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Exon 1a and 1b (Ela and Elb) encode the full-length and truncated N-terminal extracellular domains, respectively. Exon 4 encodes the fifth transmembrane area and the preliminary a part of the third intracellular loop area. However, its position in mediating the consequences of progastrin and incompletely processed gastrins underneath pathological circumstances such as malignancies remains controversial. Akt, in turn, phosphorylates a big selection of proteins concerned in cell proliferation, survival, and motility. In addition, the parietal cells are morphologically immature, and insensitive to acute stimulation with exogenous gastrin, histamine, or the muscarinic/cholinergic agonist, carbachol. Infusion of gastrin alone transiently enhanced parietal cell maturation and function, whereas mixed infusion of each peptides produced a sustained recovery, suggesting that an interaction between the 2 peptides is important to maintain regular parietal cell maturation and performance. Many of the physiological actions of gastrin occur because of its regulation of specific gene expression. Increasing proof suggests that gastrin can regulate the expression of genes through both cell autonomous and paracrine mechanisms. These proinflammatory features were observed when the mesentery was superinfused with gastrin in a concentration- and time-dependent method, and in hypergastrinemic states, such as therapy with omeprazole or H. Evidence signifies that gastrin also can modulate immune cell functions by each inter- and intracellular processes. However, in distinction to G17, where sulfation inhibits its destruction by neutral endopeptidase 24. It does this by (1) stimulating gallbladder contractions and pancreatic exocrine secretion and (2) inhibiting gastric emptying and meals consumption. It does this by slowing gastric emptying and inhibiting the ingestion of further meals by inducing a sense of satiation. Finally, wild-type mice, in response to a lipid meal, confirmed an inhibition of gastric acid secretion and decreased gastric emptying. Luyer and colleagues showed that dietary fats decreases the discharge of inflammatory cytokines. Inhibition of nicotinic receptors (by chlorisondamine administration) in high-fat fed rats caused elevated bacterial translocation to distant organs and elevated plasma endotoxin ranges. These agonists have been used for the inhibition of tumor cell proliferation and the suppression of the signs associated to carcinoid syndrome, corresponding to diarrhea and flushing. Using the same quantity scheme, the signal sequence of the preprohormone is numbered from 102 (translation initiation methionine) to 79 (glycine). The numbers on the high of the diagrams symbolize the amino-acid (aa) sequence for preprosomatostatin (beginning with 102 and ending with 14). The numbers at the backside of the diagram represent the aa sequence for prosomatostatin (1�92). The N-terminal portion of prosomatostatin is highly conserved between human and rat, differing solely by 4 residues. D cells are plentiful in both the oxyntic mucosa (fundus) and antrum the place they exhibit prolonged cytoplasmic processes which would possibly be in close proximity to their target cells. Patients with acromegaly are handled with octreotide to attenuate symptoms related to development hormone extra. Reports of unwanted effects on this affected person population embrace gradual large bowel transit time. Prolonged large bowel transit time increases the proportion of deoxycholic acid in fasting serum and in bile, resulting in an general enhance in biliary ldl cholesterol supersaturation and gallstone formation among sufferers with acromegaly. Somatostatin receptors associate with L-type calcium channels and couple to Gi2 proteins, causing calcineurin activation locally and depriming of granules situated subsequent to the L-type calcium channels. These neoplasms are of endodermal origin (neuroendocrine cells) and most express neural cell markers together with chromogranin A, neuronspecific enolase, and synaptophysin. In uncommon cases of practical pancreatic endocrine neoplasms, somatostatinomas (oversecretion of somatostatin by neoplastic D cells of the pancreas), may cause signs of hyperglycemia, steatorrhea, and gallstones.

