Background: Gastric cancer is the fourth most common malignancy in the world. Honey is a complex mixture of special biological active constituents. Honey possesses antioxidant and anti- tumor properties. Nutritional studies have indicated that consumption of honey modulates the risk of developing gastric cancer. On the other hand, apoptosis has been reported to play a deci- sive role in precancerous changes. Our chief study was conducted to assess the relationship be- tween consumption of honey and apoptosis in human gastricmucosa.
Helicobacter pylori infects the gastricmucosa of half the world’s population and the infection is considered to be an impor- tant factor in the pathogenesis of peptic ulcer (1,2), distal gastric carcinoma (3) and mu- cosa-associated lymphoid tissue lymphoma (4). The reason why most infected subjects remain asymptomatic whereas only a few develop the related diseases is controversial. Besides environmental and bacterial viru- lence factors, differences in the host genet- ics may influence the type of tissue inflam- matory reaction and subsequently the out- come of infection.
On the host side, host counteracts H. pylori infection by alteration in different aspects. Secretion of antibacterial substances and gastric mucosal barrier are the important defense mechanisms of the stomach to limit the proliferation of H. pylori. Lactoferrin inhibits bacterial growth by restricting the availability of extracellular iron ions, and Lactoferrin also has antibacterial characteristics . Components of the gastric mucin can inhibit biosynthesis of the H. pylori wall. Neutrophils and macrophages produce large amounts of reactive oxygen species (ROS) and nitric oxide (NO) which can produce reactive nitrogen species (RNS) by reacting with O2 ˙- [16–18]. ROS and RNS can directly kill bacteria. In addition, host inflammatory and immunological reaction to H. pylori increases. The chronic infection was characterized by increasing the numbers of lymphocytes, macro- phages, neutrophils, mast cells and dendritic cells, and the infiltration of inflammatory cells into the sub-epithelial gastric lamina propria. A humoral immune response to H. pylori is elicited in nearly all H. pylori -infected humans. IFN-c, TNF, IL-6, IL-7, IL-8, IL-10 and IL-18 levels are increased in the gastricmucosa [19–20]. Monocyte-derived human dendritic cells release cyto- kines and increase expression of major histocompatibility class II proteins . Moreover, H. pylori infection can enhance cell proliferation [8,22] as to retrieve gastricmucosa damage and apoptosis of gastric epithelial cells [18,23]. Thus, to counteract H. pylori infection, host activates gene transcription involved in defense mechanism, inflammatory and immunological reaction, cell proliferation and apoptosis.
ABSTRACT. Background. Chronic gastritis process of cell renewal in the mucosa is disturbed, leading to rapid movement of the generative cell zone without full differentiation into mature specialized area accommodation epithelial cells. The result of this process is the inability to fully function gastric glands. Crucial in the diagnosis of gastritis given the nature of the mor- phological changes of the gastricmucosa and preferential localization of these changes. Objective. To assess histological changes of gastricmucosa in patients with clinically different types of functional dyspepsia. Methods. Adult patients (18-65 years) with confirmed diagnosis of functional dyspepsia were eligible to participate. Biopsy specimens were taken from sto- mach due to the Houston-updated gastric biopsy sampling protocol for the next histological examination. One expert ga- strointestinal pathologist assessed all tissue samples. Atrophy was assessed due to Operative Link for Gastritis Assessment (OLGA) staging system. Results. 75 patients were recruited, 42 of which had epigastric pain (I group) and 33 – postprandial distress syndrome (II group) due to Rome III criteria (2006). Antral and corpus atrophy were detected at the same frequency in both groups (p>0.05), however the stage of atrophy didn’t exceed I in all cases. Complete antral metaplasia was revealed in 11 (26.2%) patients of the I group and 11 (33.3%) patients of the II one. Incomplete antral metaplasia was seen in 2 (4.7%) patients of the I group and 2 (6.1%) patients of the II one. No cases of corpus metaplasia or dysplasia were found. Conclu- sion. Our study didn’t reveal statistically significant correlation between stage of gastritis, atrophic or metaplastic changes and clinical symptoms of functional dyspepsia.
