HepPar-1 and Arginase-1 Immunohistochemistry in Adenocarcinoma of the Small Intestine and Ampullary Region

2015 ◽  
Vol 139 (6) ◽  
pp. 791-795 ◽  
Author(s):  
Stephen Lagana ◽  
Susan Hsiao ◽  
Fei Bao ◽  
Antonia Sepulveda ◽  
Roger Moreira ◽  
...  
Keyword(s):  
Small Intestine ◽  
Intestinal Morphology ◽  
Small Intestinal Mucosa ◽  
Control Groups ◽  
Arginase 1 ◽  
Normal Human ◽  
Small Intestinal ◽  
Upper Gastrointestinal ◽  
Colorectal Adenocarcinomas ◽  
Diffuse Positivity

Context HepPar-1 and Arginase-1 are urea cycle enzymes used to distinguish hepatocellular carcinoma from other carcinomas. HepPar-1, but not Arginase-1, is known to be immunoreactive with normal human small intestine. Objectives To better define and compare the immunohistochemical staining patterns of HepPar-1 and Arginase-1 in adenocarcinomas arising in the small intestine, including the ampullary region. Design Staining for HepPar-1 and Arginase-1 was performed on 20 nonampullary small intestinal adenocarcinomas and 32 adenocarcinomas from the ampullary region. Ampullary adenocarcinomas were divided into intestinal morphology (15), pancreatobiliary morphology (14), and unclassifiable (3). Nonneoplastic small intestinal mucosa and colorectal adenocarcinomas were used as control groups. Results HepPar-1 stained 12 of 20 nonampullary small intestinal adenocarcinomas, with a median of 63% of cells staining in positive cases. It also stained 11 of 15 ampullary carcinomas with intestinal morphology, with a median of 75% of cells staining in positive cases. Two of 14 ampullary carcinomas with pancreatobiliary morphology were positive for HepPar-1. Arginase-1 showed positivity in 2 ampullary region carcinomas and diffuse positivity in 1 duodenal adenocarcinoma. Two of 22 colorectal carcinomas stained for HepPar-1 with none positive for Arginase-1. Conclusions HepPar-1, but not Arginase-1, usually shows positivity in small intestinal adenocarcinomas and ampullary adenocarcinomas with intestinal morphology, but only rarely shows positivity in ampullary adenocarcinomas with pancreatobiliary morphology. HepPar-1 positivity in metastatic adenocarcinoma with intestinal morphology is suggestive of an upper gastrointestinal primary site.

Carbohydrase activity in the pancreatic tissue and small intestine mucosa of sheep fed dried-grass or ground maize-based diets

1985 ◽  
Vol 104 (2) ◽  
pp. 435-443 ◽  
Author(s):  
A. N. Janes ◽  
T. E. C. Weekes ◽  
D. G. Armstrong
Keyword(s):  
Small Intestine ◽  
Amylase Activity ◽  
Total Activity ◽  
Pancreatic Tissue ◽  
Proximal Region ◽  
Small Intestinal Mucosa ◽  
Intestine Mucosa ◽  
Ruminant Animals ◽  
Specific Activities ◽  
Small Intestinal

SummaryTwo groups of six sheep were fed either dried-grass or ground maize-based diets for at least 4 weeks before slaughter. Samples of the small intestinal mucosa and spancreatic tissue were assayed for a-amylase, glucoamylase, maltase and oligo-l,6-glucosidase.The pancreatic tissue contained high activities of α-amylase and much lower activities of glucoamylase, maltase and oligo-1,6-glucosidase. There was no effect of diet on the specific activities of any of these enzymes in the pancreatic tissue.The activity of α-amylase adsorbed on to the mucosa of the small intestine was greatest in the proximal region of the small intestine, the activity generally declining with increasing distance away from the pylorus. There was no diet effect on the absorbed α-amylase activity.Similar patterns of distribution along the small intestine were observed for maltase, glucoamylase and oligo-1,6-glucosidase with the highest activities in t he jejunum. There was no overall effect of diet on glucoamylase or maltase specific activities and glucoamylase total activity, although the total activities of maltase and oligo-1,6-glucosidase were significantly greater for the sheep fed the ground maize-based diet (P < 0·05).It is suggested that ruminant animals may be capable of digesting large amounts of starch in the small intestine through an adaptation in the activity of the host carbohydrases.

