Effects of psychological stress on small intestinal motility and expression of cholecystokinin and vasoactive intestinal polypeptide in plasma and small intestine in mice

AIM: To investigate the effects of psychological stress on small intestinal motility and expression of cholecystokinin (CCK) and vasoactive intestinal polypeptide (VIP) in plasma and small intestine, and to explore the relationship between small intestinal motor disorders and gastrointestinal hormones under psychological stress. METHODS: Thirty-six mice were randomly divided into psychological stress group and control group. A mouse model with psychological stress was established by housing the mice with a hungry cat in separate layers of a two-layer cage. A semi-solid colored marker (carbon-ink) was used for monitoring small intestinal transit. CCK and VIP levels in plasma and small intestine in mice were measured by radioimmunoassay (RIA). RESULTS: Small intestinal transit was inhibited (52.18±19.15% vs70.19±17.79%, P<0.01) in mice after psychological stress, compared to the controls. Small intestinal CCK levels in psychological stress mice were significantly lower than those in the control group (0.75±0.53 μg/g vs1.98±1.17 μg/g, P<0.01), whereas plasma CCK concentrations were not different between the groups. VIP levels in small intestine were significantly higher in psychological stress mice than those in the control group (8.45±1.09 μg/g vs7.03±2.36 μg/g, P<0.01), while there was no significant difference in plasma VIP levels between the two groups. CONCLUSION: Psychological stress inhibits the small intestinal transit, probably by down-regulating CCK and up-regulating VIP expression in small intestine.

Exogenous carbon monoxide attenuates inflammatory responses in the small intestine of septic mice

AIM： To determine whether the carbon monoxide （CO）-releasing molecules （CORM）-Iiberated CO sup- press inflammatory responses in the small intestine of septic mice. METHODS： The C57BL/6 mice （male, n = 36; weight 20±2 g） were assigned to four groups in three re- spective experiments. Sepsis in mice was induced by cecal ligation and puncture （CLP） （24 h）. Tricarbonyl- dichlororuthenium （Ⅱ） dimer （CORM-2） （8 mg/kg, i. v.） was administrated immediately after induction of CLP. The levels of inflammatory cytokines [interleukin-1β （IL-1β） and tumor necrosis factor-α （TNF-α）] in tis- sue homogenates were measured with enzyme-linked immunosorbent assay. The levels of malondialdehyde （MDA） in the tissues were determined. The levels of nitric oxide （NO） in tissue homogenate were measured and the expression levels of intercellular adhesion mol- ecule 1 （ICAM-1） and inducible nitric oxide synthase （iNOS） in the small intestine were also assessed. NO and IL-8 levels in the supernatants were determined after the human adenocarcinoma cell line Caco-2 was stimulated by lipopolysaccharide （LPS） （10 g/mL） for 4 h in vitro. RESULTS： At 24 h after CLP, histological analysis showed that the ileum and jejunum from CLP mice in- duced severe edema and sloughing of the villous tips, as well as infiltration of inflammatory cells into the mu- cosa. Semi-quantitative analysis of histological samples of ileum and jejunum showed that granulocyte infil- tration in the septic mice was significantly increased compared to that in the sham group. Administration of CORM-2 significantly decreased granulocyte infiltration. At 24 h after CLP, the tissue MDA levels in the mid- ileum and mid-jejunum significantly increased com- pared to the sham animals （103.68 ± 23.88 nmol/ml vs 39.66 ± 8.23 nmol/mL, 89.66±9.98 nmol/mL vs 32.32 ± 7.43 nmol/mL, P 〈 0.01）. In vitro administra- tion of CORM-2, tissue MDA levels were significantly decreased （50.65±11.46 nmol/mL, 59.32 ± 6.62 nmol/mL, P 〈 0.05）. Meanwhile, the tissue IL-1β and TNF-α levels in the mid-ileum significantly increased compared to the sham animals （6.66±1.09 pg/mL vs 1.67±0.45 pg/mL, 19.34±3.99 pg/mL vs 3.98 ± 0.87 pg/mL, P 〈 0.01）. In vitro administration of CORM-2, tissue IL-1β and TNF-α levels were significantly de- creased （3.87 ± 1.08 pg/mL, 10.45±2.48 pg/mL, P 〈 0.05）. The levels of NO in mid-ileum and mid-jejunum tissue homogenate were also decreased （14.69 ± 2.45 nmol/mL vs 24.36 ± 2.97 nmol/mL, 18.47 ± 2.47 nmol/mL vs 27.33 ± 3.87 nmol/mL, P 〈 0.05）. The ex- pression of iNOS and ICAM-1 in the mid-ileum of septic mice at 24 h after CLP induction significantly increased compared to the sham animals. In vitro administration of CORM-2, expression of iNOS and ICAM-1 were sig- nificantly decreased. In parallel, the levels of NO and IL-8 in the supernatants of Caco-2 stimulated by LPS was markedly decreased in CORM-2-treated Caco-2 cells （2.22 ± 0.12 nmol/mL vs 6.25±1.69 nmol/mL, 24.97 ± 3.01 pg/mL vs 49.45± 5.11 pg/mL, P 〈 0.05）. CONCLUSION： CORM-released CO attenuates the inflammatory cytokine production （IL-1β and TNF-α）, and suppress the oxidative stress in the small intestine during sepsis by interfering with protein expression of ICAM-1 and iNOS.

