Relevant bibliographies by topics / Hereditary behaviour

Academic literature on the topic 'Hereditary behaviour'

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Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "Hereditary behaviour"

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Schwarzer, Gudrun, Susanne Huber, Martina Grüter, Thomas Grüter, Cornelia Groß, Melanie Hipfel, and Ingo Kennerknecht. "Gaze behaviour in hereditary prosopagnosia." Psychological Research 71, no. 5 (June 10, 2006): 583–90. http://dx.doi.org/10.1007/s00426-006-0068-0.

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Usmonov, Botir. "A Numerical Solution of Hereditary Equations with a Weakly Singular Kernel for Vibration Analysis of Viscoelastic Systems / Vienâdojumu Ar Vâjo Singulâro Kodolu Skaitliskais Risinâjums Iedzimto Viskoelastîgo Sistçmu Vibrâciju Analîzei." Proceedings of the Latvian Academy of Sciences. Section B. Natural, Exact, and Applied Sciences. 69, no. 6 (December 1, 2015): 326–30. http://dx.doi.org/10.1515/prolas-2015-0048.

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Abstract Viscoelastic, or composite materials that are hereditary deformable, have been characterised by exponential and weakly singular kernels in a hereditary equation. An exponential kernel is easy to be numerically implemented, but does not well describe complex vibratory behaviour of a hereditary deformable system. On the other hand, a weakly singular kernel is known to describe the complex vibratory behaviour, but is nontrivial to be numerically implemented. This study presents a numerical formulation for solving a hereditary equation with a weakly singular kernel. Recursive algebraic equations, which are numerically solvable, are formulated by using the Galerkin method enhanced by a numerical integration and elimination of weak singularity. Numerical experiments showed that the present approach with a weakly singular kernel is well fitted into a realistic vibratory behaviour of a hereditary deformable system under dynamic loads, as compared to the same approach with an exponential kernel.
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Di Paola, Mario, and Michele Fabio Granata. "Fractional model of concrete hereditary viscoelastic behaviour." Archive of Applied Mechanics 87, no. 2 (November 18, 2016): 335–48. http://dx.doi.org/10.1007/s00419-016-1196-7.

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Levina, Anna S., Nina A. Bondarenko, Natalia V. Shiryaeva, Alexander I. Vaido, and Natalia A. Dyuzhikova. "Hereditary determined diving behaviour in rats as a factor of fitness." Ecological genetics 18, no. 3 (October 9, 2020): 317–28. http://dx.doi.org/10.17816/ecogen25817.

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Background. Rats natural ability to swim and dive provides adaptation in the wildlife and is widely applied as an instrument in experimental physiology. Nevertheless theres little scientific evidence on diving behaviour in rats itself. Meanwhile this behavioural pattern might be a notable trait to shed light on functional features of the nervous system, the higher nervous activity structure and evolutional adaptability in animals, including inherited ones. Materials and methods. In the present work we compared the performance of the spontaneous diving behaviour in the Morris water maze and forced diving behaviour in the Extrapolation escape task in two selected rat strains genetically differing in the nervous system excitability threshold. Results. We found a greater extent and adaptive pattern of both types of the diving behaviour in the high-excitable LT strain. This may be due to such basic features of this strain as high exploratory activity and an increased level of fear reactions. It was also shown that the second, low-excitable HT rat strain, demonstrates maladaptive jumping behaviour in the Extrapolation escape task due to higher anxiety level in the stress conditions. Conclusion. Observed differences between two strains allow us to consider the diving behaviour performed by high-excitable rats an inherited strain characteristic resembling adaptive rat behaviours in the wild and look forward to investigate its genetic mechanisms.
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Ermakov, Pavel. "Hemispheric asymmetry of aggressive behaviour and hereditary factors." International Journal of Psychophysiology 94, no. 2 (November 2014): 143. http://dx.doi.org/10.1016/j.ijpsycho.2014.08.654.

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Iglauer, F., C. Beig, J. Dimigen, S. Gerold, A. Gocht, A. Seeburg, S. Steier, and F. Willmann. "Hereditary compulsive self-mutilating behaviour in laboratory rabbits." Laboratory Animals 29, no. 4 (October 1, 1995): 385–93. http://dx.doi.org/10.1258/002367795780740140.

