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Books on the topic 'Genes families'

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Published: 2 February 2024

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1

Knowles, Jonathan. Cellulase families and their genes. New York: Elsevier, 1987.

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2

Hannigan, Emma. Designer genes. Dublin, Ireland: Poolbeg, 2009.

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Hannigan, Emma. Designer genes. Dublin, Ireland: Poolbeg, 2009.

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4

Michaels, Rune. Nobel genes. New York: Atheneum Books for Young Readers, 2010.

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5

Nobel genes. New York: Atheneum Books for Young Readers, 2010.

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6

Michaels, Rune. Nobel genes. New York: Atheneum Books for Young Readers, 2010.

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7

Dozens of cousins: Blue genes, horse thieves, and other relative surprises in your family tree. Berkeley: Ten Speed Press, 1999.

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8

King, Susan. Eating pomegranates: A memoir of mothers, daughters and genes. [Toronto]: Bond Street Books, 2009.

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9

International, Congress on Genes Gene Families and Isozymes (13th 2005 Shanghai China). Proceedings of the XIII International Congress on Genes, Gene Families, and Isozymes: Shanghai, China, September 17-21, 2005. Bologna: MEDIMOND, International Proceedings, 2003.

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10

Moffat, Bobbie Wells. Inherited genes: Including families; Wells, Price, Sharpe, Alexander, McKnight, Wallace, Hoyl, Costner, Lattimore, Stockton, Peeler, Redwine, Carlock, Ray, Norman, Dodd, Hill, Halbert, Miller, Baty, Harris. Salem, MA: Higginson Book Co., 2000.

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11

Genograms: The new tool for exploring the personality, career, and love patterns you inherit. Chicago: Contemporary Books, 1989.

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12

Alexakēs, Eleutherios P. Manē: Genē kai oikogeneia. 2nd ed. Athēna: Trochalia, 1998.

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13

Behling, Katja. Martha Freud: Die Frau des Genies. Berlin: Aufbau Taschenbuch Verlag, 2002.

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14

Behling, Katja. Martha Freud: Die Frau des Genies. Berlin: Aufbau Taschenbuch Verlag, 2002.

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15

Kuster, Friederike. Rousseau - die Konstitution des Privaten: Zur Genese der bürgerlichen Familie. Berlin: Akademie Verlag, 2005.

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16

Six, Jacob. De genen van de kunstverzamelaar: 50 collecties in de familie. Zwolle: Waanders Uitgevers, 2016.

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17

Papadopoulou, Antigonē. Hē metexelixē tēs kypriakēs oikogeneias: Aphēgēseis apo treis genies gynaikōn. [Nicosia?]: Antigonē Perikleous Papadopoulou, 2014.

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18

Cesare, Peschle, Fondazione internazionale Menarini, Istituto superiore di sanità (Italy), and World Health Organization, eds. Normal and neoplastic blood cells: From genes to therapy. New York, N.Y: New York Academy of Sciences, 1987.

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19

Un pas, un sentier, une vie: Roman. Plantagenet, ON: Chardon bleu, 2010.

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20

Aile, Kurultayı (1994 Ankara Turkey). Aile Kurultayı: Değişim sürecinde aile, toplumsal katılım ve demokratik değerler : 16-18 Kasım 1994 : açış konuşmaları, genel bildiriler, oturumlar. Ankara: T.C. Başbakanlık Aile Araştırma Kurumu Başkanlığı, 1995.

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21

Irving vs. Irving: Canada's feuding billionaires and the stories they won't tell. Toronto, Ontario, Canada: Viking, 2014.

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22

David, Sankoff, and Nadeau J. H, eds. Comparative genomics: Empirical and analytical approaches to gene order dynamics, map alignment and the evolution of gene families. Dordrecht: Kluwer Academic, 2000.

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23

Die aufgeklärte Familie: Untersuchungen zur Genese, Funktion und Realitätsbezogenheit des familialen Wertsystems im Drama der Aufklärung. Tübingen: M. Niemeyer, 1988.

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24

Hébert, Carmen Labarre. The origins of Jacques Genest dit Labarre and his first years in New-France. Drummondville, Québec: Carmen Labarre-Hébert, 2007.

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25

1924-, Smith George F., and National Down Syndrome Society (U.S.). Symposium, eds. Molecular structure of the number 21 chromosome and Down syndrome. New York, N.Y: New York Academy of Sciences, 1985.

