Academic literature on the topic 'Intestines, embryology'

Gastrointestinal caeca, which are unique structures of fish, are located at the junction between the stomach and intestine. The postembryonic development of caeca in the bluegill was traced in relation to the source of nutrition (endogenous, endoexogenous, or exogenous). During the mesolarval stage a constriction appears at the gastrointestinal junction, which first gives origin to bulges, which eventually become the stomach and the intestine. The gastrointestinal constriction deepens and obstructs the rapidly branching mucosa of the intestine. The obstructed mucosal folds extend outward and are transformed into caecal buds. It was found that both the formation and the number of the caeca are related to the magnitude of the gastrointestinal constriction and the degree of splitting of the obstructed mucosal folds. The absence of mucosal division in the stomach at the time of the caecal buds' origin also establishes that the caeca develop from the intestinal mucosal folds and not from the stomach.

Intestinal malrotation occurs if midgut does not complete or partially completes its 270° counter-clockwise rotation around the superior mesenteric artery during embryologic life. In general, it frequently manifests with vomiting due to duodenal obstruction and volvulus in the initial months of life, and it is very rare to manifest in the adulthood. A 20-year-old male patient who had severe abdominal pain, nausea, vomiting, and distention for one day was evaluated at the emergency department. On abdominal tomography “swirling appearance of structures around the superior mesenteric artery” was reported. CT appearance was considered compatible with a rotational anomaly. Emergency surgery was planned for the patient. In laparotomy, it was observed that an approximately 100 cm long small intestine segment was rotated around a band (Ladd) and ischemia was developed in this segment due to rotation of its mesentery. The rotation of the small intestinal mesentery was corrected by opening the bands. After the warm application to the intestinal mesenteric ischemia for a while, the color and the peristalsis of the intestines became normal. The patient was discharged on postoperative day 2 with suggestions.

