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Aim. To assess of adaptive immunity of the duodenal mucosa in neonates with sepsis. Methods. A study of duodenal biopsy specimens obtained during duodenoscopy from neonates who had signs of suspected ulcerative lesions of the digestive tract. Five of them were obtained from infants with clinical and laboratory signs of neonatal sepsis (NS), two from infants without sepsis (comparison group). Immunohistochemical staining was performed using the Novolink Polymer Detection System imaging system with commercial antibodies to CD4, CD8, CD20 and Bcl-2, and the CSAII Biotin-free Tyramide Signal Amplification System imaging system with commercial antibodies to caspase-3 and caspase-9 in accordance with the manufacturers instructions. Results. It was found that the number of CD4+ T-lymphocytes of the duodenal mucosa in neonatal sepsis group in 4 of 5 infants did not differ from the control group. The number of CD8+ lymphocytes in neonates with sepsis in 3 of 5 cases was even higher than in the control group. The number of CD20+ B-lymphocytes in 4 infants with sepsis was significantly less compared with the control. Activation of apoptosis in mucosal cells was detected, which was manifested by a large number of caspase-3-positive cells (in 4 of 5 cases) in comparison with the control group. The number of caspase-9-positive cells in the studied groups was almost equal. A substantial decrease in the number of Bcl-2-positive mucosal cells in all 5 infants with sepsis was noted as compared with the control indicators. Conclusion. The study revealed moderate immunosuppression in the duodenal mucosa in neonates with sepsis, manifested by low values of CD20+ B-lymphocytes in the absence of a significant decrease in the number of CD4+ and CD8+ T-lymphocytes. The detected moderate activation of apoptosis processes against the background of reduced antiapoptotic potential creates the conditions for a possible translocation of the intestinal microbiota into the bloodstream.

A black-spotted duodenal mucosa was observed during endoscopy of a man with several comorbidities including hypertension and end-stage kidney disease. Histopathological examination revealed pigment-laden macrophages in the lamina propria of the duodenal villi, which was consistent with duodenal pseudomelanosis.

The work is devoted to the study of structural changes of enterocytes in the mucous membrane of the duodenum in a burn injury of the skin of a rat under conditions of experimental streptozotocin induced diabetes. The study was carried out on laboratory white adult rats-males weighing 180-210 g. The control group consisted of 21 animals without somatic pathology, the first experimental group consisted of 21 rats with skin burn injury, the second experimental group cleared 21 rats with skin burn and experimental streptozotocin induced diabetes. A model of experimental diabetes mellitus was reproduced by administering streptozotocin intraperitoneally once in dose of 50 mg/kg to rats. In an experimental simulation of a skin burn, two copper plates in the form of an ellipse were kept in water at 100oC for 10 minutes and, under ether anesthesia conditions, were applied simultaneously symmetrically on both exposed parts of the body of rats with an exposure for 10 seconds. Burn skin damage in rats was II-AB degrees – dermal surface burn (according to the old classification III-A degree) with a total area of 21-23% of the body surface with the development of burn shock. For morphological studies, the duodenum was taken, fragments of which were processed using conventional light and electron microscopy. The main criteria for assessing damage the enterocytes of the duodenal mucosa were the results studies of histological and ultrastructural data over 7, 14 and 21 days after a skin burn. The results of the studies showed that the damage of the enterocytes of the duodenal mucosa is based on deep destructive changes, which after 21 days (at the stage of septic toxemia), as a rule, are not reversible and develop against the background of significant intoxication of the organism. In the mucous membrane of the duodenum with burn injury of the skin associated with diabetes mellitus, there is a deterioration of the manifestations of the adaptive response and prolongation of destructive processes, accompanied by a violation of intercellular interactions in cytoarchitectically modified and deformed villi and crypts.

Background & Aims Acid hypersensitivity is claimed to be a symptomatic trigger in functional dyspepsia (FD); however, the neuroimmune pathway(s) and the mediators involved in this process have not been investigated systematically. Palmitoylethanolamide (PEA) is an endogenous compound, able to modulate nociception and inflammation, but its role in FD has not been assessed. Methods Duodenal biopsy specimens from FD and control subjects, and peroxisome proliferator-activated receptor-α (PPARα) null mice were cultured at a pH of 3.0 and 7.4. Mast cell (MC) number, the release of their mediators, and the expression of transient receptor potential vanilloid receptor (TRPV)1 and TRPV4, were evaluated. All measurements also were performed in the presence of a selective blocker of neuronal action potential (tetradotoxin). FD and control biopsy specimens in acidified medium also were incubated in the presence of different PEA concentrations, alone or combined with a selective PPARα or PPAR-γ antagonist. Results An acid-induced increase in MC density and the release of their mediators were observed in both dyspeptic patients and controls; however, this response was amplified significantly in FD. This effect was mediated by submucosal nerve fibers and up-regulation of TRPV1 and TRPV4 receptors because pretreatment with tetradotoxin significantly reduced MC infiltration. The acid-induced endogenous release of PEA was impaired in FD and its exogenous administration counteracts MC activation and TRPV up-regulation. Conclusions Duodenal acid exposure initiates a cascade of neuronal-mediated events culminating in MC activation and TRPV overexpression. These phenomena are consequences of an impaired release of endogenous PEA. PEA might be regarded as an attractive therapeutic strategy for the treatment of FD., Graphical abstract

Gastric mucosa has been widely studied during the pre/post-Helicobacter pylori (Hp) era. Excluding peptic ulcer disease (PUD), the duodenal mucosa has not been thoroughly analyzed, even less so in functional dyspepsia (FD). We would like to make some comments after studying 161 dyspeptic patients with samples taken from the gastric body, antrum, proximal and distal duodenum.

