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This paper evaluated the behavioural performance to coating mortar water with rubberized tyres. #0.60 mm and #1.19 mm grain sizes have been used with the incorporation of 10 and 20% (in volume), replacing the small units. The methodology has elapsed with capillary and drying tests; humidification and drying procedures with mass control, infrared thermography and measurement of humidity. The results indicated that in capillarity and drying the trace A20F (#0.60 mm particle size and incorporation of 20%) had have a low absorption rate and helped in the process of water disposal. In the humidification and drying process, both active as well as passive, the rubber possibly blocks the pores of mass, for the grain traits size #0.60 mm (A10F and primarily A20F) have proven easy to lose water, suggesting that the majority of water absorbed would be concentrated on the surface part of the composite. [ABSTRACT FROM AUTHOR]

Background The aim of this study is to clarify whether acotiamide and rabeprazole combination therapy can improve clinical symptoms, gastric emptying, and satisfaction with treatment in functional dyspepsia (FD) patients more effectively than acotiamide or rabeprazole monotherapy alone. We also aimed to determine whether acotiamide affects these changes via its effect on gastric emptying and appetite-related hormones such as ghrelin. Methods We used Rome III criteria to evaluate upper abdominal symptoms and anxiety by the State-Trait Anxiety Inventory ( STAI). Gastric motility was evaluated by the 13C-acetate breath test. Eighty-one FD patients were treated with acotiamide (300 mg/day) ( n = 35), acotiamide (300 mg/day) and rabeprazole (10 mg/day) ( n = 28), or rabeprazole (10 mg/day) ( n = 18) for a period of 4 weeks and followed after 4 weeks of no treatment. Adenocorticotropic hormone (ACTH), cortisol, leptin and ghrelin levels were measured in all FD patients. Key Results Acotiamide and rabeprazole combination therapy significantly improved postprandial distress syndrome (PDS)-like symptoms ( p = 0.018, p = 0.04 and p = 0.041, respectively) and epigastric pain ( p = 0.024) as wells as STAI-state scores ( p = 0.04) compared to rabeprazole monotherapy. Both acotiamide monotherapy, and acotiamide taken in combination with rabeprazole, significantly ( p = 0.001 and p = 0.02, respectively) improved satisfaction with treatment, compared to rabeprazole monotherapy. Acotiamide and rabeprazole combination therapy had no significant effect on ACTH and cortisol levels in FD patients. Of interest, acotiamide monotherapy, and acotiamide and rabeprazole combination therapy, significantly ( p < 0.0001 and p = 0.018, respectively) increased acylated ghrelin/total ghrelin ratios and significantly ( p = 0.04) improved impaired gastric emptying compared to rabeprazole monotherapy. Conclusions & Inferences Further studies are warranted to clarify how acotiamide treatment improves clinical symptoms in FD patients. [ABSTRACT FROM AUTHOR]

Copyright of Archives of Veterinary Science is the property of Archives of Veterinary Science and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Archives of Veterinary Science is the property of Archives of Veterinary Science and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Nitrite (NO2-) is a substrate for both oxidative and reductive microbial metabolism. NO2- accumulates at the base of the euphotic zone in oxygenated, stratified open-ocean water columns, forming a feature known as the primary nitrite maximum (PNM). Potential pathways of NO2- production include the oxidation of ammonia (NH3) by ammonia-oxidizing bacteria and archaea as well as assimilatory nitrate (NO3-) reduction by phytoplankton and heterotrophic bacteria. Measurements of NH3 oxidation and NO3- reduction to NO2- were conducted at two stations in the central California Current in the eastern North Pacific to determine the relative contributions of these processes to NO2- production in the PNM. Sensitive (< 10 nmol L-1), precise measurements of [NH4+] and [NO2-] indicated a persistent NH maximum overlying the PNM at every station, with concentrations as high as 1.5 µmol L-1. Within and just below the PNM, NH3 oxidation was the dominant NO2- producing process, with rates of NH3 oxidation to NO2- of up to 31 nmol L-1 d-1, coinciding with high abundances of ammonia-oxidizing archaea. Though little NO2- production from NO3- was detected, potentially nitrate-reducing phytoplankton (photosynthetic picoeukaryotes, Synechococcus, and Prochlorococcus) were present at the depth of the PNM. Rates of NO2- production from NO3- were highest within the upper mixed layer (4.6 nmol L-1 d-1 ) but were either below detection limits or 10 times lower than NH3 oxidation rates around the PNM. One-dimensional modeling of water column NO2- production agreed with production determined from 15N bottle incubations within the PNM, but a modeled net biological sink for NO2- just below the PNM was not captured in the incubations. Residence time estimates of NO2- within the PNM ranged from 18 to 470 days at the mesotrophic station and was 40 days at the oligotrophic station. Our results suggest the PNM is a dynamic, rather than relict, feature with a source term dominated by ammonia oxidation. [ABSTRACT FROM AUTHOR]