Carbon liberated from CO-releasing molecules attenuates leukocyte infiltration in the small intestine of thermally injured mice

AIM： To determine whether Carbon （CO） liberated from CO-releasing molecules attenuates leukocyte infiltration in the small intestine of thermally injured mice. METHODS： Thirty-six mice were assigned to four groups. Mice in the sham group （n = 9） were underwent to sham thermal injury; mice in the burn group （n = 9） received 15% total body surface area full-thickness thermal injury; mice in the burn ＋ CORM-2 group （n = 9） were underwent to the same thermal injury with immediate administration of tricarbonyldichlororut henium （11） dimer CORM-2 （8 mg/kg, i.v.）; and mice in the burn＋DMSO group （n = 9） were underwent to the same thermal injury with immediate administration of 160 IJL bolus injection of 0.5% DMSO/saline. Histological alterations and granulocyte infiltration of the small intestine were assessed. Polymorphonuclear neutrophil （PMN） accumulation （myeloperoxidase assay） was assessed in mice mid-ileum. Activation of nuclear factor （NF）-KB, expression levels of intercellular adhesion molecule-1 （ICAM-1） and inducible heme oxygenase in mid-ileum were assessed. RESULTS： Treatment of thermally injured mice with CORM-2 attenuated PMN accumulation and prevented activation of NF-kB in the small intestine. This was accompanied by a decrease in the expression of ICAM-1. In parallel, burn-induced granulocyte infiltration in mid- ileum was markedly decreased in the burn mice treated with CORM-2. CONCLUSION： CORM-released CO attenuates leukocyteinfiltration in the small intestine of thermally injured mice by interfering with NF-KB activation and protein expression of ICAM-1, and therefore suppressing the pro-adhesive phenotype of endothelial cells.

The dynamic distribution of nitric oxide synthase in the small intestine of mice with intestinal radiation sickness

in order to understand the dynamic change of nitric oxide (NO) and its pathological significance during intestinal radiation sickness, we gave mice 60Co γ-ray irradiation and sacrificed them after different periods of survival.The dynamic distribution of nitric oxide synthase (NOS) in the small intestines (duodenum, jejunum and ileum) was studied by using NADPH-diaphorase histochemistry. The results showed that in the animal groups that survived 48 h and 72 h after irradiation (the 48 h and 72 h groups), the number of NOS-positive neuronal bodies and the density of NOS-positive fibers increased obviously in the myenteric plexus and deep muscular plexus as compared with the control group. The neuronal bodies and fibers were stained intensely. The NOS-positive reaction product in the glandular cavities of the intestines and on the mucosa also increased. The results suggest that the activation of NOS or increase of NO production might be one of the main causes of intestinal and vascular dilatation during intestinal radiation sickness.