Сучасне довкілля забруднене ксенобіотиками, що здатні викликати розвиток патологічних процесів. Один із ксенобіотиків – епіхлоргідрин (ЕПХГ). Вплив цього ксенобіотика викликає зміни стану різних органів, зокрема органів травної системи. Наслідки дії ЕПХГ на дванадцятипалу кишку (ДК) не досліджені.Мета роботи – дослідити характер змін стану ворсин слизової оболонки (СО) ДК і мітотичної активності клітин епітелію СО ДК за умов тривалої дії ЕПХГ, а також оцінити можливість, ефективність використання екстракту ехінацеї пурпурової і тіотріазоліну для корекції цих змін.Матеріали та методи. Експериментальне дослідження виконали на самцях білих щурів. Сформували 6 експериментальних груп. Після завершення 2-місячного введення ЕПХГ, екстракту ехінацеї пурпурової (ЕП) і тіотріазоліну на 1, 7, 15, 30, 60 добу з експерименту виводили по 6 щурів із кожної експериментальної групи. Висоту ворсин СО ДК і мітотичну активність клітин СО ДК оцінювали за допомогою лабораторного мікроскопа серії МС 100 фірми Micros (Австрія).Результати. Після завершення тривалого введення ЕПХГ у морфофункціональній організації CO ДК щурів відбувалися зміни, що проявлялися у зменшенні висоти ворсин і мітотичної активності клітин епітелію СО ДК. З часом виразність змін зменшувалася. Введення екстракту ЕП і введення тіотріазоліну щурам, які не отримували ЕПХГ, супроводжується збільшенням висоти ворсин. У разі застосування тіотріазоліну цей ефект є тривалішим.Застосування екстракту ЕП, а також використання тіотріазоліну під час інгаляцій ЕПХГ зменшує виразність і тривалість зменшення висоти ворсин і мітотичної активності клітин епітелію СО ДК, що викликані цією хімічною речовиною.Висновки. Тривалий вплив ЕПХГ супроводжується негативними змінами стану СО ДК. Тіотріазолін ефективніше, ніж екстракт ЕП корегує наслідки негативного впливу ЕПХГ., Introduction. The modern environment is polluted by xenobiotics which can cause the development of pathological processes. One of xenobiotics is epichlorohydrin (ECH). The impact of this xenobiotic causes changes in the state of various organs, including the organs of the digestive system. However, the effects of ECH on the duodenum have not been investigated.The aim of the study is to investigate the changes in the state of the duodenal villi in rats and changes in mitotic activity of mucous epithelial cells under ECH influence as well as to evaluate a possibility and effectiveness of Echinacea purpurea (EP) extract and thiotriazoline use for these changes correction.Material and methods. An experimental study was performed on male white rats. Six experimental groups were created. Six rats from each experimental group were removed from the experiment on the 1st, 7th, 15th, 30th, 60th days after the end of the two-month administration of ECH, EP extract and thiotriazoline. The height of the villi of the duodenal mucosa and changes in mitotic activity of mucous epithelial cells were estimated using a microscope of the MS 100 series of Micros (Austria).Results. Morphofunctional organization of duodenal mucosa in rats was changed after the long-term introduction of ECH. The height of villi and mitotic activity of mucous epithelial cells were reduced. Over time, the expressiveness of the changes diminished. Introduction of EP extract and thiotriazoline administration to rats which did not receive ECH was accompanied by an increase in the height of villi. In the case of thiotriazoline administration, this effect was longer. The use of EP extract as well as the use of thiotriazoline during ECH inhalations reduced the severity and duration of the decrease in the height of villi and mitotic activity of mucous epithelial cells caused by this chemical. The negative effects of ECH were corrected more effectivelly by thiotriazoline than by EP extract.Conclusions. Prolonged action of ECH is accompanied by negative changes in the state of duodenal mucosa. The negative effects of ECH were corrected more effectivelly by thiotriazoline than by EP extract., Современная окружающая среда загрязнена ксенобиотиками, которые способны вызвать развитие патологических процессов. Одним из ксенобиотиков является эпихлоргидрин (ЭПХГ) Влияние этого ксенобиотика вызывает изменения состояния различных органов, в том числе органов пищеварительной системы. Последствия действия ЭПХГ на двенадцатиперстную кишку (ДК) не исследованы.Цель работы – изучить характер изменений состояния ворсин слизистой оболочки (СО) ДК и митотической активности клеток эпителия СО ДК в условиях длительного действия ЭПХГ, а также оценить возможность и эффективность использования экстракта эхинацеи пурпурной (ЭП) и тиотриазолина для коррекции этих изменений.Материалы и методы. Экспериментальное исследование выполнено на самцах белых крыс. Сформировали 6 экспериментальных групп. После завершения 2-месячного введения ЭПХГ, экстракта ЭП и тиотриазолина на 1, 7, 15, 30 и 60 сутки из эксперимента выводили по 6 крыс из каждой экспериментальной группы. Высоту ворсин СО ДК и митотическую активность клеток эпителия СО ДК оценивали с помощью лабораторного микроскопа серии МС 100 фирмы Micros (Австрия).Результаты. После окончания длительного введения ЭПХГ в морфофункциональной организации CO ДК крыс происходили изменения, которые проявлялись в уменьшении высоты ворсин и митотической активности клеток эпителия СО ДК. Со временем степень изменений уменьшалась. Введение экстракта ЭП и введение тиотриазолина крысам, которые не получали ЭПХГ, сопровождалось увеличением высоты ворсин. В случае применения тиотриазолина этот эффект является более длительным. Применение экстракта ЭП, а также использование тиотриазолина во время ингаляций ЭПХГ уменьшало выраженность и длительность уменьшения высоты ворсин и митотической активности клеток эпителия СО ДК, вызванной этим химическим веществом.Выводы. Длительное воздействие ЭПХГ сопровождается негативными изменениями состояния СО ДК. Тиотриазолин более эффективно, чем экстракт ЭП, корректирует последствия негативного влияния ЭПХГ.

INTRODUCTION: Duodenal epithelial barrier impairment and immune activation may play a role in the pathogenesis of functional dyspepsia (FD). This study was aimed to evaluate the duodenal epithelium of patients with FD and healthy individuals for detectable microscopic structural abnormalities. METHODS: This is a prospective study using esophagogastroduodenoscopy enhanced with duodenal confocal laser endomicroscopy (CLE) and mucosal biopsies in patients with FD (n = 16) and healthy controls (n = 18). Blinded CLE images analysis evaluated the density of epithelial gaps (cell extrusion zones), a validated endoscopic measure of the intestinal barrier status. Analyses of the biopsied duodenal mucosa included standard histology, quantification of mucosal immune cells/cytokines, and immunohistochemistry for inflammatory epithelial cell death called pyroptosis. Transepithelial electrical resistance (TEER) was measured using Ussing chambers. Epithelial cell-to-cell adhesion proteins expression was assessed by real-time polymerase chain reaction. RESULTS: Patients with FD had significantly higher epithelial gap density on CLE in the distal duodenum than that of controls (P = 0.002). These mucosal abnormalities corresponded to significant changes in the duodenal biopsy samples of patients with FD, compared with controls, including impaired mucosal integrity by TEER (P = 0.009) and increased number of epithelial cells undergoing pyroptosis (P = 0.04). Reduced TEER inversely correlated with the severity of certain dyspeptic symptoms. Furthermore, patients with FD demonstrated altered duodenal expression of claudin-1 and interleukin-6. No differences in standard histology were found between the groups. DISCUSSION: This is the first report of duodenal CLE abnormalities in patients with FD, corroborated by biopsy findings of epithelial barrier impairment and increased cell death, implicating that duodenal barrier disruption is a pathogenesis factor in FD and introducing CLE a potential diagnostic biomarker in FD.

The article presents results of histological, histochemical investigations of duodenal mucosa of broilers, which were fed 36 days in a row with were fed 36 days in a row with fodder mixed of probiotic supplements «Probion forte» in doses of 100 g/kg. At 36 day of the experiment 10 chickens from each group were taken out from the experiment, was performed autopsy and selected models of duodenum, which are fixed in 10% of solution neutral formalin, Karnua liquid, followed by pouring into paraffin. It was produced histological sections, were stained with hematoxylin-eosin, by Stidmen, McManus. Prolonged feeding of poultry with probiotic supplements «Probion forte» in excessive dose of 100 g/kg has caused structural and functional changes in the mucosa of the duodenum, expressed the formation of ugly bifurcated broad villi and reflected a decrease in productive indexes of poultry.