The purpose of our research was to study the effects of probiotic feed supplement “Bio-Mos” on the structure changes of digestive apparatus of two-year-old channel catfish and carp. Materials and methods of research. Studies on the influence of a probiotic supplement on the organism of two-year-old channel catfish were conducted on the basis of the Prydniprovsky industrial warm-water fish farm under the conditions of the State Enterprise "Nyvka" of the Institute of Fisheries of the National Academy of Agrarian Sciences of Ukraine. Carp and channel catfish intestines were investigated during the growing season (May-September). Fish received a probiotic additive “Bio-mos” with feed. The preparation was fed for carp in a concentration of 2%, and for channel catfish – 5% of the feed weight. For histological studies, the samples of biological material were carried out using an express method of modification of the pouring of fish tissues into paraffin mixtures. Histometry of objects (determination of linear dimensions of histological objects) was carried out according to Avtandilov G. G. For microscopic histocyte studies, a manual "Atlas of histology and embryology of industrial fish of Ukraine", "Atlas of microscopic structure of fish liver", "Atlas of histology and histochemistry of freshwater fish" and "Fish Histology and Histopathology" were used. Results of the research. As histologic studies revealed the complex use of the preparation "Bio-mos" in the composition of feedstuffs had a positive effect on the development of certain sections of the fish intestinal tube. Probably this may be explained by the synergy of the individual components of the diet. Concerning the two-year-old species of the channel catfish, we can say that the histostructure of the wall of the esophagus and the thick intestine in the control and experimental individuals were almost identical and did not reveal any changes in the entire length of the sites. Separate modifications at the microlevel were recorded in the stomach wall. Our studies showed that usage of the drug "Bio-mos" in the composition of feed in the area of large curvature of stomach of investigated individuals increased secretory activity of the glandular structures. It was also found in fish that received feed supplement, enlightenment of most gastric glands, somewhat expanded. It should be noted that exorcinocytes, due to the influence of individual components of the drug "Bio-mos", gain increased secretory activity. It was noted that the increase of secretory activity of the gastric wall of experimental fish had a focal character, which shows an increase in the intensity of the body as a whole. Investigation of the structure of the thin intestine of carp and channel catfish at the microlevel revealed a number of common features that were observed within the studied species: The cell walls of a single-layered high prismatic epithelium of the mucous membrane were almost obscured indifferently, in connection with which the entire cellular layer was observed in the form of a homogeneous, optically homogeneous mass. Cytoplasm of epithelial cells was characterized by increased oxyfilm. At the apical end of the cells there was a low rim, formed by a huge amount of cytoplasmic processes that had its own type of dark strip. The nuclei of the epitheliocytes were oval or highly elongated, oriented closer to the basal end; in them there were clearly visible lumps of chromatin and sharply oxyphilic nucleols. Occasionally there were mitotic cells. Among the prismatic cells were often glandulotsity. Under the epithelium was a plate of mucous membrane, represented by a layer of loose connective tissue or the same, it consisted of collagen membranes that form a three-dimensional barely noticeable network. The muscle layer of the mucous membrane was represented only by separate elongated very thin smooth muscle cells with rod-shaped cores lying under the epithelium. The muscle of the intestinal tube was two-layer. The inner layer of the circular muscle on the histopreparation was cut along. The nucleus of the muscle cells was round, lying in the center and surrounded by a light rim of the cytoplasm (where the incision did not take the nucleus, nuclear-free sites were visible). Between the circular and longitudinal layers of smooth muscle lied the intermucosal layer of fine puffy connective tissue, in it – the capillaries, which were determined by the nuclei of the endothelium. On the histological preparations of the small intestine of the carp, it was noted that the circular muscle layers, the own plate of the mucosa with accompanying intramural ganglia, vascular elements and connective tissue, as well as the components of the intestinal folds within the studied groups, were morphologically identical. In fish of the control group, the vast majority of intestinal folds were in a free state, at the same time, in the majority of experimental individuals, peculiar anastomoses of the folds were observed in the mucous membrane of the small intestine. This phenomenon had a local character, but it clearly illustrated the increase in surface area of absorption. The experimental group was found to change the intestinal fold and had a relatively developed capillary network, indicating optimization of metabolic processes in the intestinal tube. The own plate of the fold of the mucous membrane had a pronounced hyperchromatosis. Probably, their concentration within this histological structure was stable in nature – this fact clearly reflected an increase in the immune status of fish, and, consequently, an improvement in the health indicators of individuals. It should be noted that in the investigated fish, modification changes in the form of individual centers are considered also in the caudal direction of the intestinal tube, but were not expressed in such contrast. Conclusions. Investigation the influence of the probiotic drug "Bio-mos" on the intestines of the channel catfish were established changes in its structure, and in particular noted that exorcinocytes, as a result of the influence of individual components of the drug become elevated secretory activity. This phenomenon is focal in nature, and shows an increase in the intensity of the body as a whole. In carps, that received the drug Bio-mos in the composition of feed, the length of the intestinal folds exceeds the length of the individuals in the control group (an average of 1.6 times). Accordingly, the change in length increases the surface area of absorption. Complex use of the preparation "Bio-mos" in the composition of feed for fish, has a modifying effect on the mucous membrane of the intestinal tube in the form of stimulation of secretory activity of the glands of the stomach, increasing the area of the absorbent surface of the small intestine, accelerating blood flow and modulating the immune status of fish organism in whole.

Nucleotide-binding oligomerization domain, leucine-rich repeat and pyrin domain-containing proteins (NRLPs) are central components of the inflammasome. Accumulating evidence has shown that a reproductive clade of NRLPs is predominantly expressed in oocyte to cleavage stage embryos and participates in mammalian preimplantation development as a component of a multiprotein complex known as the subcortical maternal complex (SCMC). Nlrp9s belong to the reproductive class of NLRPs; Nlrp9b is unique in acting as an inflammasome against rotavirus in intestines. Here we generated mice carrying mutations in all three members of the Nlrp9a/b/c gene (Nlrp9 triple mutant (TMut) mice). When crossed with WT males, the Nlrp9 TMut females were fertile, but deliveries with fewer pups were increased in the mutants. Consistent with this, blastocyst development was retarded and lethality to the preimplantation embryos increased in the Nlrp9 TMut females in vivo. Under in vitro culture conditions, the fertilized eggs from the Nlrp9 TMut females exhibited developmental arrest at the two-cell stage, accompanied by asymmetric cell division. By contrast, double-mutant (DMut) oocytes (any genetic combination) did not exhibit the two-cell block in vitro, showing the functional redundancy of Nlrp9a/b/c. Finally, Nlrp9 could bind to components of the SCMC. These results show that Nlrp9 functions as an immune or reproductive NLRP in a cell-type-dependent manner.