Background/Aims: In this crossover study, we investigated whether nizatidine, a H2-receptor antagonist, can alleviate clinical symptoms and gastric emptying in patients with Rome III-based functional dyspepsia (FD) with or without impaired gastric emptying. Methods: We enrolled 30 patients presenting with FD symptoms (epigastric pain syndrome, n = 6; postprandial distress syndrome, n = 24). Rome III-based FD patients were treated with nizatidine (300 mg/day) or placebo for 4 weeks in a crossover trial. Gastric motility was mainly evaluated with the Tmax value using the 13C-acetate breath test. Meal-related symptoms were defined as postprandial fullness and early satiation. Gastroesophageal symptom was defined as a burning feeling rising from the stomach or lower chest up toward the neck. Acylated- and desacylated ghrelin levels were evaluated by the ELISA method. Clinical symptoms, gastric emptying and ghrelin levels were evaluated at three different points during the study (pretreatment, after 4 weeks former treatment and after 4 weeks later treatment). The primary end point of this study was to determine whether nizatidine would improve clinical symptoms and gastric emptying in FD patients with or without impaired gastric emptying via affecting ghrelin levels. Results: Meal-related symptoms of the patients treated with nizatidine improved significantly (21/30; 70%) compared to those treated with placebo (3/30; 10%). In addition, nizatidine treatment also significantly improved gastroesophageal symptoms (16/30; 53%) compared to those treated with placebo (0/30; 0%). Nizatidine treatment in patients with FD accompanied by impaired gastric emptying significantly improved clinical symptoms and Tmax value as a marker of gastric emptying (10/11, 91%; 9/11, 82%) compared to placebo therapy, respectively. There were no significant differences in ghrelin levels between nizatidine treatment and placebo therapy. Conclusion: Nizatidine administration significantly improved both gastric emptying and clinical symptoms in FD patients with impaired gastric emptying. Copyright © 2012 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

The article presents a study on carprofen's efficacy administered by different routes in experimental uveitis in dogs. The researchers used 12 mongrel dogs and 20 poodles aging from 11 to 14 months. They found that topical route is preferred for uveitis management because it is simple to use and offers desirable intraocular drug concentration.

Background: In healthy subjects who inspire deeply the lower esophagus usually opens, and the esophageal palisade vessels (EPVs) become visible. However, in patients with achalasia, the full extent of the EPVs does not become visible and, in addition, rosette-like esophageal folds appear in the lower esophagus. The aim of this study was to investigate whether or not these changes at the lower esophagus are characteristic findings of achalasia.Methods: A total of 34 patients with achalasia and no esophageal dilatation following deep inspiration were compared with 34 sex- and age-matched control subjects. Following a deep inspiration, the lower esophagus of all study cohorts was evaluated on (1) whether or not the full extent of the EPVs was visible, (2) whether or not rosette-like esophageal folds appeared in the lower esophagus, and (3) whether or not there were any gastric lesions.Results: One patient had secondary achalasia, and the remaining 33 patients had primary achalasia. In the control subjects, the full extent of the EPVs was clearly visible after a deep inspiration, and no esophageal folds appeared in the lower esophagus. In contrast, in the achalasia patients, EPVs were not observed in all patients after a deep inspiration, and rosette-like esophageal folds appeared in 33 of the 34 patients.Conclusion: After a deep inspiration, the non-visibility of the EPVs and the appearance of rosette-like esophageal folds at the lower esophagus, which we have called "esophageal rosette", are characteristic endoscopic findings of primary achalasia. [ABSTRACT FROM AUTHOR]