What are the effects of proton pump inhibitors on the small intestine?

Generally, proton-pump inhibitors(PPIs) have great benefit for patients with acid related disease with less frequently occurring side effects. According to a recent report, PPIs provoke dysbiosis of the small intestinal bacterial flora, exacerbating nonsteroidal anti-inflammatory drug-induced small intestinal injury.Several meta-analyses and systematic reviews have reported that patients treated with PPIs, as well as post-gastrectomy patients, have a higher frequency of small intestinal bacterial overgrowth(SIBO) compared to patients who lack the aforementioned conditions.Furthermore, there is insufficient evidence that these conditions induce Clostridium difficile infection. At this time, PPI-induced dysbiosis is considered a type of SIBO. It now seems likely that intestinal bacterial flora influence many diseases, such as inflammatory bowel disease, diabetes mellitus, obesity, nonalcoholic fatty liver disease, and autoimmune diseases.When attempting to control intestinal bacterial flora with probiotics, prebiotics, and fecal microbiota transplantation, etc., the influence of acid suppression therapy, especially PPIs, should not be overlooked.

Titanium dioxide induced inflammation in the small intestine

AIM:To investigate the effects of titanium dioxide (TiO2) nanoparticles (NPTiO 2 ) and microparticles (MPTiO 2 ) on the inflammatory response in the small intestine of mice. METHODS: Bl 57/6 male mice received distilled water suspensions containing TiO 2 (100 mg/kg body weight) as NPTiO 2 (66 nm), or MPTiO 2 (260 nm) by gavage for 10 d, once a day; the control group received only distilled water. At the end of the treatment the duodenum, jejunum and ileum were extracted for assessment of cytokines, inflammatory cells and titanium content. The cytokines interleukin (IL)-1b, IL-4, IL-6, IL-8, IL-10, IL-12, IL-13, IL-17, IL-23, tumor necrosis factor-α (TNF-α), intracellular interferon-γ (IFN-γ) and transforming growth factor-β (TGF-β) were evaluated by enzyme-linked immunosorbent assay in segments of jejunum and ileum (mucosa and underlying muscular tissue). CD4 + and CD8 + T cells, natural killer cells, and dendritic cells were evaluated in duodenum, jejunum and ileum samples fixed in 10% formalin by immuno-histochemistry. The titanium content was determined by inductively coupled plasma atomic emission spectrometry. RESULTS: We found increased levels of T CD4 + cells (cells/mm 2 ) in duodenum:NP 1240 ± 139.4, MP 1070 ± 154.7 vs 458 ± 50.39 (P < 0.01); jejunum:NP 908.4 ± 130.3, MP 813.8 ± 103.8 vs 526.6 ± 61.43 (P < 0.05); and ileum:NP 818.60 ± 123.0, MP 640.1 ± 32.75 vs 466.9 ± 22.4 (P < 0.05). In comparison to the control group, the groups receiving TiO 2 showed a statistically significant increase in the levels of the inflammatory cytokines IL-12, IL-4, IL-23, TNF-α, IFN-γ and TGF-β. The cytokine production was more pronounced in the ileum (mean ± SE):IL-12: NP 33.98 ± 11.76, MP 74.11 ± 25.65 vs 19.06 ± 3.92 (P < 0.05); IL-4: NP 17.36 ± 9.96, MP 22.94 ± 7.47 vs 2.19 ± 0.65 (P < 0.05); IL-23: NP 157.20 ± 75.80, MP 134.50 ± 38.31 vs 22.34 ± 5.81 (P < 0.05); TNFα: NP 3.71 ± 1.33, MP 5.44 ± 1.67 vs 0.99± 019 (P < 0.05); IFNγ: NP 15.85 ± 9.99, MP 34.08 ± 11.44 vs 2.81 ± 0.69 (P < 0.05); and TGF-β: NP 780.70 ± 318.50, MP 1409.00 ± 502.20 vs 205.50 ± 63.93 (P < 0.05). CONCLUSION:Our findings indicate that TiO2 particles induce a Th1-mediated inflammatory response in the small bowel in mice.