scholarly journals Enteral arginase II provides ornithine for citrulline synthesis

2011 ◽  
Vol 300 (1) ◽  
pp. E188-E194 ◽  
Author(s):  
Juan C. Marini ◽  
Bettina Keller ◽  
Inka Cajo Didelija ◽  
Leticia Castillo ◽  
Brendan Lee
Keyword(s):  
Small Intestine ◽  
Stable Isotope ◽  
Transgenic Mice ◽  
Small Intestinal Mucosa ◽  
Wild Type ◽  
Proline Utilization ◽  
Small Intestinal ◽  
Arginase Ii ◽  
Citrulline Synthesis

The synthesis of citrulline from arginine in the small intestine depends on the provision of ornithine. To test the hypothesis that arginase II plays a central role in the supply of ornithine for citrulline synthesis, the contribution of dietary arginine, glutamine, and proline was determined by utilizing multitracer stable isotope protocols in arginase II knockout (AII−/−) and wild-type (WT) mice. The lack of arginase II resulted in a lower citrulline rate of appearance (121 vs. 137 μmol·kg−1·h−1) due to a reduced availability of ornithine; ornithine supplementation was able to restore the rate of citrulline production in AII−/− to levels comparable with WT mice. There were significant differences in the utilization of dietary citrulline precursors. The contribution of dietary arginine to the synthesis of citrulline was reduced from 45 to 10 μmol·kg−1·h−1 due to the lack of arginase II. No enteral utilization of arginine was observed in AII−/− mice (WT = 25 μmol·kg−1·h−1), and the contribution of dietary arginine through plasma ornithine was reduced in the transgenic mice (20 vs. 13 μmol·kg−1·h−1). Dietary glutamine and proline utilization were greater in AII−/− than in WT mice (20 vs. 13 and 1.4 vs. 3.7 μmol·kg−1·h−1, respectively). Most of the contribution of glutamine and proline was enteral rather than through plasma ornithine. The arginase isoform present in the small intestinal mucosa has the role of providing ornithine for citrulline synthesis. The lack of arginase II results in a greater contribution of plasma ornithine and dietary glutamine and proline to the synthesis of citrulline.

scholarly journals Morphology of small intestinal mucosa and intestinal weight change with metabolic type of cattle

2008 ◽  
Vol 53 (No. 10) ◽  
pp. 525-532 ◽  
Author(s):  
R. Zitnan ◽  
J. Voigt ◽  
S. Kuhla ◽  
J. Wegner ◽  
A. Chudy ◽  
...  
Keyword(s):  
Body Weight ◽  
Small Intestine ◽  
Intestinal Mucosa ◽  
High Energy ◽  
Proximal Jejunum ◽  
Small Intestinal Mucosa ◽  
Apparent Digestibility ◽  
Cattle Breeds ◽  
Metabolic Type ◽  
Small Intestinal

The objective of this study was to investigate rumen fermentation, apparent digestibility of nutrients, and morphology of ruminal und intestinal mucosa in two cattle breeds of different metabolic type. From each breed six purebred German Holstein (H) bulls representing the secretion type and six Charolais (CH) bulls representing the accretion type were raised and fattened under identical conditions with <I>semi ad libitum</I> feeding of a high energy diet. The animals were used for a digestion trial started at nine months of age and animals were slaughtered at 18 months of age. Body weight (668 vs. 764 kg, <I>P</I> = 0.011), body weight gain (1 223 vs. 1 385 g/day, <I>P</I> = 0.043), and body protein gain (93 vs. 128 g/day, <I>P</I> = 0.001) were lower in H compared to CH bulls. Protein expense per kg protein accretion was higher in H bulls (13.8 vs. 10.2, <I>P</I> = 0.001). No significant differences were found in concentration and pattern of ruminal short chain fatty acid and in apparent digestibility of organic matter, crude fibre, and N-free extracts. There were no significant differencs in all morphometric traits of rumen mucosa between both cattle breeds. Compared to H, the villi of CH bulls were higher in duodenum (586 vs. 495 &mu;m, <I>P</I> = 0.001) and proximal jejunum (598 vs. 518&mu;m, <I>P</I> < 0.001), the crypt were deeper in duodenum (295 vs. 358, <I>P</I>< 0.001) and proximal jejunum (292 vs. 344 &mu;m, <I>P</I> = 0.020). In contrast, the villi in ileum were higher in H (522 vs. 471 &mu;m, <I>P</I> = 0.006). The weight of total small intestine, as percentage of total body weight, was 1.1 in H and 0.8 in CH (<I>P</I> = 0.002). The utilization of food crude protein was positively related to the duodenal (<I>P</I> = 0.001) and proximal jejunal villus height (<I>P</I> = 0.003) and to the duodenal crypt depth (<I>P</I> < 0.001) and negatively related to weight of small intestine (<I>P</I> = 0.004). It is concluded, that the higher growth potential and feed efficiency in CH bulls compared to H bulls is not caused by differences in digestion processes, but in size of small intestine, and morphology of small intestinal mucosa. Obviously the duodenum and proximal jejunum of CH bulls adapt to increase the absorptive surface due to the increase in nutrient demand.