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26

E, Angel Peter, and Herrlich Peter 1940-, eds. The fos and jun families of transcription factors. Boca Raton: CRC Press, 1994.

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27

1960-, Gibbon Ann, ed. Steinberg : le démantèlement d'un empire familial. Montréal, Qué: Libre Expression, 1990.

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28

Sonnenblick, Jordan. Dodger & me. New York: Feiwel and Friends, 2008.

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29

Michaels, Rune. Nobel Genes. Simon & Schuster Children's Publishing, 2010.

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30

Michaels, Rune, and Frederic Basso. Nobel Genes. Audible Studios on Brilliance Audio, 2017.

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31

Nobel genes. Simon & Schuster, 2010.

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32

Nobel Genes. Simon & Schuster, 2011.

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33

Hertz, Rosanna, and Margaret K. Nelson. Random Families. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190888275.001.0001.

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This is a book about unprecedented families—networks of strangers linked by genes, medical technology, and the human desire for affinity and identity. It chronicles the chain of choices that couples and single mothers make—how to conceive, how to place sperm donors in their family tree, and what to do when it suddenly becomes clear that there are children out there that share half their child’s DNA. Do shared genes make you family? Do children find anything in common? What becomes of the random networks that arise once the members of the families of donor siblings find one another? Based on over 350 interviews with children and parents from all over the United States, Hertz and Nelson explore what it means to children to be a donor sibling and what it’s like to be a parent who discovers four, six, or even a dozen children who share half the DNA of one’s own child. At the heart of their investigation are remarkable relationships woven from tenuous bits of information and fueled by intense curiosity. The authors suggest that donor siblings are expanding the possibilities for extended kinship in the United States.
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34

King, Susan. Eating Pomegranates: A Memoir of Mothers, Daughters and Genes. Penguin Random House, 2010.

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35

King, Susan. Eating Pomegranates: A Memoir of Mothers, Daughters, and Genes. Doubleday Canada, 2011.

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36

Gabriel, Sarah. Eating Pomegranates: A Memoir of Mothers, Daughters and Genes. Vintage, 2010.

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37

Elhossiny, Ayman. Family Tree Secrets! Diseases That Run in the Families: Prevalence of a Disease According to Gender, Race, and Genes. Independently Published, 2020.

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38

Heidet, Laurence, Bertrand Knebelmann, and Marie Claire Gubler. Thin glomerular basement membrane nephropathy and other collagenopathies. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0325_update_001.

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The discovery of a thin glomerular basement membrane in a renal biopsy without any other abnormalities can be explained in a number of ways. This could be an early biopsy in a patient with Alport syndrome, or it could be an individual who is a carrier for an Alport gene. These carriers are at increased risk of significant renal disease in their lifetime and some have proteinuria as well as haematuria, so they can no longer be equated with the historic label of benign familial haematuria. Some families with a thin glomerular basement membrane and haematuria inherited in an autosomal dominant fashion do not appear to have linkage to COL4 genes. Others have variable renal disease that has sometimes given rise to a label of mild but autosomal dominant Alport syndrome. This territory might also attract the label basement membrane 345 collagenopathy. Other uncommon conditions affecting the glomerular basement membrane include nail patella syndrome.
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39

Marini, Carla, and Renzo Guerrini. Biological Basis of Primary Generalized Epilepsies—Genetics. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0036.

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Primary generalized epilepsies account for 30% of all epilepsies. These age-related epilepsies without structural brain lesions and normal development have a high heritability. Based on the main seizure type and their age of onset, four main subsyndromes are recognized. Rare autosomal dominant families carry mutations in a few genes involved in ion channel functions, whereas common genes are yet to be discovered. The complex inheritance involving multiple genes is the major limiting factor preventing to uncover their genetic architecture. Understanding genetic determinants is the key to unraveling the neurobiology and to improve therapies for these disorders.
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40

Distel, Marijn A., and Marleen H. M. de Moor. Genetic Influences on Borderline Personality Disorder. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199997510.003.0007.