Common mesentery is an anatomical abnormality resulting from a defect in the embryonic development of the digestive tract, resulting in a fetal disposition of the intestine in patients. It is mostly revealed during the neonatal period and in children with severe accidents of occlusion. At the anatomo-embryological level, the common mesentery is the consequence of malrotation and attachment of the primary intestinal loop during its embryological development. Attachment abnormalities may or may not be associated with rotation abnormalities (the latter favor them), and they are of 2 types: excessive attachments or attachments defects.We report the case of an 8-years-old female patient received in the emergency room for severe abdominal pain, inability to pass stools and gas, and bilious and incoercible vomiting for 2 days. The surgical exploration showed a volvulus of the small bowel with a 270° clockwise rotation, and the presence of a complete common mesentery and numerous mesenteric lymphadenopathies. The stomach and colon were distended, with adhesions between the colon and the small bowel, but no ischemia or intestinal perforation was noted. The operative procedures consisted of untwisting the volvulated loops in an anti-clockwise direction(270°), a release of adhesions, an appendectomy. We also emptied the small intestine and repositioned it.Common mesentery is a rare pathological state and its incidence is poorly understood due to clinical latency. But a good knowledge of embryology, attentive listening to patients and an accurate reading of the various radiological examinations can lead us thinking about malrotation. The occurrence of occlusive accidents is the main frequent cause of discovery of this abnormality.

Enteric duplication is rare in dogs. Here, we report the rarest form of duplication in which two segments are parallel and share a wall for most of their lengths. A nine-year-old spayed female Yorkshire terrier was referred to the Veterinary Medical Teaching Hospital at Gyeongsang National University due to anorexia and diarrhoea. Physical examination, haematological examination, radiography, and ultrasonography were performed. On physical examination, dry, pale mucous membrane was identified. Moderate anaemia with decreased packed cell volume was detected in complete blood count. Serum urea nitrogen and creatinine levels were mildly increased. Radiographic images revealed no significant findings. On ultrasonographic examination, a multi-layered appearance of a focal small intestinal segment was identified in the left mid abdomen. Following the lesion, it was divided into two small intestinal segments. Based on imaging findings, intussusceptions or enteric duplication were suspected. To resect the abnormal small intestinal segment, enterectomy was performed. Follow-up was not performed because the patient expired during the postoperative recovery time. The histopathological diagnosis was non-communicating small intestinal duplication. Non-communicating intestinal duplication is related to embryologic abnormalities and is usually concurrent with other anomalies such as vertebral malformations and urogenital duplications. However, this case had no other anomalies associated with the malformation of the intestine.

Midgut malrotation is a congenital anomaly seen usually in childhood. Its presentation as an acute intestinal obstruction is extremely rare in adults usually identified intra operatively. A high index of suspicion is always required when dealing with any case of acute intestinal obstruction. We report a case of young adult who presented with symptoms of acute intestinal obstruction and was diagnosed intra-operatively as cecal volvulus with impending perforation caused by midgut malrotation. Malrotation of the intestinal tract is seen due to aberrant embryology. The presentation of intestinal malrotation in adults is very rare. Contrast enhanced Computed tomography (CT) can show the abnormal anatomy clearly. Anomalies like midgut malrotation can present as an operative dilemma and awareness regarding these conditions can help surgeons deal with these conditions.

Intestinal duplications are rare anomalies that usually present in childhood. Of these, duodenal duplications are among the most uncommon. Although these usually present with obstructive symptoms or bleeding, pancreatitis may occur. A case of duodenal duplication cyst causing recurrent pancreatitis in a 12-year-old girl is presented. The literature on duodenal duplications, and their epidemiology, embryology and pathophysiology is reviewed.

