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Journal articles on the topic 'ADNFLE'

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Author: Grafiati

Published: 9 March 2023

Last updated: 10 March 2023

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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.

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11

Itier, Valérie, and Daniel Bertrand. "Mutations of the neuronal nicotinic acetylcholine receptors and their association with ADNFLE." Neurophysiologie Clinique/Clinical Neurophysiology 32, no. 2 (April 2002): 99–107. http://dx.doi.org/10.1016/s0987-7053(02)00294-0.

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12

Bonati, Maria Teresa, Rosanna Asselta, Stefano Duga, Luigi Ferini-Strambi, Alessandro Oldani, Marco Zucconi, Massimo Malcovati, Leda Dalprà, and Maria Luisa Tenchini. "Refined mapping of CHRNA3/A5/B4 gene cluster and its implications in ADNFLE." NeuroReport 11, no. 10 (July 2000): 2097–101. http://dx.doi.org/10.1097/00001756-200007140-00008.

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13

Picard, F., D. Bruel, D. Servent, W. Saba, C. Fruchart-Gaillard, M. A. Schöllhorn-Peyronneau, D. Roumenov, et al. "Alteration of the in vivo nicotinic receptor density in ADNFLE patients: a PET study." Brain 129, no. 8 (June 30, 2006): 2047–60. http://dx.doi.org/10.1093/brain/awl156.

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14

Rodrigues‐Pinguet, Nivalda, Li Jia, Maureen Li, Antonio Figl, Alwin Klaassen, Anthony Truong, Henry A. Lester, and Bruce N. Cohen. "Five ADNFLE Mutations Reduce the Ca 2+ Dependence of the Mammalian α4β2 Acetylcholine Response." Journal of Physiology 550, no. 1 (July 2003): 11–26. http://dx.doi.org/10.1113/jphysiol.2003.036681.

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15

Labate, A., L. Mumoli, A. Fratto, A. Quattrone, and A. Gambardella. "Hippocampal sclerosis worsens autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) phenotype related to CHRNB2 mutation." European Journal of Neurology 20, no. 3 (August 17, 2012): 591–93. http://dx.doi.org/10.1111/j.1468-1331.2012.03839.x.

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16

Tenchini, M. L., S. Duga, M. T. Bonati, R. Asselta, A. Oldani, M. Zucconi, M. Malcovati, L. Dalprà, and L. Ferini-Strambi. "SER252PHE and 776INS3 Mutations in the CHRNA4 Gene are Rare in the Italian ADNFLE Population." Sleep 22, no. 5 (August 1999): 637–39. http://dx.doi.org/10.1093/sleep/22.5.637.

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17

Yamada, Junko, Gang Zhu, Motohiro Okada, Shinichi Hirose, Shukuko Yoshida, Yuko Shiba, Keisuke Migita, et al. "A novel prophylactic effect of furosemide treatment on autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE)." Epilepsy Research 107, no. 1-2 (November 2013): 127–37. http://dx.doi.org/10.1016/j.eplepsyres.2013.08.018.

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18

Bouchardy, I., O. Steinlein, R. Combi, L. Ferini-Strambi, A. Gambardella, G. Rudolf, M. A. Morris, and F. Picard. "Mutations of the orexin system, a regulator of sleep arousal, are not a common cause of ADNFLE." Neurology 76, no. 14 (April 4, 2011): 1272–73. http://dx.doi.org/10.1212/wnl.0b013e31821434f0.

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19

Saberi, Behzad. "Pore-Forming M2 Domains of CHRNA4 and CHRNB2 Mutations In Autosomal Dominant Nocturnal Frontal Lobe Epilepsy (ADNFLE) Phenotype." American Journal of Biomedical Science & Research 1, no. 5 (March 8, 2019): 222–23. http://dx.doi.org/10.34297/ajbsr.2019.01.000547.

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20

Aminkeng, F. "KCNT1mutations in ADNFLE and MMPSI: a new driver in the etiology and pathophysiology of early-onset epileptic syndromes." Clinical Genetics 83, no. 4 (April 2013): 319–20. http://dx.doi.org/10.1111/cge.12082.

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21

Gu, Wenli, Daniel Bertrand, and Ortrud K. Steinlein. "A major role of the nicotinic acetylcholine receptor gene CHRNA2 in autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) is unlikely." Neuroscience Letters 422, no. 1 (July 2007): 74–76. http://dx.doi.org/10.1016/j.neulet.2007.06.006.