Background: Changes in food constituent during suckling, weaning and post-weaning periods documented histological and functional adaptation in rat small intestine. Objectives: identify histological changing events, which represent such adaptation in the rat duodenal mucosa. Material and methods: Twenty four male rat pups are divided into equal 4 groups including day one, 7 &15 (pre-weaning) and day 21 (weaning). In addition, two other groups including 12 male adult rats equally divided, aged 45 days (post-weaning) and 90 days, were used. The animals are euthanized at the fore mentioned days and the duodenum is processed for light and scanning electron microscopic examination. Paraffin sections are stained with haematoxylin & eosin and combined alcian blue/ PAS. Computer image analysis and statistical study are done for the height of the villi, depth of the crypts and villous / crypt ratio. Results: The villi are broadening with the advance of age. The height of the villi and the depth of the crypts show a statistical non-significant increase in the pre-weaning groups. At weaning, there is a significant decrease in the height of the villi with a decrease of the villous/crypt ratio. The villi are covered by brushed columnar enterocytes and some vacuolated enterocytes are seen only in pre-weaning period. Acidic and neutral mucin positive stained goblet cells are distributed on villi and within the crypts of pre-weaning pups. At weaning, goblet cells are positive for acidic mucin only. Crypts are lined with pyramidal enterocytes and paneth cells are dominating in day 21. Both villi and crypts at postnatal day 21(weaning) acquire structural appearance similar to that of adult.

Diclofenac Sodium (DS) as one of Non-steroidal Anti-inflammatory Drugs (NSAIDS) is a commonly used and may be used in high or toxic doses by mistake or postoperatively. Consequently, the present study was designed to evaluate the possible protectiverole of Moringa Oleifera (MO) on the experimentally induced microscopical changes of duodenal mucosa of adult rats following administration of different high doses of DS. Forty five rats were divided into the following groups (15 each): Group I was served as a control group, Group II was subgrouped to IIa, b and c, that were administered oral 50, 100 and 150 mg/kg of DS respectively for 2 days after fasting for 20 hours. Group III was subgrouped to IIIa, b and c. These rats were maintained on oral MO (500mg/kg) daily for one week, and then they were administered the same doses as in the previous group. A variety of histological changes was observed in group II. The changes were ranged from loss of the brush border to cellular lysis, destruction of villi, monocellular infiltrations and basal glandular ulcerations. The PAS stained sections showed focal negative expression of the brush border together. Although the goblet cells appeared significantly decreased in number, they had increased acidic mucin secretion. In conclusion, the current study suggested that MO may have a limited and partial protective effect on the duodenal mucosa in cases of high dose administration.

Aim An evaluation of the efficacy of endoscopic methods for the diagnosis and correction of surgical and immunological complications after retroperitoneal pancreas transplantation. Materials and methods From October 2011 to March 2015, 27 patients underwent simultaneous retroperitoneal pancreas-kidney transplantation (SPKT). Diagnostic oesophagogastroduodenoscopy (EGD) with protocol biopsy of the donor and recipient duodenal mucosa and endoscopic retrograde pancreatography (ERP) were performed to detect possible complications. Endoscopic stenting of the main pancreatic duct with plastic stents and three-stage endoscopic haemostasis were conducted to correct the identified complications. Results Endoscopic methods showed high efficiency in the timely diagnosis and adequate correction of complications after retroperitoneal pancreas transplantation. This article is protected by copyright. All rights reserved.

Background Endoscopy is performed for direct inspection of the mucosa and acquisition of biopsies in dogs with inflammatory bowel disease (IBD). Aim To evaluate the interobserver agreement in the endoscopic assessment of duodenal mucosa in dogs with IBD. Methods Thirty-five archived endoscopic images of grossly normal (n = 6) and inflamed (n = 29) duodenal mucosa were displayed to 3 expert and 5 trainee endoscopists. Each image was assessed independently by endoscopists for mucosal abnormalities using established indices (of hyperemia, granularity, friability, lymphatic dilatation, and erosions) or interpreted as normal mucosa (trial 1). A repeated trial (trial 2) was performed with the same images presented in random order 1 month later, and accompanied by a visual template. Results There was slight interobserver agreement in initial mucosal assessment for expert and trainee endoscopists in trial 1 (kappa ≤ 0.02, P > .05). Interobserver agreement improved in trial 2 for both expert and trainee endoscopists (kappa = 0.2, P > .05) for experts and (P

Ghrelin is a hormone discovered relatively recently, the effect of which is associated with the normal activity of the digestive tract. It is the most abundant in the gastric mucosa, but also occurs in other parts of the digestive system, sexual organs and some glands. Many authors associate the action of ghrelin with appetite and weight gain or weight loss. The purpose of this study was by immunohistochemical methods to localize grelin-pozitive cells in the duodenal mucosa and comparatively to determine their amount. We use Ghrelin (H-40) antibody (Santa Cruz-USA), and for the visualization of the results - detection system EnVisionTM FLEX Mini Kit, High Ph (DAKO - k8024 HRP). Histomorphometric study performed by Michael Vinther Image Analyzer, Version 1.33 (Mee Soft, Germany).

Background/Aims Duodenal immune alterations have been reported in a subset of patients with functional dyspepsia (FD). The aim of this study was to investigate the effect of acute stress on immune cell counts and the expression of tight junction proteins in the duodenal mucosa. Methods Twenty-one male rats were divided into the following three experimental groups: 1) the nonstressed, control group, 2) the 2-hour-stressed group, and 3) the 4-hour-stressed group. Eosinophils, mast cells and CD4+ and CD8+ T lymphocytes in the duodenal mucosa were counted. The protein and mRNA expressions of occludin and zonula occludens-1 (ZO-1) were examined. Results Eosinophils, mast cells and CD8+ T lymphocyte counts did not differ between the stressed and control groups. The number of CD4+ T lymphocytes and the protein and mRNA expressions of occludin and ZO-1 were significantly lower in the 4-hour-stressed group compared with the control group. The plasma adrenocorticotrophic hormone and cortisol levels of the 4-hour-stressed group were significantly higher than those of the control group. Conclusions Acute stress reduces the number of CD4+ T lymphocytes and the expression of tight junction proteins in the duodenal mucosa, which might be associated with the duodenal immune alterations found in a subset of FD patients.