Morphological and molecular response of small intestine to lactulose and hydrogen-rich water in female piglets fed Fusarium mycotoxins contaminated diet

Background: Following the intake of Fusarium mycotoxin-contaminated feed,small intestines may be exposed to high levels of toxic substances that can potentially damage intestinal functions in livestock.It is well known that Fusarium mycotoxins will lead a breakdown of the normally impeccable epithelial barrier,resulting in the development of a "leaky" gut.H2 administration with different methods has been proved definitely potentials to prevent serious intestinal diseases.The goal of this study is to investigate the roles of lactulose(LAC) and hydrogenrich water(HRW) in preventing intestinal dysfunction in piglets fed Fusarium mycotoxin-contaminated feed.Methods: A total of 24 female piglets were evenly assigned to 4 groups: negative control(NC) group,mycotoxincontaminated(MC) feed group,MC feed with LAC treatment(MC + LAC),and MC feed with HRW treatment(MC +HRW),respectively.Piglets in the NC group were fed uncontaminated control diet,while remaining piglets were fed Fusarium mycotoxin-contaminated diet.For the NC and MC groups,10 mL/kg body weight(BW) of hydrogen-free water(HFW) was orally administrated to piglets twice daily;while in the MC + LAC and MC + HRW groups,piglets were treated with the same dose of LAC solution(500 mg/kg BW) and HRW twice daily,respectively.On d 25,serum was collected and used for biochemical analysis.Intestinal tissues were sampled for morphological examination as well as relative genes and protein expression analysis.Results: Our data showed that Fusarium mycotoxins induced higher serum diamine oxidase(DAO) activities(P < 0.05),D-lactic acid levels(P < 0.01),and endotoxin status(P < 0.01),lower villus height(P < 0.01) and ratio of villus height to crypt depth(P < 0.05) in small intestine,greater apoptosis index and higher mRNA expression related to tight junctions(P < 0.05).In addition,the distribution and down-regulation of claudin-3(CLDN3) protein in the small intestinal was also observed.As expected,oral administrations of HRW and LAC were found to remarkably provide beneficial effects against Fusarium mycotoxin-induced apoptosis and intestinal leaking.Moreover,either HRW or LAC treatments were also revealed to prevent abnormal intestinal morphological changes,disintegrate tight junctions,and restore the expression and distribution of CLDN3 protein in the small intestinal mucosal layer in female piglets that were fed Fusarium mycotoxins contaminated diet.Conclusions: Our data suggest that orally administrations of HRW and LAC result in less Fusarium mycotoxininduced apoptosis and leak in the small intestine.Either HRW or LAC treatments could prevent the abnormal changes of intestinal morphology and molecular response of tight junctions as well as restore the distribution and expression of CLDN3 protein of small intestinal mucosa layer in female piglets that were fed Fusarium mycotoxins contaminated diet.