Materials and Methods: Thirty-two rats were randomly assigned into 4 groups (8 in each), including: the control group, HCl (10 mM) treated group, HCl (100 mM) treated group, and one group to study the effect of Nω-Nitro-L-arginine methyl ester hydrochloride (L-NAME). Anesthetized rats underwent tracheostomy and midline laparotomy. Ninety min after the instillation of neutral or acidic solutions, animals were sacrificed and the gastricmucosa was collected to measure the H 2 S concentration by ELISA method and to quantify mRNA expression of
In the present study, we have characterized the expression of histo‐blood group antigens in the normal canine gastricmucosa to define the gastric glycosylation profile of dogs (Table 2). The expression pattern of type 1 and type 2 Lewis antigens in the canine gastricmucosa revealed a different distribution when compared with the human gastricmucosa. Normal canine mucosa showed minor expression of type 1 Lewis antigens, with absence of Leb and sLea expression and only a sparse expression of Lea in the body of one of the animals tested. In the human normal gastricmucosa, and depending on the secretor status of the individual, Lea and Leb are highly expressed in the superficial foveolar epithelium 23, 35, where MUC5AC mucin is co‐expressed 36. The normal canine mucosa demonstrated expression of Lewis type 2 antigens characterized by expression of Lex and Ley, along with a minor expression of sLex. In the canine gastricmucosa this expression was mostly observed in the superficial and foveolar epithelium, with Ley expression extending to the deeper portions of the gastric gland. In the human gastricmucosa, the expression of Lewis type 2 antigens is generally restricted to the deeper part of the gastric glands, where MUC6 mucin is co‐expressed 37, 38. Knowing that type 1 fucosylated structures are receptors for H. pylori in human stomach, the different expression patterns of type 1 and 2 Lewis antigens observed may play a role in differences in prevalence of gastric helicobacters in both mammalian species.
Because of the potential role of SLC6A4 in FD, DNA methylation status of SLC6A4 gene was examined in the gastricmucosa of FD patients. Methylation status of SLC6A4 PCGI has been reported to have influence on serotonin transporter mRNA levels . Recent research has also gradually revealed that change in methylation patterns across the gene (so-called intragenic or gene body methylation) may have a role in several pathologic state . Thus, to obtain detailed information about Figure 2. Methylation status of SLC6A4 gene in the gastricmucosa in relation to the distance from transcriptional start site. Average methylation of each sites analyzed were expressed as mean +/2SEM.
Figure 3. Box-plot showing the average distribution of cyclooxy- genase-2 (COX-2) Yamauchi et al. (21) score in 30 normal speci- mens, 12 ectopic gastricmucosa (EGM) and 10 Barrett’s esopha- gus. (Error bars are ± SD and horizontal lines are medians). The value obtained for normal specimens was zero, since there was no COX-2 expression in the normal tissue.
This work investigated the frog gastricmucosa response to hydrogen peroxide and ethanol induced injury. Acid and mucus secretion were estimated “in vitro” in control animals with intragastric absolute ethanol (1ml/30min. or 2ml/60min.) and hydrogen peroxide. The gastricmucosa morphological conditions were assessed “in vivo”, concerning lesion area, pH and mucus. Ethanol (1ml/30min.) was observed to cause hyperemia, cell damage, rupture, edema, erosions, necrosis in gastricmucosa and significant increase in acid secretion. Absolute ethanol (2ml/60min.) caused a decrease in acid secretion due to alcalinization and an increase of mucus and pH. Intragastric hydrogem peroxide provoked gastric unwrinkling and hyperemia, acid secretions were not increased, mucus fragmented and the pH was decreased. The results indicate an increase of mucus and acid in response to ethanol and unwrinkling and hyperemia to hydrogen peroxide.
were generally negative, while mucosa-as- sociated lymphoid tissue (MALT) and folli- cular lymphomas were frequently positive (92 and 64%, respectively). Later studies have shown that sensitivity to apoptosis by the CD95 pathway might be altered, as none of the lymphomas studied by Plumas et al. (6), regardless of their level of CD95 expres- sion, had apoptosis induced by the anti-CD95 monoclonal antibody. These investigators confirmed the low expression of CD95 in chronic lymphocytic leukemia and mantle cell lymphomas, and its high expression in follicular lymphomas.
Os microrganismos espiralados (helicobactérias) têm sido observados no estômago de cães há mais de um século (Happonen et al., 2000; Hwang et al., 2002). Porém, apenas após a descoberta do envolvimento do Helicobacter pylori (H. pylori), com a gênese de gastrites, úlceras pépticas, e neoplasias gástricas em seres humanos (Happonen et al., 1998; Simpson et al., 1999), é que se intensificaram os estudos sobre a incidência e a implicação clínica, da presença desses microrganismos gástricos em animais domésticos, especialmente em cães e gatos. Até o presente momento, contudo, não pode ser estabelecida uma associação positiva entre a presença desses microrganismos e alterações na mucosa gástrica desses indivíduos (Eaton et al., 1996). Os objetivos desta comunicação foram descrever a prevalência, a distribuição e densidade de colonização, de helicobactérias gástricas em cães saudáveis e caracterizar os aspectos microscópicos e macroscópicos da mucosa estomacal desses indivíduos.