The secretion of HCO3(-) in the duodenum is increased by mucosal acidification, and this process is modulated by gas mediators such as nitric oxide (NO), hydrogen sulfide (H2S), and carbon monoxide (CO), in addition to prostaglandins (PGs). The secretion is increased by NOR3 (NO donor), NaHS (H2S donor), and CORM-2 (CO donor). The HCO3(-) responses to NOR3 and CORM-2 are attenuated by indomethacin, while that to NaHS is mitigated by indomethacin and L-NAME as well as sensory deafferentation. NOR3 and CORM-2 increase mucosal PGE2 production, while H2S increases mucosal PGE2 content and luminal NO release. The HCO3(-) response to mucosal acidification is attenuated by indomethacin, propargylglycine, and SnPP, each inhibiting PG, H2S and CO production, respectively. The acid-induced duodenal damage is worsened when either PG, H2S or CO is lacking. These findings suggest that 1) NO, H2S, and CO, generated endogenously or exogenously, stimulate HCO3(-) secretion in the duodenum; 2) the stimulatory action of NO and CO is mediated, at least partly, by endogenous PGs, while that of H2S is mediated by PGs and NO as well as sensory neurons; 3) these gas mediators are involved in the local regulation of acid-induced HCO3(-) secretion, in addition to endogenous PGs; 4) the acid-induced duodenal damage is worsened by agents inhibiting the endogenous production of NO, H2S or CO. It is assumed that these gas mediators play a role in maintaining the integrity of the duodenal mucosa by modulating the secretion of HCO3(-).

The aim of this study is to evaluate the effect of probiotic supplementation associated to different levels of crude protein (CP) on the count of intraepithelial lymphocytes (IELs) in the duodenum of meat quails. A total of 2304 quails were distributed in a completely randomized design in a 2 x 4 factorial scheme (with and without probiotic and four levels of CP - 15, 20, 25 and 30%), with two replicates per treatment in two experimental periods, in a total of 32 experimental units. At seven days old, two quails from each experimental unit were euthanized to harvest the duodenum segment. Semi-serial 7-μm histological sections were obtained, which were subsequently stained with hematoxylin-eosin to perform the IEL count. For the calculation, first 2500 epithelial cells were counted from the mucosa of each animal, and then the IELs present between these cells were counted, with the results expressed in amounts of IELs/100 epithelial cells. No differences were found in the IEL count among the treatments. Under the experimental conditions, it can be concluded that the use of probiotic associated to different levels of CP supplementation does not alter the IEL count in the duodenum of meat quails.

We report a case of lipoma in the antum of the stomach which prolapsed into the duodenal bulb and caused a duodenal ulcer, speculated to have been induced by the friction of its top against the duodenal mucosa. Although the ulcer healed after the administration of a proton pump inhibitor, the symptom of epigastric discomfort continued, suggested to be due to prolapsing. Therefore, a laparoscopic operation was conducted. The incidence of lipoma of the stomach is rare, and cases of its prolapse into the duodenum are very few. Furthermore, it is extremely rare for it to cause a duodenal ulcer. Because these features made this case clinically interesting, we report it here.

Ten patients with progressive systemic sclerosis (PSS), 4 patients with other gastro-intestinal diseases and 5 normal controls, underwent small intestinal biopsy procedure. The biopsy material was incubated with tritiated thymidine and processed for auto-radiography. The labelling index (LI) in the small intestinal mucosa was estimated. The LI in PSS patients with duodenal involvement was significantly higher than the LI in PSS patients without duodenal involvement. In the latter group, the LI was at the same level as in normal controls. The LI in patients with other gastro-intestinal diseases, with diarrhoea as a main symptom, was not significantly different from the LI found in duodenal PSS.

Leptin is secreted into the gastric juice by epithelial Chief cells and reaches the duodenum in a biologically intact active form. We assessed the possibility that this gastric leptin crosses the intestinal mucosa by transcytosis through enterocytes to reach blood circulation. Endogenous gastric leptin secretion was triggered by cholinergic stimulation. In another set of experiments, recombinant leptin was inserted in vivo into the duodenal lumen. Plasma levels of leptin were assessed by enzyme immunoassay and Western blot, and duodenal tissue was processed for immunocytochemistry. We first observed that leptin was found inside duodenal enterocytes from fed rats but not inside those from fasted ones. Stimulation of gastric secretion by a cholinergic agent led to rapid increases in plasma leptin levels (202 ± 39%) except when the pylorus was clamped. Insertion of recombinant leptin into the duodenal lumen raised plasma leptin concentrations (558 ± 34%) quite rapidly, whereas carrier solution without leptin had no effect. The use of FITC-tagged leptin reinforced these results. Light and electron microscopy revealed the cellular compartments involved in its transcytosis, namely, the enterocyte microvilli, the endocytotic vesicles, the Golgi complex, and the basolateral interdigitations. Leptin was also present in the lamina propria, in capillary endothelial cell plasmalemmal vesicles, and in capillary lumina. These results demonstrate that gastric exocrine leptin is internalized by duodenal enterocytes and delivered to the lamina propria and blood circulation. It may thus be able to play important paracrine and endocrine functions for the control of gastric emptying and nutrient absorption.

Strong: recurrent episodes of documented acute pancreatitis (typical pain, increased serum amylase) in patients with congenital pancreas divisum or other variants of a dominant dorsal duct (absent duct of Wirsung, filamentous communication to duct of Wirsung).

The objective of this study was to investigate the effect of docosahexaenoic acid (DHA) supplementation on blood and intestinal DHA levels and lung function in mild/moderately affected adult CF patients with the ΔF508 genotype. Background Cystic Fibrosis (CF) patients often present with plasma fatty acid levels indicating low levels of linoleic (18:2 n −6) and docosahexaenoic (22:6 n −3) acids and an increased level of arachidonic acid (20:4 n −6). Improved dietary fat intake or reducing fat malabsorption with pancreatic enzymes has failed to normalize this biochemical deficiency of DHA. Methods Five CF patients, aged 18–43, received 70 mg of DHA/kg body weight/d for six weeks. At baseline and at six weeks a physical exam, lung function, 3-day dietary intake, duodenal mucosal biopsy and blood sample were assessed. The blood was analyzed for plasma vitamin A, D and E levels, liver function tests, clinical chemistry (CBC, differential and electrolytes). Plasma and red blood cell fatty acid levels were also analyzed. At three weeks, assessment included a physical exam, lung function test and fasting blood sample (vitamin levels, liver function and clinical chemistry only). Results Pre- and post-measurements were compared for the four subjects who completed the study. An increase in DHA content (% w/w) was observed in all phospholipid fractions of plasma, red blood cell and mucosal samples. No significant differences in vitamin levels, liver function or lung function were observed. Conclusions The study proves the concept that an increase in tissue DHA levels in CF patients can be achieved by supplementing for six weeks with 70 mg/kg/d DHA.