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During the last few years an increasing number of cases of extensive automutilation has been observed in a rabbit breeding colony of Checkered crosses. Digits and pads of the front feet were traumatized. No other behavioural abnormalities or signs of disease were evident. Self-mutilation was seen both in stock, breeding and experimental animals, in rabbits kept singly in cages and in those housed in groups on the ground, in rabbits kept in different buildings and under the care of different staff members. This behavioural abnormality of Checkered crosses has also been observed in animals after being placed into other institutions or private homes. No evidence of an agent responsible for the occurrence of self-injury could be found with parasitological, mycological, histological, clinical or haematological examination. Twelve to 16 animals are affected yearly in a colony varying in size between 130 and 230 rabbits. Following complete healing, relapses occurred up to 3 times per year, on either the same or the opposite front foot. In the last 21 cases episodes of automutilation could be regularly interrupted with the dopamine antagonist, haloperidol. Similar signs of automutilation were never seen in animals of another breeding line kept in the same building and under the same conditions nor in animals brought in from other breeding colonies. A relatively high coefficient of inbreeding can be presupposed in this 15-year-old breeding colony of Checkered crosses. A genetic predisposition for the behavioural anomaly described appears very likely.
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Tchuraev, Rustem N. "Epigenes — overgenes level hereditary units." Ecological genetics 8, no. 4 (December 15, 2010): 17–24. http://dx.doi.org/10.17816/ecogen8417-24.

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The theoretical and experimental aspects concept of epigenes are considered. In epigenes part of the heritable information is preserved, coded and trasmitted in generations out of the primary structure of genomic DNA. The behaviour under crosses simples modelic epigenes is demonstrated. The variants of molecular-genetics mechanisms of epigenes and original results of experimental construction artificials epigenes by methods gene-engenering are presented. The ontogenetic and phylogenetic roles of epigene systems are discussed. It has been shown, that even simplest epigene systems can provide key events of ontogeny. The epigenes systems can provide non-Darwinian evolutionary strategy by means of “remember” relatively unsuccesful muves of evolution and preservation reserved variants of ontogeny.
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PALKA, P. "Biventricular diastolic behaviour in patients with hypertrophic and hereditary hemochromatosis cardiomyopathies." European Journal of Echocardiography 5, no. 5 (October 2004): 356–66. http://dx.doi.org/10.1016/j.euje.2004.01.003.

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Pridmore, Saxby, Gyaneshwar Rao, and Prosper Abusah. "Hereditary Spastic Paraplegia with Dementia." Australian & New Zealand Journal of Psychiatry 29, no. 4 (December 1995): 678–82. http://dx.doi.org/10.3109/00048679509064985.

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Objective: Hereditary spastic paraplegia (HSP) with dementia is a very rare condition. The aim of the paper is to present the first report of HSP in a Fijian Indian family. Method: A psychiatrist and a general physician examined the affected members of the family on five occasions over three years. Results: There are three affected individuals In a sibship of seven. The parents are without symptoms and the marriage is non-consanguineous. The course of the disease has been remarkably similar. All subjects were healthy and performing well in the early years of school. In two, symptoms of cognitive loss preceded difficulty with ambulation and in the third, these symptoms appeared concurrently. All subjects had both symptoms by 13 years of age; they were unable to ambulate independently by the mid to late teens, at which time there was dysarthria spastic paraplegia and dementia. One subject suffered a three month episode of hypomanic behaviour. Over the three-year study period deterioration was slight but noticeable. Conclusions: It is possible that HSP is more commonly associated with pre-senile dementia than is currently recognised. HSP with dementia is a very rare cause of failing school performance. Physical examination of the patient and other family members is indicated if this diagnosis is being considered.
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KALBE, M., B. HABERL, J. HERTEL, and W. HAAS. "Heredity of specific host-finding behaviour in Schistosoma mansoni miracidia." Parasitology 128, no. 6 (May 13, 2004): 635–43. http://dx.doi.org/10.1017/s0031182004005037.

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Two strains of Schistosoma mansoni were used to investigate the hereditary basis of species-specific host recognition by analysing behavioural responses of miracidia to snail-conditioned water. An Egyptian strain of S. mansoni, capable of distinguishing its host snail Biomphalaria alexandrina from other snails was cycled repeatedly through Biomphalaria glabrata, the intermediate host of a Brazilian strain known to respond even to non-susceptible snails with high intensity. After 5 cycles in the non-natural host, miracidia of the Egyptian strain still retained their preference for the original host snail. In a second experiment, host-finding behaviour of hybrids between these two parasite strains was studied. In the F1 generation, hybrids of both parental combinations showed the same low degree of specificity as the pure-bred Brazilian strain. Approximately one quarter of F2 hybrids proved to be as discriminatory as the Egyptian strain, confirming dominant Mendelian inheritance of non-specificity in schistosome miracidial host-finding behaviour. Moreover, hybrids seem to have lost the ability to develop in B. alexandrina, possibly suggesting a link between host recognition and host compatibility. The heredity of this behavioural trait is of evolutionary and epidemiological significance, since a shift to low host-finding specificity might have been a prerequisite for S. mansoni to acquire new host snails after being introduced to South America by the slave trade.
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Dissertations / Theses on the topic "Hereditary behaviour"

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Loxton, Natalie, and n/a. "The Contribution of Reinforcement Sensitivity Theory and Family Risk to Dysfuntional Eating and Hazardous Drinking." Griffith University. School of Applied Psychology, 2005. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20060112.111417.

