOUS) (three associated and three isolated fetal IUGRs). Conclusion: We described one of the largest studies evaluating Ion Proton-based NIPS and the first clinical study reporting pregnancy outcome in a large series of patients. This platform is highly efficient in detecting the three most common trisomies. Our protocol is robust and can be implemented easily in any medical genetics’ laboratory. Our second study highlighted the added value of CMA in the case of associated fetal IUGR with an incremental yield of 6.1% (4/65) over karyotyping. No pathogenic CNVs were reported in the isolated fetal IUGR group. Could NIPS supplant CMA in isolated fetal IUGR? The development of the NIPS test has reduced prenatal invasive testing and therefore its complications [...]
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Göbel, Nora [Verfasser]. "Chlamydia psittaci und Lymphome der okulären Adnexe - besteht ein Zusammenhang? / vorgelegt von Nora Göbel." 2008. http://d-nb.info/991176863/34.
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Vidal, Andreas [Verfasser]. "Ejakulatveränderungen beim chronischen Beckenschmerzsyndrom (chronische Prostatitis) : Entzündungseinfluss auf das Spermiogramm und sekretorische Parameter der männlichen Adnexe / vorgelegt von Andreas Vidal." 2003. http://d-nb.info/968641156/34.
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Busse, Claudia [Verfasser]. "Erbliche Erkrankungen der okulären Adnexe, des Bulbus und des vorderen Augenabschnittes beim Hund : eine Literaturstudie und Übersicht über den derzeitigen Stand züchterischer Maßnahmen der Rassezuchtvereine bei verschiedenen Augenerkrankungen / vorgelegt von Claudia Busse." 2007. http://d-nb.info/987881418/34.
Full textBooks on the topic "ADNFLE"
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Dziama, Antoni. Przek¿adnie ze ·bate. 2nd ed. Warszawa: Wydaw. Nauk. PWN, 1995.
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Schwarz, Yom Tov. Sefer Sheʼelot u-teshuvot Adne neḥoshet. Nu York: Yom Ṭov ha-Leṿi Shṿarts, 1990.
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Schwarz, Yom Tov. Sefer Sheʼelot u-teshuvot Adne neḥoshet. Nu York: Yom Ṭov ha-Leṿi Shṿarts, 1990.
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Spain. Ministerio de Defensa. Dirección General de Infraestructura. Instrucción para la redacción de ADNE y ficha técnica. [Madrid]: Ministerio de Defensa, Secretaría General Técnica, 1990.
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ʻAbu, Eliyahu Ben. Adne zahav: ʻal masekhet Bava batra, ʻiyunim ṿe-ḥidushim ... Ḥefah: E. Ben-ʻAbu, 2003.
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Meśaś, Yosef. Sefer Mayim ḥayim: Otsar 314 teshuvot benuyot ʻal adne O.ḥ. ... [Brooklyn?: ḥ. mo. l., 1993.
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Huss, Boaz. ʻAl adne paz: Ha-Ḳabalah shel R. Shimʻon ibn Lavi. Yerushalayim: Y.L. Magnes, 2000.
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Efrayim ben Shemuʼel Zanṿil Heḳsher. Shut ṿe-ḥidushe Adne paz. Shut Koaḥ Shor. Shishah zerʻone ʻarugah. [Monroe, N.Y: ha-sefer, Hotsaʼat sifre posḳim rishonim, 1985.
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Sefer Bikure Yehudah: ʻal Masekhet Shevuʻot : beʼurim neḥmadim ʻal adne ha-peshat ... 3rd ed. [Brooklyn, N.Y.?]: Yehudah Meʼir Yaʻaḳov Laikhtag, 2007.
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Perlmuṭer, Ben Tsiyon Menaḥem Mendl. Sefer Niṭʻe Eliyahu: Tokhno meyusad ʻal adne ḳodesh vi-yedaber ʻal ʻinyanim shonim ... Yerushalayim: Ben Tsiyon Menaḥem Mendl Perlmuṭer, 2001.
Find full textBook chapters on the topic "ADNFLE"
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Dose, J., and F. Jänicke. "Adnexe." In Die Gynäkologie, 439–77. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-662-11496-4_25.
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Kaufmann, M. "Adnexe." In Die Gynäkologie, 659–64. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-662-11496-4_37.
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Germer, U. "Adnexe." In Ultraschalldiagnostik in Geburtshilfe und Gynäkologie, 845–77. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-53662-9_33.
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Schwarz, J., S. Mahner, and F. Jänicke. "Adnexe." In Die Gynäkologie, 529–64. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-20923-9_30.
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Kaufmann, M. "Adnexe." In Die Gynäkologie, 829–35. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-20923-9_46.
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Germer, Ute. "Adnexe." In Ultraschalldiagnostik in Geburtshilfe und Gynäkologie, 749–78. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-29633-8_32.
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Both, Marcus, Anja Eckstein, Joachim Esser, Thomas Neß, and Bernhard Nölle. "Extraokular/Adnexe." In Entzündliche Augenerkrankungen, 47–70. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-38419-6_2.
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Hampel, Christian. "Uterus und Adnexe." In Komplikationen in der Urologie, 393–403. Berlin, Heidelberg: Springer Berlin Heidelberg, 2021. http://dx.doi.org/10.1007/978-3-662-60625-4_31.
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Serno, J., T. Papathemelis, and N. Maass. "Entzündliche Erkrankungen der Adnexe." In Weiterbildung Gynäkologie und Geburtshilfe, 39–45. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-662-44424-5_5.
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Hautmann, Maximilian. "Vaginosonographische Darstellung der Adnexe." In Atlas der Vagino- und Hysterosonographie, 76–85. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74648-2_20.
Full textConference papers on the topic "ADNFLE"
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Wang, Kai, Chunxu Shen, Chaoyun Zhang, and Wenye Ma. "AdnFM: An Attentive DenseNet based Factorization Machine for Click-Through-Rate Prediction." In ICCDE 2022: 2022 The 8th International Conference on Computing and Data Engineering. New York, NY, USA: ACM, 2022. http://dx.doi.org/10.1145/3512850.3512852.
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Champ, Julien, and Vincent Boudet. "ADNL: Accurate distributed node localization algorithm in Wireless Sensor Networks." In 2010 European Wireless Conference (EW). IEEE, 2010. http://dx.doi.org/10.1109/ew.2010.5483437.
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Sitnikov, A. A., S. A. Ivanov, P. P. Zhugan, and E. V. Ageenkov. "Aqual Survey by the Differential-Normalized Method of Electrical Prospecting (Adnme) and Continuous Dipole Electromagnetic Sounding (Ndemz) for Oil and Gas Exploration and Geological-Engineering Works." In Marine Technologies 2019. European Association of Geoscientists & Engineers, 2019. http://dx.doi.org/10.3997/2214-4609.201901804.
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