BACKGROUND: There is no known preventive agent against nonsteroidal anti-inflammatory drug (NSAID) induced small-intestinal injury. OBJECTIVE: To evaluate by capsule endoscopy whether coadministration of prostaglandin (PG) can prevent small-intestinal damage induced by short-term NSAID treatment. DESIGN: Single-blind, randomized, controlled trial. SETTING: All procedures were performed at Nippon Medical School. SUBJECTS: Thirty-four healthy male volunteers. METHODS: All subjects were randomly assigned to 2 groups: an NSAID-control group, who underwent NSAID (diclofenac sodium, 25 mg 3 times daily) and omeprazole (20 mg once daily) treatment, and an NSAID-PG group, who received PG (misoprostol, 200 microg 3 times daily) in addition to the same NSAID-omeprazole treatment. Eligible subjects, 15 per group, underwent capsule endoscopy before and 14 days after treatment. MAIN OUTCOME MEASUREMENTS: The number of mucosal breaks at capsule endoscopy. RESULTS: NSAID treatment significantly increased the mean (SD) number of mucosal breaks per subject, from a basal level of 0.1 +/- 0.3 up to 2.9 +/- 6.3 lesions in the NSAID-control group (P = .012). In contrast, there was no significant change in the mean number of mucosal breaks before and after PG cotreatment (P = 0.42). Thus, the mean number of posttreatment mucosal breaks per subject was significantly higher in the NSAID-control group than in the NSAID-PG group (P = .028). There was a significant increase in the percentage of subjects in the NSAID-control group, with at least 1 mucosal break after treatment (from 6.7% to 53.3%), whereas there was no change in the incidence of mucosal breaks in the NSAID-PG group, which remained at 13.3%. (P = .002). LIMITATIONS: Single-center, open-label study. CONCLUSIONS: PG cotherapy reduced the incidence of small-intestinal lesions induced by a 2-week administration of diclofenac sodium. [ABSTRACT FROM AUTHOR]

BACKGROUND: The prevalence of gastroesophageal reflux disease has been increasing in Japan as it has in Western countries, but Barrett's esophagus (BE) is less common in Japan than in Western countries. The aim of this study, therefore, was to investigate esophageal motility and clinical characteristics in Japanese patients with BE. METHODS: Ten patients with BE were compared with ten patients with mild reflux esophagitis (RE), ten patients with severe RE, and ten healthy subjects of comparable age and sex. The prevalence of Helicobacter pylori was investigated in the patients with BE. The intraluminal microtransducer method was used to test for esophageal motility. Basal lower esophageal sphincter (LES) pressure was assessed by the rapid pull-through method. The esophageal wave after ten repeated 5-ml water swallowings at 30-s intervals was measured at 3, 8, 13, and 18 cm above the LES. RESULTS: The basal LES pressure, the amplitude of the esophageal wave at 3 and 8 cm above the LES, and the frequency of primary peristalsis in the severe RE group and BE group were significantly lower than the values in the healthy subjects and the mild RE group. The amplitude of the esophageal wave 13 cm above the LES in the BE group was significantly lower than that in the healthy subjects and the mild RE group. There was no difference between the severe RE group and the BE group in the basal LES pressure and the amplitude of the esophageal wave. The frequency of primary peristalsis in the BE group, however, was significantly lower than that in the severe RE group. Nine of the ten patients with BE were H. pylori-negative. CONCLUSIONS: Our conclusions are that esophageal dysmotility in Japanese patients with BE represents an advanced stage of severe RE, and that most Japanese patients with BE are H. pylori-negative. [ABSTRACT FROM AUTHOR]