AbstractThe survival rate of newborns with gastroschisis (GS) has been increasing in the past decades; however, the morbidity continues to be high, mainly related to the length of hospitalization due to disturbances of motility, absorption, and risk of intestinal infections. The development of basic research with the creation of experimental models has provided enormous advances in the understanding of the pathophysiology of the disease. These models allowed the study of the target genes involved in the embryology of the defect, the influence of the amniotic fluid, and the use of drugs and fetal therapies in an attempt to reduce the intestinal damage and to provide a rapid return of intestinal motility. Our aim was to describe the main GS models and the translational, historical impact of these research advances on the disease.

Le gène Cdx2 exerce de nombreuses fonctions au cours du développement embryonnaire. Son expression est maintenue spécifiquement dans l’épithélium intestinal adulte. Cdx2 est diminué dans les cancers colorectaux (CCR), favorisant la migration et la dissémination des cellules tumorales. Cette diminution de Cdx2 est réversible, suggérant une dérégulation du gène. Nous avons étudié d’une part les fonctions intestinales de Cdx2 au cours du développement et surtout chez l’adulte, et d’autre part les mécanismes moléculaires associés à la dérégulation de Cdx2 dans les CCR.Une approche d’invalidation conditionnelle de Cdx2 chez la souris a été choisie. Nous montrons que Cdx2 est nécessaire pour l’établissement de l’identité intestinale au cours du développement. De plus, dans l’intestin adulte il contribue au maintien de l’identité des cellules souches et intervient dans la différenciation terminale des cellules épithéliales. Le croisement du modèle murin transgénique pCdx2-9LacZ avec le modèle de cancérogénèse colique spontanée Apc∆14/+ indique que les éléments nécessaires à la diminution d’expression de Cdx2 dans les CCR sont sur le promoteur de 9kb de Cdx2. Par ailleurs, nous montrons une corrélation d’expression entre les protéines HNF4α, régulateur transcriptionnel de Cdx2, et Cdx2 dans des échantillons de tumeurs intestinales humaines et murines. L’invalidation conditionnelle de Hnf4α dans l’intestin est associée à une réduction d’expression de Cdx2 et à une plus grande susceptibilité des animaux à la tumorigenèse colique chimio-induite. HNF4α constitue un facteur important de la dérégulation de Cdx2 dans les CCR et exerce une fonction suppresseur de tumeur dans l’intestin
The Cdx2 gene exerts many functions during embryonic development. Its expression is maintained specifically in the adult intestinal epithelium. Cdx2 expression is reduced in colorectal cancers (CRC); moreover, this reduction promotes migration and the spread of colon tumor cells. The alteration of Cdx2 in CRC is reversible, suggesting a deregulation of the gene. The objectives of my project were to study the functions of Cdx2 during intestinal development and in adults and to study the molecular mechanisms associated with the deregulation of Cdx2 in CRC. An approach of conditional invalidation of Cdx2 in mice has been used. We show that Cdx2 plays a key role in establishing the intestinal identity during development. In addition, at the adult stage Cdx2 is involved in the maintaining of the intestinal stem cells identity and in the control of terminal differentiation of intestinal epithelial cells. Crossing the transgenic mouse model pCdx2-9LacZ with spontaneous colon carcinogenesis model ApcΔ14/+ indicates that the elements necessary for the decrease of Cdx2 expression are located on the Cdx2 promoter of 9kb. Earlier team works have highlighted HNF4α as a transcriptional regulator of Cdx2 expression. In this work, we have demonstrated a correlation between HNF4α and Cdx2 protein expression in samples of human and mouse intestinal tumors. The conditional invalidation of Hnf4α in the intestine is associated with a reduction of Cdx2 expression, and a greater susceptibility for mice to chemo-induced colonic tumorigenesis. HNF4α is an important factor in the deregulation of Cdx2 in CRC and it exerts itself a tumor suppressor function in the gut