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The fluid (1) absorbs jolts, (2) prevents adherence of the embryo to the am nion, and (3) allows for fetal actions. Fetal uri�e is added daily to the am niotic fluid within the flfth m onth, however this uri�e is m ostly water because the placenta is functioning as an trade for metabolic wastes. During childbirth, the am niochorionic membrane types a hydrostatic wedge that helps to dilate the cervical canal. These changes include (1) an increase in fibrous tissue in the core of the villus, (2) thickening of basem ent membranes in fetal capillaries, (3) obliterative changes in small capillaries of the villi, and (4) deposition of fibrinoid on the surface of the villi within the junctional zone and within the chorionic p�ate. Excessive fibrinoid formation regularly causes infarction of an intervillous lake or sometimes of an entire cotyledon. The m issing a rte ry eithe r fa ils to fo rm [agenesis] or degenerates early in developm ent. Both conditions are associated with an increase in th e incidence of start defects. Prim ary causes of hydram nios embody idiopathic causes (35%), m aternal diabetes (25%], and congenital m alform ations, including central nervous system issues. The lack of fluid in the am niotic cavity m ay constrict the fe tu s or there m ay be too littie fluid fo r th e fetus to " breathe" into its lungs resulting in lung hypoplasia. They outcome from simultaneous shedding of two oocytes and fertilization by completely different spermatozoa. The zygotes implant individually within the uterus, and often each develops its own placenta, amnion, and chorionic sac. Similarly, the walls of the chorionic sacs may come into ci�se apposition and fuse. Occasionally, every dizygotic twin possesses purple blood cells of two dif ferent types (erythrocyte mosaicism), indicating that fusi�n of the two placentas was so intimate that purple cells had been exchanged. The two embryos have a typical placenta and a typical chorionic cavity but separate amniotic cavities. In rare instances, the separation occurs on the bilaminar germ disc stage, just before the appearance of the primitive stieak. This method of splitting leads to formation of two partners with a single placenta and a typical chorionic and amniotic sac. Although triplets are uncommon (about 1 per 7,600 pregnancies), delivery of quadruplets, quintuplets, and so forth is rarer. In current years, m�ltiple births have occurred more regularly in mothers given gonadotiopins (fertility drugs) forovulatoryfailure. During the last 2 to four weeks of pregnancy, nonetheless, this tissue undergoes a transitional phase in preparation for the onset of labor. Ultimately, this section ends with a thickening of the myometrium in the upper regi�n of the uterus and a softening and thinning of the lower regi�n and cervix. Labor itself is divided into three phases: (1) e�facement (thinning and shortening) and dilatation of the cervix (this stage ends when the cervix is fully dilated), (2) supply of the fetus, and (3) delivery of the placenta and fetal m em branes. Stage 1 is produced by uterine contractions that forc� the amniotic sac against the cervical canal like a wedge, or if the membranes have ruptured, then strain shall be exerted by the presenting a half of the fetus, normally the pinnacle. Stage 2 is also assisted by uterine contractions, however crucial forc� is supplied by elevated intra-abdominal stress from contraction of abdominal muscular tissues. Stage three requires uterine contractions and is aided by increasing intra-abdominal stress. As the uterus contracts, the higher half retracts, making a smaller and smaller lumen, while the lower half expands, thereby producing path to the forc�. Contractions normally start about 10 minutes aside; then, during the second stage of labor, they may happen < 1 m in ute aside and last from 30 to ninety seconds. Monozygotic Twins the second type of twins, which develops from a single fertilized ovum, is monozygotic, or identical, twins. The earliest separation is believed to happen on the twocell stage, during which case two separate zygotes develop.