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22

Shiba, Yuko, Fumiaki Mori, Junko Yamada, Keisuke Migita, Yoshikazu Nikaido, Koichi Wakabayashi, Sunao Kaneko, Motohiro Okada, Shinichi Hirose, and Shinya Ueno. "Spontaneous epileptic seizures in transgenic rats harboring a human ADNFLE missense mutation in the β2-subunit of the nicotinic acetylcholine receptor." Neuroscience Research 100 (November 2015): 46–54. http://dx.doi.org/10.1016/j.neures.2015.06.003.

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23

Halász, Péter, Anna Kelemen, and Anna Szűcs. "Physiopathogenetic Interrelationship between Nocturnal Frontal Lobe Epilepsy and NREM Arousal Parasomnias." Epilepsy Research and Treatment 2012 (May 10, 2012): 1–8. http://dx.doi.org/10.1155/2012/312693.

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Aims. To build up a coherent shared pathophysiology of NFLE and AP and discuss the underlying functional network. Methods. Reviewing relevant published data we point out common features in semiology of events, relations to macro- and microstructural dynamism of NREM sleep, to cholinergic arousal mechanism and genetic aspects. Results. We propose that pathological arousals accompanied by confused behavior with autonomic signs and/or hypermotor automatisms are expressions of the frontal cholinergic arousal function of different degree, during the condition of depressed cognition by frontodorsal functional loss in NREM sleep. This may happen either if the frontal cortical Ach receptors are mutated in ADNFLE (and probably also in genetically not proved nonlesional cases as well), or without epileptic disorder, in AP, assuming gain in receptor functions in both conditions. This hypothesis incorporates the previous “liberation theory” of Tassinari and the “state dissociation hypothesis” of Bassetti and Terzaghi). We propose that NFLE and IGE represent epileptic disorders of the two antagonistic twin systems in the frontal lobe. NFLE is the epileptic facilitation of the ergotropic frontal arousal system whereas absence epilepsy is the epileptic facilitation of burst-firing working mode of the spindle and delta producing frontal thalamocortical throphotropic sleep system. Significance. The proposed physiopathogenesis conceptualize epilepsies in physiologically meaningful networks.

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24

Indurthi, Dinesh C., Taima Qudah, Vivian W. Liao, Philip K. Ahring, Trevor M. Lewis, Thomas Balle, Mary Chebib, and Nathan L. Absalom. "Revisiting autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) mutations in the nicotinic acetylcholine receptor reveal an increase in efficacy regardless of stochiometry." Pharmacological Research 139 (January 2019): 215–27. http://dx.doi.org/10.1016/j.phrs.2018.11.031.

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25

Sone, Daichi, Takayuki Sugawara, Eisuke Sakakibara, Yu Tomioka, Go Taniguchi, Yoshiko Murata, Masako Watanabe, and Sunao Kaneko. "A case of autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) coexisting with pervasive developmental disorder harboring SCN1A mutation in addition to CHRNB2 mutation." Epilepsy & Behavior 25, no. 2 (October 2012): 192–95. http://dx.doi.org/10.1016/j.yebeh.2012.07.027.

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26

Picard, F., D. Bruel, D. Servent, E. Brodtkorb, S. Zuberi, A. Gambardella, B. Steinborn, H. Valette, and M. Bottlaender. "20. In vivo PET study of the mutated nicotinic receptors using [18F]-A-85380 in patients with autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE)." Clinical Neurophysiology 120, no. 9 (September 2009): e192-e193. http://dx.doi.org/10.1016/j.clinph.2009.07.024.

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27

Guo, Yuxiong, Qinfei Miao, Yuxin Zhang, Chun Wang, Mingjuan Liang, Xueping Li, Weifeng Qiu, Gangan Shi, Qiongxiang Zhai, and Zhihong Chen. "A novel missense creatine mutant of CaBP4, c.464G>A (p.G155D), associated with autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE), reduces the expression of CaBP4." Translational Pediatrics 11, no. 3 (March 2022): 396–402. http://dx.doi.org/10.21037/tp-22-54.

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28

O'Neill, Heidi C., Duncan C. Laverty, Natalie E. Patzlaff, Bruce N. Cohen, Carlos Fonck, Sheri McKinney, J. Michael McIntosh, et al. "Mice expressing the ADNFLE valine 287 leucine mutation of the Β2 nicotinic acetylcholine receptor subunit display increased sensitivity to acute nicotine administration and altered presynaptic nicotinic receptor function." Pharmacology Biochemistry and Behavior 103, no. 3 (January 2013): 603–21. http://dx.doi.org/10.1016/j.pbb.2012.10.014.