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This thesis details a continuing body of research investigating the contribution of personality to disordered eating and alcohol abuse in young women. There is growing evidence of high levels of reward sensitivity in women with both disorders, and high levels of punishment sensitivity in dysfunctional eating women. However, it is unlikely that personality alone accounts for the development of such dysfunctional behaviour. Two studies were conducted to further examine the contribution of reward and punishment sensitivity to these disorders. In the first study, 443 university women completed self-report measures of alcohol use, dysfunctional eating, reinforcement sensitivity, parental drinking, family environment and maternal eating. Reward and punishment sensitivity were better predictors of disordered behaviour than family factors, although maternal dysfunctional eating significantly increased the risk of daughters' dysfunctional eating. Punishment sensitive daughters of bulimic mothers reported the highest level of bulimic symptoms themselves. Punishment sensitivity also functioned as a partial pathway variable between family risk and disordered eating. Given the stronger contribution of personality to disordered behaviour, a second study was conducted in which 131 women completed behavioural tasks under conditions of reward and punishment. Performance on a computerised measure of punishment sensitivity was associated with greater levels of dysfunctional eating but not drinking. However, performance on a card-sorting task of reward sensitivity failed to correlate with self-reported reward sensitivity or disordered behaviour. It was concluded that an innate sensitivity to reward increases the risk of disorders characterised by strong approach tendencies, whilst high punishment sensitivity, perhaps due to a chaotic family, increases the risk of dysfunctional eating, particularly daughters of eating disordered mothers.
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Loxton, Natalie. "The Contribution of Reinforcement Sensitivity Theory and Family Risk to Dysfuntional Eating and Hazardous Drinking." Thesis, Griffith University, 2005. http://hdl.handle.net/10072/365289.

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This thesis details a continuing body of research investigating the contribution of personality to disordered eating and alcohol abuse in young women. There is growing evidence of high levels of reward sensitivity in women with both disorders, and high levels of punishment sensitivity in dysfunctional eating women. However, it is unlikely that personality alone accounts for the development of such dysfunctional behaviour. Two studies were conducted to further examine the contribution of reward and punishment sensitivity to these disorders. In the first study, 443 university women completed self-report measures of alcohol use, dysfunctional eating, reinforcement sensitivity, parental drinking, family environment and maternal eating. Reward and punishment sensitivity were better predictors of disordered behaviour than family factors, although maternal dysfunctional eating significantly increased the risk of daughters' dysfunctional eating. Punishment sensitive daughters of bulimic mothers reported the highest level of bulimic symptoms themselves. Punishment sensitivity also functioned as a partial pathway variable between family risk and disordered eating. Given the stronger contribution of personality to disordered behaviour, a second study was conducted in which 131 women completed behavioural tasks under conditions of reward and punishment. Performance on a computerised measure of punishment sensitivity was associated with greater levels of dysfunctional eating but not drinking. However, performance on a card-sorting task of reward sensitivity failed to correlate with self-reported reward sensitivity or disordered behaviour. It was concluded that an innate sensitivity to reward increases the risk of disorders characterised by strong approach tendencies, whilst high punishment sensitivity, perhaps due to a chaotic family, increases the risk of dysfunctional eating, particularly daughters of eating disordered mothers.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Applied Psychology
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Svensson, Idor. "Phonological dyslexia : cognitive, behavioural and hereditary aspects /." [Göteborg] : Dept. of Psychology, Göteborg University, 2003. http://catalogue.bnf.fr/ark:/12148/cb399169814.

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Kechik, Joy E. "Comparing Family Sharing Behaviors in BRCA Carriers with PALB2 Carriers." Scholar Commons, 2019. https://scholarcommons.usf.edu/etd/7825.

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Identifying individuals with hereditary cancer predisposition can improve health outcomes for patients and their family members through early cancer detection and prevention strategies. Prior research about family sharing of genetic test results among those with hereditary breast cancer has overwhelmingly been limited to the BRCA1 and BRCA2 genes. The present study sought to compare family sharing behaviors in women with pathogenic BRCA variants to women with pathogenic variants in the more recently identified and characterized PALB2 gene. A total of 18 BRCA carriers and 13 PALB2 carriers were interviewed about family sharing practices using a semi-structured guide based on the Integrated Behavioral Model. Barriers and facilitators to family sharing were similar for both BRCA and PALB2 carriers, with logistical difficulties and emotional struggles related to anticipated negative reactions from relatives being the most salient barriers. The most important facilitators were: attitude that sharing enables health protection, provider recommendation, strong family relationships, confidence in sharing basic information, knowledge of what to share and how to share, and belief that sharing is highly important. Given similar attitudes, norms, and control beliefs related to family sharing, similar, but tailored interventions may be effective at increasing family disclosures among both groups. Such interventions should involve a discussion of patients’ attitudes towards sharing with healthcare providers to strengthen motivations and address barriers and provision of informational resources to increase confidence and knowledge. Family sharing resources should clearly specify which relatives need to be informed, why sharing is important, and how at-risk relatives may benefit.
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Chadwell, Sarah E. B. S. "Factors Influencing Clinical Follow-up for Individuals with a Personal History of Breast and/or Ovarian Cancer and Previous Negative or Uncertain BRCA1 and BRCA2 Testing." University of Cincinnati / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1491317215551797.

