BACKGROUND: One of the most artificial sweeteners is Aspartame which is commonly  used in a variety of foodstuffs. Objectives: This study has been carried out in order to evaluate the effects of Aspartame on histology and histometry of duodenum. Methods: Forty female Balb/C mice, 21 days of age were selected and initial weight was determined. The treatment groups received 100, 200 and 400 mg/kg of Aspartame for 6 weeks, control group received only distilled water. At the end of experiment, the mice were reweighed. Then the duodenal tissue sections were prepared and stained with H&amp;E. Besides the histological study, histometric data were collected by a light microscope equipped with Axiovision software. Results: The body weights in treatment groups (100, 200 and 400 mg/kg) were 5.57±1.18, 4.47±0.89 and 5.84±0.57 respectively, which in comparison with the control group (9.38±0.81) showed a significant difference (p<0.05). The histological study showed that the rate of destruction in the cells and mucosal structures, at the dose of 200 mg/kg compared to the dose of 100 and 400 mg/kg has been increased. In histometric aspect, abundance of duodenal villi, height of the villi and thickness of duodenal mucosa, only in the experimental group of 200 mg/kg were significantly increased compared to the control group (p<0.05). Whereas the width of villi (width of the apex, body and the base), in all of the experimental groups showed a significant decrease compared to the control group (p<0.05). The thickness of musculature of duodenum in experimental groups had no significant differences with the control group. Conclusions: Based on this study, it can be concluded that Aspartame can cause some histological and histometrical changes in duodenum.

There is a balance between oxidative stress, antioxidant capacity and immune response. Their roles in physiological and behavioural mechanisms are important for the maintenance of the organism’s internal equilibrium. This study aimed to evaluate the antioxidant effects of the exogenous alga Spirulina platensis (Arthrospira platensis) in a stress-induced rat model, and to describe its possible mechanism of action. Thirty-six adult male Sprague Dawley rats were separated into four groups: control (C), stress (S), S. platensis (Sp), and S. platensis + stress (SpS). The rats in groups Sp and SpS were fed with 1,500 mg/kg b.w./day Spirulina platensis for 28 days. All rats were exposed to prolonged light phase conditions (18 h light : 6 h dark) for 14 days. The SpS and S groups were exposed to stress by being kept isolated and in a crowded environment. Blood samples were obtained by puncturing the heart on the 28th day. The effect of stress on serum corticosterone, oxidative stress markers (TOS, TAC, PON1, OSI) and immunological parameters (IL-2, IL-4, IFN-ɣ) were tested. Also, the brain, heart, intestines (duodenum, ileum, and colon), kidney, liver, spleen, and stomach of the rats were weighed. Serum corticosterone levels were higher in the S group than in the C group, and significantly lower in the SpS group than in the S group. Mean total antioxidant capacity were lower in the S group than in the C group, and Spirulina reversed this change. Although not significantly different, IL-2 was lower in the S group than in the C group. However, in the SpS group, IL-2 increased due to Spirulina platensis mitigating effects of stress. Male rats fed a diet with Spirulina platensis could experience significantly milder physiological changes during stress, although stress patterns may be different. Exogenous antioxidant supplements merit further investigation in animals and humans where the endogenous defence mechanism against stress may not be sufficient.

Coinfection of goose parvovirus (GPV) and duck circovirus (DuCV) occurs commonly in field cases of short beak and dwarfism syndrome (SBDS). However, whether there is synergism between the two viruses in replication and pathogenicity remains undetermined. We established a coinfection model of GPV and DuCV in Cherry Valley ducks. Tissue samples were examined histopathologically. The viral loads in tissues were detected by qPCR, and the distribution of the virus in tissues was detected by immunohistochemistry (IHC). Coinfection of GPV and DuCV significantly inhibited growth and development of ducks, and caused atrophy and pallor of the immune organs and necrosis of the liver. GPV and DuCV synergistically amplified pathogenicity in coinfected ducks. In the early stage of infection, viral loads of both pathogens in coinfected ducks were significantly lower than those in monoinfected ducks (P < 0.05). With the development of the infection process, GPV and DuCV loads in coinfected ducks were significantly higher than those in monoinfected ducks (P < 0.05). Extended viral distribution in the liver, kidney, duodenum, spleen, and bursa of Fabricius was consistent with the viral load increases in GPV and DuCV coinfected ducks. These results indicate that GPV and DuCV synergistically potentiate their replication and pathogenicity in coinfected ducks.