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The full course of apoptosis, from its initiation to the final fragmenting of the cell, usually requires several hours. At the start of apoptosis, dense chromosome condensation occurs at the periphery of the nucleus. The nucleus turns into fragmented, and the cell breaks up into membrane-bound apoptotic our bodies, that are phagocytosed by surrounding cells. Morphologically the defining feature of apoptosis is that the contents of the cell are never launched however remain membrane bound. Autophagy was first described in the Nineteen Sixties to explain the finding of cytoplasmic elements within membranebound our bodies in liver and kidney cells. The course of is analogous in yeast,three,four the roundworm, Caenorhabditis elegans4 and mammals5 and begins with the formation of a membrane sac referred to as the phagophore, or isolation membrane, which engulfs a portion of the cytoplasm. This membrane then elongates and closes to type an autophagosome, which accommodates an indiscriminate portion of the cytoplasm. The autophagosome is then transported to and fuses with a lysosome to kind the autolysosome where the cytoplasmic contents are digested. Triggered by nutrient deprivation, autophagy is important to surviving hunger as a result of its recycling of amino acids, which may be used for gluconeogenesis, protein synthesis, or a source of energy for metabolism. Cells present process extreme autophagy present a complete destruction of the cytosolic compartment so that solely the nucleus stays. In distinction to programmed cell demise, in cells undergoing necrosis in response to tissue injury, the plasma membrane turns into permeable early in the process. The cells sometimes swell and burst, releasing their contents and sometimes triggering an inflammatory response. Detection of cells present process necrosis is predicated on the early enhance in membrane permeability. Small charged molecules, similar to propidium iodide and numerous nucleic acid dyes, would normally be excluded from the cell, but enter and may be detected by their fluorescence. Identification of those proteins and the molecular mechanisms concerned was largely the results of genetic studies in the roundworm C. Mammals have developed similar groups of proteins that fill the roles of effector, adaptor, and regulator. Both of those enzymes are constitutively present and sure to inhibitory proteins and are released by the action of the caspases. Many of those are involved within the upkeep of the cytoskeleton and embrace actin, -catenin, gelsolin, fodrin, and spectrin. Actin is the main cytoskeletal protein responsible for the form of the cell and cell motility. Early during the apoptotic course of, phosphatidyl serine is externalized to the plasma membrane offering a phagocytotic ("eat me") signal to other cells. Annexin V binds to phosphatidyl serine and, conjugated to fluorochromes, offers one other means to detect apoptotic cells via fluorescent microscopy or move cytometry. Colorimetric and fluorogenic substrates are available for all of the caspases, or Western blotting can be used to find out the shift in the amount of procaspase to the energetic type. Another such molecule is cytochrome c, which is released from mitochondria through the apoptotic course of. The apoptosome then recruits and binds procaspase 9, which is proteolytically cleaved to form lively caspase 9. The morphological hallmarks of apoptosis within the nucleus, chromatin condensation, and nuclear fragmentation are initiated by caspase cleavage of specific proteins. Caspases 3 and 6 cleave lamin and varied nuclear proteins answerable for the structural integrity of the nucleus. In addition to inducing cell dying in some types of cells, it also elicits a variety of physiological responses, similar to inflammation, cell proliferation, and differentiation. Although a lot of the results of p53 are believed due to its actions as a transcription issue, a current report by Chipuk et al. Cleavage converts Bid to the energetic, truncated type, t-Bid, which is able to binding to Bcl-2 and causing apoptosis. In part, that is due to the lack of a clear understanding of the mechanisms and signaling pathways concerned in autophagy. At instances autophagy can shield cells from apoptosis, and the inhibition of autophagy will lead to apoptosis.

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Characterization of fat-induced neurotensin-like immunoreactivity in plasma using column liquid chromatography and radioimmunoassay. Skov Olsen P, Holst Pedersen J, Kirkegaard P, Stadil F, Fahrenkrug J, Christiansen J. Neurotensin slows gastric emptying by a transient inhibition of gastric and a chronic inhibition of duodenal motility. Interaction of neurotensin, secretin and cholecystokinin on pancreatic exocrine secretion in acutely aware dogs. Interaction of neurotensin, cholecystokinin, and secretin within the stimulation of the exocrine pancreas within the dog. Analysis of the management of intestinal motility in fasted rats, with special reference to neurotensin. Ameliorative effects of bombesin and neurotensin on trinitrobenzene sulphonic acid-induced colitis, oxidative harm and apoptosis in rats. Differential effects of intestine hormones on pancreatic and intestinal growth throughout administration of an elemental food plan. Neurotensin induces hyperplasia of the pancreas and development of the gastric antrum in rats. Effect of intracerebroventricular infusion of neurotensin in glucose-dependent insulinotropic peptide secretion in canines. Peripheral and central administration of xenin and neurotensin suppress meals intake in rodents. Identification of xenin, a xenopsin-related peptide, in the human gastric mucosa and its impact on exocrine pancreatic secretion. Alcohol and fatty acid stimulation of neurotensin release from rat small gut. Synchronous oscillations within the basal secretion of pancreatic-polypeptide and gastric acid. Depression by cholinergic blockade of pancreatic-polypeptide concentrations in plasma. The use of a rat isolated ileal preparation to investigate the discharge of neurotensin. Regulation of pancreastatin release from a human pancreatic carcinoid cell line in vitro. The role of protein kinase D in neurotensin secretion mediated by protein kinase C-alpha/-delta and Rho/Rho kinase. Neuropeptide Y family of peptides: structure, anatomical expression, operate, and molecular evolution. Development of neuropeptide Y-related peptides in the digestive organs during the larval stage of Japanese flounder, Paralichthys olivaceus. Characterization, sequence, and expression of the cloned human neuropeptide Y gene. Presence, distribution, and pharmacological results of neuropeptide Y in mammalian gastrointestinal tract. The distribution and origin of a novel mind peptide, neuropeptide Y, in the spinal twine of a quantity of mammals. Distribution of neuropeptide Y-like immunoreactivity within the normoganglionic and aganglionic segments of human colon. Distribution, quantitation, and origin of immunoreactive neuropeptide Y within the human gastrointestinal tract. High ranges of neuropeptide Y in peripheral noradrenergic neurons in varied mammals together with man. Distribution, pathways and reactions to drug remedy of nerves with neuropeptide Y- and pancreatic polypeptidelike immunoreactivity in the guinea-pig digestive tract. Nerve fibers in the intestine and pancreas of the rat displaying neuropeptide-Y immunoreactivity. Enteric neuronal circuitry and transmitters controlling intestinal motor operate. Neuropeptide Y-like immunoreactive buildings within the rat stomach with special reference to the noradrenaline neuron system.

