Um die anderen Arten von Veröffentlichungen zu diesem Thema anzuzeigen, folgen Sie diesem Link: Developmental neurophysiology Genetic aspects.

Zeitschriftenartikel zum Thema „Developmental neurophysiology Genetic aspects“

Geben Sie eine Quelle nach APA, MLA, Chicago, Harvard und anderen Zitierweisen an

Wählen Sie eine Art der Quelle aus:

Machen Sie sich mit Top-50 Zeitschriftenartikel für die Forschung zum Thema "Developmental neurophysiology Genetic aspects" bekannt.

Neben jedem Werk im Literaturverzeichnis ist die Option "Zur Bibliographie hinzufügen" verfügbar. Nutzen Sie sie, wird Ihre bibliographische Angabe des gewählten Werkes nach der nötigen Zitierweise (APA, MLA, Harvard, Chicago, Vancouver usw.) automatisch gestaltet.

Sie können auch den vollen Text der wissenschaftlichen Publikation im PDF-Format herunterladen und eine Online-Annotation der Arbeit lesen, wenn die relevanten Parameter in den Metadaten verfügbar sind.

Sehen Sie die Zeitschriftenartikel für verschiedene Spezialgebieten durch und erstellen Sie Ihre Bibliographie auf korrekte Weise.

1

Winter, R. M. „Genetic Aspects of Developmental Pathology“. Journal of Medical Genetics 25, Nr. 2 (01.02.1988): 141. http://dx.doi.org/10.1136/jmg.25.2.141.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
2

Scharloo, W. „Canalization: Genetic and Developmental Aspects“. Annual Review of Ecology and Systematics 22, Nr. 1 (November 1991): 65–93. http://dx.doi.org/10.1146/annurev.es.22.110191.000433.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
3

Regehr, Sonya M. „The genetic aspects of developmental dyslexia.“ Canadian Journal of Behavioural Science / Revue canadienne des sciences du comportement 19, Nr. 3 (1987): 239–53. http://dx.doi.org/10.1037/h0079988.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
4

Postma, Alex V., Lukas R. C. Dekker, Alexandre T. Soufan und Antoon F. M. Moorman. „Developmental and Genetic Aspects of Atrial Fibrillation“. Trends in Cardiovascular Medicine 19, Nr. 4 (Mai 2009): 123–30. http://dx.doi.org/10.1016/j.tcm.2009.07.003.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
5

Paoli, Marco, und Giovanni C. Galizia. „Olfactory coding in honeybees“. Cell and Tissue Research 383, Nr. 1 (Januar 2021): 35–58. http://dx.doi.org/10.1007/s00441-020-03385-5.

Der volle Inhalt der Quelle
Annotation:
Abstract With less than a million neurons, the western honeybee Apis mellifera is capable of complex olfactory behaviors and provides an ideal model for investigating the neurophysiology of the olfactory circuit and the basis of olfactory perception and learning. Here, we review the most fundamental aspects of honeybee’s olfaction: first, we discuss which odorants dominate its environment, and how bees use them to communicate and regulate colony homeostasis; then, we describe the neuroanatomy and the neurophysiology of the olfactory circuit; finally, we explore the cellular and molecular mechanisms leading to olfactory memory formation. The vastity of histological, neurophysiological, and behavioral data collected during the last century, together with new technological advancements, including genetic tools, confirm the honeybee as an attractive research model for understanding olfactory coding and learning.
APA, Harvard, Vancouver, ISO und andere Zitierweisen
6

Alkhzouz, Camelia, Simona Bucerzan, Maria Miclaus, Andreea-Manuela Mirea und Diana Miclea. „46,XX DSD: Developmental, Clinical and Genetic Aspects“. Diagnostics 11, Nr. 8 (30.07.2021): 1379. http://dx.doi.org/10.3390/diagnostics11081379.