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Russell, Mark C. "Heredity and the Human Condition: A Study of 20th Century Genetic Accounts of Alcoholism." Diss., Virginia Tech, 2002. http://hdl.handle.net/10919/11092.

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This dissertation takes as its starting point some curious historical parallels in research on the heritability of alcoholism from opposite ends of the 20th century, and the underlying continuity in assumptions implicated by these parallels. Rather than review mainstream historical narratives on the origins of genetic research and alcoholism studies, I examine evidence and developments as yet unexplored by scholars. First I examine the origins of recent research models and diagnostic criteria that provide evidence for the hereditary nature of alcoholism. Then I consider the assumption of genetic determinism and its relationship to strategies of propaganda employed by the Eugenics movement early in the century. Using these historical "snapshots" I draw out conceptual and philosophical problems with the genetic explanation of alcoholism that continue to confront researchers today. These limitations suggest two possible avenues of resolution: either we develop finer-grained strategies for distinguishing social deviance from physical disorders, or we develop an integrated understanding of the complex interplay of human biological and cultural systems by extending the approach known as Developmental Systems Theory. In the conclusion, I explore these options and their potential ramifications for our understanding of alcoholism in hereditary and human contexts.
Ph. D.
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Massicot, France. "Etudes pharmacologiques et toxicologiques d'un régulateur métabolique : le chlorhydrate de chloro-4 phénoxyacétate d'hydroxyméthyl-3 N-méthyl pipéridine (PM 170)." Paris 7, 1986. http://www.theses.fr/1986PA077090.

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Shelton, Heath W. "The Effects of Two Novel Anti-Inflammatory Compounds On Prepulse Inhibition and Neural Microglia Cell Activation in a Rodent Model of Schizophrenia." Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/etd/3537.

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Recent studies have shown elevated neuroinflammation in a large subset of individuals diagnosed with schizophrenia. A pro-inflammatory cytokine, tumor necrosis factor-alpha (TNFα), has been directly linked to this neuroinflammation. This study examined the effects of two TNFα modulators (PD2024 and PD340) produced by our collaborators at P2D Bioscience, Inc., to alleviate auditory sensorimotor gating deficits and reduce microglial cell activation present in the polyinosinic:polycytidylic (Poly I:C) rodent model of schizophrenia. Auditory sensorimotor gating was assessed using prepulse inhibition and microglial activation was examined and quantified using immunohistochemistry and confocal microscopy, respectively. Both PD2024 and PD340 alleviated auditory sensorimotor gating deficits and reduced microglia activation and thereby demonstrated the ability to treat both the behavioral and neuroinflammatory aspects of the disorder. These results are significant and suggest that neural TNFα is a potential pharmacological target for the treatment of schizophrenia.
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Jiang, Yan. "Chromatin Remodeling in Transgenic Mouse Brain: Implications for the Neurobiology of Depression: A Dissertation." eScholarship@UMMS, 2009. https://escholarship.umassmed.edu/gsbs_diss/423.

