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Статті в журналах з теми "Embryonic Structures physiology"
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KIMURA, HIROSHI, IKUO TOHYAMA, KOUNOSUKE MIZUTANI, and JUNZO OCHI. "Fibronectin-like immunoreactive structures in embryonic rat brain." Acta Histochemica et Cytochemica 22, no. 2 (1989): 243–58. http://dx.doi.org/10.1267/ahc.22.243.
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POLUEKTOV, M. G., and P. V. PCHELINA. "SLEEP IN CHILDREN: FROM PHYSIOLOGY TO PATHOLOGY." Medical Council, no. 9 (July 18, 2017): 97–102. http://dx.doi.org/10.21518/2079-701x-2017-9-97-102.
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Circadian rhythms and the mechanisms of sleep and wakefulness begin to form in the embryonic period and undergo many stages of development before acquire characteristics typical for an adult. Structure of sleep disturbances in children also differs from that in the adult population. Most sleep disorders in children are the result of immaturity of certain brain structures and mechanisms: primary sleep disorders, pediatric behavioral insomnia, sleepwalking, night terrors, enuresis. These disorders are benign, and usually disappear by adulthood. Treatment of benign sleep disorders in children should primarily be based on the methods of behavioral therapy, the rules of sleep hygiene and the purpose of light sedation.
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Jacobson, A. G., and A. K. Sater. "Features of embryonic induction." Development 104, no. 3 (November 1, 1988): 341–59. http://dx.doi.org/10.1242/dev.104.3.341.
Повний текст джерелаАнотація:
The patterned distribution of different organs in the amphibian embryo begins with the establishment of two domains, the animal and vegetal regions, that differ in developmental potency. Differences amplify as inductive interactions occur across boundaries between areas of different potency. Embryonic induction establishes a temporally and spatially dynamic area of developmental potency - a morphogenetic field. The final arrangement and differentiation of cell types within the field emerge from subsequent interactions occurring primarily within the field. These principles are illustrated in a review of the induction of the lens and the heart. Recent studies show that the induction of the lens of the eye and the induction of the heart begin early in development. Most of lens inductions occurs before the formation of the optic vesicle, and the heart appears to be part of a complex of dorsal structures whose formation is dependent upon the establishment of the dorsoventral axis. Suppressive as well as inductive tissue interactions occur during the determination of both of these organs, affecting their position and time of appearance. The complex processes of induction defined by the past nine decades of experimental work present many challenging questions that can now be addressed, especially in terms of the molecular events, cellular behaviour and regulatory physiology of the responding tissue.
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Yamamoto, Makoto, Li Cui, Kohei Johkura, Kazuhiko Asanuma, Yasumitsu Okouchi, Naoko Ogiwara, and Katsunori Sasaki. "Branching ducts similar to mesonephric ducts or ureteric buds in teratomas originating from mouse embryonic stem cells." American Journal of Physiology-Renal Physiology 290, no. 1 (January 2006): F52—F60. http://dx.doi.org/10.1152/ajprenal.00001.2004.
Повний текст джерелаАнотація:
Ureteric bud epithelial cells and metanephric mesenchymal cells that comprise the metanephric kidney primordium are capable of producing nephrons and collecting ducts through reciprocal inductive interaction. Once these cells are induced from pluripotent embryonic stem (ES) cells, they have the potential to become powerful tools in the regeneration of kidney tissues. In this study, we investigated these renal primordial cells and structures in mouse ES cell outgrowths and their transplants. Gene expression essential for early kidney development was examined by RT-PCR in embryoid body (EB) outgrowths and their transplants in adult mice. Histochemical detection of kidney primordial structures and gene expression analysis coupled with laser microdissection were performed in transplant tissues. RT-PCR analysis detected gene expression of Pax-2, Lim-1, c-Ret, Emx2, Sall1, WT-1, Eya-1, GDNF, and Wnt-4 in the EB outgrowths from days 6–9 of expansion onward, and also in the teratoma tissues 14 and 28 days after transplantation. Histochemical analysis 14 days after transplantation showed that some ducts were positive for Pax-2, endo A cytokeratin, kidney-specific cadherin, and Dolichos biflorus agglutinin and that dichotomous branching of these ducts had occurred. These staining patterns and morphological features are intrinsic for mesonephric ducts and ureteric buds. In long-term survival of 28 days, Pax-2-immunoreactivity disappeared in some renal primordia-like structures, indicating their differentiation. Some ducts were accompanied by mesonephric nephron-like convoluted tubules. RT-PCR analysis of those structures collected by microdissection confirmed that they expressed kidney development-related genes. In conclusion, these data suggest the potential of ES cells to produce renal primordial duct structures and provides an insight into the regeneration of kidney tissues.
