Penetration of insecticides through isolated sections of the mouse digestive system: effects of age and region of intestine.
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The effects of various levels of acetic or propionic acid supplementation on feed intake and the gastrointestinal tract were studied in female broiler chicks. Voluntary feed intake and body weight gain decreased with the inclusion of the acids. Results indicate that acetic and propionic acids exert a similar anorectic effect on chicks fed diets differing in energy content. The inhibitory effect of these acids on voluntary feed intake could not be attributed to alterations in feed utilization, to differences in pancreatic alpha-amylase activity, or to differences in the acid-base balance. The increase in cecal capacity and volatile fatty acid (VFA) content is probably due to increased utilization of nonstarch polysaccharides at that site, the latter compensating for feed inhibition. This reflects a slight adaptive response of the cecum to anorectic agents.
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A 27 year-old man who underwent an intestinal segmental resection for small bowel perforation was hospitalized for chronic abdominal pain with weight loss. Coeliac and mesenteric stenosis was diagnosed and laparotomy was performed. Histologic findings were consistent with Buerger's disease. One month later, he developed intermittent claudication of the left leg, and 8 years later amputation of a toe was performed. Since 1956, 25 cases of abdominal Buerger's disease has been reported in the literature. In eight cases, intestinal involvement inaugurated the disease. The clinical presentation can be various: chronic abdominal pain, mesenteric infartus, occlusion, perforation. Small bowel, colon and rectum can be concerned. The literature points out a mortality rate of 25% in intestinal Buerger's disease, contrasting with a mortality rate of 4% in peripheral forms of the disease. Although rare, intestinal form of Buerger's disease should be diagnosed early, because of its high mortality rate. Doppler of mesenteric arteries may contribute to the early diagnosis.
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The epidemiologic aspects of esophageal cancer are well known. The extreme geographical variations in incidence of the disease, the variability in the sex ratio, and the secular trends have been described frequently. The etiology of cancer of the esophagus is known to be complex and composed of multiple factors, those caused by the environment being of greatest importance. The disease preferentially attacks groups with a low socioeconomic status or those hindered by poverty. The esophageal cancer belt has been frequently studied to provide clues to the etiology of esophageal cancer but no definite culprit has yet been found. The majority of the factors so far implicated in cancer of the esophagus appear to act directly on the esophagus rather than systemically. This is an unusual situation in that it enables the disease to be prevented by primary means. There appears to be an enormous disparity in the etiology of the disease among various countries. This disparity may be more apparent than real if the epidemiologic data are interpreted to mean that there is a two-stage process involved, with multiple etiologies for each stage. If we assume that nutritional deficiencies, even subtle ones, predispose the esophagus to influence by carcinogenic substances, the geographic differences fade. Nutritional deficiencies can develop by chronic alcohol use as well as by poverty and lack of an adequate food supply, but diet does not explain the whole picture. External carcinogens are necessary to effect the end result. The culprit may be tobacco in one culture and fungal elements in another. The South African studies which showed an association with tobacco and not alcohol could be explained if we assume that the population's nutritional deficiencies already predisposed the esophagus for the effect of an external carcinogen, thereby making alcohol usage superfluous. It would be helpful if the relationship between esophagitis and nutritional status were elucidated and if it were determined that the condition could be improved or eliminated by dietary factors. The association between nutrition and esophagitis may suggest methods of primary prevention of esophageal cancer and provide a chance of lowering the incidence of this deadly disease.
In 1930, stomach cancer was the leading cause of death due to cancer among men in the United States. Among women it was the third leading cause of cancer deaths. Although it is well known that death rates for stomach cancer have diminished dramatically over the past 50 years, stomach cancer still has the third poorest 5-year relative survival rate of the different cancers, after pancreatic and lung cancer. Most evidence indicates that environmental factors play an important role in the development of stomach cancer. The remarkable decrease in stomach cancer mortality over the past 50 years and the results of a variety of migrant studies support this review. Several published case-control studies have shown positive associations with preserved meat and salted and pickled food in general. However, there are negative associations with vegetables, fruits and milk; vitamin C is implicated. Milk has both positive and negative associations. This points to the possibility of a carcinogen produced by traditional preservation methods such as salting and suggests that fresh vegetables and fruits and high intakes of vitamin C may reduce the risk. What specific role/s the diet plays in the incidence of stomach cancer remains to be seen. There is a need to elaborate the relationship of such factors as age, sex, migration, geography, environmental factors, and diet to the carcinogenic process that produces cancer of the stomach.
Colon cancer accounts for over 10% of all cancers diagnosed from 1973 to 1976 in the United States. Many factors have been identified as having a role in its etiology, including the intestinal microflora, colonic mutagens, bile acids, cholesterol, estrogens, and diet. The evidence supporting or refuting the importance of each of these factors and others is discussed. Dietary factors appear to be the most important risk determinants for colon cancer. In particular, a high-fat, low-fiber diet has been most consistently incriminated as a promoting agent of this cancer. The incidence of colon cancer and consumption of total fat and animal protein are highly correlated internationally. However, further epidemiologic studies have given equivocal results. A high-fiber diet has been proposed as being protective against colon cancer although the mechanism of protection remains unclear. A major correlational study has shown that dietary fiber consumption was higher in areas with low incidence of colon cancer than in those areas with high incidence. A few case-control studies have been supportive of the fiber hypothesis but many more have shown no difference among cases and controls in their fiber consumption. More epidemiological studies are needed to clarify the role of diet in the etiology of colon cancer. Before a dietary change is recommended, the competing risks of other cancers and other diseases should be extensively researched.