Protective effects of Ligustrazine,Kakonein and Panax Notoginsenoside on the small intestine and immune organs of rats with severe acute pancreatitis

BACKGROUND:Severe acute pancreatitis (SAP) is characterized by fatal pathogenic conditions and a high mortality.It is important to study SAP complicated with multiple organ injury.In this study we compared the protective effects of three traditional Chinese medicines (Ligustrazine,Kakonein and Panax Notoginsenoside) on the small intestine and immune organs (thymus,spleen and lymph nodes) of rats with SAP and explored their mechanism of action.METHODS:One hundred forty-four rats with SAP were randomly divided into model control,Ligustrazine-treated,Kakonein-treated,and Panax Notoginsenoside-treated groups (n=36 per group).Another 36 normal rats comprised the sham-operated group.According to the different time points after operation,the experimental rats in each group were subdivided into 3-,6-and 12-hour subgroups (n=12).At various time points after operation,the mortality rate of rats and pathological changes in the small intestine and immune organs were recorded and the serum amylase levels were measured.RESULTS:Compared to the model control groups,the mortality rates in all treated groups declined and the pathological changes in the small intestine and immune tissues were relieved to different degrees.The serum amylase levels in the three treated groups were significantly lower than those in the model control group at 12 hours.The pathological severity scores for the small intestinal mucosa,thymus and spleen (at 3 and 12 hours) in the Ligustrazine-treated group,for the thymus (at 3 and 12 hours) and spleen (at 3 and 6 hours) in the Kakonein-treated group,and for the thymus (at 3 hours)and spleen (at 3 hours) in the Panax Notoginsenoside-treated group were significantly lower than those in the model control group.The pathological severity scores of the small intestinal mucosa (at 6 and 12 hours) and thymus (at 6 hours) in the Ligustrazine-treated group were significantly lower than those in the Kakonein-and Panax Notoginsenoside-treated groups.CONCLUSIONS:All the three traditional Chinese drugs significantly alleviated the pathological changes in the small intestine and immune organs of SAP rats.Ligustrazine was the most effective one among them.

Epidemiology of cancer of the small intestine

Cancer of the small intestine is very uncommon.There are 4 main histological subtypes:adenocarcinomas,carcinoid tumors,lymphoma and sarcoma.The incidence of small intestine cancer has increased over the past several decades with a four-fold increase for carcinoid tumors,less dramatic rises for adenocarcinoma and lymphoma and stable sarcoma rates.Very little is known about its etiology.An increased risk has been noted for individuals with Crohn's disease,celiac disease,adenoma,familial adenomatous polyposis and Peutz-Jeghers syndrome.Several behavioral risk factors including consumption of red or smoked meat,saturated fat,obesity and smoking have been suggested.The prognosis for carcinomas of the small intestine cancer is poor(5 years relative survival < 30%),better for lymphomas and sarcomas,and best for carcinoid tumors.There has been no signif icant change in longterm survival rates for any of the 4 histological subtypes.Currently,with the possible exceptions of obesity and cigarette smoking,there are no established modifiable risk factors which might provide the foundation for a prevention program aimed at reducing the incidence and mortality of cancers of the small intestine.More research with better quality and sufficient statistical power is needed to get better understanding of the etiology and biology of this cancer.In addition,more studies should be done to assess not only exposures of interest,but also host susceptibility.

Effect of emodin on small intestinal peristalsis of mice and relevant mechanism

AIM: To investigate the effect of emodin on small intestinal peristalsis of mice and to explore its relevant mechanisms.METHODS: The effect of emodin on small intestinal peristalsis of mice was observed by charcoal powder propelling test of small intestine. The contents of motilin and somatostatin in small intestine of mice were determinated by radioimmunoassay. The electrical potential difference (PD) related to Na+ and glucose transport was measured across the wall of reverted intestinal sacs. Na+-K+-ATPase activity of small intestinal mucosa was measured by spectroscopic analysis.RESULTS: Different dosages of emodin can improve small intestinal peristalsis of mice. Emodin increased the content of motilin, while reduced the content of somatostatin in small intestine of mice significantly. Emodin 0.2, 0.4, 0.8, and 1.6 g/L decreased PD when there was glucose. However, emodin had little effect when glucose was free. The Na+-K+-ATPase activity of small intestinal mucosa of mice in emodin groups was inhibited obviously. CONCLUSION: Emodin can enhance the function of small intestinal peristalsis of mice by mechanisms of promoting secretion of motilin, lowering the content of somatostatin and inhibiting Na+-K+-ATPase activity of small intestinal mucosa.