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29

Rozycka, Agata, Jolanta Dorszewska, Barbara Steinborn, Bartosz Kempisty, Margarita Lianeri, Kamila Wisniewska, and Paweł P. Jagodzinski. "Original article A transcript coding for a partially duplicated form of α7 nicotinic acetylcholine receptor is absent from the CD4 + T-lymphocytes of patients with autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE)." Folia Neuropathologica 1 (2013): 65–75. http://dx.doi.org/10.5114/fn.2013.34198.

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30

Kandemir, Ali, Marco L. Longana, Tulio H. Panzera, Gilberto G. del Pino, Ian Hamerton, and Stephen J. Eichhorn. "Natural Fibres as a Sustainable Reinforcement Constituent in Aligned Discontinuous Polymer Composites Produced by the HiPerDiF Method." Materials 14, no. 8 (April 10, 2021): 1885. http://dx.doi.org/10.3390/ma14081885.

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Sustainable fibre reinforced polymer composites have drawn significant attention in many industrial sectors as a means for overcoming issues with end-of-life regulations and other environmental concerns. Plant based natural fibres are considered to be the most suitable reinforcement for sustainable composites since they are typically from renewable resources, are cheap, and are biodegradable. In this study, a number of plant based natural fibres-curaua, flax, and jute fibres-are used to reinforce epoxy, poly(lactic acid) (PLA), and polypropylene (PP) matrices to form aligned discontinuous natural fibre reinforced composites (ADNFRC). The novel HiPerDiF (high performance discontinuous fibre) method is used to produce high performance ADNFRC. The tensile mechanical, fracture, and physical (density, porosity, water absorption, and fibre volume fraction) properties of these composites are reported. In terms of stiffness, epoxy and PP ADNFRC exhibit similar properties, but epoxy ADNFRC shows increased strength compared to PP ADNFRC. It was found that PLA ADNFRC had the poorest mechanical performance of the composites tested, due principally to the limits of the polymer matrix. Moreover, curaua, flax (French origin), and jute fibres are found to be promising reinforcements owing to their mechanical performance in epoxy and PP ADNFRC. However, only flax fibre with desirable fibre length is considered to be the best reinforcement constituent for future sustainable ADNFRC studies in terms of mechanical performance and current availability on the market, particularly for the UK and EU.

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31

Serno, J., T. Papathemelis, and N. Maass. "Entzündliche Erkrankungen der Adnexe." Der Gynäkologe 46, no. 5 (April 27, 2013): 331–38. http://dx.doi.org/10.1007/s00129-013-3156-4.

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32

Mohr, Ch, and B. Hoffmeister. "Tumoren der okulären Adnexe." Der Onkologe 5, no. 9 (September 17, 1999): 771–80. http://dx.doi.org/10.1007/s007610050438.

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33

Kakkassery, V., N. Stübiger, I. A. Adamietz, I. Tischoff, A. Baraniskin, and I. M. Wunderlich. "Lymphome der okulären Adnexe." Der Ophthalmologe 112, no. 3 (February 20, 2015): 210–16. http://dx.doi.org/10.1007/s00347-014-3205-y.

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34

Köstlin, R., and I. Hoffmann. "Die sonographische Untersuchung des vorderen Augenabschnittes beim Kleintier." Tierärztliche Praxis Ausgabe K: Kleintiere / Heimtiere 32, no. 03 (2004): 175–79. http://dx.doi.org/10.1055/s-0037-1622408.