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Borderline personality disorder (BPD) tends to “run in families.” Twin and twin family studies show that BPD is moderately heritable, with some evidence for nonadditive gene action. BPD co-occurs with Axis I and other Axis II disorders, as well as with a certain profile of normal personality traits. Multivariate twin (family) studies have shown that these phenotypic associations are partly due to genetic associations, and this is observed most strongly for BPD and neuroticism. Candidate gene-finding studies for BPD suggest the possible role of genes in the serotonergic and dopaminergic system, but this needs to be confirmed in larger genome-wide studies. Future studies will complement the knowledge described in this chapter to enable us to move toward a comprehensive model of the development of BPD in which biological and environmental influences on BPD are integrated.
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41

Samuels, Jack, Marco A. Grados, Elizabeth Planalp, and O. Joseph Bienvenu. Genetic Understanding of OCD and Spectrum Disorders. Edited by Gail Steketee. Oxford University Press, 2012. http://dx.doi.org/10.1093/oxfordhb/9780195376210.013.0025.

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This chapter reviews the evidence for the genetic etiology of OCD and spectrum conditions. A genetic basis is supported by the familial aggregation of OCD; evidence for involvement of genes of major effect in segregation analyses; and higher concordance for OCD in identical than non-identical twins. Recent studies also support linkage of OCD to specific chromosomal regions and association of OCD with specific genetic polymorphisms. However, specific genes causing OCD have not yet been firmly established. The search for genes is complicated by the clinical and etiologic heterogeneity of OCD, as well as the possibility of gene–gene and gene–environmental interactions. Despite this complexity, developments in molecular and statistical genetics, and further refinement of the phenotype hold promise for further deepening our genetic understanding of OCD and spectrum disorders in the coming decade.
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42

Kanno, Hiroshi, and Joachim P. Steinbach. Familial tumour syndromes: von Hippel–Lindau disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199651870.003.0016.

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Von Hippel–Lindau (VHL) disease, an autosomal dominant familial tumour syndrome, is often associated with haemangioblastoma of the central nervous system. In the presence of oxygen, VHL protein serves to prevent the accumulation of hypoxia-inducible factor (HIF) protein by targeting it to the proteasomal pathway, while biallelic inactivation of the VHL gene blocks degradation of HIF and leads to constitutive activation of the HIF pathway although oxygen is present. HIF-target genes are involved in angiogenesis, proliferation, and metabolism enabling tumour growth. Haemangioblastoma is a highly vascularized, begin tumour commonly associated with a cyst, but it is linked with neurological morbidity and mortality based on its location and multiplicity. Haemangioblastoma in VHL is diagnosed according to symptoms and signs, past and family histories, laboratory data, neuroradiological findings, pathological findings, and genetic testing. Surgical treatment is usually the most recommended therapy for haemangioblastomas, and using well-defined microsurgical techniques, the majority can be resected safely.
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43

Bingham, Coralie. Hepatocyte nuclear factor-1B. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0315_update_001.

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Hepatocyte nuclear factor-1B (HNF1B, also known as TCF2) is a transcription factor that is involved in renal development, and in the transcription of several genes implicated in other genetic renal diseases. Mutations in HNF1B cause maturity onset diabetes of the young, renal cysts and diabetes syndrome, and some cases of familial juvenile hyperuricaemic nephropathy. They also account for a large proportion of developmental renal disorders included abnormalities detected antenatally. The various abnormalities associated with the gene may occur in isolation or together in the same patient.
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44

Walsh, Richard A. Siblings with Instability. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190607555.003.0015.

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Over the past 5 years, there has been a shift in the approach to searching for a genetic diagnosis in familial ataxic syndromes. Whereas in the past, a limited but expensive search through a selection of commercially available genes using Sanger sequencing was performed, there is now widespread availability of gene panels utilizing next-generation sequencing techniques. This is an efficient and powerful approach that may achieve a diagnosis in more than 30% of patients with a familial ataxia that remain undiagnosed. However, accurate phenotyping remains critical to allow interpretation of sequence variants of uncertain significance, to identify biomarkers that may be useful to monitor future therapies, and to assist with the identification of underlying pathophysiology.
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45

Liede-Schumann, Sigrid, Ulrich Meve, Gildas Gâteblé, Gabrielle Barriera, and Silvio Fici. Apocynaceae pro parte, Phellinaceae, Capparaceae : Flore de la Nouvelle Calédonie, volume 27. Publications scientifiques du Muséum, Paris ; IRD, Marseille, 2020. http://dx.doi.org/10.5852/fft49.