Der volle Inhalt der Quelle
Annotation:
Differences in sex development (DSD) in patients with 46,XX karyotype occur by foetal or postnatal exposure to an increased amount of androgens. These disorders are usually diagnosed at birth, in newborns with abnormal genitalia, or later, due to postnatal virilization, usually at puberty. Proper diagnosis and therapy are mostly based on the knowledge of normal development and molecular etiopathogenesis of the gonadal and adrenal structures. This review aims to describe the most relevant data that are correlated with the normal and abnormal development of adrenal and gonadal structures in direct correlation with their utility in clinical practice, mainly in patients with 46,XX karyotype. We described the prenatal development of structures together with the main molecules and pathways that are involved in sex development. The second part of the review described the physical, imaging, hormonal and genetic evaluation in a patient with a disorder of sex development, insisting more on patients with 46,XX karyotype. Further, 95% of the etiology in 46,XX patients with disorders of sex development is due to congenital adrenal hyperplasia, by enzyme deficiencies that are involved in the hormonal synthesis pathway. The other cases are explained by genetic abnormalities that are involved in the development of the genital system. The phenotypic variability is very important in 46,XX disorders of sex development and the knowledge of each sign, even the most discreet, which could reveal such disorders, mainly in the neonatal period, could influence the evolution, prognosis and life quality long term.
APA, Harvard, Vancouver, ISO und andere Zitierweisen
7

Srivastava, Deepak. „Developmental and genetic aspects of congenital heart disease“. Current Opinion in Cardiology 14, Nr. 3 (Mai 1999): 263. http://dx.doi.org/10.1097/00001573-199905000-00011.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
8

Levy, Avraham A., Anne Bagg Britt, Kenneth R. Luehrsen, Vicki L. Chandler, Christine Warren und Virginia Walbot. „Developmental and genetic aspects ofMutator excision in maize“. Developmental Genetics 10, Nr. 6 (1989): 520–31. http://dx.doi.org/10.1002/dvg.1020100611.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
9

Veenma, D. C. M., A. de Klein und D. Tibboel. „Developmental and genetic aspects of congenital diaphragmatic hernia“. Pediatric Pulmonology 47, Nr. 6 (29.03.2012): 534–45. http://dx.doi.org/10.1002/ppul.22553.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
10

MORSE, ANDREW C., JOHN L. BEARD und BYRON C. JONES. „A Genetic Developmental Model of Iron Deficiency: Biological Aspects“. Proceedings of the Society for Experimental Biology and Medicine 220, Nr. 3 (März 1999): 147–52. http://dx.doi.org/10.1046/j.1525-1373.1999.d01-22.x.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
11

Morse, A. C., J. L. Beard und B. C. Jones. „A Genetic Developmental Model of Iron Deficiency: Biological Aspects“. Experimental Biology and Medicine 220, Nr. 3 (01.03.1999): 147–52. http://dx.doi.org/10.3181/00379727-220-44357.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
12

Jablonka, Eva, und Marion J. Lamb. „Bridging the gap: The developmental aspects of evolution“. Behavioral and Brain Sciences 30, Nr. 4 (August 2007): 378–89. http://dx.doi.org/10.1017/s0140525x07002361.

Der volle Inhalt der Quelle
Annotation:
AbstractThe commentaries onEvolution in Four Dimensionsreflect views ranging from total adherence to gene-centered neo-Darwinism, to the acceptance of non-genetic and Lamarckian processes in evolution. We maintain that genetic, epigenetic, behavioral, and cultural variations have all been significant, and that the developmental aspects of heredity and evolution are an important bridge that can unite seemingly conflicting research programs and different disciplines.
APA, Harvard, Vancouver, ISO und andere Zitierweisen
13

Hughes, Imelda, und Richard Newton. „Genetic Aspects of Cerebral Palsy“. Developmental Medicine & Child Neurology 34, Nr. 1 (12.11.2008): 80–86. http://dx.doi.org/10.1111/j.1469-8749.1992.tb08568.x.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
14

Wynne-Davies, Ruth. „GENETIC ASPECTS OF IDIOPATHIC SCOLIOSIS“. Developmental Medicine & Child Neurology 15, Nr. 6 (12.11.2008): 809–11. http://dx.doi.org/10.1111/j.1469-8749.1973.tb04919.x.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
15

Avdjieva-Tzavella, D. „Genetic and Non Genetic Aspects of Autism Spectrum Disorders“. Balkan Journal of Medical Genetics 11, Nr. 1 (01.01.2008): 3–10. http://dx.doi.org/10.2478/v10034-008-0012-2.