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Antes, Lisa M., Monica M. Villar, Sylvia Decker, Roberto F. Nicosia, and Dean A. Kujubu. "A serum-free in vitro model of renal microvessel development." American Journal of Physiology-Renal Physiology 274, no. 6 (June 1, 1998): F1150—F1160. http://dx.doi.org/10.1152/ajprenal.1998.274.6.f1150.
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The differentiation and organization of the embryonic renal vasculature is a crucial event in renal development. To study this process, we developed a serum-free in vitro model of renal microvessel development. Mouse embryonic kidney explants, when embedded specifically in type I collagen, demonstrate outgrowth of microvascular structures when stimulated by the phorbol ester 12- O-tetradecanoylphorbol 13-acetate (TPA, 10–50 ng/ml). Other polypeptide growth factors stimulated little, if any, microvessel outgrowth from the explants. Similar outgrowths were not observed when other embryonic tissue explants were used. The number of microvessels observed depended on the gestational age of the explants. We hypothesize that TPA induces the in situ differentiation of metanephric mesenchymal cells into endothelial cell precursors and that specific matrix proteins and cell-matrix interactions are necessary for the organization of these precursors into microvessels. Our model will allow us to examine in detail the responsiveness of metanephric kidney cells to both growth factors and extracellular matrix molecules and to understand how they influence renal endothelial cell differentiation.
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Kuwahara, M., T. Ogaeri, R. Matsuura, H. Kogo, T. Fujimoto, and S. Torihashi. "In vitro organogenesis of gut-like structures from mouse embryonic stem cells." Neurogastroenterology and Motility 16, s1 (April 2004): 14–18. http://dx.doi.org/10.1111/j.1743-3150.2004.00468.x.
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Northcutt, R. Glenn. "The use and abuse of developmental data." Behavioral and Brain Sciences 26, no. 5 (October 2003): 565–66. http://dx.doi.org/10.1017/s0140525x03340129.
Повний текст джерелаАнотація:
Structural similarity is helpful in recognizing homologous structures, but it does not define them. Such structures must also have phylogenetic continuity, a criterion that is ignored by Aboitiz et al. and by proponents of “field homology.” “Similar” structures, as well as “field homologues” from “the same” embryonic field, are not necessarily homologous, and an outgroup analysis of developmental stages should be performed to establish homologies.
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Driehuis, Else, and Hans Clevers. "CRISPR/Cas 9 genome editing and its applications in organoids." American Journal of Physiology-Gastrointestinal and Liver Physiology 312, no. 3 (March 1, 2017): G257—G265. http://dx.doi.org/10.1152/ajpgi.00410.2016.
Повний текст джерелаАнотація:
Organoids are three-dimensional (3D) structures derived from adult or embryonic stem cells that maintain many structural and functional features of their respective organ. Recently, genome editing based on the bacterial defense mechanism CRISPR/Cas9 has emerged as an easily applicable and reliable laboratory tool. Combining organoids and CRISPR/Cas9 creates exciting new opportunities to study organ development and human disease in vitro. The potential applications of CRISPR in organoids are only beginning to be explored.