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L’exceptionnelle richesse floristique de la Nouvelle-Calédonie est mondialement connue. Plus de 3 400 espèces de plantes vasculaires indigènes y sont répertoriées, dont les trois-quarts sont endémiques de l’archipel. L’endémisme ne concerne pas seulement les espèces, mais aussi les genres (près d’une centaine) et même trois familles. La diversité se décline aussi sur le plan écologique, en lien avec l’histoire géologique originale de la Nouvelle-Calédonie, qui a favorisé le micro-endémisme et les espèces inféodées aux substrats ultramafiques. De nouvelles espèces continuent à être découvertes, aussi reste-t-il nécessaire de poursuivre prospections et recherches botaniques, afin de mieux comprendre l’origine et l’évolution de cette flore, et contribuer à sa préservation. Le présent volume regroupe trois familles d’Angiospermes. Celle des Apocynaceae dont la classification a été profondément remaniée depuis la publication en 1981 du fascicule « Apocynaceae », volume 10 de la Flore de la Nouvelle-Calédonie et Dépendances : les trois sous-familles traitées ici (Periplocoideae, Secamonoideae et Asclepiadoideae) formaient auparavant la famille des Asclepiadaceae. Les Phellinaceae qui, avec 10 espèces ligneuses, constituent l’une des trois familles endémiques du territoire. Enfin, la Nouvelle-Calédonie héberge quelques espèces de la famille cosmopolite des Capparaceae, toutes appartenant au genre du câprier (Capparis). Conformément à la ligne éditoriale de la collection, cet ouvrage comporte, pour chaque famille traitée indépendamment : une présentation générale suivie de descriptions détaillées des genres et des espèces ; des clés d’identification, en français et en anglais ; une illustration variée comprenant des dessins au trait et des photographies des plantes vivantes ; des cartes de répartition et une évaluation des besoins de conservation selon les critères de l’UICN.
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46

Is It In Your Genes: How Genes Influence Common Disorders and Diseases That Affect You and Your Family. Cold Spring Harbor Laboratory Press, 2004.

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47

Kuster, Friederike. Rousseau - Die Konstitution des Privaten: Zur Genese der Bürgerlichen Familie. de Gruyter GmbH, Walter, 2009.

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48

Stallings, Michael C., Ian R. Gizer, and Kelly C. Young-Wolff. Genetic Epidemiology and Molecular Genetics. Edited by Kenneth J. Sher. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199381678.013.002.

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The tools of genetic epidemiology—family, adoption, and twin studies—show convincingly that substance use behavior and substance use disorders are influenced by both genetic and familial and extrafamilial environmental factors. Environmental factors appear to play a more influential role in the early stages of substance use, whereas genetic factors become more important in the development of problem use and substance use disorder. Moreover, some genetic effects are likely conditional on conducive environments; research employing both behavior genetic approaches and measured genes point to important gene–environment interactions that promote substance use and dependence. Consequently, a full understanding of the addiction process requires investigating substance use behavior within its comorbid context. The identification of specific genetic mechanisms underlying these heritable influences is elusive. These findings have prompted the development of new strategies for testing the joint effect of multiple genetic variants in gene-based or gene pathway analyses.
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49

Allen, Shelley J. Pathophysiology of Alzheimer’s disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198779803.003.0002.

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We now know that the onset of the pathological processes leading to Alzheimer’s disease (AD) may be 15–20 years before symptoms appear. This focuses attention on synaptic changes and the early role of tau, and less on the hallmark amyloid plaques (Aβ‎) and neurofibrillary tau tangles. Sensitive biomarkers to allow early screening will be essential. Familial autosomal AD is the result of mutations in one of three genes (APP, PSEN1, or PSEN2), each directly related to increased Aβ‎, and informs pathological mechanisms in common sporadic cases, but are also subject to influence by many risk genes and environmental factors. The essential role of apolipoprotein E in neuronal repair and Aβ‎ clearance provides a therapeutic target but also a challenge in carriers of the risk gene APOE4. Current treatments are symptomatic, derived from neurotransmitter deficits seen; particularly cholinergic, but emerging data suggest alternative targets which may prove more productive.
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50

Is It in Your Genes?: The Influence of Genes on Common Disorders and Diseases That Affect You and Your Family. Cold Spring Harbor Laboratory Press, 2004.

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