scholarly journals Obscure Gastrointestinal Bleeding Due to a Small Intestinal Gastrointestinal Stromal Tumor in a Young Adult

2016 ◽  
Vol 10 (3) ◽  
pp. 668-673 ◽  
Author(s):  
Mami Yamamoto ◽  
Kentaroh Yamamoto ◽  
Hirotaka Taketomi ◽  
Fumio Yamamoto ◽  
Hiroshi Yamamoto
Keyword(s):  
Small Intestine ◽  
Gastrointestinal Tract ◽  
Gastrointestinal Bleeding ◽  
Gastrointestinal Stromal Tumor ◽  
Stromal Tumor ◽  
Intestinal Tumors ◽  
Small Bowel Tumors ◽  
Vascular Abnormalities ◽  
Small Intestinal ◽  
Upper Gastrointestinal

The source of most cases of gastrointestinal bleeding is the upper gastrointestinal tract. Since bleeding from the small intestine is very rare and difficult to diagnose, time is required to identify the source. Among small intestine bleeds, vascular abnormalities account for 70–80%, followed by small intestine tumors that account for 5–10%. The reported peak age of the onset of small intestinal tumors is about 50 years. Furthermore, rare small bowel tumors account for only 1–2% of all gastrointestinal tumors. We describe a 29-year-old man who presented with obscure anemia due to gastrointestinal bleeding and underwent laparotomy. Surgical findings revealed a well-circumscribed lesion measuring 45 × 40 mm in the jejunum that initially appeared similar to diverticulosis with an abscess. However, the postoperative pathological diagnosis was a gastrointestinal stromal tumor with extramural growth.

scholarly journals Influence of ethanol on the activity of glycosidases in rats exposed to cadmium (Cd2+).

1995 ◽  
Vol 42 (3) ◽  
pp. 297-299
Author(s):  
L P Arciuch ◽  
A Omasta ◽  
K Rostkowska ◽  
M Gałazyn-Sidorczuk ◽  
J Moniuszko-Jakoniuk ◽  
...  
Keyword(s):  
Small Intestine ◽  
Intestinal Mucosa ◽  
Small Intestinal Mucosa ◽  
Distinct Effect ◽  
Small Intestinal ◽  
Beta Galactosidase

Inhibition by ethanol of the activities of lysosomal exoglycosidases in stomach, small intestine, liver and brain of rats exposed to cadmium (Cd2+) was determined. Out of the glycosidases tested the most distinct effect of Cd2+ and ethanol administered to the rats in vivo was observed in the small intestinal mucosa in a decreasing order: N-acetyl-beta-hexosaminidase, beta-galactosidase and alpha-fucosidase.

scholarly journals Lentinan Attenuates Damage of the Small Intestinal Mucosa, Liver, and Lung in Mice with Gut-Origin Sepsis

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Zhongshen Kuang ◽  
Tingting Jin ◽  
ChangYi Wu ◽  
Yanan Zong ◽  
Panpan Yin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Small Intestine ◽  
Liver Function ◽  
Signaling Pathway ◽  
Intestinal Mucosa ◽  
Bacterial Translocation ◽  
Sham Operation ◽  
Small Intestinal Mucosa ◽  
Stress Injury ◽  
Small Intestinal