Der volle Inhalt der Quelle
Annotation:
Genetic and Non Genetic Aspects of Autism Spectrum DisordersChromosome abnormalities have long been recognized as an important cause of learning disabilities and multiple malformation syndromes. About 0.8% of live born infants have numerical or structural chromosomal anomalies that result in an abnormal phenotype. Identification of such anomalies is important clinically and also for accurate genetic counseling. Recently, molecular cytogenetic and array-based techniques have enabled higher resolution screens for chromosome anomalies. This brief review of the etiology of autism spectrum disorders (ASD) focuses on the heritable and non heritable risk factors that underlie this major neuro-developmental disorder. Since all patients with a chromosomal imbalance are dysmorphic, the association of ASD with a facial dysmorphism seems to be a good indication for chromosomal anomaly screening.
APA, Harvard, Vancouver, ISO und andere Zitierweisen
16

Lichtenstein, Anatoly V. „Cancer: evolutionary, genetic and epigenetic aspects“. Clinical Epigenetics 1, Nr. 3-4 (14.09.2010): 85–100. http://dx.doi.org/10.1007/s13148-010-0010-6.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
17

Krausz, Csilla, und Leendert H. J. Looijenga. „Genetic aspects of testicular germ cell tumors“. Cell Cycle 7, Nr. 22 (15.11.2008): 3519–24. http://dx.doi.org/10.4161/cc.7.22.6980.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
18

Graw, Jochen. „Genetic aspects of embryonic eye development in vertebrates“. Developmental Genetics 18, Nr. 3 (1996): 181–97. http://dx.doi.org/10.1002/(sici)1520-6408(1996)18:3<181::aid-dvg1>3.0.co;2-5.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
19

Dilcher, Roxane, Roula Jamous, Adam Takacs, Eszter Tóth-Fáber, Alexander Münchau, Shu-Chen Li und Christian Beste. „Neurophysiology of embedded response plans: age effects in action execution but not in feature integration from preadolescence to adulthood“. Journal of Neurophysiology 125, Nr. 4 (01.04.2021): 1382–95. http://dx.doi.org/10.1152/jn.00681.2020.

Der volle Inhalt der Quelle
Annotation:
Different aspects of an action need to be integrated to allow smooth unfolding of behavior. We examine developmental effects in these processes and show that mechanisms of action execution and speed, but not those of action feature binding, are subject to age-related changes between the age of 10 and 30 yr.
APA, Harvard, Vancouver, ISO und andere Zitierweisen
20

Cinar, C., C. Beyazyurek, G. Ozgon, S. Ozkan, B. Ismailoglu, O. Oner, F. Fiorentino und S. Kahraman. „4.002 Genetic aspects of male infertility in assisted reproduction“. Reproductive BioMedicine Online 16 (Januar 2008): s38. http://dx.doi.org/10.1016/s1472-6483(10)61385-5.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
21

Hackstein, JHP. „Genetic and evolutionary aspects of methanogenesis“. Reproduction Nutrition Development 37, Suppl. 1 (1997): 5–8. http://dx.doi.org/10.1051/rnd:19970702.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
22

Comings, David E. „Genetic aspects of childhood behavioral disorders“. Child Psychiatry and Human Development 27, Nr. 3 (März 1997): 139–50. http://dx.doi.org/10.1007/bf02353694.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
23

Bis-Brewer, Dana M., Sarah Fazal und Stephan Züchner. „Genetic modifiers and non-Mendelian aspects of CMT“. Brain Research 1726 (Januar 2020): 146459. http://dx.doi.org/10.1016/j.brainres.2019.146459.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
24

Paul, Lynn K., Warren S. Brown, Ralph Adolphs, J. Michael Tyszka, Linda J. Richards, Pratik Mukherjee und Elliott H. Sherr. „Agenesis of the corpus callosum: genetic, developmental and functional aspects of connectivity“. Nature Reviews Neuroscience 8, Nr. 4 (April 2007): 287–99. http://dx.doi.org/10.1038/nrn2107.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
25

