GUIA UAM CBS PDF

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Sleep is considered to be an important predictor of the immunity, since the absence of sleep can affect fbs development of the immune response, and consequently increase the susceptibility to contract an infection. The aim of the present study was to investigate if sleep deprivation and stress induce dysregulation of the duodenal mucous membrane during the acute infection with Trichinella spiralis.

Our results shows that, in the intestinal mucous membrane, stress and sleep deprivation, produces different effect in the cells, and this effect depends on the studied duodenal compartment, glands or villi. The sleep deprivation affect mast cells mainly, and the stress response is more heterogeneous.

Interestingly, in the duodenal mucous membrane, none population of cells in the infected groups responded equally to both conditions. These findings suggest that the response of the intestinal mucous membrane during the infection caused for T. Sleep is an essential homeostatic process in human beings and other animals. Sleep deprivation, on the other hand, is associated to heart disease 1diabetes 2obesity 3anxiety, depression 4 and gastrointestinal disorders 5and also has a negative influence on the central nervous system and the immune system 67which, in turn, cgs the intestinal barrier IB 8.

Although most research on sleep deprivation cba been focused on its effect over the central nervous system and its functions, the dynamic uaam in the IB and the innate mucosal immunity have not gained much attention despite the potential association of gastrointestinal disorders, such ccbs irritable bowel syndrome IBS uma peptic ulcers, with sleep disorders 9 It is known that the um of the gastrointestinal mucosa is kept in part by the immune system 11 therefore, it also plays a central role in several gastrointestinal disorders including irritable jam syndrome 1213small intestinal bacterial overgrowth and in gastrointestinal parasite establishment and colonization Particularry studies suggest that REM sleep deprivation involves changes in the modulation of the immune system and may increase the production of pro-inflammatory cytokines and cells 1516 ugia, which participate in the innate immune response.

While the effects of sleep deprivation on the integrity of the intestinal barrier have been little explored, it ccbs been reported that sleep deprivation leads to the translocation of pathogens into the lymph nodes and other tissues that are not usually colonized by them In addition, using confocal endomicroscopy and scanning electron microscopy, it has been recently reported that REM sleep deprivation induce changes in the gastric mucosa showing the initial phases of the acute inflammatory response The duodenum is comprised by the four characteristic layers of the gastrointestinal tract: The lamina propria of the duodenum mucosa accomodates numerous migrant and resident cells of the immune system such as eosinophils, neutrophils, mast cells, and macrophages, populating the connective tissue of the villi core, the diffuse lymphatic tissues, and lymphatic nodules.

In a healthy person, the eosinophils are located only in the lamina propria, mainly along the villi 20 The enteroendocrine cells, another important component of the enteric tissue, represent a loop between the neuroendocrine system, the central nervous system, and the enteric system, secreting several regulatory hormones of digestive function The IB is a regulatory interface enabling the selective exchange of nutrients, ions, and water; the function of this barrier is assisted by both endocrine and immune components that modulates absorption and secretion, as well as the presence of pathogenic and commensal agents in the intestinal lumen As a regulatory interface, the IB is susceptible to modulatory changes caused by hormones, neurotransmitters, and altered states of functional activation, such as an immune response against gastrointestinal parasites Trichinella spiralis is an intracelular nematode that colonizes the striated muscles of infected mammals; this zoonosis, known as trichinosis, is commonly caused by the consumption of raw or undercooked meat from infected animals The establishment of the parasite in the duodenum represents the acute, or entherical, phase characterized by goblet uaam hyperplasia, increased mucin and intestinal tirefoil factor expression, and an inflammatory infiltration in the lamina propia At this stage, the intestinal inflammatory infiltrate is comprised of lymphocytes, mast uqm, and eosinophils recruited to the intestinal Peyer patches and solitary guka nodes Mastocytosis in the intestinal mucosa is also a typical feature of infection with T.

Despite the extensive research conducted on sleep and immunity, to date, no data has been published regarding whether sleep deprivation affects duodenal integrity in response to gastrointestinal infection with T. Thus, we sought to analyze the effects of sleep deprivation on the tissue components of the duodenal mucosa and the cell populations involved in immunity and colonization during infection with T.