This study is aimed at exploring the effects of lentinan on small intestinal mucosa as well as lung and liver injury in mice with gut-origin sepsis. Cecal ligation and perforation (CLP) were used to construct a mouse model of gut-origin sepsis. The mice were randomly divided into six groups: sham operation group (sham), gut-origin sepsis model group (CLP), ulinastatin-positive drug control group (UTI), lentinan low concentration group (LTN-L, 5 mg/kg), lentinan medium concentration group (LTN-M, 10 mg/kg), and lentinan high concentration group (LTN-H, 20 mg/kg). H&E staining was used to detect the pathological damage of the small intestine, liver, and lung. The serum of mice in each group was collected to detect the expression changes of inflammatory cytokines, oxidative stress biomarkers, and liver function indexes. In vitro assessment of bacterial translocation was achieved through inoculated culture media. Western blot and RT-qPCR were used to detect the expression of molecules related to the NF-κB signaling pathway in the small intestine tissues of mice. The results showed that compared with the CLP group, the injury degree of the small intestine, liver, and lung in mice with gut-origin sepsis was improved with the increase of lentinan concentration. In addition, TNF-α, IL-1β, IL-6, and HMGB1 were decreased with the increase of lentinan concentration, but the expression of IL-10 was increased. Lentinan could also reduce the expression of oxidative stress injury indexes and liver function indexes and inhibit bacterial translocation to liver and lung tissues. Further mechanism investigation revealed that lentinan downregulated the expression of the NF-κB signaling pathway molecules (NF-κB, TLR4, and Bax) and upregulated the expression of occludin and Bcl-2. In conclusion, lentinan inhibits the activity of the NF-κB signaling pathway, thus attenuating injuries of small intestinal mucosa and liver and lung in mice with gut-origin sepsis and reducing the inflammatory response in the process of sepsis.

Essential fatty acid deficiency in mice impairs lactose digestion

2008 ◽  
Vol 295 (3) ◽  
pp. G605-G613 ◽  
Author(s):  
S. Lukovac ◽  
E. L. Los ◽  
F. Stellaard ◽  
E. H. H. M. Rings ◽  
H. J. Verkade
Keyword(s):  
Small Intestine ◽  
Fatty Acid ◽  
Mrna Expression ◽  
Essential Fatty Acid ◽  
Intestinal Mucosa ◽  
Intestinal Morphology ◽  
Lactase Activity ◽  
Intestinal Histology ◽  
Fat Malabsorption ◽  
Small Intestinal

Essential fatty acid (EFA) deficiency in mice induces fat malabsorption. We previously reported indications that the underlying mechanism is located at the level of the intestinal mucosa. We have investigated the effects of EFA deficiency on small intestinal morphology and function. Mice were fed an EFA-deficient or control diet for 8 wk. A 72-h fat balance, the EFA status, and small intestinal histology were determined. Carbohydrate absorptive and digestive capacities were assessed by stable isotope methodology after administration of [U-13C]glucose and [1-13C]lactose. The mRNA expression and enzyme activity of lactase, and concentrations of the EFA linoleic acid (LA) were measured in small intestinal mucosa. Mice fed the EFA-deficient diet were markedly EFA-deficient with a profound fat malabsorption. EFA deficiency did not affect the histology or proliferative capacity of the small intestine. Blood [13C6]glucose appearance and disappearance were similar in both groups, indicating unaffected monosaccharide absorption. In contrast, blood appearance of [13C]glucose, originating from [1-13C]lactose, was delayed in EFA-deficient mice. EFA deficiency profoundly reduced lactase activity (−58%, P < 0.01) and mRNA expression (−55%, P < 0.01) in mid-small intestine. Both lactase activity and its mRNA expression strongly correlated with mucosal LA concentrations ( r = 0.77 and 0.79, respectively, P < 0.01). EFA deficiency in mice inhibits the capacity to digest lactose but does not affect small intestinal histology. These data underscore the observation that EFA deficiency functionally impairs the small intestine, which in part may be mediated by low LA levels in the enterocytes.

scholarly journals Notch2 signaling is required for proper mast cell distribution and mucosal immunity in the intestine