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Rungarunlert, S., W. Chakritbudsabong, S. Pamonsupornvichit, L. Sariya, R. Pronarkngver, S. Chaiwattanarungruengpaisan, J. N. Ferreira, et al. "184 Establishment of Porcine Induced Pluripotent Stem Cell Lines by Adding LIN 28 Transcription Factor." Reproduction, Fertility and Development 30, no. 1 (2018): 232. http://dx.doi.org/10.1071/rdv30n1ab184.
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The establishment of porcine induced pluripotent stem cells (piPSC) is important in the field of human biomedical regenerative medicine. The pig model is a more representative model than current rodent models because it better mimics human physiology in different organ systems. The piPSC can be traditionally generated by reprogramming somatic cells using 4 transcription factors (4TF: OCT4, SOX2, KLF4, and c-MYC), similarly in human. However, it is difficult to maintain the pluripotent state of reprogrammed cells and they exhibit poor differentiation capacity. Hence, the 4TF may be not enough to reprogram porcine somatic cells. This study aimed to establish piPSC by adding LIN28 (referred to as 5TF) to the traditional 4TF, via retroviral vector. Here, we report the successful establishment of 3 piPSC lines by using the 5TF. All 5TF-piPSC lines exhibited a normal karyotype (38, XY) and a typical mouse embryonic stem cell (ESC) morphology, including tightly packed and dome-like shape, even after they were propagated over 40 passages. All 5TF-piPSC lines were positive for alkaline phosphatase staining and expressed high levels of ESC-like markers (OCT4, SOX2, NANOG, and SSEA-1). Importantly, the 5TF-piPSC lines showed pluripotent capacity, as evidenced by differentiation into 3 germ layers in vitro following cystic embryoid body formation, as well as by efficiently forming teratomas containing all 3 embryonic germ layers in vivo. Moreover, the 5TF-piPSC lines showed spontaneously contractile cardiomyocytes and expressed cardiomyocyte markers (cardiac troponin T) during spontaneous cardiac differentiation using cell aggregation into spherical-like structures referred to as embryoid bodies. Thus, the addition of LIN28 TF promoted long-term pluripotency of piPSC and enhanced the ability to differentiate towards 3 embryonic germ layers and cardiac lineage. This research project is supported by grants from the Mahidol University, Thailand.
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Tkatchenko, Tatiana V., Ricardo A. Moreno-Rodriguez, Simon J. Conway, Jeffery D. Molkentin, Roger R. Markwald, and Andrei V. Tkatchenko. "Lack of periostin leads to suppression of Notch1 signaling and calcific aortic valve disease." Physiological Genomics 39, no. 3 (November 2009): 160–68. http://dx.doi.org/10.1152/physiolgenomics.00078.2009.
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The Postn gene encodes protein periostin. During embryonic development, it is highly expressed in the outflow tract (OFT) endocardial cushions of the developing heart, which give rise to several structures of the mature heart including the aortic valve. Periostin was previously implicated in osteoblast differentiation, cancer metastasis, and tooth and bone development, but its role in cardiac OFT development is unclear. To elucidate the role that periostin plays in the developing heart we analyzed cardiac OFT phenotype in mice after deletion of the Postn gene. We found that lack of periostin in the embryonic OFT leads to ectopic expression of the proosteogenic growth factor pleiotrophin ( Ptn) and overexpression of delta-like 1 homolog (Dlk1), a negative regulator of Notch1, in the distal (prevalvular) cushions of the OFT. This resulted in suppression of Notch1 signaling, strong induction of the central transcriptional regulator of osteoblast cell fate Runx2, upregulation of osteopontin and osteocalcin expression, and subsequent calcification of the aortic valve. Our data suggest that periostin represses a default osteogenic program in the OFT cushion mesenchyme and promotes differentiation along a fibrogenic lineage. Lack of periostin causes derepression of the osteogenic potential of OFT mesenchymal cells, calcium deposition, and calcific aortic valve disease. These results establish periostin as a key regulator of OFT endocardial cushion mesenchymal cell fate during embryonic development.