L'immunité innée représente la première ligne de défense contre les infections et ses mécanismes ont été conservés au cours de l'évolution. Elle repose sur la reconnaissance de structures microbiennes conservées absentes des cellules de l'hôte (Microbe Associated Molecular Patterns) par des récepteurs spécifiques (Pattern Récognition Receptors). La drosophile est dépourvue de système immunitaire adaptatif et ne dispose que d'un système immunitaire inné pour lutter contre les infections microbiennes. Chez la drosophile, les facteurs NF-KappaB (Nuclear Factor-KappaB) sont activés au cours de la réponse immunitaire par les voies de signalisation Toll et IMD. La voie IMD est induite en réponse aux infections par des bacilles et régule l'expression de peptides antibactériens ; la voie Toll est principalement activée après infection par des coques et des champignons et régule l'expression de peptides antifongiques et d'un nombre restreint de peptides antibactériens. Des mutations inactivant ces deux voies bloquent l'expression de gènes codant les peptides antimicrobiens, causant une susceptibilité accrue aux infections microbiennes. Une comparaison des cascades gouvernant NF-KappaB chez la drosophile et les mammifères montre des parallèles saisissants entre la voie IMD et la voie TNF-R1 (Tumour Necrosis Factor receptor-1). Mon projet de thèse consiste en l'étude de la régulation des facteurs NF-KappaB chez la drosophile. Mon objectif était d'identifier de nouveaux régulateurs de la voie IMD par une approche génétique. Des données préliminaires obtenues lors de cribles effectués à partir de cellules en culture par ARN interférence (ARNi) avaient suggéré un rôle d'une protéine à domaine RING appelée DIAP2 (Drosophila Inhibitor of Apoptosis 2) dans la voie IMD. Nous avons montré qu'une délétion de diap2 induit chez la drosophile une susceptibilité accrue aux infections par des bactéries à Qram négatif associée à un défaut d'expression des gènes codant les peptides antibactériens. Des expériences d'épistasie ont démontré que DIAP2 est un régulateur positif de la voie IMD qui agit en aval de la protéine adaptatrice IMD. Pris dans son ensemble, mon travail a montré que DIAP2 est un nouveau composant de la voie IMD. Le laboratoire de Pascal Meier (Cancer Institute, Londres) a identifié une nouvelle protéine appelée PIMS (PGRP-LC-interacting Inhibitor of IMD Signaling) capable d'interagir en culture de cellules avec PGRP-LC, le récepteur de la voie IMD. J'ai étudié la fonction de PIMS à l'aide d'approches ARNi et génétique. Ainsi l'inactivation de PIMS in vivo provoque gne activation constitutive de la voie IMD dans l'intestin en absence d'infection et une suractivâtion de cette même voie après infection bactérienne orale. Mon travail établit que PIMS régule négativement la voie IMD, empêchant son activation inappropriée par la flore intestinale ou lors d'une infection. Nos collaborateurs anglais ont par ailleurs montré que PIMS pourrait agir dans le recyclage du récepteur à la membrane et réguler son interaction avec la protéine adaptatrice IMD/ou affecterait la stabilité ou la localisation du récepteur PGRP-LC à la membrane. Ce travail nous a permis d'identifier un nouveau régulateur négatif de la voie IMD qui participe à l'homéostasie du système immunitaire au niveau de l'intestin. Chez les vertébrés, la famille des facteurs de transcription de type NF-KappaB joue un rôle majeur lors des phénomènes d'immunité, d'inflammation, de prolifération cellulaire et d'apoptose. Bien que ces facteurs soient l'objet de nombreuses études, de nombreux aspects de leur fonction et de leur régulation chez les mammifères ne sont toujours pas élucidés. La réponse immunitaire de la drosophile présente de fortes analogies avec l'immunité innée des mammifères et la compréhension de ses mécanismes de régulation peut donc apporter un éclairage nouveau sur la régulation de l'inflammation chez l'homme
Drosophila represents an ideal model System in which to study host-pathogen interactions since insects have a particularly effective immune System that appears to be evolutionarily conserved. It relies solely on an innate immune response. NF-KappaB is a family of structurally related and evolutionarily conserved transcription factors. In response to microbial challenge, these factors are responsible for the antimicrobial response in drosophila. Indeed two NF-KappaB signalling pathways regulate the expression of antimicrobial peptides in response to bacterial infection. The Toll pathway is activated by gram-positive bacteria, while the IMD pathway responds to gram-negative bacteria. Activation of either Toll or IMD signalling results in the activation of distinct NF-KappaB-like transcription factors. Similarly in mammals, members of the NF-KappaB protein family play a central role in the regulation of inflammatory and innate immune responses. The IMD pathway of drosophila is highly similar to the mammalian TNF-R1 pathway. The conservation of the NF-KappaB regulatory mechanisms between organisms as diverse as insects and mammals indicate that the regulation of the innate immune response is evolutionarily conserved. The aim of my thesis was to study the regulation of the IMD pathway activation. Preliminary data in cultured cells suggested that DIAP2 protein may be involved in the IMD pathway activation. An in vivo genetic approach revealed that a loss of function of this gene is responsible for a higher susceptibility to infection and a decrease in antimicrobiel peptide production. Epistatic studies showed DIAP2 is a positive regulator of the IMD signalling that acts upstream or in parallel of TAK1. Therefore DIAP2 is a new component of this pathway. Secondly, Pascal Meier's team identified a new protein called PIMS (PGRP-LC-interacting Inhibitor of IMD Signalling) that interacts in cultured cells with the PGRP-LC receptor. Its inactivation induces the constitutive activation of the IMD signalling in vivo in the gut without an overt infection. After an oral infection it leads to the overactivation of the IMD signalling. This work shows that PIMS negatively régulates the IMD signalling. PIMS interacts with the peptidoglycane récognition protein (PGRP-LC), causing its depletion from the plasma membrane and shutdown of IMD signalling. Moreover, it also prevents the activation of this pathway by the commensal flora. Thus PIMS is required to establish immune tolerance to commensal bacteria and to maintain a balanced IMD response following exposure to bacterial infections

