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Journal articles on the topic 'Developmental neurophysiology Genetic aspects'

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Published: 4 June 2021
Last updated: 28 January 2023

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1

Winter, R. M. "Genetic Aspects of Developmental Pathology." Journal of Medical Genetics 25, no. 2 (February 1, 1988): 141. http://dx.doi.org/10.1136/jmg.25.2.141.

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2

Scharloo, W. "Canalization: Genetic and Developmental Aspects." Annual Review of Ecology and Systematics 22, no. 1 (November 1991): 65–93. http://dx.doi.org/10.1146/annurev.es.22.110191.000433.

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3

Regehr, Sonya M. "The genetic aspects of developmental dyslexia." Canadian Journal of Behavioural Science / Revue canadienne des sciences du comportement 19, no. 3 (1987): 239–53. http://dx.doi.org/10.1037/h0079988.

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4

Postma, Alex V., Lukas R. C. Dekker, Alexandre T. Soufan, and Antoon F. M. Moorman. "Developmental and Genetic Aspects of Atrial Fibrillation." Trends in Cardiovascular Medicine 19, no. 4 (May 2009): 123–30. http://dx.doi.org/10.1016/j.tcm.2009.07.003.

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5

Paoli, Marco, and Giovanni C. Galizia. "Olfactory coding in honeybees." Cell and Tissue Research 383, no. 1 (January 2021): 35–58. http://dx.doi.org/10.1007/s00441-020-03385-5.

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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.
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6

Alkhzouz, Camelia, Simona Bucerzan, Maria Miclaus, Andreea-Manuela Mirea, and Diana Miclea. "46,XX DSD: Developmental, Clinical and Genetic Aspects." Diagnostics 11, no. 8 (July 30, 2021): 1379. http://dx.doi.org/10.3390/diagnostics11081379.

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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.
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7

Srivastava, Deepak. "Developmental and genetic aspects of congenital heart disease." Current Opinion in Cardiology 14, no. 3 (May 1999): 263. http://dx.doi.org/10.1097/00001573-199905000-00011.

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8

Levy, Avraham A., Anne Bagg Britt, Kenneth R. Luehrsen, Vicki L. Chandler, Christine Warren, and Virginia Walbot. "Developmental and genetic aspects ofMutator excision in maize." Developmental Genetics 10, no. 6 (1989): 520–31. http://dx.doi.org/10.1002/dvg.1020100611.

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9

Veenma, D. C. M., A. de Klein, and D. Tibboel. "Developmental and genetic aspects of congenital diaphragmatic hernia." Pediatric Pulmonology 47, no. 6 (March 29, 2012): 534–45. http://dx.doi.org/10.1002/ppul.22553.

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10

MORSE, ANDREW C., JOHN L. BEARD, and BYRON C. JONES. "A Genetic Developmental Model of Iron Deficiency: Biological Aspects." Proceedings of the Society for Experimental Biology and Medicine 220, no. 3 (March 1999): 147–52. http://dx.doi.org/10.1046/j.1525-1373.1999.d01-22.x.

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11

Morse, A. C., J. L. Beard, and B. C. Jones. "A Genetic Developmental Model of Iron Deficiency: Biological Aspects." Experimental Biology and Medicine 220, no. 3 (March 1, 1999): 147–52. http://dx.doi.org/10.3181/00379727-220-44357.

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12

Jablonka, Eva, and Marion J. Lamb. "Bridging the gap: The developmental aspects of evolution." Behavioral and Brain Sciences 30, no. 4 (August 2007): 378–89. http://dx.doi.org/10.1017/s0140525x07002361.

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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.
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13

Hughes, Imelda, and Richard Newton. "Genetic Aspects of Cerebral Palsy." Developmental Medicine & Child Neurology 34, no. 1 (November 12, 2008): 80–86. http://dx.doi.org/10.1111/j.1469-8749.1992.tb08568.x.

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14

Wynne-Davies, Ruth. "GENETIC ASPECTS OF IDIOPATHIC SCOLIOSIS." Developmental Medicine & Child Neurology 15, no. 6 (November 12, 2008): 809–11. http://dx.doi.org/10.1111/j.1469-8749.1973.tb04919.x.

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15

Avdjieva-Tzavella, D. "Genetic and Non Genetic Aspects of Autism Spectrum Disorders." Balkan Journal of Medical Genetics 11, no. 1 (January 1, 2008): 3–10. http://dx.doi.org/10.2478/v10034-008-0012-2.