Дисертації з теми "Embryonic Structures physiology"
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Liu, Yanhe. "Human oocytes and embryos viewed by time-lapse videography, and the development of an embryo deselection model." Thesis, Edith Cowan University, Research Online, Perth, Western Australia, 2016. https://ro.ecu.edu.au/theses/1787.
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Despite its wide application today, in vitro fertilization (IVF) treatment continues to have relatively low efficacy, largely due to inaccuracy in selecting the best quality embryo(s) from the cohort for transfer. Novel methodologies for improved selection are being developed, and time-lapse observation of human embryos is gaining increasing popularity due to the more detailed morphokinetic information obtained plus uninterrupted culture conditions. The morphokinetic information enables the use of quantitative timings in developmental milestones of embryos and qualitative measures of abnormal biological events, to assist embryo selection/deselection. This project aimed to identify current limitations in the use of such measures and to develop recommendations for improvement in clinical application.
In the current study, most data were collected retrospectively from infertile couples seeking IVF treatment at a fertility clinic, with consent to use time-lapse incubation (Embryoscope) for embryo culture. Comparisons of time-lapse measures were made between embryos with confirmed implantation and non-implantation outcomes following uterine transfers. Thereafter, an embryo deselection model was proposed based on the retrospective findings, followed by prospective validation.
It was found in the current study that the reference starting time point (t0) in certain existing time-lapse systems was inaccurate due to (i) the early biological variations between sibling oocytes, (ii) technical limitations in current equipment and protocols, and (iii) different insemination methods used (Papers 1&2). The above variations may be minimized by using pronuclear fading (PNF, a biological time point) as t0 rather than insemination (a procedural time point) (Paper 2). An example of such application was the comparison of embryo development between patients with high and low serum progesterone levels on the trigger-day (Paper 3). Furthermore, the growth rate of embryos reported in the literature is subject to multiple clinical or laboratory factors, and this was in agreement with the present study where a published time-lapse algorithm emphasizing quantitative timing parameters was shown to lose its discriminatory power in implantation prediction when applied in two different laboratories (Paper 4). Interestingly, the qualitative measures seemed to have better inter-laboratory transferability due to the embryo growth patterns appearing independent of clinical and technical factors (Paper 4). Two novel qualitative measures were reported in the present study, namely reverse cleavage and less than 6 intercellular contact points at the end of the 4-cell stage, showing negative correlations with embryo implantation outcomes (Papers 5&6). A qualitative embryo deselection model was therefore proposed, including several qualitative measures with implantation rates being potentially increased from 22.4% to 33.6% (Paper 6). Finally, an embryo deselection model combining both qualitative and quantitative measures was reported with the use of PNF as t0, showing significant prediction of implantation outcomes in embryos regardless of insemination method (Paper 7).
In conclusion, this thesis demonstrates the usefulness of time-lapse embryo selection during IVF treatment in one specific laboratory. However, any new time-lapse parameter or model for embryo selection requires external validation by properly designed large-scale studies. Future clinical research and the development of integrated engineering and computer technology may further improve the efficacy of time-lapse selection of human embryos.
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Barblett, Hamish. "Factors affecting the survival and implantation of human blastocysts following vitrification." Thesis, Edith Cowan University, Research Online, Perth, Western Australia, 2019. https://ro.ecu.edu.au/theses/2228.