Several studies have demonstrated the role of free radicals in causing esophagus-gastro-duodenal mucosal injury. The present study has been designed to investigate: whether acid, bile salts and a combination of bile + acid could determine the production of O2-derived free radicals by oesophageal, gastric and duodenal mucosa; which agent is capable of producing more free radicals and if O2-derived free radicals production depends on the duration of contact with acid, bile salts and their combination. Wistar rats' gastro-intestinal mucosa were perfused with bile, acid and a combination of bile + acid at pH4 and pH2 for 1 hour and 2 hours. Free radical production (FRP) was assessed by chemoluminescence. After 1 hour, the increase in FRP in comparison with control reached statistical significance (P < 0.05) at all tested pH levels in the duodenum, at pH1, 2 and 3 in the esophagus, and at pH1 in the stomach. Comparing different segments, both the esophagus and duodenum behaved similarly, producing more free radicals than the stomach at all pH values. However, this difference reached statistical significance at pH1 and 2 only. In comparison to control, FRP was increased by bile (pH7) infusion after 1 and 2 hours. There was increased FRP in all segments after the infusion of bile at pH2 and 4 in comparison to control. Infusion of bile at pH2 stimulates more FRP than infusion of bile at pH4 in all segments. This increased FRP reaches statistical significance in the esophagus after 2 hours of infusion, in the stomach after 1 and 2 hours of infusion, but in the duodenum it does not reach statistical significance. Acid, bile and bile + acid at pH2 and 4 can cause free radical production in esophageal, gastric and duodenal mucosa. Their role in producing free radicals is different according to the segment and the chemical composition of the solution.

Background: The aim of the present study was to examine the presence of motilin in the duodenal epithelial cells of premature infants of

Objective. To assess safety of nimesulid in rheumatic pts with history of ulcer or multiple erosions (ME) of stomach and/or duodenal mucosa. Methods. 42 pts with rheumatic diseases aged 22-73 years were included. AH had gastric or duodenal ulcers or ME (n>10) connected with NSAID treatment and confirmed by endoscopy no more than 6 months before the beginning of the study. Pts were included after healing of ulcers and erosions. The pts were randomized to receive Nimesulid 200 mg/day (group 1) or Diclofenac suppositoria 100 mg/day + ranitidine 150 mg/day (group 2). Esophagogastroduodenoscopy was performed before and 12 weeks after the beginning of treatment. Results. Relapse of stomach ulcer was observed in I pts of group 1 (5,6%). Relapse of NSAID-induced ulcers and ME was noted in 6 pts of group 2 (33,3%): in 4 cases stomach ulcers, in 1 case stomach ME, in 1 case duodenal ulcer (p=0,0424). Presence of gastralgias and dyspepsia was noted in 36,8% pts of group 1 and in 20% pts of group 2 (p=0,0539). In 1 pts of group 2 gastralgias were the reason for premature endoscopy. Conclusion. Nimesil (Nimesulid) can be considered as a more safe drug than classical NSAIDs with smaller risk of serious gastroduodenal complications development in rheumatic pts with ulcer history. The results of the study allow to recommend Nimesulid as a drug of choice for treatment of pts with history of NSAID-induced gastropathy.

Although anti-endomysial antibodies (EmA) have been found in the supernatants of cultured intestinal mucosa from patients with coeliac disease (CD), in no study has the clinical reliability of this new diagnostic tool been investigated. Our aims were to evaluate the clinical usefulness of the in vitro production of EmA in CD diagnosis in consecutive patients with suspected CD, and to evaluate the reliability of the in vitro challenge in CD patients on a gluten-free diet (GFD).For the former aim, consecutive patients who were due to undergo intestinal biopsy for suspected diagnosis of CD were enrolled: according to the final diagnosis, these patients were divided into two groups: Group 1 comprised 91 newly diagnosed CD patients (40 males; age range 7 months to 84 years), Group 2 included 100 subjects with diseases other than CD (44 males; age range 9 months to 76 years). For the latter aim, we also studied 21 CD patients on a gluten-free diet after 16-123 months (8 males; age range 3-51 years), with normal intestinal architecture (Group 3) and 22 patients who served as controls (12 males; age range 4-60 years) with gastroesophageal reflux disease-like symptoms (Group 4). All patients underwent determination of serum anti-gliadin (AGA) and EmA antibodies, histology evaluation of the intestinal biopsies and EmA assay in the supernatants of in vitro gliadin-challenged duodenal mucosa.EmA assay in the supernatants showed a sensitivity and specificity of 96% and 100%, respectively; these were not significantly different from those observed for serum EmA (88% and 99%, respectively). However, EmA assay in the supernatants was useful in CD patients with mild intestinal histology lesions (infiltrative/hyperplastic type): in this subgroup it was positive in 9/12 of cases, but serum EmA was positive in only 2/12. As regards the reliability of the in vitro gliadin challenge, EmA production in supernatants was recorded only in 10/21 CD patients on a gluten-free diet. The patients with a positive in vitro challenge had a higher number of intra-epithelial lymphocytes than patients with a negative challenge.1) EmA assay in the medium of cultured intestinal biopsy can detect gluten-sensitive enteropathy, characterized by an infiltrative/hyperplastic histological pattern, which is often associated with negative serum EmA. 2) The in vitro challenge in CD patients on a gluten-free diet detects EmA production in the culture medium only in half of the cases and other studies must be performed to evaluate whether EmA production after in vitro challenge can be considered a reliable test for confirming CD diagnosis.

We examined the effect of celecoxib, a selective COX-2 inhibitor, on duodenal HCO3- and ulcerogenic responses caused by acid in rats, in comparison with indomethacin and loxoprofen (nonselective COX inhibitors) or SC-560 (a selective COX-1 inhibitor). Methods: Male SD rats were used after 18 h fasting. Under urethane anesthesia, the duodenal loop was perfused with saline, and the HCO3- secretion was measured at pH 7.0 using a pH-stat method. Results: Mucosal acidification (exposure to 10 mM HCl for 10 min) stimulated HCO3- secretion with an increase of mucosal PGE2 contents in the duodenum. These responses were significantly attenuated by pretreatment with indomethacin, loxoprofen or SC-560, while celecoxib had no effect. Perfusion of the loop with 100 mM HCl for 4 h produced mild hemorrhagic damage, and the severity of these lesions was significantly aggravated by indomethacin, loxoprofen and SC-560 but not celecoxib. COX-2 was not expressed in the duodenal mucosa after acidification, while COX-1 was exp...

We studied the role of duodenal cellular ion transport in epithelial defense mechanisms in response to rapid shifts of luminal pH. We used in vivo microscopy to measure duodenal epithelial cell intracellular pH (pHi), mucus gel thickness, blood flow, and HCO[Formula: see text] secretion in anesthetized rats with or without the Na+/H+exchange inhibitor 5-( N, N-dimethyl)-amiloride (DMA) or the anion transport inhibitor DIDS. During acid perfusion pHidecreased, whereas mucus gel thickness and blood flow increased, with pHiincreasing to over baseline (overshoot) and blood flow and gel thickness returning to basal levels during subsequent neutral solution perfusion. During a second brief acid challenge, pHidecrease was lessened (adaptation). These are best explained by augmented cellular HCO[Formula: see text] uptake in response to perfused acid. DIDS, but not DMA, abolished the overshoot and pHiadaptation and decreased acid-enhanced HCO[Formula: see text] secretion. In perfused duodenum, effluent total CO2output was not increased by acid perfusion, despite a massive increase of titratable alkalinity, consistent with substantial acid back diffusion and modest CO2back diffusion during acid perfusions. Rapid shifts of luminal pH increased duodenal epithelial buffering power, which protected the cells from perfused acid, presumably by activation of Na+-HCO[Formula: see text] cotransport. This adaptation may be a novel, important, and early duodenal protective mechanism against rapid physiological shifts of luminal acidity.