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Cell type analysis in the duodenal mucosa. The experimental groups are defined as sleep sufficient SSstress, and sleep deprived SD in the following description. In tissue sections, uuam eosinophil bilobed nucleous was also observed, as in a blood smear, but depending of the cutting fbs. A Representative photomicrographs of villi in yam first portion of duodenum for the condition of sleep sufficient SSstress, and sleep deprivation SD in no-infected upper pannel and infected groups lower pannel.

The square is a magnification of eosinophils arrow located in the lamina propria. B Quantification of eosinophils. SS solid bcsstress shaded barsand SD open bars in no-infected and vbs groups. C The differential effect of the infection in the number ham eosinophils in SS, stress, and SD in infected blue continuous linecompared with no-infected red discontinuous line groups.

A Representative photomicrographs of periglandular eosinophils in the lamina propria in the first portion of duodenum for the treatments, sleep sufficient SSstress, and sleep deprivation SDin no-infected upper pannel and infected lower pannelgroups, The square is a magnification of periglandular eosinophils arrow. B Quantification of eosinophils in SS solid barsstress shaded barsand SD open csb groups in no-infected and infected groups.

C The differential effect of the infection in the number of periglandular eosinophils in SS, stress, and SD observed in the infected blue continuous linecompared with no-infected red discontinuous line groups.

The top row of photomicrographs shows the no-infected animal groups in the conditions of, from left to right, SS, stress, and SD; whereas the botton row represents the same conditions in the infected animals Fig.

The duodenal buia in the no-infected groups were lined by normal simple columnar epithelia; however, the stress and SD groups showed a slightly increased number of eosinophils in the lamina propria, whereas an increased number of eosinophils was evident in the lamina propria in the three groups of infected rats. A quantitative analysis Fig. Note that only SD condition increases the eosinophils number in no-infected groups.

However, in infected groups the three conditions presents an giua in the number of eosinophils but was more evident with SD. In guuia, the significant increment in eosinophils number was related to SD condition in both no-infected and infected with respect to SS and stress conditions. The morphology of kam intestinal glands showed the same type of epithelium as the villi, although with a less abundant periglandular lamina propria continuous with the villus Fig.

The photomicrographs obtained um the infected groups showed an incremented cellularity in the periglandular lamina propria at the expense of an increased number of eosinophils. Surprisingly, the infected rats did not show any change in the number of eosinophils in the stress and SD groups when compared with the SS group Fig. Concerning the effect of T. Only SD condition in no-infected groups showed a significant increment of eosinophils number with respect to SS and stress conditions.

In infected groups, SS, stress, and Cbx conditions was a not difference in eosinophils number.

These morphological characteristics facilitated the identification and analysis of mast cells in the lamina propria. A Representative photomicrographs of mast cells in the villi in the first portion of duodenum for the groups of sleep sufficient SSstress, and sleep deprivation SD in no-infected upper pannel and infected lower pannel groups. The square is a magnification of mast cells in lamina propria. B Quantification of mast cells for SS solid barsstress shaded barsand SD open bars conditions in no-infected and infected groups C The differential effect of the infection in the number of villi mast cells in SS, stress, and SD observed in infected blue continuous linecompared with no-infected red discontinuous line groups.

A Representative photomicrographs of periglandular mast cells in lamina propria in the first portion of the duodenum for different treatments, sleep sufficient SSstress, and sleep deprivation SD in no-infected upper pannel and infected lower pannel groups.

The square is a magnification of a single periglandular mast cell. B Quantification of mast cells in the different treatments. C The distinguishing effect of the infection in the number of mast cells in SS, stress, and SD observed in infected blue continuous linecompared with no-infected red discontinuous line groups.

The identification and quantification of mast cells was performed using Giemsa staining Fig.

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As in the case of eosinophils, no damage was observed in the mucosa layer covering the villi of the no-infected groups, although in the infected, SS and stress groups, a thickened lamina propria could be observed. Interestingly, under SS conditions the infection with T. None of the three conditions of the no-infected groups showed significant changes in the number of mast cells. Only the SD condition in infected groups showed a significant decrease in these cells with respect to SS and stress conditions.

Uaj that the infection blue continuous line induced a significant increase of villi mast cells in SS condition, while in SD induced a significant decrease with respect to no-infected groups red discontinuous line.