Korochkin, L. I. „Aspects of the genetic control of development of the autonomous nervous system“. Russian Journal of Developmental Biology 31, Nr. 2 (März 2000): 71–88. http://dx.doi.org/10.1007/bf02758810.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
26

Kaufman, Jim, und Thomas L. Koppenheffer. „Session 3: Molecular and genetic aspects of the MHC, and complement“. Developmental & Comparative Immunology 13, Nr. 4 (September 1989): 371–73. http://dx.doi.org/10.1016/0145-305x(89)90079-7.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
27

Rinkevich, B., und I. L. Weissman. „3.5 Some genetic aspects of chimera resorption in a colonial tunicate“. Developmental & Comparative Immunology 13, Nr. 4 (September 1989): 376. http://dx.doi.org/10.1016/0145-305x(89)90084-0.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
28

Aliev, Gjumrakch, Narasimha M. Beeraka, Vladimir N. Nikolenko, Andrey A. Svistunov, Tatyana Rozhnova, Svetlana Kostyuk, Igor Cherkesov et al. „Neurophysiology and Psychopathology Underlying PTSD and Recent Insights into the PTSD Therapies—A Comprehensive Review“. Journal of Clinical Medicine 9, Nr. 9 (12.09.2020): 2951. http://dx.doi.org/10.3390/jcm9092951.

Der volle Inhalt der Quelle
Annotation:
Post-traumatic stress disorder (PTSD) is a well-known psychiatric disorder that affects millions of people worldwide. Pharmacodynamic and cognitive-behavioral therapies (CBT) have been used to treat patients with PTSD. However, it remains unclear whether there are concurrent changes in psychopathological and neurophysiological factors associated with PTSD patients. Past reports described those PTSD patients with efficient fatty acid metabolism, neurogenesis, mitochondrial energy balance could improve ability to cope against the conditioned fear responses and traumatic memories. Furthermore, cognitive, behavioral, cellular, and molecular evidence can be combined to create personalized therapies for PTSD sufferers either with or without comorbidities such as depression or memory impairment. Unfortunately, there is still evidence lacking to establish a full understanding of the underlying neurophysiological and psychopathological aspects associated with PTSD. This review has extensively discussed the single nucleotide polymorphism (SNPs) of genetic factors to cause PTSD, the implications of inflammation, neurotransmitter genomics, metabolic alterations, neuroendocrine disturbance (hypothalamus-pituitary-adrenal (HPA) axis), mitochondrial dynamics, neurogenesis, and premature aging related to PTSD-induced psychopathology and neurophysiology. In addition, the review delineated the importance of CBT and several pharmacodynamic therapies to mitigate symptomatology of PTSD.
APA, Harvard, Vancouver, ISO und andere Zitierweisen
29

Björn, Marko Henrik, Werner Ravyse, Chrisna Botha-Ravyse, Jonne M. Laurila und Tuula Keinonen. „A Revised Pedagogy Model for Simulator-Based Training with Biomedical Laboratory Science Students“. Education Sciences 11, Nr. 7 (01.07.2021): 328. http://dx.doi.org/10.3390/educsci11070328.

Der volle Inhalt der Quelle
Annotation:
Methods based on simulation pedagogy are widely used to practice hands-on skills in safety environment. The usability of an EEG simulator on clinical neurophysiology course was evaluated. Second-year biomedical laboratory science students (N = 35) on this course were included in the study. They were divided into three groups. Two groups used the EEG simulator with different feedback modes and one group did not use the simulator. Results were expected to reveal a correlation between user experience and learning outcomes. This study made used of a mixed method study design. During the study, students were asked to keep a learning diary throughout the course on their experience. Diaries were analyzed qualitatively based on content analyses. Quantitative analyses based on an UX questionnaire that measures classical usability aspects (efficiency, perspicuity, dependability) and user experience aspects (novelty, stimulation) and the students’ feelings to use simulator. The quantitative data was analyzed using SPSSTM software. The quantitative and qualitative analyses showed that the use of the EEG simulator, which was evaluating teaching–learning process, has an extra benefit in clinical neurophysiology education and students felt that the simulator was useful in learning. The simulation debriefing session should be followed by a full theoretical and practical session. Students compared their learning from the simulator with that of the actual placement which fosters the reflective practice of learning, again deepening the understanding of the EEG electrode placement and different wave patterns.
APA, Harvard, Vancouver, ISO und andere Zitierweisen
30

