The Probiotic, ID-JPL934, Attenuates Dextran Sulfate Sodium-Induced Colitis in Mice Through Inhibition of Proinflammatory Cytokines Expression.

Despite the increasing prevalence of inflammatory bowel disease (IBD), classified as immune-mediated disorders, the exact biological mechanisms leading to its development are undetermined, and treatment strategies remain elusive. Probiotics have been proposed as potential alternatives for treating IBD. The purpose of this research was to find therapeutic candidates of probiotics for colitis. We adopted dextran sulfate sodium (DSS)-induced colitis model to demonstrate the therapeutic effects of ID-JPL934, a mixture of three live bacterial strains at a 1:1:1 ratio: Lactobacillus johnsonii IDCC9203, Lactobacillus plantarum IDCC3501, and Bifidobacterium animalis subspecies lactis IDCC4301, on IBD. The severity was scored according to the disease activity index (DAI) for colitis by observing body weight (BW) and stool status of each mouse once a day. BALB/c mice given 3.5% DSS in drinking water suffered from symptoms of colitis such as weight loss, diarrhea, and bloody excrement. In our study, administration of ID-JPL934 reduced the DAI scores in a dose-dependent manner, and treatments with ID-JPL934 108 and 109 colony-forming unit per mouse per day showed similar inhibition compared with those of sulfasalazine 500 mg per kg BW per day. Moreover, the contraction of colon length improved. ID-JPL934 also suppressed inflammatory lesions such as infiltration of immune cells in mucosa and submucosa, severe crypt damage, and loss of goblet and epithelial cells on the histological analysis. These results might be due to downregulation of the expression of proinflammatory cytokines, including tumor necrosis factor-α, interleukin (IL)-1ß, and IL-6. From these results, ID-JPL934 might be an effective therapeutic candidate for IBD.

Therapeutic effect of tyndallized Lactobacillus rhamnosus IDCC 3201 on atopic dermatitis mediated by down-regulation of immunoglobulin E in NC/Nga mice.

The therapeutic effect of oral administration of Lactobacillus rhamnosus IDCC 3201 tyndallizate (RHT3201) on atopic dermatitis (AD)-like skin lesions in NC/Nga mice were investigated. After induction of dermatitis in NC/Nga mice with house-dust mite extract, each group was fed RHT3201 with 1 × 10(8) , 1 × 10(9) , or 1 × 10(10) cells orally once a day for 8 weeks. Dermatitis scores and frequency of scratching were improved by oral feeding with RHT3201. In contrast to the control group, RHT3201-fed mice showed significantly down-regulated mast cell numbers and serum immunoglobulin E (IgE) concentrations had significantly less IL4 in their axillary lymph node cells. The therapeutic effect of RHT3201 was found to be dose-dependent. These findings indicate that RHT3201 has potential for treating AD.

Endosonographic Features of Gastric Schwannoma: A Single Center Experience.

BACKGROUND/AIMS: Gastric schwannomas are rare benign mesenchymal tumors that are difficult to differentiate from other mesenchymal tumors with malignant potential, such as gastrointestinal stromal tumors. This study aimed to evaluate the characteristic findings of gastric schwannomas via endoscopic ultrasonography (EUS). METHODS: We retrospectively reviewed the EUS findings of 27 gastric schwannoma cases that underwent surgical excision at Pusan National University Hospital during 2007 to 2014. RESULTS: Gastric schwannomas were mainly located in the middle third of the stomach with a mean tumor size of 32 mm. All lesions exhibited hypoechoic echogenicity, and 24 lesions (88.9%) exhibited heterogeneous echogenicity. Seventeen lesions (63.0%) exhibited decreased echogenicity compared to the normal proper muscle layer. Distinct borders were observed in 24 lesions (88.9%), lobulated margins were observed in six lesions (22.2%), and marginal haloes were observed in 24 lesions (88.9%). Hyperechogenic spots were observed in 21 lesions (77.8%), calcifications were observed in one lesion (3.7%), and cystic changes were observed in two lesions (7.4%). CONCLUSIONS: During EUS, gastric schwannomas appear as heterogeneously hypoechoic lesions with decreased echogenicity compared to the normal proper muscle layer. These features may be helpful for differentiating gastric schwannomas from other mesenchymal tumors.