After reviewing all cases, the patients were separated into 4 groups: Group I – patients presenting normal gastricmucosa or gastricmucosa with minimal inlammatory changes; Group II – chronic gastritis with mild inlammatory activity; Group III – chronic gastritis with moderate or severe (patent) inlammatory activity; Group IV – patients presenting atrophic body gastritis. The degree of inlammatory activity was based on the general pattern polymorphonuclear neutrophils (PMNs) iniltrate the lamina propria. Moderate or severe activity indicates presence of numerous PMNs diffuse along the section, frequently invading the epithelium of the glands, and sometimes forming tiny abscesses. Mild activity indicates presence of few PMNs in lamina propria, frequently with regional distribution or just forming inlammatory focus of activity.
The atrophy of specialized glands of the gastricmucosa associated with chronic inflammation is a common pathological condition in humans. In general, the more severe cases of atrophy of the gastricmucosa do not involve diagnostic difficulties by the two methods commonly used, i.e., endoscopic and histopathological examinations. The current importance of the recognition of gastric mucosal atrophy is the frequency at which this condition is associated with the development of precancerous lesions, i.e., intestinal metaplasia and dysplasia of the gastric epithelium, which may develop into gastric cancer in the sequence known as Correa cascade (4) . The two
C. lutea fractions interrupt diethyldithiocarbamate (DTC) induces antral lesions in earlier report by 68.79% (Nwidu and Nwafor 2009). DTC is reported to initiates its effects by mobilization of superoxide and hydroxyl radicals (oxygen derived free radicals) (Oka et al., 1990). Superoxide radical and hydrogen peroxide play pathogenic role in this ulcer model Salim (1989). The low RSA observed in our study could not be explained in light of present findings. Gastric cyto-protection may be mediated by at least two different mechanisms. The first one is by stimulation of release of prostaglandins (PG) and the second one by Michael’s acceptor interaction with sulfhydryl-containing compounds of the mucosa. The latter, mechanism of cyto-protection might be mediated by CLL EAF, at least in part, by the reaction between electrophilic moiety on the trans-cinnamic acid and sulfhydryl- containing compounds of the gastricmucosa (Donadel et al., 2005). In this mechanism of cyto-protection, antioxidant activity might be mediated by the reaction between the electrophilic acceptor, trans-cinnamic acid, (which constitute 21.9% of isolated compounds) from the EAF with sulfhydryl-containing compounds of the gastricmucosa (Marıa et al., 2000). Trans-cinnamic acid (Michael’s acceptor) and electron donation by sulphydryl moiety present in proteins or oxidants containing compounds has form a new basis of cytoprotection (Souza-Brito et al., 1998; Hiruma- Lima et al., 1999; Hiruma-Lima et al., 2001; Melo et al., 2003; Yesilada et al., 2004; Hamauzu et al., 2008).
To check the patients’ antioxidant and oxidative stress marker levels, 10 mL of blood was taken from the brachial vein. The blood samples were stored in -80°C until the markers were measured. After the patients’ examinations, a biopsy was obtained from each participant. According to the previous studies, during endoscopy biopsy samples of gastric antrum were taken for H. pylori urease culture tests. Stomach antrum and corpus biopsies were also taken for histological examination. In general, if one of the results of the three tests of H. pylori urease culture and histopathological examination was negative, the patient was considered as negative for H. pylori infection. Meanwhile, if all three of the test results were positive, the patient was considered as positive for H. pylori infection. Patients with positive H. pylori cultures were attributed into the treatment group, and patients with negative H. pylori cultures and normal gastricmucosa, after histopathological ex- aminations, were selected for control group. Eligible patients were divided into two groups: a triple therapy group (control) and a triple therapy + curcumin group (treatment). Triple therapy was given as a one-week course of an omeprazole-based triple regi- men (omeprazole/20 mg, amoxicillin/1 g, and metronidazole/800 mg, each given orally twice a day (OAM – manufactured by The Government Pharmaceutical Organization, Bangkok, Thailand). In this study, for curcumin administration, we used the Turmeric Tablet (Khaolaor Laboratory; Bangkok, Thailand) (700 mg orally three times a day) for 4 weeks (8) . The control group received no