Blood ◽  
2011 ◽  
Vol 117 (1) ◽  
pp. 128-134 ◽  
Author(s):  
Mamiko Sakata-Yanagimoto ◽  
Toru Sakai ◽  
Yasuyuki Miyake ◽  
Toshiki I. Saito ◽  
Haruhiko Maruyama ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Mast Cell ◽  
Small Intestine ◽  
Mast Cells ◽  
Lamina Propria ◽  
Conditional Knockout ◽  
Small Intestinal Mucosa ◽  
Epithelial Layer ◽  
Strongyloides Venezuelensis ◽  
Small Intestinal

Abstract Notch receptor-mediated signaling is involved in the developmental process and functional modulation of lymphocytes, as well as in mast cell differentiation. Here, we investigated whether Notch signaling is required for antipathogen host defense regulated by mast cells. Mast cells were rarely found in the small intestine of wild-type C57BL/6 mice but accumulated abnormally in the lamina propria of the small-intestinal mucosa of the Notch2-conditional knockout mice in naive status. When transplanted into mast cell–deficient Wsh/Wsh mice, Notch2-null bone marrow-derived mast cells were rarely found within the epithelial layer but abnormally localized to the lamina propria, whereas control bone marrow-derived mast cells were mainly found within the epithelial layer. After the infection of Notch2 knockout and control mice with L3 larvae of Strongyloides venezuelensis, the abundant number of mast cells was rapidly mobilized to the epithelial layer in the control mice. In contrast, mast cells were massively accumulated in the lamina propria of the small intestinal mucosa in Notch2-conditional knockout mice, accompanied by impaired eradication of Strongyloides venezuelensis. These findings indicate that cell-autonomous Notch2 signaling in mast cells is required for proper localization of intestinal mast cells and further imply a critical role of Notch signaling in the host-pathogen interface in the small intestine.

scholarly journals Effect of a High-Fat Diet on the Small-Intestinal Environment and Mucosal Integrity in the Gut-Liver Axis

Cells ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 3168
Author(s):  
Takashi Nakanishi ◽  
Hirokazu Fukui ◽  
Xuan Wang ◽  
Shin Nishiumi ◽  
Haruka Yokota ◽  
...  
Keyword(s):  
Small Intestine ◽  
Bile Acids ◽  
High Fat Diet ◽  
Small Intestinal Mucosa ◽  
High Fat ◽  
Mucosal Permeability ◽  
Mucosal Integrity ◽  
Junction Molecules ◽  
Intestinal Contents ◽  
Small Intestinal

Although high-fat diet (HFD)-related dysbiosis is involved in the development of steatohepatitis, its pathophysiology especially in the small intestine remains unclear. We comprehensively investigated not only the liver pathology but also the microbiome profile, mucosal integrity and luminal environment in the small intestine of mice with HFD-induced obesity. C57BL/6J mice were fed either a normal diet or an HFD, and their small-intestinal contents were subjected to microbial 16S rDNA analysis. Intestinal mucosal permeability was evaluated by FITC-dextran assay. The levels of bile acids in the small-intestinal contents were measured by liquid chromatography/mass spectrometry. The expression of tight junction molecules, antimicrobial peptides, lipopolysaccharide and macrophage marker F4/80 in the small intestine and/or liver was examined by real-time RT-PCR and immunohistochemistry. The abundance of Lactobacillus was markedly increased and that of Clostridium was drastically decreased in the small intestine of mice fed the HFD. The level of conjugated taurocholic acid was significantly increased and those of deconjugated cholic acid/secondary bile acids were conversely decreased in the small-intestinal contents. The expression of occludin, antimicrobial Reg IIIβ/γ and IL-22 was significantly decreased in the small intestine of HFD-fed mice, and the intestinal permeability was significantly accelerated. Infiltration of lipopolysaccharide was significantly increased in not only the small-intestinal mucosa but also the liver of HFD-fed mice, and fat drops were apparently accumulated in the liver. Pathophysiological alteration of the luminal environment in the small intestine resulting from a HFD is closely associated with minimal inflammation involving the gut-liver axis through disturbance of small-intestinal mucosal integrity.

Sign in / Sign up

Export Citation Format

Share Document