Zafeiriou, Dimitrios I., Efterpi L. Pavlidou und Euthymia Vargìami. „Diverse Clinical and Genetic Aspects of Craniofrontonasal Syndrome“. Pediatric Neurology 44, Nr. 2 (Februar 2011): 83–87. http://dx.doi.org/10.1016/j.pediatrneurol.2010.10.012.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
31

Vigevano, Federico, Lucia Fusco, Matteo Di Capua, Stefano Ricci, Rosella Sebastianelli, Pierpaolo Lucchini, Tiziana Granata et al. „Benign infantile familial convulsions: Clinical and genetic aspects“. Pediatric Neurology 11, Nr. 2 (September 1994): 94–95. http://dx.doi.org/10.1016/0887-8994(94)90183-x.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
32

Trifu, Simona Corina, Anca Vlăduţi und Antonia Ioana Trifu. „Genetic aspects in schizophrenia. Receptoral theories. Metabolic theories“. Romanian Journal of Morphology and Embryology 61, Nr. 1 (2020): 25–32. http://dx.doi.org/10.47162/rjme.61.1.03.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
33

Goldsmith, H. H., Kathryn S. Lemery, Kristin A. Buss und Joseph J. Campos. „Genetic analyses of focal aspects of infant temperament.“ Developmental Psychology 35, Nr. 4 (Juli 1999): 972–85. http://dx.doi.org/10.1037/0012-1649.35.4.972.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
34

Eisenberg, Vered H., und Joseph G. Schenker. „Genetic engineering: Moral aspects and control of practice“. Journal of Assisted Reproduction and Genetics 14, Nr. 6 (Juni 1997): 297–316. http://dx.doi.org/10.1007/bf02765833.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
35

Kwon, Ahreum, und Ho-Seong Kim. „Congenital hypogonadotropic hypogonadism: from clinical characteristics to genetic aspects“. Precision and Future Medicine 5, Nr. 3 (30.09.2021): 97–105. http://dx.doi.org/10.23838/pfm.2021.00093.

Der volle Inhalt der Quelle
Annotation:
Congenital hypogonadotropic hypogonadism (CHH) is a rare disorder caused by a deficiency in gonadotropin-releasing hormone (GnRH). CHH is characterized by delayed puberty and/or infertility; this is because GnRH is the main component of the hypothalamic-pituitary-gonadal (HPG) axis, which is a key factor in pubertal development and reproductive function completion. However, since the development of sexual characteristics and reproduction begins in the prenatal period and is very complex and delicate, the clinical characteristics and involved genes are very diverse. In particular, the HPG axis is activated three times in a lifetime, and the symptoms and biochemical findings of CHH vary by period. In addition, related genes also vary according to the formation and activation process of the HPG axis. In this review, the clinical characteristics and treatment of CHH according to HPG axis activation and different developmental periods are reviewed, and the related genes are summarized according to their pathological mechanisms.
APA, Harvard, Vancouver, ISO und andere Zitierweisen
36

Weiss, Norbert, und Gerald W. Zamponi. „Genetic T-type calcium channelopathies“. Journal of Medical Genetics 57, Nr. 1 (19.06.2019): 1–10. http://dx.doi.org/10.1136/jmedgenet-2019-106163.

Der volle Inhalt der Quelle
Annotation:
T-type channels are low-voltage-activated calcium channels that contribute to a variety of cellular and physiological functions, including neuronal excitability, hormone and neurotransmitter release as well as developmental aspects. Several human conditions including epilepsy, autism spectrum disorders, schizophrenia, motor neuron disorders and aldosteronism have been traced to variations in genes encoding T-type channels. In this short review, we present the genetics of T-type channels with an emphasis on structure-function relationships and associated channelopathies.
APA, Harvard, Vancouver, ISO und andere Zitierweisen
37

Eriksson, Johan G. „Developmental pathways and programming of diabetes: epidemiological aspects“. Journal of Endocrinology 242, Nr. 1 (Juli 2019): T95—T104. http://dx.doi.org/10.1530/joe-18-0680.