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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.
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16

Lichtenstein, Anatoly V. "Cancer: evolutionary, genetic and epigenetic aspects." Clinical Epigenetics 1, no. 3-4 (September 14, 2010): 85–100. http://dx.doi.org/10.1007/s13148-010-0010-6.

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17

Krausz, Csilla, and Leendert H. J. Looijenga. "Genetic aspects of testicular germ cell tumors." Cell Cycle 7, no. 22 (November 15, 2008): 3519–24. http://dx.doi.org/10.4161/cc.7.22.6980.

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18

Graw, Jochen. "Genetic aspects of embryonic eye development in vertebrates." Developmental Genetics 18, no. 3 (1996): 181–97. http://dx.doi.org/10.1002/(sici)1520-6408(1996)18:3<181::aid-dvg1>3.0.co;2-5.

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19

Dilcher, Roxane, Roula Jamous, Adam Takacs, Eszter Tóth-Fáber, Alexander Münchau, Shu-Chen Li, and 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, no. 4 (April 1, 2021): 1382–95. http://dx.doi.org/10.1152/jn.00681.2020.

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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.
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20

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

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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.

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22

Comings, David E. "Genetic aspects of childhood behavioral disorders." Child Psychiatry and Human Development 27, no. 3 (March 1997): 139–50. http://dx.doi.org/10.1007/bf02353694.

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23

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

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24

Paul, Lynn K., Warren S. Brown, Ralph Adolphs, J. Michael Tyszka, Linda J. Richards, Pratik Mukherjee, and Elliott H. Sherr. "Agenesis of the corpus callosum: genetic, developmental and functional aspects of connectivity." Nature Reviews Neuroscience 8, no. 4 (April 2007): 287–99. http://dx.doi.org/10.1038/nrn2107.

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25

Korochkin, L. I. "Aspects of the genetic control of development of the autonomous nervous system." Russian Journal of Developmental Biology 31, no. 2 (March 2000): 71–88. http://dx.doi.org/10.1007/bf02758810.

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26

Kaufman, Jim, and Thomas L. Koppenheffer. "Session 3: Molecular and genetic aspects of the MHC, and complement." Developmental & Comparative Immunology 13, no. 4 (September 1989): 371–73. http://dx.doi.org/10.1016/0145-305x(89)90079-7.

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27

Rinkevich, B., and I. L. Weissman. "3.5 Some genetic aspects of chimera resorption in a colonial tunicate." Developmental & Comparative Immunology 13, no. 4 (September 1989): 376. http://dx.doi.org/10.1016/0145-305x(89)90084-0.

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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, no. 9 (September 12, 2020): 2951. http://dx.doi.org/10.3390/jcm9092951.

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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.
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29

Björn, Marko Henrik, Werner Ravyse, Chrisna Botha-Ravyse, Jonne M. Laurila, and Tuula Keinonen. "A Revised Pedagogy Model for Simulator-Based Training with Biomedical Laboratory Science Students." Education Sciences 11, no. 7 (July 1, 2021): 328. http://dx.doi.org/10.3390/educsci11070328.

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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.
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30

Zafeiriou, Dimitrios I., Efterpi L. Pavlidou, and Euthymia Vargìami. "Diverse Clinical and Genetic Aspects of Craniofrontonasal Syndrome." Pediatric Neurology 44, no. 2 (February 2011): 83–87. http://dx.doi.org/10.1016/j.pediatrneurol.2010.10.012.

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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, no. 2 (September 1994): 94–95. http://dx.doi.org/10.1016/0887-8994(94)90183-x.

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32

Trifu, Simona Corina, Anca Vlăduţi, and Antonia Ioana Trifu. "Genetic aspects in schizophrenia. Receptoral theories. Metabolic theories." Romanian Journal of Morphology and Embryology 61, no. 1 (2020): 25–32. http://dx.doi.org/10.47162/rjme.61.1.03.

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33

Goldsmith, H. H., Kathryn S. Lemery, Kristin A. Buss, and Joseph J. Campos. "Genetic analyses of focal aspects of infant temperament." Developmental Psychology 35, no. 4 (July 1999): 972–85. http://dx.doi.org/10.1037/0012-1649.35.4.972.

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34

Eisenberg, Vered H., and Joseph G. Schenker. "Genetic engineering: Moral aspects and control of practice." Journal of Assisted Reproduction and Genetics 14, no. 6 (June 1997): 297–316. http://dx.doi.org/10.1007/bf02765833.