Modest acute hypovolaemia in rats markedly decreases the duodenal mucosal alkaline secretion via neurohumoral links. The present study was undertaken to investigate if such a procedure influences the morphological changes observed following an acid challenge of the duodenal mucosa. Experiments were performed on anaesthetized male Sprague-Dawley rats. HCI (10 or 100 mM) was infused during 15 min into the duodenum via a luminally situated catheter. Time controls were compared with animals bled 10% of total blood volume. Mucosal damage was evaluated by light microscopic morphometry on transverse sections and by scanning electron microscopy of the luminal surface. Perfusion with either 10 mM or 100 mM HCI reduced villus length by about 30%. The villus area was unaffected by 10 mM HCI, but was reduced significantly by 10% by 100 mM HCI as compared with NaCI time controls. Hypovolaemia did not influence the morphometrical changes induced by 10 mM HCI but reduced significantly both villus length (-28%) and villus area (-10%) as compared with the unbled 100 mM HCI group. Scanning electrone microscopy (SEM)-based visual damage score was not influenced by the hypovolaemia procedure in any of the acidities. Morphological changes of the duodenal mucosa, induced by moderate intra-luminal acidity (10 mM HCl), is not influenced by hypovolaemia. However, at higher acidities (100 mM HCl) the hypovolaemia contributes to more severe mucosal damage.

Background/Aim: It is well known that Helicobacter pylori changes its shapes according to various environmental conditions. The aim of this study was to examine the morphological differences between H. pylori in the duodenum and that in the stomach. Methods: Duodenal biopsy specimens were obtained from patients with duodenal mucosal lesions, and these specimens were then histopathologically examined. Morphological and genetic properties of cultured H. pylori isolates were analyzed. Results:H. pylori was identified in 16 out of 50 duodenal biopsy specimens. Along with the regular form, we found a fine form of H. pylori in the gastric metaplastic mucosa of ten duodenal specimens that was shorter in length and thinner in diameter than the regular helical form. There were no detectable differences between the ureA-ureB polymorphism of the duodenal fine form and that of gastric regular form in a single patient. As compared with patients without H. pylori in the duodenum, the prevalence of recurrent duodenal ulcers significantly increased in patients with the fine form (p < 0.05), but not in patients with the regular form. Conclusion: The fine form of H. pylori in the metaplastic duodenal mucosa could result from its adaptation to the duodenal environment and may be associated with the recurrence of a duodenal ulcer.

Summary An unusual location for pyogenic granuloma is reported. The lesions were found during endoscopy in the duodenum of a 13 year old boy with a history of acute myeloid leukaemia and portal hypertension who had undergone a bone marrow transplant. 4 red, raised, polypoid masses measuring 0.7cm were seen in the second and third portions of the duodenum and were resected endoscopically. Histological findings were typical of pyogenic granuloma. To our knowledge, this is the first case report of this condition occurring in the duodenal mucosa of a child.

To determine whether glutamine acutely stimulates protein synthesis in the duodenal mucosa, five healthy growing dogs underwent endoscopic biopsies of duodenal mucosa at the end of three 4-h primed, continuous intravenous infusions ofl-[1-13C]leucine on three separate days, while receiving intravenous infusion of 1) saline, 2)l-glutamine (800 μmol ⋅ kg−1 ⋅ h−1), and 3) isonitrogenous amounts of glycine. The three infusions were performed after 24 h of fasting, a week apart from each other and in a randomized order. Glutamine infusion induced a doubling in plasma glutamine level, and glycine caused a >10-fold rise in plasma glycine level. During intravenous infusions of [13C]leucine, the plasma leucine labeling attained a plateau value between 3.22 and 3.68 mole % excess (MPE) and [13C]ketoisocaproate ([13C]KIC) of 2.91–2.84 MPE; there were no significant differences between glutamine, glycine, and saline infusion days. Plasma leucine appearance rate was 354 ± 33 (SE), 414 ± 28, and 351 ± 35 μmol ⋅ kg−1 ⋅ h−1(not significant) during glycine, saline, and glutamine infusion, respectively. The fractional synthetic rate (FSR) of duodenal mucosa protein was calculated from the rise in protein-bound [13C]leucine enrichment in the biopsy sample, divided by time and with either plasma [13C]KIC or tissue free [13C]leucine as precursor pool enrichment. Regardless of the precursor pool used in calculations, duodenal protein FSR failed to rise significantly during glutamine infusion (65 ± 11%/day) compared either with saline (84 ± 18%/day) or glycine infusion days (80 ± 15%/day). We conclude that 1) plasma [13C]KIC and tissue free [13C]leucine can be used interchangeably as precursor pools to calculate gut protein FSR; and 2) short intravenous infusion of glutamine does not acutely stimulate duodenal protein synthesis in well-nourished, growing dogs.

Ten newborn kids were used to evaluate the relationship between apoptosis and passive immune transfer in neonatal enterocytes. Kids were slaughtered in groups of 2 at birth, 1, 2, 3, or 60 d postpartum, and samples of duodenal epithelium collected from each animal. Samples were fixed, dehydrated, and embedded in paraffin wax. Sections were assessed for apoptotic cells and immunostained for IgG. Our results suggest that IgG absorption is mediated by apoptotic enterocytes. Thus, delaying apoptosis may improve the success of passive immune transfer.

Background: The prevalence of biliopancreatic disorders is high in patients with periampullary diverticula. However, endoscopic retrograde cholangiopancreatography (ERCP) in patients with the papilla deep inside duodenal diverticula is difficult. Methods: Two patients were included in this study, each with the papilla deep inside a diverticulum and in whom an initial ERCP was unsuccessful. A biopsy forceps to pinch the duodenal mucosa distal to the papilla and pull the papilla out of the diverticulum and a cannula were inserted into the working channel of a duodenoscope together (the two-devices-in-one-channel method). With coordination of the two instruments, cannulation of the bile duct was attempted. Results: In both patients ERCP was successful using this procedure and no complications followed. Conclusions: The two-devices-in-one-channel method is useful when performing ERCP in patients with the papilla inside juxtapapillary diverticula.

The occurrence of early gastric carcinoma with invasion to the duodenum is supposed to be very low, although advanced cancers arising in the antrum can often invade the duodenal area. Generally, malignant invasion of the duodenum is difficult to diagnose preoperatively, as spread of gastric cancer to the duodenum is often infiltrative and invades through the submucosal or subserosal layer. We report an unusual case of an intramucosal gastric carcinoma with extensive duodenal invasion that was preoperatively diagnosed by endoscopy.

