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Paediatric clinical pharmacology
Published in Evelyne Jacqz-Aigrain, Imti Choonara, Paediatric Clinical Pharmacology, 2021
Evelyne Jacqz-Aigrain, Imti Choonara
In childhood, drug metabolising hepatic enzyme activity changes with age and development [3]. This is covered by the term ontogeny. In general, neonates have very low intrinsic enzyme activity. The activity increases to levels above that found in adults in the toddler years. Most enzymes have decreased to adult levels by the teenage years. This has implications for the dosing of children throughout childhood and may explain why many doses in children cannot be simply scaled down linearly for adults.
Regulation of the Pituitary Gland by Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
The embryonic development of the hypothalamo-pituitary complex has been primarily studied in rodents, using a combination of morphological, biochemical and genetic approaches. Information on the process of ontogeny has also benefitted from the availability of naturally occurring mutations and transgenic animal models. For an in-depth coverage of pituitary cell differentiation, the interested reader is referred to two reviews [29,43].
Phylogeny of Normal and Abnormal Hemoglobin Genes
Published in S. K. Dutta, DNA Systematics, 2019
The second developmental feature which is striking is that the genes are arranged on the chromosome in order of expression. This is true not only for man but also for the rabbit, the mouse, various primates, sheep, and goats4,20,22 and may therefore be a widespread and perhaps universal characteristic. The significance of this observation remains something of a mystery. One of the hoary maxims of classical descriptive biology is that “ontogeny recapitulates phylogeny” — a reference to the at least superficial resemblance between various developmental stages and the lower forms which preceded man on the evolutionary scale. Whether this observed parallel between position and development carries any as yet undeciphered message of phylogenetic importance remains to be seen.
Influencing tumor-associated macrophages in malignant melanoma with monoclonal antibodies
Published in OncoImmunology, 2022
Rebecca Adams, Gabriel Osborn, Bipashna Mukhia, Roman Laddach, Zena Willsmore, Alicia Chenoweth, Jenny L C Geh, Alastair D MacKenzie Ross, Ciaran Healy, Linda Barber, Sophia Tsoka, Victoria Sanz-Moreno, Katie E Lacy, Sophia N Karagiannis
Melanoma-associated macrophages can derive either from embryonic-derived tissue resident macrophages (Res-TAMs), recruited and maintained by colony-stimulating factor-1 (CSF-1) binding its receptor CSF1R,25 or through the recruitment of circulating monocytes via the CCL2/CCR2 chemokine pathway, which can differentiate into monocyte-derived macrophages (mo-TAMs).26–28 The exact contributions of each origin pool are still being explored, with a paucity of information on how macrophage ontogeny affects TAM function within melanoma. Much knowledge of ontogeny derives from mouse studies, due to the inability to undertake fate-mapping studies in humans. Alongside this, genetic similarities and a lack of markers that can help distinguish tissue-resident from monocyte-derived macrophages render further exploration into this area quite challenging.29 It appears that tissue resident macrophages are the first to be influenced by factors secreted from tumors. However, in the cancer types studied so far, the contribution of Res-TAMs and mo-TAMs appears organ specific:29–31 in pancreatic cancer models, Res-TAMs appeared to promote tumor growth; in human glioma samples mo-TAMs correlate with tumor grade; and in mouse models of lung cancer, macrophages of both origins appear to contribute to tumor growth. No such comparative studies of how macrophage origin can affect function have been carried out in melanoma.
The foraging gene as a modulator of division of labour in social insects
Published in Journal of Neurogenetics, 2021
Christophe Lucas, Yehuda Ben-Shahar
Over 50years ago, the pioneering ethologist Niko Tinbergen published his seminal paper entitled “On aims and methods of ethology” (Burkhardt, 2014; Tinbergen, 1963). With brilliant simplicity, Tinbergen argued that if biologists want to really understand “behaviour” then they need to ask the following four questions (rephrased): (1) What is the studied trait good for (its impact on fitness)? (2) How does it develop during the lifetime of an individual (development/ontogeny)? (3) How did it evolve over the history of the species (trait phylogeny)? (4) How does it work (mechanism/causation)? The emergence of modern neuroscience and neurogenetics followed in the footsteps of ethology by providing a mechanistic framework as a powerful approach to the design of behavioural studies and their interpretation in the context of brain functions (Tinbergen question #4).
Early social deprivation does not affect cortisol response to acute and chronic stress in zebrafish
Published in Stress, 2021
Soaleha Shams, Aysha Khan, Robert Gerlai
Nevertheless, distinction between social development that is dependent on presence of appropriate social cues in the early environment and not on absence of aliments (as well as shelter, cleanliness, temperature regulation, etc.), can help us better understand both ontogeny of typical social behavior and the protective effects typical socialization has against poor health outcomes later in life. Recall that early adversity is associated with high prevalence of inflammation, immune dysfunction, and psychopathology in humans (Avitsur et al., 2015; Chiang et al., 2015; Fisher et al., 2016; Gerritsen et al., 2017; Gershon et al., 2013; Struber et al., 2014), and zebrafish has been increasingly used in modeling and analysis of these conditions (Garcia-Moreno et al., 2019; McCammon & Sive, 2015; Novoa & Figueras, 2012; Shams et al., 2018b; Stewart et al., 2012; Varga et al., 2018). Additionally, while zebrafish and humans share the same adrenal stress hormone (cortisol), the main stress hormone in rodents is slightly different (corticosterone) and extensive research has shown similarities in consequences of early social deprivation in human and rodent (Brett et al., 2015; Cacioppo et al., 2011; Hawkley et al., 2012). Further characterization of behavior and physiology of isolated animals and systematic comparisons of social isolation literature in altricial vs precocial species is needed to identify regulators and mechanisms by which early social environment plays a role in mediating the risk, onset, and exacerbation of later illness.