Повний текст джерелаАнотація:
The increased cell numbers, presence of the blastocoel and rapid cell re-organisation have required the development of specific survival criteria post warm to effectively select the most viable blastocyst for transfer. Pre-freeze blastocyst expansion and post warm re-expansion have been shown to contribute significantly to the chances of an implantation and subsequent live birth. The aim of this study was to explore factors that influence the outcome of blastocyst transfers after vitrification and warming, and hopefully improve outcomes by further applying improvements in future cycles. Variables from 8 years of vitrified/warmed blastocysts were retrospectively compiled and analysed to determine the most significant contributors to outcome. There were 2466 transfers of either 1 or 2 vitrified/warmed blastocysts resulting in 796 (32.3%) clinical pregnancies and 751 (30.5%) live born babies. The patient/cycle specific variables of age: ≤38 years (OR: 2.01, 95% CI:1.48-2.73), transfer order: ≤ 2 (OR:1.32, 95% CI:1.10- 1.59) and cycle type: non-HRT (OR: 1.38, 95% CI:1.15-1.66) significantly influenced the live birth outcome. Blastocysts vitrified on day 5 of development had significantly improved outcomes to day 6 blastocysts (OR: 1.80, 95% CI: 1.37-2.35). A greater degree of blastocyst expansion on Day 5 further improved these outcomes (OR: 1.47, 95% CI:1.17-1.86). A grade 1 morphology rating significantly improved the outcomes of day 5 expanded blastocysts (OR: 1.51, 95% CI:1.24-1.85). The composition of the warming media and possibly the concentrations of osmotic buffer contributed to the survival of warmed blastocysts. Post warming assessment of the blastocyst showed that if the level of cell degeneration in the surviving and transferred embryo was less than 5%, this significantly influenced the outcome (OR:1.57, 95% CI:1.22-2.03). There was no significant difference if a blastocyst with ≥ 95% cell survival commenced re-expansion within 30 or 60 minutes after the warm (OR: 1.13, 95% CI:0.87-1.46). This study highlights the significance of even a small number of degenerative cells in the warmed blastocyst despite early commencement of re-expansion and warrants further prospective analysis.
Книги з теми "Embryonic Structures physiology"
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Alvarez-Bolado, G. Developmental brain maps: Structure of the embryonic rat brain. New York: Elsevier, 1996.
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Larsen's Human Embryology. Churchill Livingstone, 2014.
Знайти повний текст джерелаЧастини книг з теми "Embryonic Structures physiology"
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Benarroch, Eduardo E., Jeremy K. Cutsforth-Gregory, and Kelly D. Flemming. "Diencephalon." In Mayo Clinic Medical Neurosciences, edited by Eduardo E. Benarroch, Jeremy K. Cutsforth-Gregory, and Kelly D. Flemming, 627–56. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190209407.003.0018.
Повний текст джерелаАнотація:
The supratentorial level includes all structures located within the skull and above the tentorium cerebelli. These structures develop from the embryonic prosencephalon and, therefore, include derivatives of the diencephalon and telencephalon. The visual system, a derivative of the diencephalon, provides input to the cerebral cortex for image formation and to subcortical structures to trigger the light reflex and entrain the circadian rhythm. This chapter discusses the anatomy, physiology, and clinical correlates of the diencephalic components of systems at the supratentorial level.
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Lingvay, Ildiko, and Shelby A. Holt. "The Thyroid." In Textbook of Endocrine Physiology. Oxford University Press, 2011. http://dx.doi.org/10.1093/oso/9780199744121.003.0015.