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Although apoptosis had been acknowledged as a form of cell demise for many years, and was described as pyknosis, the term itself was proposed by Kerr et al. Withdrawal of development factors or trophic substances also results in apoptosis of some cells. The binding of ligands to cell membrane receptors of the tumor necrosis issue family is liable for cytokine induced apoptosis. Numerous Atg (autophagy related) proteins have been identified in yeast with counterparts in mammals which were shown to congregate at a site close to the vacuolar membrane where autophagosomes originate. The Atg proteins are regarded as liable for recruiting membrane elements to the phagophore, nucleation, and elongation of the phagosome. Many indicators that activate apoptosis additionally induce autophagy, whereas inhibitors of apoptosis also inhibit autophagy. Lysosomal proteases, cathepsin B, D, and L, have been shown to mediate apoptosis in a variety of cell varieties. However, the fundamental mechanisms involved in autophagy and the particular roles performed by these proteins in sequestering vesicle formation remain to be elucidated. In addition, the roles of autophagy in physiology and pathology of mammalian cells are only starting to be realized. There are actually differences involving apoptosis, and the primary one is the excessive incidence of colon cancer compared to cancer of the small bowel, but there are additionally many similarities. The comparisons and contrasts between the two tissues keep away from redundancy and sometimes provide obvious explanations of differences in physiology and pathology. The intestinal epithelium offers an attention-grabbing yet complicated model in which to check apoptosis. This tissue has some of the fast turnover rates identified, as cells are misplaced into the lumen and replaced by the progeny of stem cells. Apoptosis plays a job both in the lack of cells and in regulating the number of stem cells. Both proliferation and apoptosis are affected by the hormones, progress factors, and influences that regulate the growth of all tissues within the physique. In addition, nevertheless, the lining of the gut Chapter thirteen Programmed Cell Death in the Gastrointestinal Tract 385 is subjected to luminal contents within the form of nutrients, digestion merchandise, micro organism, and growth factors. For essentially the most part, these studies have centered on describing spontaneous apoptosis and harm or stress-induced apoptosis. Many of those have recognized the roles of members of the Bcl-2 household of proteins and p53. However, there have been few research which have examined the overall regulatory means of apoptosis in the intestine. There has been little progress in developing appropriate in vitro models of normal intestinal cells. The most widely used intestinal cell traces have been developed from tumors and are irregular. Villus three Days Enterocytes Goblet cells Enteroendocrine cells Crypt Proliferative Transit cells Stem cell(s) 13. The crypt to villus ratio varies from roughly 14 crypts per villus in the duodenum to about 6 crypts per ileal villus. The longer duodenal villi each comprise approximately 7800 cells, whereas those in the ileum contain about 2100. Numerous research in normal, transgenic and chimeric mice have proven that crypts are monoclonal and are populated by the descendants of a single stem cell anchored close to the bottom of the crypt79�84 (see 85 for review). Following division of the stem cell, one daughter cell stays anchored as the model new stem cell, whereas the other undergoes a quantity of divisions within the lower and middle thirds of the crypt. The complete variety of dividing and non-dividing cells in a crypt varies in accordance with its location, just as the variety of cells per villus varies. Duodenal crypts include roughly 530 cells, whereas the common number of cells per ileal crypt is 360. During migration, the cells mature into three of the 4 terminally differentiated cell types of the adult small intestinal epithelium: the absorptive enterocyte, the entero-endocrine cell, and the mucous-secreting goblet cell. Migration from the crypt�villus junction to the zone of extrusion at or near the villous tip takes roughly three days. Thus, every of the four main cell varieties arises from progenitors of a single multipotent stem cell.