Multiple chronic non-specific ulcer of small intestine characterized by anemia and hypoalbuminemia

A female patient with anemia and hypoalbuminemia was admitted to our hospital due to an over 20-year history of recurrent dizziness,fatigue and ankle edema.She was diagnosed as multiple chronic nonspecific ulcer of the small intestine characterized by non-specific histology and persistent gastrointestinal bleeding.

Giant primary angiosarcoma of the small intestine showing severe sepsis

Primary malignant tumors of the small intestine are rare, comprising less than 2% of all gastrointestinal tumors. An 85-year-old woman was admitted with fever of 40&#x02005;&#x02005;&#x000b0;C and marked abdominal distension. Her medical history was unremarkable, but blood examination showed elevated inflammatory markers. Abdominal computed tomography showed a giant tumor with central necrosis, extending from the epigastrium to the pelvic cavity. Giant gastrointestinal stromal tumor of the small intestine communicating with the gastrointestinal tract or with superimposed infection was suspected. Because no improvement occurred in response to antibiotics, surgery was performed. Laparotomy revealed giant hemorrhagic tumor adherent to the small intestine and occupying the peritoneal cavity. The giant tumor was a solid tumor weighing 3490 g, measuring 24 cm &#x000d7; 17.5 cm &#x000d7; 18 cm and showing marked necrosis. Histologically, the tumor comprised spindle-shaped cells with anaplastic large nuclei. Immunohistochemical studies showed tumor cells positive for vimentin, CD31, and factor VIII-related antigen, but negative for c-kit and CD34. Angiosarcoma was diagnosed. Although no postoperative complications occurred, the patient experienced enlargement of multiple metastatic tumors in the abdominal cavity and died 42 d postoperatively. The prognosis of small intestinal angiosarcoma is very poor, even after volume-reducing palliative surgery.

Opiate-induced constipation related to activation of small intestine opioid μ2-receptors

AIM： To investigate the role of opioid p-receptor subtype in opiate-induced constipation （OIC）.METHODS： The effect of Ioperamide on intestinal transit was investigated in mice. Ileum strips were isolated from 12-wk-old male BALB/c mice for identification of isometric tension. The ileum strips were precontracted with 1 μmol/L acetylcholine （ACh）. Then, decrease in muscle tone （relaxation） was characterized after cumu- lative administration of 0.1-10μ~mol/L Ioperamide into the organ bath, for a concentration-dependent study. Specific blockers or antagonists were used for pretreat- ment to compare the changes in Ioperamide-induced relaxation.RESULTS： In addition to the delay in intestinal transit, Ioperamide produced a marked relaxation in isolated ileum precontracted with ACh, in a dose-dependent manner. This relaxation was abolished by cyprodime,a selective opioid p-receptor antagonist, but not modified by naloxonazine at a dose sufficient to block opioid μ-1 receptors. Also, treatment with opioid μ-1 receptor agonist failed to modify the muscle tone. Moreover, the relaxation by Ioperamide was attenuated by glibenclamide at a dose sufficient to block ATP-sensitive K^＋ （KATP） channels, and by protein kinase A （PKA） inhibitor, but was enhanced by an inhibitor of phosphodiesterase for cyclic adenosine monophosphate （cAMP）.CONCLUSION： Loperamide induces intestinal relaxa- tion by activation of opioid μ-2 receptors via the cAMP- PKA pathway to open KATp channels, relates to OIC.