ABSTRACT - Background - Morbid obesity treatment through vertical gastroplasty Roux-en-Y gastric bypass initially used a contention ring. However, this technique may create conditions to the development of potentially malign alterations in the gastricmucosa. Although effective and previous- ly performed in large scale, this technique needs to be better evaluated in long-term studies regarding alterations caused in the gastricmucosa. Objective - To analyze the preoperative and postoperative endoscopic, histological and cell proliferation indings in the gastric antrum and body mucosa of patients submitted to the Roux-en-Y gastric bypass with a contention ring. Methods - We retrospectively evaluated all patients submitted to Roux-en-Y gastric bypass with a contention ring with more than 60 months of postoperative follow-up. We compared the preoperative (gastric antrum and body) and postoperative (gastric pouch) gastricmucosa endoscopic indings, cell proliferation index and H. pylori prevalence. We evaluated cell proliferation through Ki-67 antibody immunohistochemical expression. Results - In the study period, 33 patients were operated with the Roux-en-Y gastric bypass using a contention ring. We found a chronic gastritis rate of 69.7% in the preoperative period (gastric antrum and body) and 84.8% in the postoperative (gastric pouch). H. pylori was present in 18.2% of patients in the preoperative period (gastric antrum and body) and in 57.5% in the postoperative (gastric pouch). Preoperative cell proliferation index was 18.1% in the gastric antrum and 16.2% in the gastric body, and 23.8% in the postoperative gastric pouch. The postoperative cell proliferation index in the gastric pouch was signiicantly higher (P=0.001) than in the preoperative gastric antrum and body. Higher cell proliferation index and chronic gastritis intensity were signiicantly associated to H. pylori presence (P=0.001 and P=0.02, respectively). Conclusion - After Roux-en-Y gastric bypass with contention ring, there was a higher chronic gastritis incidence and higher cell proliferation index in the gastric pouch than in the preoperative gastric antrum and body. Mucosa inlammation intensity and cell proliferation index in the postoperative gastric pouch were associated to H. pylori presence and were higher than those found in the preoperative gastric antrum and body mucosa. HEADINGS - Morbid obesity. Gastroplasty. Roux-en-Y anastomosis. Ki-67 antigen. Helicobacter pylori.
Mutation rates in bacteria have generally been considered to be much slower than in viruses. This is partly because estimates of long-term mutation rates for the evolution of distinct species have been inappropriately used for dating divergence within species. Furthermore, the most com- monly used long-term mutation rate is based on geological dates that are no longer accepted. In addition, only few short-term mutation rates have been calculated within bacterial species, and these differ with the species by several orders of magnitude. Here, we provide robust estimates for short-term mutation and recombination rates within Helicobacter pylori, a bacterium that commonly infects the human gastricmucosa, based on serial isolates from long-term infections and on differences between isolates from multiple family members. These short-term mutation rates are 5–17-fold faster than long-term mutation rates in H. pylori that have been calibrated by parallel ancient migrations of humans. Short-term muta- tion rates in bacteria, including those for H. pylori, can be quite fast, partially overlapping with those for viruses. Future calculations of ages of bacterial species will need to account for dramatic differences in mutation rate between species and for dramatic differences between short- and long-term mutation rates.
correlation between duodenogastric reflux and the development of epithelial proliferative lesions in the pyloric mucosa. However, the lesions induced by the duodenogastric reflux were a benign condition, since they did not present cellular atypia or mural invasion and were reversible with interruption of duodenogastric reflux. Therefore, the aim of present study is to investigate if combining TV to the experimental model of duodenogastric reflux (DGR) can enhance the progression of proliferative lesions to malignancy, as well to evaluate if TV, by itself, can induce morphological alterations in the gastricmucosa.
swab samples (from 38 patients, 4 patient family members, and 27 healthy volunteers). The samples were grown in dishes and two clones from each dish were chosen for MLST analysis. All but 11 of the replicates shared the same DST; those that were different were from two gastricmucosa samples (nos. 8027 and 8066), four oral swabs from the dyspeptic patients (nos. 8027, 8113, 8203, and 8221), and five oral swabs from the healthy volunteers (nos. 2n, 42a, 157c, 287, and 287g). Details of the Candida prevalence in the healthy volunteers and the dyspeptic group are presented in Tables S1 and S2, respectively. As shown in Tables S1 and S2, 46 different DSTs were identified: 37 were identified in a single sample and nine were shared by multiple samples (DST142, DST367, DST601, DST656, DST1593, DST1594, DST1779, DST1957, and DST1971). Twenty-nine novel DSTs (DST1593, DST1594, and DST1956–1978) were submitted to the MLST database (http://calbicans.mlst.net). Their details are presented in Table S3.
Although acute lesions induced experimentally in rodents presents many different characteristics of ulcers that occur in man, the results obtained through these methodologies indicate the involvement of some factors in the protective mechanism of gastricmucosa by compounds presented in plants extracts. The aqueous extract of leaves of A. millefolium L. was able to protect the gastricmucosa against the direct necrosing action of ethanol, which can cause injury to the gastricmucosa by damaging and breaking the gelatinous layer composed of mucus and bicarbonate, which protects the stomach 9, 10 and