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Zusammenfassung: Gegenstand: Diese zweiteilige Arbeit beschreibt den Einsatz eines hochauflösenden Linear-Array-Schallkopfes mit einer Mittelfrequenz von 12 MHz zur Darstellung des vorderen Augenabschnittes und der Netzhaut-Glaskörper-Peripherie beim Kleintier. Material und Methoden: Im ersten Teil der Studie wurden die Adnexe und der vordere Augenabschnitt bei gesunden Hunden und Katzen sonographisch erfasst. Zusätzlich erfolgte eine Untersuchung des gesamten Bulbus, der Adnexe sowie der Orbita von gesunden Kaninchen und Meerschweinchen. Die Sonographie wurde unter Lokalanästhesie, in Sedation oder Allgemeinnarkose durchgeführt. Ergebnisse: Im Anschluss an die Untersuchungen traten in keinem Fall durch die Sonographie bedingte Komplikationen auf. Mit der hochauflösenden Ophthalmosonographie ließen sich anteriore und bulbuswandständige Strukturen des Augapfels und die okulären Adnexe beurteilen. Die entstehenden Bilder ähnelten histologischen Schnittbildern niedriger Vergrößerung, ohne jedoch deren Präparationsartefakte aufzuweisen. Zusätzlich konnten dabei der gesamte Bulbus und seine Adnexe sowie die Orbita mit einem Ultraschallgerät untersucht werden. Schlussfolgerung und klinische Relevanz: Die hochauflösende Ophthalmosonographie liefert Bilder vom gesunden Hunde-, Katzen-, Kaninchenund Meerschweinchenauge, die mit konventionellen Geräten bisher nicht zu erreichen sind. Limitiert ist der Einsatz der Sonde durch deren Größe, vor allem in der vertikalen Schnittebene.

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35

Arakawa, Tsutomu, Takako Niikura, Fumio Arisaka, and Yoshiko Kita. "Activity-dependent neurotrophic factor, ADNF, determines the structure characteristics of Colivelin, a fusion protein of ADNF9 and Humanin analog." Journal of Peptide Science 14, no. 5 (November 12, 2007): 631–36. http://dx.doi.org/10.1002/psc.959.

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36

Chilla, B., M. Hohl, and R. Kubik. "Raumforderungen der Adnexe – Bildgebung und Differenzialdiagnosen." Radiologie up2date 8, no. 04 (December 2008): 335–55. http://dx.doi.org/10.1055/s-2008-1077747.

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37

Auw-Hädrich, C., N. Göbel, and G. Illerhaus. "Erreger bei Tumoren der okulären Adnexe." Klinische Monatsblätter für Augenheilkunde 227, no. 07 (June 9, 2010): 530–37. http://dx.doi.org/10.1055/s-0029-1245153.

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38

Abfalter, E., H. Schröcksnadel, E. Solder, D. Peer, E. Müller-Holzner, and O. Dapunt. "Aktinomykose der Adnexe – Differentialdiagnose zum Ovarialkarzinom." Gynäkologisch-geburtshilfliche Rundschau 30, no. 1 (1990): 213–14. http://dx.doi.org/10.1159/000271447.

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39

Coupland, S. E. "Lymphoproliferative L�sionen der okul�ren Adnexe." Der Ophthalmologe 101, no. 2 (February 1, 2004): 197–217. http://dx.doi.org/10.1007/s00347-003-0854-7.

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40

Jückstock, J., T. Blankenstein, S. Mahner, and I. Mylonas. "Entzündliche Erkrankungen des Uterus und der Adnexe." Der Gynäkologe 49, no. 3 (February 19, 2016): 189–200. http://dx.doi.org/10.1007/s00129-016-3840-2.

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41

Schreiber, G., Christina Hipler, and M. Görnig. "„Entzündungen der männlichen Adnexe - Störungen der Fertilität?”." Der Hautarzt 48, no. 7 (July 22, 1997): 507–9. http://dx.doi.org/10.1007/s001050050621.

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42

Pérez, César. "La crisis financiera e institucional del Ayuntamiento del Distrito Nacional." Ciencia y Sociedad 14, no. 4 (December 1, 1989): 310–30. http://dx.doi.org/10.22206/cys.1989.v14i4.pp310-30.

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Este texto evalúa la atención sobre uno de los más apremiantes problemas de las autoridades edilicias del ADN:la falta de recursos para enfrentar la demanda de los servicios de la población capitalina.

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43

Coupland, S. E., T. Wiegel, C. Auw-Haedrich, W. R. Lee, and H. Stein. "Lymphoproliferative Läsionen der okulären Adnexe und intraokuläre Lymphome." Der Onkologe 5, no. 9 (September 17, 1999): 792–804. http://dx.doi.org/10.1007/s007610050440.

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44

Rehbock, J., and G. Kindermann. "Diagnostische Abklärung der klinisch oder sonografisch auffälligen Adnexe." Der Gynäkologe 30, no. 2 (February 27, 1997): 92–97. http://dx.doi.org/10.1007/pl00003028.