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An extra complication happens when the girl has some bleeding about 14 days after fertilization because of erosive activity by the implanting blastocyst (see Chapter four, "Day thirteen," p. By combining data on the onset of the last menstrual period with fetal size, weight, and different morphological traits typical for a given m onth of growth, a reasonable estimate of the age of the fetus could be formulated. An correct determination of fetal dimension and age is important for managing being pregnant, especially if the m different has a small pelvis or if the infant has a delivery defect. Some developmental occasions occurring in the course of the first 7 months are indicated in Table eight. During the final 2 months, the fetus obtains well-rounded contours as the outcomes of deposition of subcutaneous fats. By the top of intrauterine Ufe, the pores and skin is covered by a whitish, fatty substance (vernix caseosa) composed of secretory products from sebaceous glands. At the top of the ninth m onth, the cranium has the largest circumference of all elements of the body, an essential truth with regard to its passage by way of the birth canal. As the fetus begins the ninth week of development, its demands for nutri tional and different components improve, inflicting main adjustments in the placenta. Foremost amongst these is an increase in surface area between maternal and fetal components to facil�tate change. The disposition of fetal membranes can additionally be altered as manufacturing of amniotic fluid will increase. Changes within the Trophoblast the fetal part of the placenta is derived from the trophoblast and extraembryonic mesoderm (the chorionic p�ate); the maternal compo nent is derived from the uterine endometrium. By the start of the second month, the tro phoblast is characterized by a giant quantity of secondary and tertiary villi, which give it a radial look. Stem (anchoring) villi extend from the mesoderm of the chorionic p�ate to the cytotrophoblast shell. The capillary system developing in the core of the villous stems quickly comes in contact with capillaries of the cho rionic p�ate and connecting stalk, thus giving rise to the extraembryonic vascular system. To accomplish this process, cytotropho blast ceUs bear an epithelial-to-endothelial transition. Invasi�n of the spiral arteries by cytotrophoblast cells transforms these vessels from small-diameter, high-resistance vessels to bigger diameter, low-resistance vessels that may provide increased quantities of maternal blood to intervillous areas. During the following months, quite a few small extensions grow out from existing stem villi and extend as free villi into the surrounding lacunar or intervillous spaces. The syncytium and endothe lial wall of the blood vessels are then the only layers that separate the maternal and fetal circulations. Frequently, the syncytium becomes very thin, and huge pieces containing a quantity of nuclei might break o �f and drop into the intervillous blood lakes. These items, often identified as syncytial knots, enter the maternal circulation and normally degenerate without causing any signs. Cytotrophoblast Shell Spiral artery Intervillous house Blood vessel Cytotrophoblast^ Barrierformed by 1. The extraembryonic mesoderm penetrales the stem villi within the direction of the decidual p�ate. In many small villi, the wall of the capillaries Is in direct contact with the syncytium. As being pregnant advances, villi on the embryonic pole continu� to develop and increase, giving rise to the chorion �rondosum (bushy chorion). Villi on the abembryonic pole degenerate, and by the third month, this side of the chorion, now often known as the chorion laeve, is easy. The difFerence between the embryonic and abembryonic poles of the chorion can be reflected in the construction of the decidua, the ftinctional layer of the endometrium, which is shed during parturition. The decidua over the cho rion frondosum, the decidua basalis, consists of a compact layer of huge cells, decidual cells, with abundant amounts of lipids and glycogen. With development of the chorionic vesicle, this layer becomes stretched and degenerates. Subsequently, the chorion laeve comes into con ta d with the uterine wall (decidua parietalis) on the opposite facet of the uterus, and the 2 fuse. Henee, the only portion of the chorion taking part within the change course of is the cho rion frondosum, which, together with the de cidua basalis, makes up the placenta. Similarly, fusi�n of the amnion and chorion to type the am niochorionic membrane obliterates the chorionic cavity. This zone, characterized by de cidual and syncytial large cells, is rich in amorphous extracellular material.