Endoscopic Submucosal Dissection for Gastric Subepithelial Tumors: A Single-Center Experience.

Background and Aims. Endoscopic submucosal dissection (ESD) has been accepted as a treatment modality for gastrointestinal epithelial tumors. Recently, ESD has been applied to resect subepithelial tumors (SETs) in the gastrointestinal tract, but clinical evidence on its efficacy and safety is limited. The aim of this study was to investigate the efficacy and safety of ESD for gastric SETs and to assess possible predictive factors for incomplete resection. Patients and Methods. Between January 2006 and December 2013, a total of 49 patients with gastric SET underwent ESD at our hospital. Clinicopathologic characteristics of patients and SETs, therapeutic outcomes, complications, and follow-up outcomes were evaluated. Results. The overall rates of en bloc resection and complete resection were 88% (43/49) and 84% (43/49), respectively. Complete resection rates in tumors originating from the submucosal layer were significantly higher than those in tumors originating from the muscularis propria layer (90% versus 56%, P = 0.028). In multivariate logistic regression analyses, tumor location (upper third: odds ratio [OR] 12.639, 95% confidence interval [CI] 1.087-146.996, P = 0.043) and layer of tumor origin (muscularis propria: OR 8.174, 95% CI 1.059-63.091, P = 0.044) were independently associated with incomplete resection. Procedure-related bleeding and perforation rates were both 4%. No recurrence was observed in patients with complete resection at a median follow-up period of 29 months (range: 7-83 months). Conclusions. ESD is an effective, safe, and feasible treatment for gastric SETs. The frequency of incomplete resection increases in tumors located in the upper third of the stomach and in those originating from the muscularis propria layer.

Two Cases of Russell Body Gastritis Treated by Helicobacter pylori Eradication.

Russell body gastritis was first defined in 1998, but not many cases have been reported since then. The exact causes and process of this condition are unknown yet; however, considering the reported cases, it has been highly suggested to have correlation with Helicobacter pylori infection. Russell body gastritis has a non-specific clinical presentation of gastritis such as gastric mucosal edema in the macroscopic view. It can be mistaken as xanthoma, signet ring cell carcinoma, or a malignant lymphoma including mucosa-associated lymphoid tissue lymphoma and plasmocytoma. Russell body gastritis features polyclonal immunoglobulin and is differentiated from Mott cancer, of which immune globulin has monoclonal aspect. Authors report here two cases of Russell body gastritis with examined endoscopic findings as well as a review of related literature on the association of all reported cases of Russell body gastritis with H. pylori infection.

[A case of colonic collision tumor (adenocarcinoma and neuroendocrine carcinoma)].

Collision tumors of the colon are rare. A 54-year-old man was referred to our hospital for the evaluation of hematochezia. Colonoscopy demonstrated the presence of about 3 cm sized mass in the rectosigmoid junction. After surgical resection, the colonic lesion was histologically composed of two discrete lesions: adenocarcinoma in the superficial layer and poorly differentiated neuroendocrine carcinoma in the deeper layer. We report this case of colonic collision tumor (adenocarcinoma and neuroendocrine carcinoma) with a review of the literature.

Molecular analysis of constitutive mutations in ermB and ermA selected in vitro from inducibly MLSB-resistant enterococci.

Frequencies of spontaneous mutation from inducible resistance to constitutive resistance were determined for the four clinical isolates of erythromycin-resistant enterococci, including one isolate with ermB gene and three clinical isolates with ermA gene. The rate of ermB mutation was higher than that of ermA mutation by more than 10 fold. Sequence analysis of the regulatory regions of erm genes revealed that mutation type of ermB was just point mutation, by contraries the mutation type of ermA was either deletion or tandem duplication. These results showed distinct characteristics in mutation patterns of ermB and ermA.