The Developing Human Embryology Pdf Download: An Illustrated Guide to Normal and Abnormal Developmen

Understanding the complex concepts of a developing human is not easy. This book explains all of the stages of a developing human being in order to highlight the details of the development of various organs and their continued growth. Furthermore, this book explains all of the fundamental concepts of embryology in a clear and easy-to-understand manner, making it ideal for medical students.

The Developing Human Embryology Pdf Download

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Because of the extensive details about embryo development and growth, students find this subject challenging. The developing human is a fantastic book that organizes all of the details of embryology in a user-friendly format. In addition, with a pictorial illustration, this book provides a thorough explanation of all the details. It organizes all of the details of the weeks in relation to their normal development as well as their congenital abnormalities. This book includes diagrammatic representations, summaries, clinical aspects, and keynotes to cover all aspects of embryology.

Accessing human developmental samples is constrained by general and geographically specific ethical and legal challenges. These include issues relating to donation, access to and research use of legally defined developing human tissue material, regulatory approvals processes and cultural sensitivities. Research on human embryos and fetuses is supported within European and national regulations, such as the UK National Research Ethics Service (NRES) and the French Agence de Biomédecine. In the UK, studies on preimplantation human embryos (up to 14 days after conception) are governed by the Human Fertilisation and Embryology Authority and a research ethics committee (such as NRES). However, in the USA, research on donated human embryonic and fetal materials has increasingly been restricted over the past two decades, despite the existence of similar regulatory oversight.

The advantages of whole tissue or organ profiling compared to lineage-centric analysis include comprehensive cellular analysis and the discovery of emergent biological properties. For example, the developing liver functions as a haematopoietic organ during early gestation until the middle of the second trimester, before it functionally transitions into a metabolic organ similar to the adult liver54. To meet the high demand for erythropoiesis during development, the human skin and adrenal glands can also support erythrocyte maturation during the first trimester54,55.

In contrast to our terrestrial postnatal life, the human embryo and fetus exist in an aquatic environment: our lung, gut and skin are exposed to amniotic fluid. In contrast to the postnatal lung, the developing lung does not perform oxygen transfer or receive the same volume of blood through the pulmonary veins. The effect of these physiological factors on individual tissues and the role of the placenta and maternal decidua in supporting human embryogenesis and fetal life are emerging56,57.

The syncytiotrophoblast implants the blastocyst in the decidual epithelium by projections of chorionic villi, forming the embryonic part of the placenta. The placenta develops once the blastocyst is implanted, connecting the embryo to the uterine wall. The decidua here is termed the decidua basalis; it lies between the blastocyst and the myometrium and forms the maternal part of the placenta. The implantation is assisted by hydrolytic enzymes that erode the epithelium. The syncytiotrophoblast also produces human chorionic gonadotropin, a hormone that stimulates the release of progesterone from the corpus luteum. Progesterone enriches the uterus with a thick lining of blood vessels and capillaries so that it can oxygenate and sustain the developing embryo. The uterus liberates sugar from stored glycogen from its cells to nourish the embryo.[16] The villi begin to branch and contain blood vessels of the embryo. Other villi, called terminal or free villi, exchange nutrients. The embryo is joined to the trophoblastic shell by a narrow connecting stalk that develops into the umbilical cord to attach the placenta to the embryo.[13][17]Arteries in the decidua are remodelled to increase the maternal blood flow into the intervillous spaces of the placenta, allowing gas exchange and the transfer of nutrients to the embryo. Waste products from the embryo will diffuse across the placenta.

Sarcomeric myosins present in mammalian striated muscle are class II or conventional myosins, each myosin molecule consisting of two heavy chains (MyHCs), two essential light chains (MLCs), and two regulatory MLCs. Both MyHCs and MLCs are present in different isoforms encoded by different genes. A total of 11 MyHCs is coded by 6 myosin heavy chain (MYH) genes which are widely expressed in body muscles and 5 other genes with limited expression in specialized skeletal muscles. Five essential MLCs are coded by four myosin light chain (MYL) genes, and two regulatory MLCs by two other MYL genes (Table 1) (see [1]). Most of these genes are also expressed in the developing skeletal muscle, including two MyHC isoforms, called embryonic and neonatal (or perinatal) myosins, coded by MYH3 and MYH8, respectively, and myosin light chain 1 embryonic/atrial, coded by the MYL4 gene, which are present at high levels in the initial stages of muscle development, are downregulated after birth, and are re-expressed during muscle regeneration. Here, we review the pattern of expression of myosin genes during muscle development, focusing especially on embryonic and neonatal MyHCs. In addition, we discuss the human pathologies due to mutation of MYH3 and MYH8 and the unsettled question of the functional significance of these myosins.