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The major stem of the pulmonary vein that opens into the left atrium sends two branches to every lung. Then, as expansi�n of the left atrium contin�es, the main stem is included into the posterior wall until the point where branching of the vessel happens, resulting in 4 separate openings for pulmonary veins into the atrial chamber. At the end of the fourth week, a sickle-shaped crest grows from the roof of the widespread atrium into die lumen. The opening between the lower rim of the septum primum and the endocardial cushions is the ostium primum. With fiirther growth, extensions of the superior and infe rior endocardial cushions develop alongside the edge of the septum primum, closing the ostium primum. Before closure is full, however, cell dying produces perforations in the higher portion of the septum primum. Coalescence of these perforations varieties the ostium secundum, making certain free blood circulate from the proper to the left primitive atrium. When the lumen of the right atrium expands because of incorporation of the sinus horn, a new crescent-shaped fold appears. At this stage, the central portion of the mesocardium breaks down such that oniy the tw o ends of the guts tube stay connected. Initially, oniy the principle stem of the pulmonary vein enters the left atrium, but, as the atrlal partitions expand, this stem is included into the left atrium to the polnt the place its four branches diverge to go to the lungs. Consequently, as quickly as the method of atrlal expansi�n is complete, there are 4 openings for pulmonary veins into the left atrium. Both the wall of the proper sinus horn [blue] and the pulmonary vein [red] are incorpo rated Into the heart to type the sm ooth-w ailed parts of the atria. In the absolutely developed coronary heart, the original em bryonic right atrium becom es the trabeculated proper atrial appendage containing the pectinate muscular tissues, whereas the smooth-walled sinus venarum originates from the proper horn of the sinus ve nosus. The unique em bryonic left atrium is represented by little m ore than the trabeculated atrial appendage, whereas the At the tip of the fourth week, four atrioven tricular endocardial cushions seem: one on all sides plus one at the dorsal (superior) and one on the ventral (inferior) border of the atrioventricular canal. Initially, the atrioventricular canal gives access solely to the primitive left ventricle and is separated from the bulbus cordis by the bulbo (cono) ventricular flange. Near the top of the fifth week, nevertheless, the posterior extremity of the flange terminates almost midway alongside the bottom of the dorsal endocardial cushion and is way much less promenade inent than before. Because the atrioventricular canal enlarges to the proper, blood passing via the atrioventricular orifice now has direct access to the primitive left in addition to the primitive proper ventricle. In addition to the dorsal and ventral endo cardial cushions, two lateral atrioventricular cushions appear on the best and left borders of the canal. The dorsal and ventral cushions, in the meantime, project additional into the lumen and fuse, resulting in a whole divisi�n of the canal into right and left atrioventricular ori�ces by the end of the fifth week. A trioventricular Valves After the atrioventricular endocardial cush ions fuse, every atrioventricular ori�ce is surrounded by native proliferations of mesenchymal tissue derived from the endocardial cushions. At this stage of growth, blood from the atrial cavity enters the prim itive left ventricle as nicely as the prim itive right ventrlcle. Finally, muscular tissue within the cords degenerates and is replaced by dense connective tissue. They are related to thick muscular trabeculae within the wall of the ventricle, the papillary muscle tissue, by means of chordae tendineae. In this manner, two valve leaflets, constituting the bicuspid (or m itral) valve, kind in the left atrioventricular canal, and three, constituting the tricuspid valve, form on the right facet. The valves are hollowed out from the ventricular facet but stay connected to the ventricular wall by the chordae tendineae. It m ay be caused by extreme cell d ea th and res o rp tio n of th e septum prim u m. On the best, the ventricle could be very small, the pulm onary artery is affected and may be atretic or stenosed and the atrium could also be small; on the left, the ventricle could be very small, the aorta may be atretic or stenotic, and the atrium could also be gotten smaller. The laterality related v/ith these defects suggests an opposed impact on specification of the le ft and proper cardiac progenitor cells at an early stage of cardiac morphogenesis.