Absorption of thiamine and nicotinic acid in the rat intestine during fasting and immobilization stress

By perfusion of isolated sections of intestine with a solution containing thiamine at a concentration of 3.1 micromole, it was established that thiamine absorption in animals fasted for 72 hours decreased by 28 percent, whereas absorption increased by 12 percent in rats after 24 hour immobilization. After immobilization, absorption of label in the intestinal mucosa increased. Na K ATPase activity in the intestinal mucosa decreased by 10 percent during fasting, and it increased with immobilization of the animals. Activity of Na K ATPase in the intestinal mucosa cells determined the absorption rate of thiamine and nicotinic acid at the level of vitamin transport through the plasma membranes of the enterocytes

Chronic intestinal pseudo-obstruction in a Bernese Mountain Dog

Chronic Intestinal Pseudo-Obstruction (CIPO) is a rare syndrome characterized by chronic intestinal dilation and dysmotility in the absence of mechanical obstruction. A definite diagnosis of CIPO can only be made after histological examination of intestinal tissues. The present case describes a CIPO in a 2.5-year-old Bernese Mountain dog with a history of recurrent gastro-intestinal complaints suggestive for pseudo-obstruction. Histological lesions of small intestinal samples consisted of severe loss of smooth muscle cells of the tunica muscularis and diffuse infiltration of mononuclear cells. In addition, a hypertrophy of the lamina muscularis mucosa of the small intestinal tract was present. On the basis of these findings and the results of immunohistochemistry, a myopathic form of CIPO was diagnosed

Does CDX2 expression predict Barrett's metaplasia in oesophageal columnar epithelium without goblet cells?

Background: Intestinal metaplasia (Barrett's oesophagus), but not cardiac-type mucosa in columnar-lined oesophagus, is regarded as premalignant. As intestinal metaplasia and cardiac-type mucosa are endoscopically indiscernible, it is difficult to take targeted samples from columnar-lined oesophagus with consequently a risk of having undetected intestinal metaplasia. Aim: To investigate whether the intestinal markers CDX2, MUC2 and villin can predict the presence of undetected intestinal metaplasia in columnar-lined oesophagus. Methods: Presence of intestinal metaplasia or cardiac-type mucosa was identified in 122 biopsy sets of columnar-lined oesophagus from 61 patients, collected at two subsequent follow-up upper endoscopies. CDX2, MUC2 and villin expression were determined by immunohistochemistry. Results: All intestinal metaplasia samples (55) were positive for CDX2 and MUC2 and 32 of 55 for vil

Dendritic cell subsets in the intestinal lamina propria: ontogeny and function

The intestinal mucosa is exposed to large amounts of foreign antigen (Ag) derived from commensal bacteria, dietary Ags, and intestinal pathogens. Dendritic cells (DCs) are believed to be involved in the induction of tolerance to harmless Ags and in mounting protective immune responses to pathogens and, as such, to play key roles in regulating intestinal immune homeostasis. The characterization of classical DCs (cDCs) in the intestinal lamina propria has been under intense investigation in recent years but the use of markers (including CD11c, CD11b, MHC class II), which are also expressed by intestinal MΦs, has led to some controversy regarding their definition. Here we review recent studies that help to distinguish cDCs subsets from monocyte-derived cells in the intestinal mucosa. We address the phenotype and ontogeny of these cDC subsets and highlight recent findings indicating that these subsets play distinct roles in the regulation of mucosal immune responses in vivo

Iron metabolism of in­testinal mucosa in various blood diseases

For the investigation of iron metabolism in the intestinal mucosa in various&#12288;blood diseases, intestinal biopsy (duodenum) was performed on 10 healthy controls&#12288;and 35 cases with various blood diseases. The following are&#12288;the results&#12288;of the studies on distribution of stainable&#12288;iron, amounts of non-hemin iron in the&#12288;biopsied materials, and iron uptake of the intestinal epithelial cells.&#12288;1) An evaluation of distribution of stainable iron by Berlin&#12288;blue reaction&#12288;showed none or very mild degree, if any,&#12288;inhealthy controls, an increase in&#12288;aplastic anemia,&#12288;pernicious anemia, some of leukemias and in iron deficiency anemia following iron therapy, and a decrease in&#12288;idiopathic hypochromic anemia, anchylostomiasis anemia,&#12288;anemia with cancer, myxedema, hemolytic anemia,&#12288;and in&#12288;some of leukemias. Some of anemia with cancer, however,&#12288;showed an&#12288;increase of a certain degree. In iron absorption tests, no changes were found other than a very mild increase in aplastic anemia. 2) Non-hemin iron was 70-112&#947;/g in healthy controls, increased in aplastic anemia approximately to 100-200&#947;/g, ranging 40-130&#947;/g in leukemia, and decreased in idiopathic hypochromic anemia and in anemia with cancer ranging 30-60&#947;/g and 30-50&#947;/g respectively. Amounts of non-hemin iron and serum iron or sideroblasts show a fair correlation. The fractionation of nonhemin iron in aplastic anemia didn't show any difference in relationship of each fraction from healthy controls despite the increased amount in the former. 3) A radioautographic evaluation of iron uptake by intestinal epithelium was performed by our device for evaluation of intestinal absorption capacity. The iron uptake was mild in healthy controls, almost none in aplastic anemia, and marked in iron deficiency anemia where it was decreased approximately to the level of healthy controls following iron therapy. 4) The intestinal tissue iron showed a series of changes similar to those of iron present in the serum or erythroblasts, and the non-hemin iron in the intestinal mucosa is inversely correlated with iron uptake of epithelium and is considered to regulate the absorption according to its amount.</p