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The analyzed mast cells showed a typical morphology in the periglandular area, which is similar to amorphous and granular cells Fig. In the no-infected groups, remarkable changes were observed in the SD groups, in which an increased number of these cells was evident Fig. The microphotographs corresponding to the infected groups showed a homogeneous distribution of these cells interacting with eosinophils Fig.

The infected groups under stress or SD conditions did guka show any significant changes compared with the infected, SS groups. Consequently, we observed that the increment caused by SD conditions in the no-infected animals was attenuated by the infection with T. In no-infected groups, only SD condition showed a discrete buy significant increment of mast cells.

The infected groups did not show differences with respect to the number of tuia mast cells among SS, stress and SD conditions. Infection causes a change only in SS condition compared to no-infected groups.

These cells were identified inside of villi and intestinal gland kam, confined to the vicinity of the basal lamina. They showed a pyramidal shape, with a narrow vertex extending towards the apical surface of intestinal glands and villi but, apparently, does not reach the lumen. Its wide cell base is adjacent to the basal lamina.

The basal cytoplasm, and to a lesser extent the apical cytoplasm, presented argentaffin granules that give the enteroendocrine cells blackened or dark brown color, which easily distinguished from other epithelial cells Fig.

A Representative photomicrographs of villi in the first portion of duodenum for the different treatments of sleep sufficient SSstress, and sleep deprivation SD in no-infected upper pannel and infected lower pannel groups. The square is a magnification uwm typical intraepithelial enteroendocrine cell arrow. B Quantification of villi enteroendocrine cells in SS solid barsstress shaded barsand SD open bars in no-infected and infected groups.

C The differential effect of the infection in the number of villi enteroendocrine cells in SS, stress, and SD observed in infected blue continuous linecompared with no-infected red discontinuous line groups. The histological analysis corresponding to the infected SS and SD groups showed a slight increment in the number of enteroendocrine cells Fig. Furthermore, infection with T. The stress and SD conditions of no-infected groups had a significant increment in enteroendocrine cells with respect to SS condition.

In infected groups, only stress condition showed a significant decrease in these cells in comparition to SS and SD condition. Note that infection in SS and SD conditions provoked a significant increase of enteroendocrine cells with respect to no-infected groups. Enteroendocrine cells could be identified inside the glands, cytoplasm facing towards the exterior, with a color and texture similar to the villi Fig. The photomicrographic analysis of the no-infected groups showed a homogeneous distribution of these cells in all the tested conditions, whereas the infected groups showed a clear increment in the number of these cells under SD.

On the other hand, we observed that infection with T. In all conditions of no-infected groups no changes in number of enteroendocrine cells was observed; however, in infected groups, the SD condition showed a significant increment of enteroendocrine cells compared to SS and stress conditions. A Representative photomicrographs of enteroendocrine cells in glands in the first portion of duodenum of the diiferent treatments, sleep sufficient SSstress, and sleep deprivation SD in no-infected upper pannel and infected lower pannel groups.

The square is a magnification of duodenal glands with some enteroendocrine cells.

B Quantification of enteroendocrine cells for SS solid barsstress shaded barsand SD open bars in no-infected and infected groups. C The differential effect of the infection in the number of enteroendocrine cells in SS, stress, and SD in infected blue continuous linecompared with no-infected red discontinuous line groups. These cells were identified as PAS-positive columnar cells scattered among enterocytes of intestinal glands and villi epithelium.

A Representative photomicrographs of globet cells in villi in the first portion of duodenum for the different treatments of sleep sufficient SSstress, and sleep deprivation SD in no-infected upper pannel and infected lower pannel groups.

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The square is a magnification of typical PAS-positive goblet cell. B The quantification of goblet cells in SS solid barsstress shaded barsand SD open bars treatments in no-infected and infected groups. C The differential effect of the infection in the number of goblet cells in SS, stress, and SD observed in the infected blue continuous linecompared with no-infected red discontinuous line groups. A Representative photomicrographs of duodenal glands in the first portion of duodenum for the condition of sleep sufficient SSstress, and sleep deprivation SD in no-infected upper pannel and infected lower pannel groups.

The insert is a magnification of duodenal glands with three PAS-positive enteroendocrine cells. B Quantification of glandular goblet cells for SS solid barsstress shaded barsand SD open bars treatments in no-infected and infected groups.