Background: There have been no reports that low serum cholesterol levels increase the risk of colorectal adenoma, although many studies have shown that they do increase the risk of colorectal cancer. Alcohol intake, which is associated with a risk of colorectal adenomas, and serum cholesterol levels are closely related. The purpose of this study was to evaluate the influence of alcohol consumption on the association between serum cholesterol levels and colorectal adenoma. Methods: The subjects were 1,349 male patients who underwent both barium enema examination and total colonoscopy. They answered a questionnaire regarding their alcohol consumption history, and their blood samples were analysed. The subjects were divided into three groups: those with no tumour (with neither adenoma nor adenocarcinoma), those with adenoma and those with adenocarcinoma. Among the groups, the serum total cholesterol and triglyceride levels were compared in all the patients, in the patients who did not drink daily and in the patients who did. Results: In all the patients, the serum cholesterol and triglyceride levels did not differ between the patients with and those without adenoma. In the daily drinkers, the serum cholesterol and triglyceride levels were significantly lower in patients with adenoma than in those without. Conclusions: Significantly lower levels of serum cholesterol and triglycerides were found in daily drinkers with adenoma than in those without. [ABSTRACT FROM AUTHOR]

Background: Helicobacter pylori eradication markedly improves histological inflammation and decreases peptic ulcer recurrence, but little is known about the subsequent development of gastric mucosal injury. Aim: To investigate whether acid suppression treatment after eradication influences the development of gastric erosions. Methods: Eighty-one patients (gastritis or peptic ulcer) after successful H. pylori eradication were divided into two groups: 40 received an H2-blocker for 6 months (H2-blocker-positive) and 41 received no treatment (H2-blocker-negative). Endoscopy was performed before, and at 3 and 6 months after completion of eradication. Results: Cumulative prevalence of gastric erosions in the H2-blocker-positive group was significantly lower than in the H2-blocker-negative group, 25% vs. 42%, respectively. In the H2-blocker-negative group but not the H2-blocker-positive group, the cumulative prevalence of gastric erosions after eradication was higher in patients with less severe corpus atrophy or more severe corpus gastritis. Conclusions: Development of gastric erosions after H. pylori eradication may be controlled by acid suppression treatment. Less severe atrophy or more severe gastritis in oxyntic glands before eradication may be involved in the development of gastric erosions. These results support the idea that recovery of acid secretion may be one of factors for development of gastric mucosal erosions after successful eradication. [ABSTRACT FROM AUTHOR]

Abstract Background and Aims: The classification of gastritis by using the revised Sydney system suggests that there are two types of Helicobacter pylori-related gastritis. The aim of the present study was to examine the risk factors that might be involved in the presence of either atrophic gastritis or intestinal metaplasia of the gastric corpus of Japanese patients. Methods: Biopsy samples were obtained from the gastric corpus in 154 patients with dyspepsia, and the degree of atrophy or intestinal metaplasia was determined histologically. The correlation between several variables and presence of atrophy or intestinal metaplasia was evaluated by using multivariate analysis. Results: Among the 11 variables, which included age, peptic ulcer diseases and H. pylori infection, H. pylori infection was the major risk factor associated with the presence of atrophic gastritis or intestinal metaplasia of the gastric corpus. In contrast, duodenal ulcer (DU) disease reduced the risk of contracting both conditions. Age was an independent risk factor only for intestinal metaplasia of the gastric corpus. When 128 H. pylori-positive subjects were analyzed, DU and age were similarly associated with the presence of both conditions. Conclusions: These results suggest that DU reduces the risk for contracting atrophic gastritis and intestinal metaplasia, and age is an independent risk factor for intestinal metaplasia of the gastric corpus in dyspeptic Japanese patients. [ABSTRACT FROM AUTHOR]