Tam Wing-yip.
Thesis (M.Phil.)--Chinese University of Hong Kong, 2003.
Includes bibliographical references (leaves 91-113).
Abstracts in English and Chinese.
Abstract --- p.i
Chinese Abstract --- p.iv
Acknowledgements --- p.vi
Table of Contents --- p.vii
Chapter Chapter 1 --- General Introduction --- p.1
Chapter 1.1 --- Hirschsprung's disease --- p.1
Chapter 1.2 --- Neural crest cells and enteric nervous system --- p.3
Chapter 1.3 --- Genetics of Hirschsprun´gةs disease --- p.10
Chapter 1.3.1 --- RET/GDNF/NTN signaling pathway --- p.10
Chapter 1.3.2 --- EDNRB/EDN3/ECE-1 signaling pathway --- p.13
Chapter 1.3.3 --- Dominant megacolon and Sox10 --- p.15
Chapter 1.3.4 --- Other genes involved in intestinal aganglionosis --- p.16
Chapter 1.4 --- Objectives of the present study --- p.19
Chapter Chapter 2 --- Enteric Neural Crest Cells Migration in Dominant Megacolon Mouse Embryos --- p.21
Chapter 2.1 --- Introduction --- p.21
Chapter 2.2 --- Materials and Methods --- p.26
Chapter 2.2.1 --- Animal --- p.26
Chapter 2.2.2 --- Preparation of rat serum --- p.26
Chapter 2.2.3 --- Isolation of embryos from pregnant mice --- p.27
Chapter 2.2.4 --- Preparation of wheat germ agglutinin-gold (WGA-Au) --- p.28
Chapter 2.2.5 --- Microinjection of WGA-Au conjugate --- p.28
Chapter 2.2.6 --- Whole embryo culture --- p.29
Chapter 2.2.7 --- Examination of cultured embryos --- p.30
Chapter 2.2.8 --- Histological preparation of WGA-Au injected embryos --- p.30
Chapter 2.2.9 --- Silver enhancement staining and histological examination of the sections --- p.31
Chapter 2.2.10 --- Genotyping by polymerase chain reaction --- p.32
Chapter 2.2.11 --- TUNEL assays --- p.33
Chapter 2.3 --- Results --- p.35
Chapter 2.3.1 --- In vivo development of Dominant megacolon mouse embryos of different genotypes --- p.35
Chapter 2.3.2 --- In vitro development of embryos in control and experimental groups --- p.35
Chapter 2.3.3 --- Migration of vagal neural crest cells in Dom embryos --- p.36
Chapter 2.3.4 --- Apoptotic cells detection at the vagal region by TUNEL assay --- p.37
Chapter 2.3.5 --- Migration of sacral neural crest cells in Dom embryos --- p.37
Chapter 2.3.6 --- Apoptotic cells detection at the sacral region by TUNEL assay --- p.38
Figures and Tables
Chapter 2.4 --- Discussion --- p.40
Chapter 2.4.1 --- In vitro culture system supporting the normal development of mouse embryos --- p.40
Chapter 2.4.2 --- WGA-Au as a cell marker for tracing the NCCs migration --- p.41
Chapter 2.4.3 --- Vagal neural crest cells migration in Dom mouse embryos --- p.42
Chapter 2.4.4 --- Apoptotic cell death does not contribute to the total aganglionosis in Dom homozygous embryos --- p.43
Chapter 2.4.5 --- Sacral neural crest cells migration in Dom mouse embryos --- p.45
Chapter 2.4.6 --- NCCs migration in zebrafish colourless mutant --- p.47