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Histone lysine methylation is an important epigenetic mark for regulation of gene expression and chromatin organization. Setdb1 (Set domain, bifurcate 1), one of the histone lysine methyltransferases, specifically methylates histone H3 at lysine 9 (H3K9) and participates in transcriptional repression and heterochromatin formation. The major task of my thesis work was to investigate the epigenetic roles of Setdb1 in regulating brain functions. I started my thesis work by examining Setdb1 expression pattern during mouse brain development. The most robust signal of Setdb1 was detected in the fetal brains at embryonic day 12.5, with a ubiquitous distribution in all the proliferative zones, as well as the cortical plate and other regions comprised of postmitotic neurons. The expression of Setdb1 decreased as the brain developed, and this down-regulation profile was correlated to neuronal maturation as examined in a primary culture model of mouse cortical neurons. I then generated CK-Setdb1 transgenic mice, in which a myc-tagged full length mouse Setdb1 was constantly expressed in postmitotic neurons under the control of the CaMK II alpha promoter (CK). The expression of mycSetdb1 was detected in NeuN positive cells throughout most forebrain regions including cerebral cortex, striatum and hippocampus. A sustained increase of Setdb1 in CK-Setdb1 transgenics was verified at both mRNA and protein levels. Furthermore, an increase of H3K9 trimethylation was detected at major satellite DNA repeats in CK-Setdb1forebrains, which indicated that transgene-expressed mycSetdb1 was functionally active in adult brains. The behavioral phenotype of CK-Setdb1 transgenics was examined by using two separate founder lines. Gross neurological functions including body weight, locomotion activity, motor coordination, and breeding behavior were generally normal in CK-Setdb1 mice. CK-Setdb1 mice were further subjected to behavioral paradigms related to mood and cognitive functions. Intriguingly, as compared to the littermate controls, CK-Setdb1 mice represent a lower level of depression as indicated by decreased total immobility in two different behavioral despair tests. Moreover, CK-Setdb1 mice showed an accelerated extinction in the learned helplessness paradigm after a delayed interval (7 days), indicating a faster recovery from an established status of despair. The potential confounding factors, like memory deficits, were ruled out as CK-Setdb1 mice showed normal or even improved performances in different memory-related paradigms. Anxiety scores and stimulant drug response were normal in CK-Setdb1mice. Taken together, these findings suggested that a specific antidepressant-like phenotype was elicited by the over-expression of Setdb1 in adult mice forebrains. To further study the molecular mechanism underlying Setdb1-associated antidepressant-like behavioral changes, I screened for Setdb1-binding sites in a genome-scale by ChIP-on-chip using a tiling microarray from Affymetrix. Unexpectedly, Setdb1 showed a very restricted binding profile with a high specificity towards ionotropic glutamate receptor genes including the NMDA receptor 2B subunit gene Grin2b, which is a new target for the treatment for major depression. An increase of H3K9 dimethylation at Setdb1-binding site on Grin2b locus was detected in CK-Setdb1 hippocampus, which was correlated to a decrease of Grin2b expression as well as an accelerated desensitization of NMDA receptor. Furthermore, Chromosome Conformation Capture (3C) on Grin2b locus revealed a repressive chromatin loop structure, which tethered the distal Setdb1-binding site (~ 32 Kb downstream of transcriptional start site (TSS)) to a proximal intronic region (~12 Kb downstream of TSS) that is enriched for the binding of KAP1, a well-studied Setdb1-interacting transcriptional corepressor. Taken together, our data indicated that Setdb1 repressed Grin2b expression via H3K9 hypermethylation and higher-order chromatin loop formation, which may contribute to the antidepressant-like phenotype we observed in CK-Setdb1mice. The second part of my thesis work was to investigate the role of Setdb1 in the animal model of a neurodevelopmental disorder - Rett syndrome (RTT). Loss-of-function mutations of the gene encoding methyl-CpG binding protein 2 (MECP2) is the primary cause of RTT. There is an overlap between Setdb1- and Mecp2-associated repressive chromatin machineries, which both include histone deacetylase complex, H3K9 methyltransferase, DNA methyltransferase and heterochromatin protein 1 (HP1). Moreover, in contrast to Setdb1, which is downregulated during the cortical neuronal differentiation, Mecp2 is upregulated and the expression level is positively correlated to neuronal maturation. Therefore, we hypothesized that there is a functional redundancy between Setdb1 and Mecp2, and the up-regulation of Setdb1 in mature neurons will compensate for brain deficiency due to the loss of Mecp2. To test this hypothesis, I crossed CK-Setdb1 transgenic mice with nestincre-Mecp2 conditional knockout mice (Mecp2-/y). The behavior changes of CK-Setdb1/Mecp2-/y mice, including body weight, locomotion, motor coordination, and life span, were then compared to Mecp2-/y mice. No significant improvements in behaviors or survival were observed from CK-Setdb1/Mecp2-/y mice. Because the activation of CK promoter is limited to defined population of postmitotic neurons in forebrain, I tested our hypothesis by generating another strain of Setdb1 overexpression mice – tauSetdb1, in which the expression of mycSetdb1 is under the control of an endogenous pan-neuronal active promoter Tau. However, the introduction of tauSetdb1 also failed to rescue Mecp2 deficiency. The life span of tauSetdb1/ Mecp2-/y was even shorter as compared to Mecp2-/y mice (Kaplan-Meier, p=0.07). In conclusion, up-regulation of Setdb1 in adult brain was not sufficient to rescue Mecp2deficiency in the mouse model of RTT. One of the most challenges to study neuronal dysfunctions in brain diseases is the cellular heterogeneity of central nervous system. Current techniques for chromatin studies, including chromatin immunoprecipitation (ChIP) assays, usually lack of single cell resolution and are unable to examine the neurobiological changes in defined cell populations. In the third part of my thesis work, I developed a modified protocol to isolate neuronal nuclei from brain homogenates via Fluorescence-Activated Cell Sorting (FACS). In general, total nuclei was extracted from frozen brains, neuronal nuclei were then immuno-tagged with NeuN and sorted via FACS. Besides the NeuN labeling-FACS protocol, I also generated CK-H2BeGFP transgenic mice, in which a histone H2B-eGFP (enhanced green fluorescent protein) fusion protein was expressed in the nuclei of postmitotic neurons in mouse forebrain. Nuclei extracted from CKH2BeGFP brain were directly applied for FACS sorting. By using this protocol, we routinely got around 6-8 x106neuronal nuclei from one adult mouse forebrain, which was sufficient for ChIP applications followed by single gene PCR and microarray studies. In conclusion, our protocol permits large-scale studies of chromatin modifications or any other nuclei events in defined cell populations from distinct brain regions. Taken together, my dissertation work will lead to a better understanding of the epigenetic roles of histone H3K9 methyltransferase Setdb1 in brain functions, and may provide new targets for the therapeutic treatment of major depression.
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Kennedy, Samantha F. "Possible breakdown of dopamine receptor synergism in a mouse model of Huntington's Disease." ScholarWorks@UNO, 2017. https://scholarworks.uno.edu/td/2415.