Der volle Inhalt der Quelle
Annotation:
Type 2 diabetes (T2D) is a major, rapidly increasing global public health challenge. The major risk factors for T2D include overweight and obesity, lifestyle-related factors and genetic factors. Early life exposures shape the developmental trajectories and alter susceptibility to T2D. Based on epidemiological studies it has been suggested that fetal undernutrition plays a role in the etiology of T2D. A low birth weight has been considered a proxy for fetal undernutrition. A meta-analysis reported that a 1 kg increase in birth weight is associated with a roughly 20% lower risk of T2D. Although fetal life is of major importance for future health, the period spanning the first 1000 days of life, is characterized by great plasticity and largely influencing later health. Different growth trajectories during this time period have also been associated with an increased risk of T2D. Studies assessing the association between age at BMI rebound in childhood and later risk for T2D have reported a fivefold difference in T2D according to age at BMI rebound. Developmental and epidemiological cohort studies focusing on T2D have major public health implications supporting a paradigm shift; a shift from focusing upon risk factor modification in adult life to adopting a life course perspective when studying T2D. This paradigm shift will not only help us in getting a better understanding of the pathophysiology underlying T2D, but it will also open new possibilities and opportunities in the prevention of T2D and related disorders.
APA, Harvard, Vancouver, ISO und andere Zitierweisen
38

Harsanyi, Stefan, Radoslav Zamborsky, Lubica Krajciova, Milan Kokavec und Lubos Danisovic. „Developmental Dysplasia of the Hip: A Review of Etiopathogenesis, Risk Factors, and Genetic Aspects“. Medicina 56, Nr. 4 (31.03.2020): 153. http://dx.doi.org/10.3390/medicina56040153.

Der volle Inhalt der Quelle
Annotation:
As one of the most frequent skeletal anomalies, developmental dysplasia of the hip (DDH) is characterized by a considerable range of pathology, from minor laxity of ligaments in the hip joint to complete luxation. Multifactorial etiology, of which the candidate genes have been studied the most, poses a challenge in understanding this disorder. Candidate gene association studies (CGASs) along with genome-wide association studies (GWASs) and genome-wide linkage analyses (GWLAs) have found numerous genes and loci with susceptible DDH association. Studies put major importance on candidate genes associated with the formation of connective tissue (COL1A1), osteogenesis (PAPPA2, GDF5), chondrogenesis (UQCC1, ASPN) and cell growth, proliferation and differentiation (TGFB1). Recent studies show that epigenetic factors, such as DNA methylation affect gene expression and therefore could play an important role in DDH pathogenesis. This paper reviews all existing risk factors affecting DDH incidence, along with candidate genes associated with genetic or epigenetic etiology of DDH in various studies.
APA, Harvard, Vancouver, ISO und andere Zitierweisen
39

Rajpert-De Meyts, Ewa. „Developmental model for the pathogenesis of testicular carcinoma in situ: genetic and environmental aspects“. Human Reproduction Update 12, Nr. 3 (15.03.2006): 303–23. http://dx.doi.org/10.1093/humupd/dmk006.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
40

Flodin, Nestor W. „Metabolism of Trace Elements in Man. Vol. I—Developmental Aspects. Vol. II—Genetic Implications“. Journal of the American College of Nutrition 6, Nr. 2 (April 1987): 195. http://dx.doi.org/10.1080/07315724.1987.10738106.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
41

Popova, Nina, Nikolai Dygalo und Hasan Parvez. „Genetic and developmental aspects of neuroendocrine regulation investigated by Eugene Naumenko and his colleagues“. Biogenic Amines 19, Nr. 4 (01.12.2005): 337–45. http://dx.doi.org/10.1163/156939105774647330.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
42

Mullis, Primus E. „Genetic control of growth“. European Journal of Endocrinology 152, Nr. 1 (Januar 2005): 11–31. http://dx.doi.org/10.1530/eje.1.01797.