Small intestine bacterial overgrowth and irritable bowel syndrome-related symptoms:Experience with Rifaximin

AIM： TO estimate the prevalence of small intestinal bacterial overgrowth （SIBO） in our geographical area （Western Sicily, Italy） by means of an observational study, and to gather information on the use of locally active, non-absorbable antibiotics for treatment of SIBO.METHODS： Our survey included 115 patients fulfilling the Rome II criteria for diagnosis of irritable bowel syndrome （IBS）; a total of 97 patients accepted to perform a breath test with lactulose （BTLact）, and those who had a positive test, received Rifaximin （Normix , Alfa Wassermann） 1200 mg/d for 7 d; 3 wk after the end of treatment, the BTLact was repeated.RESULTS： Based on the BTLact results, SIBO was present in about 56% of IBS patients, and it was responsible for some IBS-related symptoms, such as abdominal bloating and discomfort, and diarrhoea. 1-wk treatment with Rifaximin turned the BTLact to negative in about 50% of patients and significantly reduced the symptoms, especially in those patients with an alternated constipation/diarrhoea-variant IBS. CONCLUSION： SIBO should be always suspected in patients with IBS, and a differential diagnosis is done by means of a ＂breath test＂. Rifaximin may represent a valid approach to the treatment of SIBO.

Effects of psychological stress on small intestinal motility and bacteria and mucosa in mice

AIM: To investigate the effects of psychological stress on small intestinal motility and bacteria and mucosa in mice, and to explore the relationship between small intestinal dysfunction and small intestinal motility and bacteria and mucosa under psychological stress. METHODS: Sixty mice were randomly divided into psychological stress group and control group. Each group were subdivided into small intestinal motility group (n= 10), bacteria group (n = 10), and D-xylose administered to stomach group (n= 10). An animal model with psychological stress was established housing the mice with a hungry cat in separate layers of a two-layer cage. A semi-solid colored marker (carbon-ink) was used for monitoring small intestinal transit. The proximal small intestine was harvested under sterile condition and processed for quantitation for aerobes (Escherichia coli) and anaerobes (Lactobacilli). The quantitation of bacteria was expressed as Iog10(colony forming units/g). D-xylose levels in plasma were measured for estimating trie damage of small intestinal mucosa. RESULTS: Small intestinal transit was inhibited (39.80±9.50% vs 58.79±11.47%,P<0.01) in mice after psychological stress, compared with the controls. Psychological stress resulted in quantitative alterations in the aerobes (E.coli). There was an increase in the number of E coli in the proximal small intestinal flora (1.78±0.30 log10(CFU/g) vs 1.37±0.21 log10(CFU/g), P<0.01), and there was decrease in relative proportion of Lactobacilli and E.coli of stressed mice (0.53±0.63 vs 1.14±1.07,P<0.05), while there was no significant difference in the anaerobes (Lactobacilli) between the two groups (2.31±0.70 log10 (CFU/g) vs 2.44±0.37 log10(CFU/g), P>0.05). D-xylose concentrations in plasma in psychological stress mice were significantly higher than those in the control group (2.90±0.89 mmol/L vs 0.97±0.33 mmol/L, P<0.01). CONCLUSION: Small intestinal dysfunction under psychological stress may be related to the small intestinal motility disorder and dysbacteriosis and the damage of mucosa probably caused by psychological stress.

Multifocal stenosing ulceration of the small intestine

Several reports have described an apparently uncommon clinicopathological disorder that is characterized by multifocal stenosing small-intestinal ulceration.Compared to Crohn's disease,the ulcers are not transmural and typically remain shallow,and involve only the mucosa and submucosa.The disorder seems to be localized in the jejunum and proximal ileum only,and not the distal ileum or colon.Only nonspecif ic inflammatory changes are present without giant cells or other typical features of granulomatous inflammation.Most patients present clinically with recurrent obstructive events that usually respond to steroids,surgical resection,or both.With the development of newer imaging modalities to visualize the small-intestinal mucosa,such as double-balloon enteroscopy,improved understanding of the long-term natural history of this apparently distinctive disorder should emerge.