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The model of basal ganglia function proposed by Albin, Young and Penney (1989) describes two anatomically independent motor pathways, the direct and indirect. However, under normal conditions striatal dopamine (DA) is required for the expression of motor behavior, and DAergic control of the two pathways (via D1 and D2 receptors, respectively) is dependent on co-activation. We tested for a possible breakdown of D1/D2 synergism using transgenic R6/1 mice bearing the human huntingtin allele (Htt). Motor stereotypy, observed prior to the onset of HD-related symptoms, was rated on a 5-point scale following activation of: A) D1 receptors alone, B) D2 receptors alone, and C) stimulation of both D1 and D2 receptors. Results revealed that mice with the HD allele, like their WT litter mates, depend on the co-activation of the indirect and direct motor pathways to facilitate deliberate behavior.
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Books on the topic "Hereditary behaviour"

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Biological foundations of human behavior: HEREDITY. London: Thomson/Wadsworth, 2003.

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Rushton, J. Philippe. Race, evolution, and behavior: A life history perspective. New Brunswick, N.J., USA: Transaction Publishers, 1997.

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Rushton, J. Philippe. Race, evolution, and behavior: A life history perspective. 2nd ed. Port Huron, MI: Charles Darwin Research Institute, 2000.

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Race, evolution, and behavior: A life history perspective. 3rd ed. Port Huron, MI: Charles Darwin Research Institute, 2000.

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Rushton, J. Philippe. Race, evolution, & behavior. New Brunswick, N.J: Transaction Publishers, 1999.

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Manes, Singer Sandra, and Pauls David L, eds. The heredity of behavior disorders in adults and children. New York: Plenum Medical Book Co., 1986.

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Vandenberg, Steven G., Sandra Manes Singer, and David L. Pauls. The Heredity of Behavior Disorders in Adults and Children. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5071-2.

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Hereditary genius: An inquiry into its laws and consequences. Amherst, NY: Prometheus Books, 2005.

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Race, evolution, and behavior: A life history perspective. New Brunswick, N.J., USA: Transaction Publishers, 1995.

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Making sense of heritability: How not to think about behavior genetics. New York: Cambridge University Press, 2005.

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Book chapters on the topic "Hereditary behaviour"

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Broadhurst, P. L. "The Hereditary Base for the Action of Drugs on Animal Behaviour." In Ciba Foundation Symposium - Animal Behaviour and Drug Action, 224–37. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470719329.ch14.

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Farajdokht, Fereshteh. "Heredity." In Encyclopedia of Animal Cognition and Behavior, 1–4. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-47829-6_71-1.

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Farajdokht, Fereshteh. "Heredity." In Encyclopedia of Animal Cognition and Behavior, 3085–87. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-319-55065-7_71.

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Vandenberg, Steven G., Sandra Manes Singer, and David L. Pauls. "Hereditary Factors in Schizophrenia." In The Heredity of Behavior Disorders in Adults and Children, 95–119. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5071-2_6.

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Vandenberg, Steven G., Sandra Manes Singer, and David L. Pauls. "Hereditary Influences on Epileptic Conditions." In The Heredity of Behavior Disorders in Adults and Children, 81–94. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5071-2_5.

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Vandenberg, Steven G., Sandra Manes Singer, and David L. Pauls. "Hereditary Factors in Affective Disorders." In The Heredity of Behavior Disorders in Adults and Children, 121–39. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5071-2_7.