Celiac disease (CD), a systemic autoimmune disorder that typically involves duodenal mucosa, can also affect other intestinal areas. Duodenal and oral mucosa organ culture has already been demonstrated as a reliable procedure to identify CD. The present study investigated gluten-dependent immunological activation of colonic mucosa in CD patients. We took advantage of the numerous colonoscopies performed for various clinical conditions or only for defensive medicine.Forty-four patients with gastrointestinal symptoms or in need of colorectal cancer screening were divided into patients with serum anti-endomysium (EMA) and anti-tissue transglutaminase (anti-tTG) antibody positive results (Group A), patients with serum antibody negative results (Group B), and patients with inflammatory bowel disease (IBD) (Group C). The autoantibodies EMA and anti-tTG were evaluated in supernatants of cultured sigmoid and duodenal biopsies from patients on a gluten-containing diet.In Group A, EMA and anti-tTG resulted positive in all duodenal culture supernatants. In sigmoid culture supernatants, EMA and anti-tTG were detected in 12/16 (75 %) and 13/16 (81.3 %) patients, respectively. In Group B, none of the 17 patients showed EMA and anti-tTG positive results in both duodenal and sigmoid cultures. In Group C, all 11 patients presented EMA negative results in sigmoid cultures. Only in one patient, anti-tTG were detectable in the sigmoid culture supernatant, as expected in cases of IBD.Data confirm that the gluten-dependent immunological activation affects more intestinal tracts with different degrees of involvement, suggesting that the organ culture of colonic biopsies could represent a new tool to opportunistically detect CD.

Uptake and metabolism of fatty acids in the duodenal mucosa of the chick was studied. In vitro incubations of a mucosal homogenate with 14C-oleic acid indicated that together with glycerides, water-soluble 14C compounds and 14CO2 were formed; the latter comprised approximately one quarter of metabolites formed. Studies in chickens introducing 14C-oleic acid into the duodenum and determining appearance of label in the cannulated pancreaticoduodenal vein and brachial artery indicated that similar processes occur in vivo, with both labeled glycerides and water-soluble compounds appearing in the blood. Quantitatively, metabolism of 14C-oleic acid to nonlipid compounds amounted to some 15% of the dose after 60 min. These findings suggest that a considerable portion of ingested fatty acids are metabolized before transport to the circulation.

The aim of the present study was to summarize the evidence in support of our previous finding that ornithine decarboxylase (ODC) activity in the rat duodenal mucosa is controlled, in part, by the central nervous system. In the first experiment, we demonstrated an effect of truncal vagotomy on ODC activity in the duodenal mucosa of fasted rats. The increase of ODC activity in the duodenum just before the dark period was abolished by truncal vagotomy. In the second experiment, an effect of glycoprivation of the central nervous system induced by 2-deoxy-D-glucose was shown. Infusion of 2-deoxy-D-glucose into the third cerebroventricle activated ODC in the duodenum in a dose-dependent manner. These results indicate that the central nervous system, in addition to local factors, is related to the increase of ODC activity in the rat duodenal mucosa.

We present a novel approach of measuring optical properties with fiber optic probe from endoscopically accessible Peri-Ampullary duodenum as way to detect pancreatic cancer at early stages.

The ontogeny of the expression of specific binding sites for bombesin (BBS), vasoactive intestinal polypeptide (VIP), and gastrin in the neonatal pig was examined. Piglets were sacrificed at birth, 1 d, 1 wk, 3 wk and 4 wk, and samples of duodenal, jejunal and ileal tissue were harvested for autoradiographic analysis of saturable radioligand binding. Monoiodinated, biologically active 125I-Tyr4-BBS, VIP or gastrin (100 pM) was applied to slide-mounted sections of piglet intestinal tissue and localized using autoradiographic analysis of radioligand binding. Saturable binding sites for 125I-BBS first appeared in duodenal tissue of 7-d-old piglets, with evidence for continued presence in this tissue through 21 d. BBS binding sites were localized in duodenal mucosa, with no detectable binding in any other tissue layers. No evidence for saturable binding of 125I-Tyr4-BBS was found in intestinal sections from either newborn, 1-d-old or 4-wk-old piglets. Saturable binding sites for 125I-VIP were present in duodenal, jejunal and ileal tissues of piglets at all ages studied and were present in both the mucosa and the muscularis externa. No saturable binding sites for 125I-gastrin were observed in intestinal sections from piglets at any of the ages studied. These results suggest potential sites of direct action of VIP in newborn, suckling and newly weaned piglets. Bombesin, however, may have direct actions only on the duodenal mucosa at 7–21 d of age. Key words: Bombesin, vasoactive intestinal polypeptide, gastrin, piglet, small intestine, newborn

Currently, the diagnosis of celiac disease (CD) is based upon the combination of raised serum anti-tissue transglutaminase or anti-endomysial antibodies and the presence of histological alterations of variable degree in the duodenal mucosa. Interpretation of duodenal biopsies is subjected to a number of variables, and the lack of standardization may cause diagnostic controversy or even misdiagnosis. The aim of this overview is to solicit a standardization of the procedures of biopsy taking, orientation, processing, staining and interpretation in order to avoid or minimize misinterpretation of duodenal biopsies. Based on a literature review and extensive personal experience, the appropriate methodology of duodenal biopsy taking, orientation, fixation, processing, staining and interpretation was thoroughly reviewed, and the most common and relevant errors and artifacts were identified. To maximize the diagnostic yield of duodenal biopsy in CD, multiple specimens are best taken from different sites of the duodenum during endoscopy, and careful visual inspection of the duodenal mucosa may help identify abnormalities related to villous atrophy. Biopsy handling and orientation are of utmost importance to avoid artifacts that may impair the pathologist's ability to detect pathology and normality. Immunostaining with anti-CD3 monoclonal antibody should be carried out, and a simplified histological classification may help distinguish atrophic from non-atrophic stages of CD enteropathy. Meticulous attention to biopsy orientation, handling and processing - together with the knowledge of the most common histological artifacts - is necessary to avoid a wrong histological interpretation which, in turn, may lead to misdiagnosis in CD.

Objective: It was the aim of this study to evaluate the number of 2 lymphoid subpopulations, CD8+ cells and FOXP3+, in the duodenum mucosa from pediatric celiac patients. Methods: Tissue sections prepared from paraffin-embedded biopsies of the descending duodenum of 61 celiac patients with Marsh grade 1 (M1), M2 and M3 disease and biopsies from 21 age-matched non-celiac (NC) patients were immunohistostained with anti-CD8 or FOXP3 antibodies. Results: The histological Marsh grade correlated with the mean number of FOXP3+ cells in the lamina propria (LP) mucosa (8.9 ± 1.1, 6.8 ± 2.4, 24.5 ± 2.6 and 31.1 ± 2.8 for NC, M1, M2 and M3 biopsies, respectively; p < 0.001). Using a cutoff point of 15 cells, 95% of NC and 88% of M1 biopsies had a mean of + cells compared with 14% for M2 and 13% for M3 biopsies. The number of FOXP3+ cells in the epithelial mucosa also correlated with transglutaminase type 2 serum levels from the celiac patients. Unlike the FOXP3+ cells, CD8+ lymphocytes were present in both LP and surface epithelial mucosa and significantly different only in the LP mucosa of the M2 and M3 groups. Conclusion: The number of FOXP3+ cells is substantially increased in the mucosa of celiac patients at advanced stages. Characterization of the activity of these cells in celiac and in other inflammatory bowel diseases will enable us to understand the significance of these cells in celiac disease.

