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Quail/chick transplantation chimeras were constructed during stages of gastrulation and neurulation to follow the subsequent movement and fate of cells of the primitive streak. All grafts were placed solely within the confines of the primitive streak to prevent confusion between cells that had not yet ingressed and those that had already ingressed, and transplanted cells were distinguished from host cells on the basis of a naturally occurring cell marker. Pathways of movement of ingressing cells corresponded to their level of residence within the primitive streak. Cells residing within Hensen's node (the cranial end of the primitive streak) initially migrated mainly cranially, remaining on or near the midline, and then extended caudally along the midline as regression of Hensen's node occurred. Cells residing within the nodus posterior (the caudal end of the primitive streak) migrated caudally. Cells residing at levels of the primitive streak between Hensen's node and the nodus posterior typically migrated bilaterally, confirming that such cells had not already ingressed prior to their transplantation (in which case, they would have migrated unilaterally). Subsets of these cells residing at progressively more caudal levels of the primitive streak migrated incrementally more laterally. Hensen's node contributed cells to the gut endoderm, head mesenchyme, notochord, and median hinge-point (MHP) cells of the neural tube (future floor plate). At younger stages (i.e., stages 3a, 3b) Hensen's node contributed cells to principally the foregut endoderm and head mesenchyme, whereas at older stages (i.e., stages 3c, 3d, 4), it contributed cells to principally the notochord and MHP region. The remaining segments of the cranial half of the primitive streak contributed cells to the various mesodermal subdivisions of the embryo, and the lengths of the segments forming these subdivisions were estimated. The most cranial level of the streak (directly behind Hensen's node) contributed cells to the most medial mesodermal subdivisions (head mesenchyme, somites) and consecutively more caudal levels of the streak contributed cells to sequentially more lateral mesodermal subdivisions (intermediate mesoderm, lateral plate mesoderm). The caudal half of the primitive streak contributed cells to the extraembryonic mesoderm, with the nodus posterior contributing to the most caudal extraembryonic mesoderm, including the blood islands. Our results confirm and extend the previous avian prospective fate maps, increasing our understanding of the movement and fate of cells of the gastrula and neurula stages.
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PMID:Mesoderm movement and fate during avian gastrulation and neurulation. 160 Feb 42

The calcium antagonists are a heterogeneous class of drugs which block the inward movement of calcium into cells through 'slow channels' from extracellular sites. By inhibiting phase 0 depolarisation in cardiac pacemaker cells and phase 2 plateau in myocardium, and by depressing calcium ion flux in smooth muscle cells of blood vessels, these agents may exert profound effects on the cardiovascular system, particularly in susceptible individuals or in overdose. Sinus node depression, impaired atrioventricular (AV) conduction, depressed myocardial contractility, and peripheral vasodilatation may result. Pharmacokinetic features of calcium antagonists include rapid and complete absorption from the gastrointestinal tract, with extensive first-pass hepatic metabolism yielding generally low bioavailability. The volume of distribution is generally large and protein binding is high. Elimination is almost entirely by the liver. Impaired renal function does not affect pharmacokinetics. Verapamil is the most potent inhibitor of cardiac conduction and contractility, with diltiazem also showing such effects. Nifedipine is the most potent vasodilator, but only occasionally impairs the sinus node or AV conduction. Significant pharmacodynamic effects are common during combination therapy with calcium antagonists, especially verapamil and beta-blockers. Verapamil may significantly elevate serum digoxin concentrations and may exert additive negative effects on chronotropism and dromotropism when this combination is used. Overdoses of calcium entry blockers are becoming more frequent and reflect an extension of the known pharmacodynamic profile of these agents. Typical features include confusion or lethargy, hypotension, sinus node depression and cardiac conduction defects. Onset of symptoms may be delayed if a sustained release preparation is ingested. Management of calcium antagonist overdose includes gut decontamination with lavage and activated charcoal. All symptomatic patients and patients with a history of ingesting a sustained release preparation should be admitted for ECG monitoring. If bradycardia and/or conduction defects contribute to hypotension, atropine or isoprenaline (isoproterenol) may accelerate the ventricular rate. Transvenous pacing may be required. Depressed myocardial contractility usually responds well to calcium chloride or calcium gluconate administration, but further inotropic support may be required. Peripheral vasodilation should be managed with intravenous fluids and a pressor agent such as dopamine or norepinephrine (noradrenaline).
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PMID:Poisoning due to calcium antagonists. Experience with verapamil, diltiazem and nifedipine. 179 22