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Vandenberg, Steven G., Sandra Manes Singer, and David L. Pauls. "Hereditary Factors in Neurotic Conditions." In The Heredity of Behavior Disorders in Adults and Children, 141–62. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5071-2_8.

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Vandenberg, Steven G., Sandra Manes Singer, and David L. Pauls. "Hereditary Factors in Antisocial Personality Disorder." In The Heredity of Behavior Disorders in Adults and Children, 173–84. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5071-2_10.

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Vandenberg, Steven G., Sandra Manes Singer, and David L. Pauls. "Heredity and Alcoholism." In The Heredity of Behavior Disorders in Adults and Children, 163–72. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5071-2_9.

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Vandenberg, Steven G., Sandra Manes Singer, and David L. Pauls. "Methods for Studying Hereditary Factors in Humans." In The Heredity of Behavior Disorders in Adults and Children, 49–79. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5071-2_4.

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Conference papers on the topic "Hereditary behaviour"

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Kwong, A., and ATW Chu. "P2-13-08: A Retrospective Study on Surveillance Behaviour and Prophylaxis after Genetic Testing for Hereditary Breast and Ovarian Cancer among High-Risk Chinese Females." In Abstracts: Thirty-Fourth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 6‐10, 2011; San Antonio, TX. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/0008-5472.sabcs11-p2-13-08.

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Scharrer, I., V. Hach-Wunderle, H. Heyland, and C. Kuhn. "INCIDENCE OF DEFECTIVE T-PA RELEASE IN 158 UNRELATED YOUNG PATIENTS WITH VENOUS THROMBOSIS IN COMPARISON TO PC-, PS-, AT III-, FIBRINOGEN- AND PLASMINOGENDEFICIENCY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643047.

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The incidence of defective T-PA release in 158 young unrelated patients (<45 years old) with deep vein thrombosis was studied and compared to that of PC-, PS-, AT III-, fibrinogen- and plasminogen deficiency. Thrombotic episodes were documented using venography with contrast medium. Venous occlusion test (VO) over 20 min. was performed in all patients, 8-12 weeks after thrombosis. T-PA antigen (Biopool kit) , T-PA activity (on fibimplates) and PAI (T-PA-inhibitor, Biopool kit) were measured before and after VO in the fasting morning samples. Furthermore we investigated the functional and immunologic levels of PC,PS,AT III, fibrinogen and plasminogen. We detected 28 patients (15 females, 13 males)= 17.7% with abnormal T-PA release. In these patients the VO test was repeated three times in an interval of 6-8 weeks. Release of T-PA activity and T-PA-Ag was diminished in all these patients. PAI levels were enhanced in 12 of these 28 patients. The rate of recurrency of thrombosis was 52%. A family history of thrombosis was reported only in 20%The incidence of PC def. was 9.4%, of PS def. 6.3%, of AT III def 5%, of dysfibrinogenemia 0.6% and of plasminogen def. 1.2%. No combined defect of abnormal T-PA release with other known hereditary coagulation or fibrinolysis disorders could be detected.In 11 healthy volunteers we investigated 4 different time periods of VO, 5, 10, 15 and 20 min. in an interval of 10 days in order to find the suitable time for VO. It was striking that T-PA activity (on fibrin plates) did not decrease to the same extent as T-PA-Ag. The different behaviour is demonstrated on table 1. Decrease in % is compared to the values of 20 min. VO.
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Purnama, Ridwan. "Street Vendor: The Study of Heredity Job and Social Behaviour." In 1st UPI International Conference on Sociology Education. Paris, France: Atlantis Press, 2016. http://dx.doi.org/10.2991/icse-15.2016.78.

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Darvish, Kurosh K., and Jeff R. Crandall. "Comparison Between a Quasilinear and a Nonlinear Viscoelastic Model for Brain Tissue." In ASME 2000 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2000. http://dx.doi.org/10.1115/imece2000-2567.

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Abstract The nonlinearity of the viscoelastic behavior of brain tissue was studied. Two nonlinear constitutive models were developed using the experimental results of forced vibrations on bovine brain samples, namely a quasilinear viscoelastic model and a multiple hereditary integral model. The latter was found to be superior especially at higher frequencies (above 27 Hz).
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Paripovic, Jelena, and Patricia Davies. "Identification of the Dynamic Behavior of Surrogate Explosive Materials." In ASME 2013 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/detc2013-12755.