Early markers of angiogenesis and ischemia during bowel conduit neovascularization

Background Bowel flaps are a good and reliable method to restore the continuity of the aerodigestive tract. Radiated fields, contaminated recipient sites, or depleted recipient vessels may increase the risk for ischemic injury after transfer. During ischemic events, we believe that bowel conduits with serosa have a delayed neovascularization process at its new recipient site. We conducted an ischemia/reperfusion murine model to understand the difference among bowel conduits with and without serosa. Materials and Methods Two groups of rats were compared: control group (jejunal conduit with serosa) and a target group (jejunal conduit without serosa). These conduits were harvested from the peritoneal cavity and transferred into a subcutaneous pocket. After 72 hours of transfer and pedicle ligation, histological changes related to ischemia/reperfusion were assessed. In addition, tissue markers of angiogenesis (CD34), ischemia (lactate dehydrogenase [LDH]), and inflammation (interleukin [IL]-1β and IL-6) were analyzed. Results Two groups (n = 20) of male rats were analyzed. Histology showed intact jejunal mucosa in the target group. The control group showed decreased number of mucin, globet cells, decreased height, and fragmentation of villi with the absence of intestinal glands. Markers of angiogenesis (CD34) were higher in the target group. In addition, markers of ischemia (LDH) (p = 0.0045) and inflammation (IL-1b, p = 0.0008, and IL-6, p = 0.0008) were significantly lower in the target group as compared with the control group. Conclusions In circumstances in which the recipient site does not offer an adequate and healthy bed or a vascular insult occurs, bowel flaps with less amount of serosa may be able to neovascularize faster thereby increasing its chances of survival

To respond or not to respond - a personal perspective of intestinal tolerance

For many years, the intestine was one of the poor relations of the immunology world, being a realm inhabited mostly by specialists and those interested in unusual phenomena. However, this has changed dramatically in recent years with the realization of how important the microbiota is in shaping immune function throughout the body, and almost every major immunology institution now includes the intestine as an area of interest. One of the most important aspects of the intestinal immune system is how it discriminates carefully between harmless and harmful antigens, in particular, its ability to generate active tolerance to materials such as commensal bacteria and food proteins. This phenomenon has been recognized for more than 100 years, and it is essential for preventing inflammatory disease in the intestine, but its basis remains enigmatic. Here, I discuss the progress that has been made in understanding oral tolerance during my 40 years in the field and highlight the topics that will be the focus of future research

The pathologists’ eyes on foregut: histopathological relations in the experimental and routine diagnostics

SUMMARY I. The study aimed to investigate the incidence of duodeno-gastroesophageal reflux-induced malignoma formation in a series of duodeno-esophageal anastomosis operations in rats. This surgical method provided a model for the reflux-induced esophageal pathologies, without carcinogen administration. 30 weeks of duodeno-gastroesophageal reflux disease significantly increased the risk of the development of BE, and reflux-induced EAC formation was evident in 4 animals. In one of these particular cases, a superficial squamous cell cancer was noted in close vicinity to the adenocarcinoma formation. The results of the applied rat model afford evidence of the simultaneous activation of more than one possible carcinogenetic pathway in experimental GERD. Synchronous neoplasm formation with different growth pattern characteristics is a rarity in humans, and this phenomenon suggests that the presented model is a suitable means of mimicking the whole spectrum of human GERD pathology. II/1. The study aimed to carry out standardized histopathological analysis focusing not only on SIM but also on the presence of additional glands in the metaplastic process at 826 consecutive patients. According to standardized histopathological dataset the cases were classified and recorded by computerized method. The obtained data proved that 1) pure SIM is very rare in the Hungarian population, 2) cardiac and superficial mucous glands are good predictors for SIM, 3) pancreatic acinar and fundic metaplasias carry less severe metaplastic process, and 4) superficial mucous glands can be responsible for creating foregut-derived tissues and thus can be the origin of BE. II/2. The study aimed to assess the value of forceps biopsy sampling in establishing the correct diagnosis revealed by EMR as well as to evaluate the efficacy of this method. Fifty-six subjects with sessile gastric polyps of epithelial origin, at least 0.5 cm in diameter, and not associated with polyposis syndromes, were included. The obtained data showed that forceps biopsy is not fully representative of the entire lesion, and a simple biopsy may therefore lead to a faulty differentiation between the neoplastic and non-neoplastic lesions. EMR proposes diagnostic and staging advantage in assessing patients with EGC as compared to forceps biopsy, because it provides more intact mucosa and submucosa for histological analysis. Sessile gastric polyps should be fully resected by EMR for a final diagnosis and (depending on the lesion size and type) possibly definitive treatment

Chronic Stress, Inflammation, and Colon Cancer: A CRH System-Driven Molecular Crosstalk.

Chronic stress is thought to be involved in the occurrence and progression of multiple diseases, via mechanisms that still remain largely unknown. Interestingly, key regulators of the stress response, such as members of the corticotropin-releasing-hormone (CRH) family of neuropeptides and receptors, are now known to be implicated in the regulation of chronic inflammation, one of the predisposing factors for oncogenesis and disease progression. However, an interrelationship between stress, inflammation, and malignancy, at least at the molecular level, still remains unclear. Here, we attempt to summarize the current knowledge that supports the inseparable link between chronic stress, inflammation, and colorectal cancer (CRC), by modulation of a cascade of molecular signaling pathways, which are under the regulation of CRH-family members expressed in the brain and periphery. The understanding of the molecular basis of the link among these processes may provide a step forward towards personalized medicine in terms of CRC diagnosis, prognosis and therapeutic targeting