The irritable bowel syndrome (IBS) is a familiar problem in the clinic, but as a disease entity it remains ill defined. Much confusion has arisen in the past, because of the inappropriate inclusion within the category of IBS of almost any patient with unexplained abdominal discomfort. Recent work has established that IBS patients can be positively identified by a cluster of specific symptoms. With the use of these criteria, it seems likely that IBS patients suffer from a diffuse motor abnormality of the gut associated with visceral hypersensitivity; although there is no associated psychopathology, a central nervous system component to the disorder is possible. Better insight into IBS promises more effective management.
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PMID:The irritable bowel syndrome. 206 58

Since most of the toxicity associated with class 1B antiarrhythmic drugs is dose-related, this review examines adverse effects seen in both therapeutic practice and accidental or premeditated overdose. Toxicity is very common with these agents and can be life-threatening. A high percentage of patients must discontinue therapy because of adverse effects. Mexiletine and tocainide are structural analogues of lignocaine (lidocaine) and toxicity is similar with all 3 drugs. With gradual intoxication (the most common form) central nervous system effects such as lightheadedness, dizziness, drowsiness and confusion are seen first. Seizures and respiratory arrest can occur. Cardiovascular toxicity is manifested by progressive heart block, reduced cardiac contraction, hypotension and asystole. Both mexiletine and tocainide may have proarrhythmic effects. Gastrointestinal toxicity is also common. Shock, hypotension, cardiac failure and beta-blocker therapy reduce lignocaine clearance and enhance the risk of intoxication during routine therapy. Both lignocaine and mexiletine elimination is impaired in severe liver disease while tocainide clearance is reduced in renal failure. Management of toxicity is largely supportive and symptomatic. Lignocaine infusion must be discontinued and decontamination of the gut in the case of oral preparations is recommended. Serious intoxication requires intensive care unit admission. Haemodialysis or haemoperfusion may be helpful in serious lignocaine and tocainide poisoning. In institutions where extracorporeal circulatory assistance is available, massive lignocaine poisoning has been successfully treated with this intervention. In the therapeutic setting serious toxicity can be prevented by close clinical surveillance and appropriate dose reduction in patients with reduced drug clearance. Because of the large interindividual variation in lignocaine pharmacokinetic parameters, therapeutic drug monitoring is recommended if results can be reported quickly. Mexiletine and tocainide have stereoselective metabolism and assays do not distinguish the more active isomers. Therapeutic drug monitoring is less useful in this situation.
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PMID:Poisoning due to class 1B antiarrhythmic drugs. Lignocaine, mexiletine and tocainide. 251 64

An 8-year-old boy with a short gut had six episodes of metabolic acidosis and neurological dysfunction over a 1 month period. The neurological features consisted of a depressed conscious state, confusion, aggressive behaviour, slurred speech and ataxia. The organic acid profile of urine demonstrated increased amounts of lactic, 3-hydroxypropionic, 3-hydroxyisobutyric, 2-hydroxyisocaproic, phenyllactic, 4-hydroxyphenylacetic and 4-hydroxyphenyllactic acids. Of the lactic acid 99% was D-lactic acid. The anaerobic gut flora consisted almost entirely of Lactobacilli in unusually large numbers. A course of vancomycin prevented further episodes. A urinary organic acid profile may be diagnostic when a person with a short gut develops metabolic acidosis or an unusual encephalopathy and bacterial metabolites should be considered in other patients with unusual combinations of organic acids in the urine.
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PMID:Severe illness caused by the products of bacterial metabolism in a child with a short gut. 401 4

The sensory innervation of the esophagus is important both to physicians, for whom esophageal sensation can cause clinical confusion, and to physiologists, who wish to understand the regulation of esophageal motion. Sensory mechanisms in the gut in general are not well understood. Mechanoreceptive reflexes and their pathways, both parasympathetic and sympathetic, have been studied in the esophagus, and thermoreceptive reflex pathways that are parasympathetic have recently been described. The terminal sensory innervation of the esophagus contains several structures that may be receptors to such stimuli. Esophageal striated muscle contains muscle spindles like those of somatic muscle. Within the myenteric plexus, the bodies of certain ganglion cells themselves may be mechanoreceptive. Also, complex subcapsular laminar arborizations that arise from cells of the nodose ganglion have been described in ganglia of the esophageal myenteric plexus. Similar laminar arborizations have been found on vessels of the submucosa in the midesophagus. In the esophageal mucosa, the terminal innervation ends in structures of diverse form located both superficially and deep in the squamous epithelium. Thus, a variety of specific neural structures that seem to represent the terminals of sensory nerves exist in the esophagus and may serve the mechanoreceptive and thermoreceptive reflexes that modify esophageal motility.
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PMID:Origin of sensation in the esophagus. 636 85