Increasing evidence suggests that mesothelial cells contribute to the control of inflammation in the peritoneal cavity by secreting prostaglandins. A study has shown that cyclo­ oxygenase (COX)­2 knockout mice die partly as a result of peritonitis. To investigate the expression and location of COX in peritonitis associated with peptic ulcer perforation. Gastric and duodenal tissues were collected intraoperatively from nine and four patients, respectively, and immunohistochemical staining for COX&Shy;1 and COX­2 was performed. Histologically, all patients had severe peritonitis around the perforation sites, into which many inflammatory cells and fibroblasts had infiltrated, and reactive mesothelial cells exhibited hyperplastic change. The COX­1 protein was not detected, whereas COX­2 was abundant in reactive mesothelial cells near the perforation site and disappeared away from the site. Macrophages and fibroblasts around the perforation site also revealed Immunostaining for COX­2. Our results showed that COX­2 protein is induced in mesothelial cells, as well as in macrophages and fibrobIasts, in inflamed peritoneal tissues associated with peptic ulcer perforation, suggesting involvement of COX­2 in tissue repair. [ABSTRACT FROM AUTHOR]

Copyright of Archives of Veterinary Science is the property of Archives of Veterinary Science and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

In this review, COX-1 and COX-2 proteins have been shown to be homologous in protein structure and ability to synthesize PG, but they have been also shown to be induced differently. COX-1 mRNA and protein have been shown to be induced slowly in intestinal crypt cells in response to irradiation and suggested to be important for crypt cell survival. Therefore, the cox-1 gene is suggested to be a delayed response gene in some systems. However, in cox-1 gene knockout animals there are no pathological gastric and intestinal findings. Although the precise roles of COX-1 in epithelial proliferation and differentiation in the gastrointestinal tract are not yet known, it apparently acts as a constitutive PG producer, thereby protecting the mucosa. On the other hand, COX-2 mRNA and protein have been shown to be induced rapidly in inflammatory sites of the stomach and colon. Thus, COX-2-derived PG presumably plays a role in the repair process of gastritis, ulcers, and colitis. Furthermore, loss of apc gene function probably induces COX-2 mRNA in gastrointestinal mucosa. Thus, high expression levels of COX-2 may lead to phenotypic changes in both intestinal epithelial cells and colon cancer cells. [ABSTRACT FROM AUTHOR]

Almost completely homogenous gastric mucous epithelial cells of guinea pigs were grown to confluence in the presence of 10% fetal calf serum (FCS). FCS, epidermal growth factor (EGF), and insulin significantly increased 5-bromo-2'-deoxyuridine (BrdU) uptake by the cells and EGF together with insulin increased the cells' [3H] thymidine uptake. Basic fibroblast growth factor (bFGF) enhanced EGF-induced DNA synthesis by the cells, but vasoactive intestinal peptide (VIP), secretin, prostaglandin E2 (PGE2), and dibutyryl cyclic AMP (dbcAMP) neither induced DNA synthesis nor enhanced the effect of EGF on DNA synthesis by the cells. Gastrin, cholecystokinin-octapeptide (CCK8), and carbamylcholine chloride (CCh) also did not enhance the effect of EGF on DNA synthesis. 125I-EGF, 125I-bFGF, and 125I-gastrin binding to the gastric mucous cells revealed the presence of high-affinity receptors for EGF and bFGF, but not for gastrin. Northern blot analysis showed the expression of EGF receptor mRNA, but not gastrin receptor mRNA. These results suggest that EGF, insulin, and bFGF may cooperatively regulate gastric mucous cell growth, but that gastrin and other gastrointestinal hormones do not have a direct stimulatory effect on mucous cell growth in the guinea pig. [ABSTRACT FROM AUTHOR]

OP16.09: Cardiac output and placental perfusion in growth-restricted fetuses with cerebral blood flow redistribution Fetal cardiac output and placental blood flow in normal growing and growth-restricted fetuses were investigated focusing into functional cardiovascular alteration especially in cases with cerebral blood flow redistribution. Umbilical venous flow volume (UVFV) and UVFV/CCO was estimated from the internal diameter of intrahepatic umbilical vein and the pulsed Doppler velocity waveform. [Extracted from the article]