Soluble esterases in tissues of endodermic origin and of various developmental ages of Gallus gallus were analysed by polyacrylamide slab gel electrophoresis and characterized as carboxylesterases, acetylesterases and cholinesterases. Esterase bands were observed from day 9 in the liver and from day 6 in stomach, intestine and yolk sac. The electrophoretic profiles became more complex after hatching with concomitant increase in the staining intensity. On isoelectric focusing of liver extracts only a major form with pI 5.4 was observed. An eserine sensitive band designated EL-1 was found to be tissue (liver) and age (upon hatching) specific. EL-1-like isozymes were also observed in other species of the Galliformes order.
When 3-nitropropanol (NPOH) was injected into the rumen (30 mg/kg), abomasum (10 mg/kg) or small intestine (10 mg/kg) of sheep, it was rapidly absorbed and converted to 3-nitropropionic acid (NPA). The reticulo-rumen was the major site of absorption for the miserotoxin aglycone but the abomasum and the small intestine also had the capacity to absorb NPOH. When NPA was injected into different regions of the alimentary tract, the reticulo-rumen was also the major site of absorption. Absorption of NPA or NPOH from the small intestine was much more rapid than from the abomasum. Plasma levels of NPA and inorganic nitrite were higher after dosing with NPOH than with NPA indicating a more rapid rate of uptake of the aglycone.
Recent analysis of a novel strain of transgenic zebrafish (gutGFP) has provided a detailed description of the early morphological events that occur during the development of the liver and pancreas. In this paper, we aim to complement these studies by providing an analysis of the morphological events that shape the zebrafish intestinal epithelium. One of our goals is to provide a framework for the future characterization of zebrafish mutant phenotypes in which intestinal epithelial morphogenesis has been disrupted. Our analysis encompasses the period between 26 and 126 h post-fertilization (hpf) and follows the growth, lumen formation and differentiation of a continuous layer of endoderm into a functional intestinal epithelium with three morphologically distinct segments: the intestinal bulb, mid-intestine and posterior intestine. Between 26 hpf and 76 hpf, the entire intestinal endoderm is a highly proliferative organ. To make a lumen, the zebrafish endoderm cells undergo apical membrane biogenesis, adopt a bilayer configuration and form small cavities that coalesce without cell death. Thereafter, the endoderm cells polarize and differentiate into distinct cell lineages. Enteroendocrine cells are distinguished first at 52 hpf in the caudal region of the intestine in a new stable transgenic line, Tg[nkx2.2a:mEGFP]. The differentiation of mucin-containing goblet cells is first evident at 100 hpf and is tightly restricted to a middle segment of the intestine, designated the mid-intestine, that is also demarcated by the presence of enterocytes with large supranuclear vacuoles. Meanwhile, striking expansion of the lumen in the rostral intestine forms the intestinal bulb. Here the epithelium elaborates folds and proliferating cells become progressively restricted to a basal compartment analogous to the crypts of Lieberkühn in mammals. At 126 hpf, the posterior intestine remains an unfolded monolayer of simple columnar epithelium.
OBJECTIVE: Previous studies have investigated the role of viruses in tumor origin of head and neck cancer. Despite this, mechanis of viral carcinogenesis remain unclear. The aim of this study is to determine the prevalence of herpes simplex virus (HSV) and Epstein-Barr virus (EBV) in malignant laryngeal and oropharyngeal lesions. MATERIAL AND METHODS: Fresh frozen specimens of 28 laryngeal and oropharyngeal squamous cell carcinomas were studied. The presence or absence of HSV and EBV was determined with polymerase chain reaction (PCR) assays. RESULTS: None of the samples showed evidence for EBV DNA. One tonsilar carcinoma case (3.5%) was positive for HSV DNA detection. CONCLUSIONS: These results do not support HSV and EBV as etiological factors in head and neck cancer.
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Recent studies have suggested that the zebrafish pancreas develops from a single pancreatic anlage, located on the dorsal aspect of the developing gut. However, using a transgenic zebrafish line that expresses GFP throughout the endoderm, we report that, in fact, two pancreatic anlagen join to form the pancreas. One anlage is located on the dorsal aspect of the developing gut and is present by 24 h postfertilization (hpf), the second anlage is located on the ventral aspect of the developing gut in a position anterior to the dorsal anlage and is present by 40 hpf. These two buds merge by 52 hpf to form the pancreas. Using heart and soul mutant embryos, in which the pancreatic anlagen most often do not fuse, we show that the posterior bud generates only endocrine tissue, while the anterior bud gives rise to the pancreatic duct and exocrine cells. Interestingly, at later stages, the anterior bud also gives rise to a small number of endocrine cells usually present near the pancreatic duct. Altogether, these studies show that in zebrafish, as in the other model systems analyzed to date, the pancreas arises from multiple buds. To analyze whether other features of pancreas development are conserved and investigate the influence of surrounding tissues on pancreas development, we examined the role of the vasculature in this process. Contrary to reports in other model systems, we find that, although vascular endothelium is in contact with the posterior bud throughout pancreas development, its absence in cloche mutant embryos does not appear to affect the early morphogenesis or differentiation of the pancreas.
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