Der volle Inhalt der Quelle
Annotation:
The application of the powerful tool molecular biology has made it possible to ask questions not only about hormone production and action but also to characterize many of the receptor molecules that initiate responses to the hormones. We are beginning to understand how cells may regulate the expression of genes and how hormones intervene in regulatory processes to adjust the expression of individual genes. In addition, great strides have been made in understanding how individual cells talk to each other through locally released factors to coordinate growth, differentiation, secretion, and other responses within a tissue. In this review I (1) focus on developmental aspects of the pituitary gland, (2) focus on the different components of the growth hormone axis and (3) examine the different altered genes and their related growth factors and/or regulatory systems that play an important physiological and pathophysiological role in growth. Further, as we have already entered the ‘post-genomic’ area, in which not only a defect at the molecular level becomes important but also its functional impact at the cellular level, I concentrate in the last part on some of the most important aspects of cell biology and secretion.
APA, Harvard, Vancouver, ISO und andere Zitierweisen
43

Schlissel, Gavin, und Pulin Li. „Synthetic Developmental Biology: Understanding Through Reconstitution“. Annual Review of Cell and Developmental Biology 36, Nr. 1 (06.10.2020): 339–57. http://dx.doi.org/10.1146/annurev-cellbio-020620-090650.

Der volle Inhalt der Quelle
Annotation:
Reconstitution is an experimental strategy that seeks to recapitulate biological events outside their natural contexts using a reduced set of components. Classically, biochemical reconstitution has been extensively applied to identify the minimal set of molecules sufficient for recreating the basic chemistry of life. By analogy, reconstitution approaches to developmental biology recapitulate aspects of developmental events outside an embryo, with the goal of revealing the basic genetic circuits or physical cues sufficient for recreating developmental decisions. The rapidly growing repertoire of genetic, molecular, microscopic, and bioengineering tools is expanding the complexity and precision of reconstitution experiments. We review the emerging field of synthetic developmental biology, with a focus on the ways in which reconstitution strategies and new biological tools have enhanced our modern understanding of fundamental questions in developmental biology.
APA, Harvard, Vancouver, ISO und andere Zitierweisen
44

Holzwarth, Johanna, Nadja Minopoli, Charlotte Pfrimmer, Martin Smitka, Sabine Borrel, Janbernd Kirschner, Nicole Muschol et al. „Clinical and Genetic Aspects of Juvenile Onset Pompe Disease“. Neuropediatrics 53, Nr. 01 (01.12.2021): 039–45. http://dx.doi.org/10.1055/s-0041-1735250.

Der volle Inhalt der Quelle
Annotation:
AbstractLittle is known about clinical symptomatology and genetics of juvenile onset Pompe disease (JOPD). The aims of this study were to analyze how these children are diagnosed, what clinical problems they have, and how phenotype is related to genotype. To accomplish this, we analyzed retrospectively data of 34 patients diagnosed after their first and before completion of their 18th birthday. Median age at diagnosis was 3.9 (range 1.1–17) years. Eight patients (23.5%) developed initial symptoms in the first year, 12 (35%) between 1 and 7 years, and 6 (18%) thereafter. Eight (23.5%) had no clinical symptoms at the time of diagnosis. Indications for diagnostics were a positive family history in three (9%), hyperCKemia in eight (23.5%), motor developmental delay in three (9%), and muscle weakness and/or pain in 17 (50%). Rare clinical signs were failure to thrive, recurrent diarrhea, and suspected hepatopathy with glycogen storage. Thirty-two different mutations were identified. Twenty-seven patients (79.5%) carried the milder c.32–13T > G mutation, known to be associated with a broad range of phenotypes. Three out of eight patients manifesting within the first year of life showed generalized muscle weakness, hypertrophic cardiomyopathy, and had to be ventilated during the course of disease, thereby demonstrating clinical overlap with infantile onset Pompe disease.These findings demonstrate that the phenotype of JOPD is broad and that the differential is not only restricted to neuromuscular disorders. Genotypic analysis was useful to delineate subjects with early onset JOPD from those with IOPD, but overall genotype–phenotype correlation was poor.
APA, Harvard, Vancouver, ISO und andere Zitierweisen
45

Bretaud, Sandrine, Sarah MacRaild, Phillip W. Ingham und Oliver Bandmann. „The Influence of the Zebrafish Genetic Background on Parkinson's Disease–Related Aspects“. Zebrafish 8, Nr. 3 (September 2011): 103–8. http://dx.doi.org/10.1089/zeb.2011.0697.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
46

Thambirajah, M. S. „Developmental dyslexia: an overview“. Advances in Psychiatric Treatment 16, Nr. 4 (Juli 2010): 299–307. http://dx.doi.org/10.1192/apt.bp.108.006072.