Introduction: The aim of the experiment was to establish the enterotoxigenic Escherichia coli K88 (ETEC K88)-induced BALB/c mouse duodenum inflammation model. Material and Methods: Mice were administered different concentrations of E. coli K88 (1.0 × 107-109 CFU/mL) for 3 d by means of an esophageal catheter. Results: The results showed that the treated group expressed several significant clinical symptoms, such as reduced dietary demands and weight loss, an increased presence of IL-1α, TNF-α, and MPO in the peripheral blood, and some pathological changes in the duodenum. On the 6th-8th days, the body weight of the mice was the lowest. On the 8th day, there were significant differences in IL-1α, TNF-α, and MPO levels compared to the control group (P < 0.05), the gap between the duodenum mucous layer and the muscular layer had widened, the number of goblet cells was increased, and the inflammatory infiltrate and inflammation changes in the lamina propria and the mucous layer were the most obvious. Conclusion: The duodenum inflammation was the most severe on day 8; thus, the model was successfully established. In addition, varying concentrations of ETEC K88 did not significantly influence the duodenum inflammation (P > 0.05).

Introduction: The aim of the experiment was to establish the enterotoxigenic Escherichia coli K88 (ETEC K88)-induced BALB/c mouse duodenum inflammation model. Material and Methods: Mice were administered different concentrations of E. coli K88 (1.0 × 10⁷-10⁹ CFU/mL) for 3 d by means of an esophageal catheter. Results: The results showed that the treated group expressed several significant clinical symptoms, such as reduced dietary demands and weight loss, an increased presence of IL-1α, TNF-α, and MPO in the peripheral blood, and some pathological changes in the duodenum. On the 6ᵗʰ-8ᵗʰ days, the body weight of the mice was the lowest. On the 8ᵗʰ day, there were significant differences in IL-1α, TNF-α, and MPO levels compared to the control group (P < 0.05), the gap between the duodenum mucous layer and the muscular layer had widened, the number of goblet cells was increased, and the inflammatory infiltrate and inflammation changes in the lamina propria and the mucous layer were the most obvious. Conclusion: The duodenum inflammation was the most severe on day 8; thus, the model was successfully established. In addition, varying concentrations of ETEC K88 did not significantly influence the duodenum inflammation (P > 0.05).

In order to study the ability of Lactobacillus casei to ameliorate murine enteritis, 18 mice were randomly divided into 3 groups: the enteritis group, intervention group, and control group. The interleukin (IL)-6 and transforming growth factor-β (TGF)-β content in mouse peripheral blood and duodenum was detected using an enzyme-linked immunosorbent assay (ELISA). The number of CD4+CD25+Foxp3+ T-regulatory cells (Tregs) and CD4+IL-17A+ Th17 cells in the mesenteric lymph nodes (MLN) and spleen were detected using flow cytometry, and quantitative reverse transcription polymerase chain reaction (PCR) and western blot analysis were used to measure Foxp3 and retinoid-related orphan receptor-γ (RORγt) mRNA and protein expression in the MLN. Histological changes in the duodenum were observed. Results indicate that in the intervention group, IL-6 content in mouse peripheral blood and duodenum was significantly lower than in the enteritis group (P < 0.05), while TGF-β content was significantly increased compared to the enteritis group (P < 0.05). For the intervention group, the percentages of CD4+CD25+Foxp3+ Tregs in spleen and MLN were increased (P < 0.05), while the percentages of CD4+IL-17A+ Th17 cells were decreased compared to the enteritis group (P < 0.05). The expression of Foxp3 mRNA and protein in the intervention group was higher than in the enteritis group, while RORγt mRNA and protein were significantly lower (P < 0.05). After mice in the enteritis group were treated with L. casei, duodenal inflammation was relieved. This study demonstrated that L. casei could have possible implications for the enterotoxigenic Escherichia coli (ETEC) induced intestinal inflammation by regulating the ratio imbalance of Th17/Treg cells.

OBJECTIVE To compare expression, activity, and fecal concentration of intestinal alkaline phosphatase (IAP) between healthy dogs and dogs with chronic enteropathy (CE). ANIMALS 9 healthy university-owned Beagles and 109 healthy client-owned dogs (controls) and 28 dogs with CE (cases). PROCEDURES Cases were defined as dogs with persistent (> 3 weeks) gastrointestinal signs that failed to respond to antimicrobials and anti-inflammatory doses of prednisolone or dietary trials, did not have mechanical gastrointestinal abnormalities as determined by abdominal radiography and ultrasonography, and had a diagnosis of lymphoplasmacytic enteritis or eosinophilic gastroenteritis on histologic examination of biopsy specimens. Duodenal and colonic mucosa biopsy specimens were obtained from the 9 university-owned Beagles and all cases for histologic examination and determination of IAP expression (by real-time quantitative PCR assay) and activity (by enzyme histochemical analysis). Fecal samples were obtained from all dogs for determination of fecal IAP concentration by a quantitative enzyme reaction assay. RESULTS For dogs evaluated, IAP expression and activity were localized at the luminal side of epithelial cells in the mucosa and intestinal crypts, although both were greater in the duodenum than in the colon. Active IAP was detected in the feces of all dogs. Intestinal alkaline phosphatase expression and activity were lower for cases than for controls, and fecal IAP concentration for dogs with moderate and severe CE was lower than that for dogs with mild CE. CONCLUSIONS AND CLINICAL RELEVANCE Results indicated that dogs with CE had impaired IAP expression and activity. Additional research is necessary to elucidate the role of IAP in the pathogenesis of CE.