Chapter 2.4.7 --- Limitation of the method used in this study --- p.49
Chapter 2.4.8 --- Conclusions --- p.49
Appendices
Chapter Chapter 3 --- Migration of Enteric Neural Crest-derived Cells in the Developing Gut of Dominant Megacolon Mouse Embryos --- p.51
Chapter 3.1 --- Introduction --- p.51
Chapter 3.2 --- Materials and Methods --- p.55
Chapter 3.2.1 --- Isolation of the gut from Dom mouse embryos --- p.55
Chapter 3.2.2 --- Whole mount immunohistochemistry --- p.55
Chapter 3.3 --- Results --- p.57
Chapter 3.3.1 --- PGP9.5 immunoreactivity in the 12.5 d.p.c. Dom embryos --- p.57
Chapter 3.3.2 --- TH immunoreactivity in the 12.5 d.p.c. Dom embryos --- p.58
Chapter 3.3.3 --- PGP9.5 immunoreactivity in the 14.5 d.p.c. Dom embryos --- p.59
Figures and Tables
Chapter 3.4 --- Discussion --- p.61
Chapter 3.4.1 --- The use of PGP9.5 and TH antibodies as markers for studying the migration of enteric neural crest-derived cells --- p.61
Chapter 3.4.2 --- Incomplete migration of neural crest-derived cells within the gut of Dom heterozygous embryos --- p.62
Chapter 3.4.3 --- Failure of sacral NCCs to invade the hindgut of Dom heterozygous embryos --- p.63
Chapter 3.4.4 --- PGP9.5 and TH positive signals in the gut of Dom homozygous embryos --- p.64
Chapter 3.4.5 --- Early differentiation of neural crest-derived cells into neurons due to haploinsufficiency of Sox10 --- p.65
Chapter 3.4.6 --- Conclusions --- p.66
Chapter Chapter 4 --- Localization of Interstitial Cells of Cajal in the Gut of Dominant Megacolon Mice --- p.67
Chapter 4.1 --- Introduction --- p.67
Chapter 4.2. --- Materials and Methods --- p.72
Chapter 4.2.1 --- Isolation of the gut from mouse embryos and adult mice --- p.72
Chapter 4.2.2 --- Cryosection and immunohistochemistry --- p.73
Chapter 4.2.3 --- Whole-mount immunohistochemistry --- p.73
Chapter 4.2.4 --- Total RNA extraction --- p.74
Chapter 4.2.5 --- Reverse transcription for the first strand cDNA synthesis --- p.75
Chapter 4.2.4 --- Reverse transcription-Polymerase chain reaction (RT-PCR) --- p.76
Chapter 4.3 --- Results --- p.77
Chapter 4.3.1 --- PGP9.5 and c-kit immunoreactivity in the Dom wild type colon --- p.77
Chapter 4.3.2 --- c-kit immunoreactivity in the Dom heterozygous adult colon --- p.78
Chapter 4.3.3 --- c-kit and SCF expression during gut development --- p.78
Figures and Tables
Chapter 4.4 --- Discussion --- p.80
Chapter 4.4.1 --- The importance in studying the development of ICCs in aganglionic gut --- p.80
Chapter 4.4.2 --- ICCs development in Dominant megacolon mice --- p.81
Chapter 4.4.3 --- The relationship between enteric neurons and ICCs development --- p.83
Chapter 4.4.4 --- Advantages of using confocal microscopy and whole- mount preparations to study the ICCs development --- p.85
Chapter 4.4.5 --- Conclusions --- p.86
Chapter Chapter 5 --- General Discussion and Conclusions --- p.87
References --- p.91