Microscopic examination of a peripheral blood smear revealed ookinetes of Plasmodium vivax. This unusual finding was probably due to an excessive delay between blood collection and smear preparation. Ookinete formation normally occurs in the mosquito gut. When seen in blood smears, it can cause confusion and misidentification of the parasite.
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PMID:Plasmodium vivax ookinetes in human peripheral blood. 781 3

While the proliferative effects of gastrin in the gastric fundus are well established, there is a considerable degree of confusion regarding the role of gastrin on the growth of the small intestine and colon. The hypothesis that gastrin is trophic throughout the gut was tested by giving three doses of pentagastrin and one of gastrin 17 to rats maintained by total parenteral nutrition (TPN). The rats were fed intravenously for one week, with the various peptides added to the TPN diet. The number of vincristine arrested metaphases per gland or crypt was then scored to determine the proliferative state. Both gastrin 17 and pentagastrin were found to be trophic in the gastric fundus, but not to the gastric antrum. A proliferative response was also seen in the duodenum, but with little evidence of a dose response element. No effect on small bowel weight was seen, and no proliferative effect was noted in the mid small bowel, thus the duodenal effect could be attributed to a local action of increased acid output on the duodenum, not a general role throughout the small intestine. No proliferative effects of pentagastrin or gastrin were seen in the colon. It is therefore concluded that the trophic role of gastrin is restricted to the gastric fundus and the proximal duodenum.
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PMID:Gastrin and the growth of the gastrointestinal tract. 788 18

This paper attempts to show how leading contemporary disciplines influenced the discovery of Chagas' disease and the formation of the early disease concept. Chagas was among the first generation of Brazilian trained scientists who incorporated modern principles of tropical medicine in its research. Thus, Chagas was familiar with characteristics of vector borne tropical diseases such as malaria and yellow fever. The detection of a hitherto unknown trypanosome in the gut of a reduviid bug prompted him to search for a related vector borne disease. Among the disciplines that were influential on Chagas' discovery and early disease description were pathology, entomology and parasitology. Parasitology as a new discipline was of crucial importance to tropical medicine and had a political dimension in the context of colonial medicine. Hence, leading scientists in tropical medicine were located in European countries and in the United States of America. One of these was the German Schaudinn School of Protozoology. The early description of American Trypanosomiasis can also be seen as a reflection of the Schaudinn School of Protozoology which dominated Chagas' scientific orientation towards parasitology with regard to the interpretation of the observed phenomena of the life cycle and the morphology and biology of T. cruzi. The first Chagas' disease concept was based on research of the biology and entomology of the trypanosome and its vector as well as on pathological studies of fatal cases. This concept was characterized by a confusion of some of the chronic forms of the disease, as iodine deficiency and goitre were endemic in some rural regions in Brazil. Therefore, early concepts of the disease faced strong opposition and even raised doubts about its existence.
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PMID:The discovery of Chagas' disease and the formation of the early Chagas' disease concept. 964 26

An infection with Rickettsiella sp. was responsible for an illness causing heavy body swelling in the Oriental cockroach Blatta orientalis. Reproduction of the colony stagnated. Vacuoles with parasitic bacteria occurred mainly in the fat body, but also in nearly all other organs, such as gut epithelium, Malpighian tubules, blood cells, and ovarioles. The parasites clearly differed from the symbiotic bacteria of the genus Blattabacterium, which regularly occur in the mycetocytes of B. orientalis. The vacuoles contained four stages of Rickettsiella: (1) infectious, electron-dense, rod-like elementary bodies (mean size 300 x 145 nm); (2) an electron-dense, flat intermedium stage, called flat body (mean size 515 x 255 x 125 nm); (3) an electron-light, spherical intermedium stage, called condensing sphere (mean size 340 nm); portions of cytoplasm condensed crescent-like at the border or in the center of the cell; and (4) large, spherical, electron-light initial bodies that multiplied by binary fission (mean size 600 nm). The initial bodies had a three-layered cell boundary, but all other stages had a five-layered cell boundary. Elementary and flat bodies contained an electron-light, oblique lamella and an oval structure with an array of ribosome-like granules, respectively. In contrast to other species of Rickettsiella, crystal formation or multiple division did not occur. The described species of Rickettsiella is different from "R. blattae," which belongs to the R. popilliae group. Instead, it shares more similarities with the R. chironomi group. To avoid confusion, it was provisionally named "R. crassificans."
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PMID:Light and electron microscopic study of a Rickettsiella species from the cockroach Blatta orientalis. 1111 69


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