OBJECTIVE To characterize the expression of monocarboxylate transporters (MCTs) 1 and 4 and the ancillary protein CD147 in the intestinal tract of healthy equids and determine the cellular location of CD147 in the intestinal epithelium. ANIMALS 12 healthy horses and ponies slaughtered for meat production or euthanized for reasons unrelated to gastrointestinal tract disease. PROCEDURES The entire gastrointestinal tract was removed from each equid within 45 minutes after slaughter or euthanasia. Tissue samples were obtained from the antimesenteric side of the duodenum, jejunum, ileum, middle part of the cecum, sternal flexure of the ventral colon, pelvic flexure, sternal flexure of the dorsal colon, and descending colon (small colon). Expressions of MCT1, MCT4, and the ancillary protein CD147 were examined in tissue samples from each of the 8 intestinal locations by means of quantitative PCR assay, immunoblotting, and immunohistochemical analyses. RESULTS Expression of MCT1 was most abundant in the cecum and colonic sites, whereas expression of MCT4 was predominantly in the proximal section of the intestine (small intestinal sites and cecum). Immunohistochemical analysis revealed that MCT1 and CD147 were present in the membranes of enterocytes (in crypts and villi). CONCLUSIONS AND CLINICAL RELEVANCE The anatomic distribution of MCT1 and MCT4 in the equine intestinal tract determined in this study together with the previous knowledge of the sites of substrate absorption indicated that MCT1 might predominantly contribute to the uptake of short-chain fatty acids in the large intestine and MCT4 might predominantly contribute to the uptake of lactate in the small intestine.

Objective: To investigate contrast-enhanced ultrasonography as a minimally invasive method for the subjective and quantitative assessment of pancreatic and duodenal perfusion in healthy adult dogs, with reference to perfusion in adjacent liver tissue. Animals: 8 clinically normal adult dogs. Procedures: Contrast-enhanced ultrasonograms of the right pancreatic limb, proximal portion of the descending duodenum, and adjacent liver were acquired after IV administration of a microbubble contrast medium. Following subjective evaluation, quantitative time-intensity curves were generated from regions of interest in the pancreas, duodenum, and liver. Five contrast medium characteristics representing perfusion parameters were determined for each organ and used for statistical analysis: interval to arrival, inflow rate, peak intensity (PI), time of peak intensity (TPI), and outflow rate. Results: Significant associations between pancreatic and duodenal values were found for interval to contrast medium arrival, PI, TPI, and outflow rate. Pancreatic and duodenal inflow rates were not correlated. Inflow and outflow rates were significantly faster and TPI significantly shorter for the pancreas and duodenum, compared with values for the liver. There was no significant difference among all 3 organs for interval to arrival and PI of contrast medium. Subjective evaluation findings corresponded to quantitative analysis results. Conclusions and Clinical Relevance: Results suggested that contrast-enhanced ultrasonography may be a useful, minimally invasive method for evaluating pancreatic and duodenal perfusion in dogs. The data from healthy dogs reported here could aid in the assessment of pancreatic and duodenal conditions and their response to medical treatment.

Effects of the following treatments on abomasal and duodenal myoelectric activity in yearling cattle were studied: 2 ml of 0.9% sodium chloride solution (NACL); 0.07 mg of bethanechol (BET)/kg of body weight; 0.1 mg of metoclopramide (MET)/kg; and 0.07 mg of bethanechol and 0.1 mg of metoclopramide (BETMET)/kg. All treatments were administered SC during the early part of phase I of the migrating myoelectric complex Myoelectric signals were recorded for 4 hours after administration of the treatments from 1 electrode in the antrum and 3 electrodes in the duodenum. For the antral spike rate (ASR), there was no significant difference among treatments during the first hour, but the ASR was significantly (P < 0.05) greater during hours 2 to 4 after treatment with BETMET, compared with ASR for MET alone. The duodenal spike rate (DSR) was significantly (P < 0.05) greater during the first hour after administration of BETMET than after the other treatments. After administration of BET, DSR was significantly (P < 0.05) greater than after MET or NACL. There was no difference in DSR after MET, compared with DSR after NACL. There was no significant difference in DSR among treatments during the second and third hours. The total antegrade propagating spike (TAPS) count was greater after administration of BETMET in all hours, compared with the other treatments. The ratio of TAPS to total spikes on the orad-most duodenal electrode was significantly (P < 0.05) greater after BETMET during hours 1 and 2.