This chapter begins by discussing the basic principles of gastrointestinal embryology, gastrointestinal anatomy, and intestinal stomas,before focusing on the key areas of knowledge, namely abdominal wall hernias, Crohn’s disease, ulcerative colitis, diverticular disease, colorectal polyps, colorectal cancer, haemorrhoids, fissure in ano, perianal infection and fistula-in-ano, and other anorectal conditions. The chapter concludes with relevant case-based discussions.

This chapter begins by discussing the symptoms of gastrointestinal pathology in neonates, and defines the main examples (vomiting, issues with the abdominal wall, the abnormal passage of meconium, and gastrointestinal bleeding). Systemic effects of gastrointestinal pathologies are then explained. The chapter then goes on to explore the incidence, clinical features, and treatment of a wide range of conditions, including jaundice, parenchymal lung anomalies, foregut duplication cysts, oesophageal atresia, congenital diaphragmatic hernia, diaphragmatic eventration, pyloric stenosis, malrotation and volvus, and intestinal atresia, among others. The embryology of congenital malformations is also explained.

Gastroschisis and omphalocele are congenital defects in the abdominal wall. These two conditions have different embryologic origins, but anesthetic management is similar for both. Gastroschisis is a full-thickness abdominal wall defect resulting in extrusion of abdominal viscera into the amniotic space without amniotic membrane coverage. The defect is usually to the right of the umbilicus. Omphalocele is a defect in the abdominal wall in the umbilical area in which the extruded abdominal contents (intestine, liver, spleen, bladder) are covered in a thin sac. Infants with omphalocele often have associated syndromes or chromosomal abnormalities. With either gastroschisis or omphalocele, the extruded abdominal contents must be covered and kept moist before surgical correction.

The vomiting centre (mainly histamine and acetylcholine receptors) in the medulla oblongata can be activated by four main input systems shown in Figure 13.1: the vestibular system, the central nervous system, the chemoreceptor trigger zone (in the fourth ventricle of the brain), and cranial nerves IX and X. With these four inputs in mind, it becomes easier to understand some of the pathologies that can activate the vomiting centre and cause nausea and vomiting, as is shown in Figure 13.2. • Contents ■ Undigested: oesophageal disorders, e.g. achalasia, pharyngeal pouch ■ Partially digested: gastric outlet obstruction, gastroparesis (delayed stomach emptying, e.g. seen in diabetes mellitus) ■ Bile (green): small bowel obstruction (distal to the ampulla of Vater) ■ Faeculent: distal intestinal or colonic obstruction. Note: the only time you will see faecal (i.e. true faeces), as opposed to faeculent (i.e. foul looking), vomiting is in patients with a gastrocolonic fistula… or coprophagia ■ Blood/coffee-ground: haematemesis (see Chapter 5) ■ Large volume: less likely to be functional. • Timing ■ Early morning: classically in pregnancy and raised intracranial pressure. ■ Duration: this is useful in identifying the severity (patients with severe nausea and vomiting present early) and a longer time course makes acute pathologies such as bowel obstruction less likely, as untreated this will either deteriorate or resolve. • Association with eating? ■ Vomiting within an hour of eating suggests an obstruction high in the gastrointestinal (GI) tract proximal to the gastric outlet. If this is the case, you should ask about peptic ulcer disease (or a history of dyspepsia) as this can cause scarring and pyloric stenosis. ■ Vomiting after a longer postprandial delay is consistent with an obstruction lower in the GI tract, usually in the small bowel. ■ Early satiety, postprandial bloating, and abdominal discomfort together suggest gastroparesis or outlet obstruction. • Use the SOCRATES mnemonic to characterize the pain (see Chapter 12). • The site is indicative of certain pathologies (e.g. right upper quadrant suggests a hepatobiliary cause, epigastric suggests a pancreatic or gastroduodenal cause). However, localization of pain is far from accurate in abdominal pathology due to the neural wiring and embryology, and also anatomical variations.