Der volle Inhalt der Quelle
Annotation:
SummaryFirst described over 100 years ago, developmental dyslexia (reading disability) has been a controversial subject. There has been much confusion regarding the definition, the psychological basis, the conceptualisation and even the name. Recent research has helped us to understand the main underlying cognitive deficits that lead to poor reading. Brain imaging studies conducted during the performance of reading tasks have shed light on its biological basis and genetic studies have identified a number of genes that are associated with reading difficulties. Together, these studies have led to a redefinition and new understanding of developmental dyslexia. This article examines these recent findings. A second article to appear in Advances will focus on clinical aspects of the disorder.
APA, Harvard, Vancouver, ISO und andere Zitierweisen
47

Smith, Lawrence C., und Bruce D. Murphy. „Review: Genetic and Epigenetic Aspects of Cloning and Potential Effects on Offspring of Cloned Mammals“. Cloning and Stem Cells 6, Nr. 2 (Juni 2004): 126–32. http://dx.doi.org/10.1089/1536230041372319.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
48

Kahraman, S., G. Karlikaya, S. Sertyel, H. Karadayi und N. Findikli. „Clinical aspects of preimplantation genetic diagnosis for single gene disorders combined with HLA typing“. Reproductive BioMedicine Online 9, Nr. 5 (Januar 2004): 529–32. http://dx.doi.org/10.1016/s1472-6483(10)61637-9.

Der volle Inhalt der Quelle
APA, Harvard, Vancouver, ISO und andere Zitierweisen
49

Atchley, William R., A. Alison Plummer und Bruce Riska. „GENETIC ANALYSIS OF SIZE-SCALING PATTERNS IN THE MOUSE MANDIBLE“. Genetics 111, Nr. 3 (01.11.1985): 579–95. http://dx.doi.org/10.1093/genetics/111.3.579.

Der volle Inhalt der Quelle
Annotation:
ABSTRACT The relationship between multidimensional form of the adult mouse mandible and body size is examined from an ontogenetic perspective. The origin and ontogeny of phenotypic correlations are described in terms of genetic and environmental covariance patterns between adult skeletal morphology and growth in body weight. Different ontogenetic patterns are observed in the genetic correlations, and these can be related to the developmental as well as the functional aspects of mandibular form. The quantitative genetic aspects of craniomandibular growth and morphogenesis are explored, together with an examination of the impact of ontogenetic changes in the genetic variance-covariance structure on morphogenetic integration and evolution by selection.
APA, Harvard, Vancouver, ISO und andere Zitierweisen
50

RUSANOVSKY, E. V. „INSTITUTIONAL ASPECTS OF FORMING AN INTERFIRM STRATEGIC ALLIANCE IN THE RUSSIAN ECONOMY“. EKONOMIKA I UPRAVLENIE: PROBLEMY, RESHENIYA 3, Nr. 10 (2020): 22–27. http://dx.doi.org/10.36871/ek.up.p.r.2020.10.03.005.

Der volle Inhalt der Quelle
Annotation:
The article is devoted to the formation of integration associations of economic entities in the market of sheep products from the point of view of the institutional and genetic concept. The specifics of doing business at the moment is being formed under the influence of institutional factors synthesized by different economic systems. The impact of these factors on the domestic market for sheep products is proposed to be considered within the framework of the concept of institutional matrices by means of institutional genetic analysis of developmental characteristics.
APA, Harvard, Vancouver, ISO und andere Zitierweisen
Wir bieten Rabatte auf alle Premium-Pläne für Autoren, deren Werke in thematische Literatursammlungen aufgenommen wurden. Kontaktieren Sie uns, um einen einzigartigen Promo-Code zu erhalten!

Zur Bibliographie