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45

Hoyme, U. B. "Klinik der entzündlichen Erkrankungen des Uterus und der Adnexe." Der Gynäkologe 39, no. 12 (December 2006): 981–95. http://dx.doi.org/10.1007/s00129-006-1920-4.

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AI, MIN, QIUYI ZHONG, CHRISTOPH SCHEIDEGGER, LISONG WANG, and XINYU WANG. "Revision of Dimelaena Norman (Caliciaceae, Ascomycota) species containing usnic acid reveals a new species and a new combination from China." Phytotaxa 574, no. 4 (December 2, 2022): 259–72. http://dx.doi.org/10.11646/phytotaxa.574.4.1.

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Dimelaena tibetica is described as a species new to science, characterized by a grayish yellow surface, usually with a covering of white pruina, a crustose thallus, areolate at center, radiate-plicate at margin, adnate apothecia and lacking gyrophoric acid. It differs from other usnic acid-containing Dimelaena species by its plane marginal lobes and adnate apothecia. Based on the study of fresh specimens from the environment of the type locality, Dimelaena altissima is proposed as a new combination. A fresh specimen of Dimelaena oreina (type species of the genus Dimelaena) was collected in the Swiss Alps, in the vicinity of the area where the type material of the species presumably was collected, and a sequence was generated to confirm the phylogenetic position of this genus. All three species share common characters: usnic acid content and a yellowish green upper surface. Descriptions of these species were based on a combination of morphological and phylogenetic analyses. A key and phylogram are provided for these three Dimelaena species which produce usnic acid.

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Vizzini, Alfredo, Paolo Picciola, Eliseo Battistin, and Enrico Ercole. "Hygrocybe rubroalba (Hygrophoraceae, Agaricales), a new species of sect. Firmae from Brazil." Phytotaxa 226, no. 1 (September 9, 2015): 18. http://dx.doi.org/10.11646/phytotaxa.226.1.2.

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A new Hygrocybe species with dimorphic basidia and spores, H. rubroalba, is described based on morphological and molecular data. Its peculiar features are a dry, bright red to purplish red, not or very slightly depressed pileus surface, and pure white lamellae that are adnate or emarginate rather than decurrent. It is phylogenetically close to H. martinicensis in sect. Firmae.

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Zimmerli, Meyer, and Messerli. "Bilaterale Tränendrüsenschwellung." Praxis 93, no. 10 (March 1, 2004): 377–79. http://dx.doi.org/10.1024/0369-8394.93.10.377.

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Eine Tränendrüsenschwellung als Erstmanifestation einer Sarkoidose tritt in weniger als 1% der Fälle auf. Im Rahmen dieser Systemerkrankung werden die verschiedenen Augenabschnitte und die Adnexe unterschiedlich isoliert oder kombiniert betroffen. Unser Fallbericht zeigt, dass die Diagnostik bei einer Tränendrüsenschwellung schwierig sein kann und dass eine konklusive Diagnose eventuell erst im weiteren Krankheitsverlauf einer Multisystemerkrankung gestellt werden kann.

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Li, Mengjie, and Haisheng Yuan. "Dendrodontia hyphopaxillosa (Basidiomycota, Polyporaceae), a new species with dense hyphal pegs from southern China." Phytotaxa 156, no. 3 (January 16, 2014): 182. http://dx.doi.org/10.11646/phytotaxa.156.3.9.

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Dendrodontia hyphopaxillosa, a new epithelioid species from southern China in Polyporaceae is described and illustrated. The species is characterized by resupinate, adnate, effused basidiocarps, densely distributed cylindrical hyphal pegs, frequently branched contorted dendrohyphidia and small ellipsoid to subcylindrical basidiospores. Discriminating characters between the new species and closely related species are discussed, and an identification key to the species of Dendrodontia is provided.

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BLANCO, Oscar, Ana CRESPO, and John A. ELIX. "Two new species of Xanthoparmelia (Ascomycota: Parmeliaceae ) from Spain." Lichenologist 37, no. 2 (March 2005): 97–100. http://dx.doi.org/10.1017/s0024282905014829.

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Xanthoparmelia isidiovagans and X. subverrucigera from Spain are described as new to science. Both species are characterized by an isidiate upper surface and the presence of the stictic acid chemosyndrome in the medulla, but X. isidiovagans has a vagrant thallus with markedly revolute lobes with a black lower surface, whereas X. subverrucigera has adnate thalli with subirregular lobes and a brown lower surface.

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