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35

Kwon, Ahreum, and Ho-Seong Kim. "Congenital hypogonadotropic hypogonadism: from clinical characteristics to genetic aspects." Precision and Future Medicine 5, no. 3 (September 30, 2021): 97–105. http://dx.doi.org/10.23838/pfm.2021.00093.

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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.
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36

Weiss, Norbert, and Gerald W. Zamponi. "Genetic T-type calcium channelopathies." Journal of Medical Genetics 57, no. 1 (June 19, 2019): 1–10. http://dx.doi.org/10.1136/jmedgenet-2019-106163.

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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.
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37

Eriksson, Johan G. "Developmental pathways and programming of diabetes: epidemiological aspects." Journal of Endocrinology 242, no. 1 (July 2019): T95—T104. http://dx.doi.org/10.1530/joe-18-0680.

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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.
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38

Harsanyi, Stefan, Radoslav Zamborsky, Lubica Krajciova, Milan Kokavec, and Lubos Danisovic. "Developmental Dysplasia of the Hip: A Review of Etiopathogenesis, Risk Factors, and Genetic Aspects." Medicina 56, no. 4 (March 31, 2020): 153. http://dx.doi.org/10.3390/medicina56040153.

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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.
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39

Rajpert-De Meyts, Ewa. "Developmental model for the pathogenesis of testicular carcinoma in situ: genetic and environmental aspects." Human Reproduction Update 12, no. 3 (March 15, 2006): 303–23. http://dx.doi.org/10.1093/humupd/dmk006.

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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, no. 2 (April 1987): 195. http://dx.doi.org/10.1080/07315724.1987.10738106.

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41

Popova, Nina, Nikolai Dygalo, and Hasan Parvez. "Genetic and developmental aspects of neuroendocrine regulation investigated by Eugene Naumenko and his colleagues." Biogenic Amines 19, no. 4 (December 1, 2005): 337–45. http://dx.doi.org/10.1163/156939105774647330.

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42

Mullis, Primus E. "Genetic control of growth." European Journal of Endocrinology 152, no. 1 (January 2005): 11–31. http://dx.doi.org/10.1530/eje.1.01797.

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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.
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43

Schlissel, Gavin, and Pulin Li. "Synthetic Developmental Biology: Understanding Through Reconstitution." Annual Review of Cell and Developmental Biology 36, no. 1 (October 6, 2020): 339–57. http://dx.doi.org/10.1146/annurev-cellbio-020620-090650.

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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.
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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, no. 01 (December 1, 2021): 039–45. http://dx.doi.org/10.1055/s-0041-1735250.

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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.
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Bretaud, Sandrine, Sarah MacRaild, Phillip W. Ingham, and Oliver Bandmann. "The Influence of the Zebrafish Genetic Background on Parkinson's Disease–Related Aspects." Zebrafish 8, no. 3 (September 2011): 103–8. http://dx.doi.org/10.1089/zeb.2011.0697.

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46

Thambirajah, M. S. "Developmental dyslexia: an overview." Advances in Psychiatric Treatment 16, no. 4 (July 2010): 299–307. http://dx.doi.org/10.1192/apt.bp.108.006072.

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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.
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47

Smith, Lawrence C., and Bruce D. Murphy. "Review: Genetic and Epigenetic Aspects of Cloning and Potential Effects on Offspring of Cloned Mammals." Cloning and Stem Cells 6, no. 2 (June 2004): 126–32. http://dx.doi.org/10.1089/1536230041372319.

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48

Kahraman, S., G. Karlikaya, S. Sertyel, H. Karadayi, and N. Findikli. "Clinical aspects of preimplantation genetic diagnosis for single gene disorders combined with HLA typing." Reproductive BioMedicine Online 9, no. 5 (January 2004): 529–32. http://dx.doi.org/10.1016/s1472-6483(10)61637-9.

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49

Atchley, William R., A. Alison Plummer, and Bruce Riska. "GENETIC ANALYSIS OF SIZE-SCALING PATTERNS IN THE MOUSE MANDIBLE." Genetics 111, no. 3 (November 1, 1985): 579–95. http://dx.doi.org/10.1093/genetics/111.3.579.

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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.
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50

RUSANOVSKY, E. V. "INSTITUTIONAL ASPECTS OF FORMING AN INTERFIRM STRATEGIC ALLIANCE IN THE RUSSIAN ECONOMY." EKONOMIKA I UPRAVLENIE: PROBLEMY, RESHENIYA 3, no. 10 (2020): 22–27. http://dx.doi.org/10.36871/ek.up.p.r.2020.10.03.005.

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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.
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