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Improvised explosive devices are often made to resemble objects that are a natural part of the environment. It is hypothesized that by understanding the mechanical behavior of the explosive material it may be possible to tune an acoustic excitation to produce signatures that indicate explosives are present in an object. Here the focus is on identification of mechanical material properties and their effect on a system’s dynamic response. Energetic material surrogates were produced by embedding inert crystals within the binder. Swept-sine wave base-excitation tests were conducted to examine repeatability of the material-mass system responses. Compression test data were fitted using a two-term Ogden model but for a massmaterial base-excited system a continuous-time system identification method was used to estimate model parameters. Damping ratios of 0.11 for the 0% (no crystals) material and 0.19 for the 50% (crystal volume fraction) material were estimated. Future work includes examination of models that include a hereditary model of viscoelasticity and nonlinear terms, and experimental investigations at higher forcing levels.
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Fukunaga, Masataka, and Nobuyuki Shimizu. "Nonlinear Fractional Derivative Stress-Strain Relations for Polymer Gels Based on the Generalized Maxwell Model." In ASME 2009 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. ASMEDC, 2009. http://dx.doi.org/10.1115/detc2009-87283.

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In this paper, we formulate two nonlinear stress-strain relations including memory effect in the dynamical behavior of gels that are the kind of viscoelastic materials. The basic assumption of the model is made that the gels consist of blobs of high polymers. Hereditary response of blobs to the stress determines the average stress-strain relation of the material. Two stress-strain relations are derived for different models of gels. These stress-strain relations are compared with the fractional derivative version of Lodge’s rubber-like liquids and the empirical nonlinear fractional derivative model proposed by Fukunaga et. al. at FDA08.
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Azizi, Yousof, Patricia Davies, and Anil K. Bajaj. "Identification of Nonlinear Viscoelastic Models of Flexible Polyurethane Foam From Uniaxial Compression Data." In ASME 2012 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/imece2012-88190.

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Flexible polyethylene foam, which is used in many engineering applications, exhibits nonlinear and viscoelastic behavior. To date, several models have been proposed to characterize the complex behavior of foams from the computationally intensive microstructural models to continuum models that capture the macroscale behavior of the foam materials. A nonlinear viscoelastic model, which is an extension of previously developed models, is proposed and its ability to capture foam response in uniaxial compression is investigated. It is assumed in the model that total stress is decomposed into the sum of a nonlinear elastic component, which is modeled by a higher order polynomial, and a nonlinear hereditary type viscoelastic component. System identification procedures are developed to estimate the model parameters using uniaxial compression data from experiments conducted at different rates. The performance of this model is compared to that of other nonlinear viscoelastic models.
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Bozhchenko, Alexandr, and Vitaliy Yakushev. "Medical-forensic risk assessment of delinquency based on dermatoglyphic research method: opportunities and prospects." In Issues of determining the severity of harm caused to human health as a result of the impact of a biological factor. ru: Publishing Center RIOR, 2022. http://dx.doi.org/10.29039/conferencearticle_63a2c2a1a70d34.70678808.

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Morphogenetic markers of predisposition to delinquent behavior are considered in the article on the example of congenital signs of papillary patterns of fingers. To do this, the fingerprints of 100 serial killers who committed crimes on a sexual basis and 100 law-abiding citizens were analyzed. According to the results of the study, informative combinations of pattern types were found, which are statistically more common in the group of people who committed serial murders. The similarity of a number of established dermatoglyphic markers of serial killers with dermatoglyphics observed in congenital diseases and diseases with hereditary predisposition is shown. The obtained results are proposed to be used in the system of a comprehensive assessment of the risk of delinquency in the person being checked and the formation of a psychological portrait of the criminal.
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Azizi, Yousof, Anil K. Bajaj, and Patricia Davies. "Development of a Multi-Body Model to Predict the Settling Point of a Seat-Occupant System." In ASME 2014 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. American Society of Mechanical Engineers, 2014. http://dx.doi.org/10.1115/detc2014-35462.

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The location of the hip-joint (H-Point) of a seat occupant is an important design specification which directly affects the seat comfort. Most car seats are made of polyurethane foam so the location of the H-Point is dependent on the quasi-static behavior of foam. In this study a multi-body seat-occupant model is developed which incorporates a realistic polyurethane foam model. The seat-occupant model consists of two main components: the seat model and the occupant model. In this study the seat is represented by a series of discrete nonlinear viscoelastic elements. The nonlinear elastic behavior of these elements is expressed by a higher order polynomial while their viscoelastic behavior is described by a global hereditary type model with the parameters which are functions of the compression rate. The nonlinear elastic and viscoelastic model parameters were estimated previously using the data obtained from conducting a series of quasi-static compression tests on a car seat foam sample. The occupant behavior is described by a two-dimensional multi-body model with 5 degrees of freedom. A Lagrangian formulation is used to derive the governing equations for the seat occupant model. These differential equations are solved numerically to obtain the H-Point location. These results are then used to calculate the force distribution at the seat and the occupant interfaces. The effects of different system parameters on the system response and the interfacial pressure distribution are also studied.
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