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The thyroid gland, which is the largest endocrine organ, secretes primarily thyroid hormones that play a critical role in the normal growth and development of the maturing human. In the adult, thyroid hormones maintain metabolic stability by regulating oxygen requirements, body weight, and intermediary metabolism. Thyroid function is under hypothalamic-pituitary control, and thus, like the gonads and adrenal cortex, it serves as a classical model of endocrine physiology. In addition, the physiological effects of thyroid hormones are regulated by complex extrathyroidal mechanisms resulting from the peripheral metabolism of the hormones, mechanisms that are not under hypothalamic-pituitary regulation. Thyroid function abnormalities are very prevalent, especially in females and in certain geographic areas, and are often a result of autoimmunity or iodine deficiency. The thyroid originates from two distinct parts of the embryonic endoderm: • The follicular structures arise from a midline thickening of the anterior pharyngeal floor (the base of the tongue), adjacent to the differentiating heart. This thyroid diverticulum first expands ventrally while still attached to the pharyngeal floor by its stalk (thyroglossal duct), and then expands laterally, leading to the characteristic bilobed structure. As the developing heart descends, the thyroid gets pulled into its final position, a process that leads to the rapid stretch and degeneration of the thyroglossal duct. • The parafollicular cells are derived from the ultimobranchial bodies (originating from the neural crest) but ultimately are surrounded by the medial thyroid. The parafollicular cells represents <10 % of the adult thyroid gland. The thyroid completes its structural development by 9 weeks of gestation, the first endocrine organ to assume its definitive form during organogenesis; yet full functional maturation and integration with the hypothalamic-pituitary axis continues throughout gestation. Abnormal thyroid development can lead to persistence of the thyroglossal duct, presence of ectopic thyroid tissue (lingual thyroid, lateral aberrant thyroid), and malposition (thoracic goiter), all of which can remain clinically silent or present later in life as diagnostic challenges. The shape of the human thyroid resembles that of a butterfly.
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Wani, Khursheed Ahmad, Jamila Irfan, and Junaid Ahmad Malik. "Impact of Heat Stress on Embryonic Implantation." In Climate Change and Its Impact on Fertility, 99–112. IGI Global, 2021. http://dx.doi.org/10.4018/978-1-7998-4480-8.ch005.
Повний текст джерелаАнотація:
One of the expected effects of mammalian developmental defects is a rise in air temperature. Heat stress adversely affects embryo oogenesis, oocyte maturation, fertilization, and implantation. The number of defects caused by heat stress in all mammals is almost identical, but each species has its own particular sensitivity to specific defects. It suggests that genotype may have a significant effect on the type of defect, its occurrence, and its extent. By heat output and loss, the body temperature is usually preserved in a restricted range, but the equilibrium can be disrupted by illness, inadequate nutrition, and severe environmental temperature. Elevated maternal temperature during pregnancy, either by fever or any other means of heating, may result in embryo death, retarded development, abortion, and many embryonic defects such as cell proliferation, migration, differentiation and apoptosis or programmed cell death, structural and functional defects, and changes in maternal physiology. Maternal heat stress also reduces the levels of placental hormones. This chapter deals with the heat stress effect on reduction of reproductive function, implantation defects, etc. of different animals and humans.
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Wani, Khursheed Ahmad, Jamila Irfan, and Junaid Ahmad Malik. "Impact of Heat Stress on Embryonic Implantation." In Climate Change and Its Impact on Fertility, 99–112. IGI Global, 2021. http://dx.doi.org/10.4018/978-1-7998-4480-8.ch005.
Повний текст джерелаАнотація:
One of the expected effects of mammalian developmental defects is a rise in air temperature. Heat stress adversely affects embryo oogenesis, oocyte maturation, fertilization, and implantation. The number of defects caused by heat stress in all mammals is almost identical, but each species has its own particular sensitivity to specific defects. It suggests that genotype may have a significant effect on the type of defect, its occurrence, and its extent. By heat output and loss, the body temperature is usually preserved in a restricted range, but the equilibrium can be disrupted by illness, inadequate nutrition, and severe environmental temperature. Elevated maternal temperature during pregnancy, either by fever or any other means of heating, may result in embryo death, retarded development, abortion, and many embryonic defects such as cell proliferation, migration, differentiation and apoptosis or programmed cell death, structural and functional defects, and changes in maternal physiology. Maternal heat stress also reduces the levels of placental hormones. This chapter deals with the heat stress effect on reduction of reproductive function, implantation defects, etc. of different animals and humans.