Small intestine bleeding due to multifocal angiosarcoma

We report a case of an 84-year-old male patient with primary small intestinal angiosarcoma.The patient initially presented with anemia and melena.Consecutive endoscopy revealed no signs of upper or lower active gastrointestinal bleeding.The patient had been diagnosed 3 years previously with an aortic dilation,which was treated with a stent.Computed tomography suggested an aorto-intestinal fistula as the cause of the intestinal bleeding,leading to operative stent explantation and aortic replacement.However,an aorto-intestinal fistula was not found,and the intestinal bleeding did not arrest postoperatively.The constant need for blood transfusions made an exploratory laparotomy imperative,which showed multiple bleeding sites,predominately in the jejunal wall.A distal loop jejunostomy was conducted to contain the small intestinal bleeding and a segmental resection for histological evaluation was performed.The histological analysis revealed a lessdifferentiated tumor with characteristic CD31,cytokeratin,and vimentin expression,which led to the diagnosis of small intestinal angiosarcoma.Consequently,the infiltrated part of the jejunum was successfully resected in a subsequent operation,and adjuvant chemotherapy with paclitaxel was planned.Angiosarcoma of the small intestine is an extremely rare malignant neoplasm that presents with bleeding and high mortality.Early diagnosis and treatment are essential to improve outcome.A small intestinal angiosarcoma is a challenging diagnosis to make because of its rarity,nonspecific symptoms of altered intestinal function,nonspecific abdominal pain,severe melena,and acute abdominal signs.Therefore,a quick clinical and histological diagnosis and decisive measures including surgery and adjuvant chemotherapy should be the aim.

Heterogeneity across the murine small and large intestine

The small and large intestine of the gastrointestinal tract(GIT) have evolved to have discrete functions with distinct anatomies and immune cell composition.The importance of these differences is underlined when considering that different pathogens have uniquely adapted to live in each region of the gut.Furthermore,different regions of the GIT are also associated with differences in susceptibility to diseases such as cancer and chronic inflammation.The large and small intestine,given their anatomical and functional differences,should be seen as two separate immunological sites.However,this distinction is often ignored with findings from one area of the GIT being inappropriately extrapolated to the other.Focussing largely on the murine small and large intestine,this review addresses the literature relating to the immunology and biology of the two sites,drawing comparisons between them and clarifying similarities and differences.We also highlight the gaps in our understanding and where further research is needed.

Clinical outcomes of enteroscopy using the double-balloon method for strictures of the small intestine

AIM:To evaluate the clinical outcome of enteroscopy, using the double-balloon method, focusing on the involvement of neoplasms in strictures of the small intestine. METHODS: Enteroscopy, using the double-balloon method, was performed between December 1999 and December 2002 at Jichi Medical School Hospital, 3apan and strictures of the small intestine were found in 17 out of 62 patients. These 17 consecutive patients were subjected to analysis. RESULTS: The double-balloon enteroscopy contributed to the diagnosis of small intestinal neoplasms found in 3 out of 17 patients by direct observation of the strictures as well as biopsy sampling. Surgical procedures were chosen for these three patients, while balloon dilation was chosen for the strictures in four patients diagnosed with inflammation without involvement of neoplasm. CONCLUSION: Double-balloon enteroscopy is a useful method for the diagnosis and treatment of strictures in the small bowel.

AN ANALYTICAL SOLUTION FOR THE MODEL OF DRUG DISTRIBUTION AND ABSORPTION IN SMALL INTESTINE

According to the physiological and anatomical characteristics of small intestine,neglecting the effect of its motility on the distribution and absorption of drug and nutrient,Y.Miyamoto et al.proposed a model of two-dimensional laminar flow in a circular porous tube with permeable wall and calculated the concentration profile of drugby numerical analysis.In this paper,we give a steady-state analytical solution of the above model including deactivationterm.The obtained results are in agreement with the results of their numerical analysis. Moreover the analytical solution presented in this paper reveals the relation among the physiological parameters of the model and describes the basic absorption rule of drug and nutrient through the intestinal wall and hence pro- vides a theoretical basis for determining the permeability and reflection coefficient through in situ experiments.