A number of studies in the 1960s and 1970s reported biochemical evidence suggesting that myosins isolated from mammalian embryonic or fetal skeletal muscle differ from adult muscle myosins (see references in [2, 3]). However, Whalen et al. [2] were the first to provide unambiguous evidence for the existence of distinct developmental myosins. They identified two specific MyHCs, called embryonic and neonatal (also called perinatal) MyHCs, hereafter referred to as MyHC-emb and MyHC-neo, which precede the appearance of adult fast myosins in the developing rat skeletal muscle [2]. The corresponding MYH genes were identified [4, 5] and found to be located in the same chromosomal locus as gene coding for adult fast myosin heavy chains on chromosome 11 (mouse) or 17 (human) [6]. The gene coding for MyHC-neo (MYH8) shows considerable sequence similarity with adult fast MYH genes, whereas the gene coding for MyHC-emb (MYH3) is quite different (see [7] for a comparative sequence analysis of MYH genes). Embryonic skeletal muscles also contain a unique type of essential MLC, MLC-1emb, encoded by the MYL4 gene, which is also expressed in the developing heart and in adult atrial myocardium but not in adult skeletal muscle [8, 9].

The developmental pattern of myosin isoform expression in the human embryonic and fetal skeletal muscle has been comparatively less investigated. At week 8 of gestation, primary generation fibers with central nuclei are present in the human skeletal muscle, whereas secondary generation fibers are formed after week 10 and become the predominant fiber population by week 21 [42]. MyHC-emb, MyHC-slow, and MyHC-neo transcripts are detectable in the developing skeletal muscle at week 9 (Fig. 1). At the protein level, all primary myofibers express MyHC-emb and MyHC-slow [43, 44], with MyHC-emb being detectable before MyHC-slow in the initial myotubes [45]. The proportion of fibers staining for MyHC-slow decreases from 75 % at week 10 to 3 % at week 21 of gestation, due to the dramatic increase in secondary fibers that initially do not contain MyHC-slow [45]. Secondary generation fibers express only MyHC-emb at week 12, MyHC-neo protein being detected at later stages [45]. Quantitative RNA analysis indicates that MYH3 transcripts account for about 81 % of all MYH transcripts in the human fetal skeletal muscle at week 15 of gestation [46]. At week 16 to 17, a tertiary fiber population has been identified, initially composed of very small myofibers stained by an anti-myosin antibody reactive with adult fast but not with neonatal MyHC [44, 47]. In situ hybridization indicates that MyHC-2A transcripts are weakly expressed at week 19 and more strongly at birth, whereas MyHC-2X transcripts are barely present at birth and are clearly expressed at 30 days after birth (Fig. 1). After week 27, a proportion of secondary fibers starts to express MyHC-slow, and by week 30, about 50 % of all muscle fibers express MyHC-slow, like in adult muscle [45, 44]. In the developing human muscles, both developmental MyHC isoforms are downregulated toward the end of gestation, the corresponding MyHC transcripts are expressed at low levels at birth, and in a 1-month-old infant, MyHC-neo persists only in a few fibers [48] (Fig. 1). In conclusion, most human skeletal muscle fibers, probably more than 95 %, appear to derive from secondary and tertiary waves of myogenesis and their diversification into the fast type 2A or slow type 1 lineage occurs before birth, during the third trimester of gestation, whereas the differentiation of type 2X fibers takes place in the first week after birth.

In the developing human quadriceps, three MLC proteins can be detected by 2D gel electrophoresis between week 7 and 12 [49]. MLC-3fast becomes clearly visible at week 25, when MLC-1emb starts to decrease rapidly. The major change during the third trimester of gestation is the progressive accumulation of the slow isoforms of MLC, so that at birth, the MLC profile is similar to that of adult muscle [49]. MLC-1sa transcripts are also detectable in human skeletal muscles at week 24, though at significantly lower levels compared to adult muscle [50].

The developmental period before birth is increasingly understood as a time of preparation during which the developing human acquires the many structures, and practices the many skills, needed for survival after birth. 2ff7e9595c