Recent studies have shown that postinfectious functional dyspepsia (FD) symptoms may persist after elimination of gastrointestinal (GI) infection as well as postinfectious irritable bowel syndrome accompanying colonic inflammation. However, it is unclear whether intestinal chronic inflammation can contribute to clinical symptoms of certain FD patients such as postinfectious FD. To determine the relationship between local inflammation of the duodenum and clinical symptoms, we evaluated the infiltration of several phenotypes of duodenal inflammatory cells as well as gastric motility using (13)C urea breath test in postinfectious FD patients.We enrolled 136 consecutive patients diagnosed with FD according to Rome III criteria, and 20 healthy controls, after upper GI endoscopy. Gastric motility was evaluated by gastric emptying time (T-max) using the (13)C-acetate breath test. Upper abdominal symptoms including epigastric pain, epigastric burning, postprandial fullness, abdominal distension, and early satiety were assessed by questionnaire scores. We obtained biopsy specimens from the stomach and duodenum during upper GI endoscopy. Histological gastritis and duodenitis were assessed as mild, moderate, or severe according to previously described criteria. Characteristics of inflammatory cells and neuroendocrine cells were determined immunohistochemically with antibodies to CD3, CD68, CCR2, Vdelta1 TCR, and serotonin.Endoscopic duodenitis was observed in only 5.7% of postinfectious FD patients. However, the rates of histological duodenitis in duodenal biopsies of postinfectious FD patients were 17% for mild, 26% for moderate, and 57% for severe grades of duodenitis. The degree of histological duodenitis of postinfectious FD patients was significantly greater than that of healthy volunteers. There was a significant correlation between epigastric burning and the degree of duodenitis in postinfectious FD patients. There was no significant difference in histological duodenitis and T-max value in the postinfectious FD patients with or without Helicobacter pylori infection. In addition, CD68-positive cell number in postinfectious FD patients was significantly increased compared with the numbers in subjects with epigastric pain syndrome or postprandial distress syndrome and in healthy volunteers. CCR2-/CD68-double positive cell number in postinfectious FD patients was significantly (P=0.009) increased compared with those in healthy volunteers.Migration of inflammatory cells, in particular, duodenal CCR2-positive macrophages, may have an important function in the pathophysiology of postinfectious FD patients.

The aim of this study was to characterize bovine and porcine pancreatic development by immunohistochemistry. In the pig, staining for both glucagon and insulin was noted at day 19. In cattle, glucagon staining was observed at day 25 and insulin staining from day 26. In both species, glucagon-stained cells were abundant initially, but later insulin-stained cells became most abundant. A few cells displayed co-localization of glucagon and insulin staining during initial development in both species. Initially, most of the cells of the pancreatic primordia and the duodenal epithelium displayed Pdx-1-staining. All insulin-stained cells displayed Pdx-1-stained nuclei, whereas no glucagon-stained cells did so. Many Pdx-1-stained cells lacked insulin staining, but with development, the relative number of these cells diminished. Nkx6.1-staining was initially seen in a pattern similar to that for Pdx-1, but was lacking duodenal staining. Subsequently, the number of Nkx6.1-stained cells diminished, but increased again to a level where practically all insulin-stained cells also presented Nkx6.1-staining. Glucagon-stained cells, on the other hand, never had Nkx6.1 staining. In conclusion, the localization of the two transcription factors, Pdx-1 and Nkx6.1, demonstrated that pancreas development appears to be controlled by mechanisms comparable with those operating in humans.

Submitted by ROBERTO PAULO CORREIA DE ARAÚJO (ppgorgsistem@ufba.br) on 2017-06-01T19:15:21Z No. of bitstreams: 1 11_v.8_3.pdf: 600434 bytes, checksum: e7b46126669b1be1fbbd4677124fecc0 (MD5) Made available in DSpace on 2017-06-01T19:15:21Z (GMT). No. of bitstreams: 1 11_v.8_3.pdf: 600434 bytes, checksum: e7b46126669b1be1fbbd4677124fecc0 (MD5) Previous issue date: 2009-09 Camundongos da linhagem AKR/J infectados pelo Strongyloides venezuelensis e tratados com Ceftazidima, Dexametasona ou com ambas as drogas foram sacrificados no terceiro, sétimo e décimo segundo dia após infecção. Pulmões e intestino delgado foram processados para histologia. Verificaram-se, nos pulmões dos quatro grupos infectados, infiltrados inflamatórios (neutrófilos e mononucleares) no terceiro dia após a infecção. No sétimo e décimo segundo dia após a infecção, o processo inflamatório se torna reduzido nos animais controle e tratados com antimicrobiano, mas não nos animais imunossuprimidos (com ou sem tratamento com antimicrobiano). A análise da mucosa duodenal confirmou a presença de parasitos em todos os grupos de animais. No 7º dia após a infecção, foram observadas alterações significativas no duodeno dos grupos controle (infectados) e dos infectados e tratados com antimicrobiano, com presença de infiltrado inflamatório, constituído de mononucleares e eosinófilos na mucosa, associada a uma maior quantidade de parasitos, principalmente na região do epitélio e sub-epitélio. Os outros dois grupos (camundongos infectados e imunossuprimidos com ou sem antimicrobiano), não apresentaram processo inflamatório. A mucosa apresentou células caliciformes menos evidentes, sugerindo uma redução de produção de muco. No décimo segundo dia da infecção, os grupos não tratados e tratados apenas com antimicrobiano apresentaram um número reduzido de parasitos e um discreto processo inflamatório no duodeno, enquanto os grupos tratados com imunossupressor (com ou sem antimicrobiano) mostraram presença de um maior número do parasito no duodeno. A permanência da infecção do S. venezuelensis foi mais prolongada nos animais imunossuprimidos em relação aos demais grupos, permanecendo até o 490dia após infecção. Os resultados indicam que a interferência dos tratamentos no equilíbrio da microbiota intestinal favoreceu o parasitismo pelo S. venezuelensis. Salvador

We studied a 66-year-old female who had a dull epigastric pain. An upper gastrointestinal (GI) series revealed a cordlike protrusion in the duodenal region, and a gastroendoscopic examination was performed and revealed a mucosal tag (MT) about 3 cm in length in the duodenal bulb. The MT was resected endoscopically and was found to be lined by normal duodenal mucosa and to have developed hyperplasia of the Brunner's glands. This MT was considered to be a congenitally-developed, hamartomatous hyperplasia of the duodenal mucosa, and of the Brunner's glands in particular.

The effects on gastric and duodenal mucosa induced by cisplatin plus etoposide (PE) chemotherapy were investigated in 32 patients with lung cancer. They were submitted to gastroduodenoscopy before rec