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A man in his 60s had end-stage alcoholic cirrhosis. About six months before his death, hepatic peribiliary cysts (HPBC) rapidly increased, and he developed jaundice and liver failure. The pathological autopsy performed after his death revealed that his intrahepatic bile duct was pressured due to multiple cysts caused by HPBC, which resulted in liver failure. Some cases of HPBC have been associated with alcoholic cirrhosis;however, no other cases of increased HPBC in a short period of time have been reported. Although identifying the cause of increased HPBC in a short time is difficult in this case, it may be have been caused by continuous alcohol drinking after the onset of HPBC. Most patients with HPBC have liver cirrhosis and obstructive jaundice that may promote liver failure as in this case. Therefore, patients with HPBC should not only be instructed for abstinence but also promptly consider effective treatments in the event of obstructive jaundice to prevent liver dysfunction.

We report a case of endoscopic stent placement to alleviate afferent loop syndrome following recurrence of pancreatic cancer. A 73-year-old man who had undergone pancreatic duodenectomy with portal vein resection for pancreatic cancer had developed a local recurrence and was treated with chemotherapy. He developed a high-grade fever and general fatigue, and laboratory data revealed anemia and a high inflammatory reaction; therefore, he was admitted to our hospital. CT scans revealed intestinal stenosis and upper dilatation, known as afferent loop syndrome, caused by the recurrence. We safely implanted a metallic stent(non-covered Niti-S stent, Century Medical, Inc.)at the point of intestinal stenosis using a double balloon endoscope. As the stent was adequately expanded and the afferent loop syndrome was relieved, the patient was discharged with a better quality of life and there were no complications associated with the stent until he died 6 months later.

We report the case of a man in his 50s who was diagnosed with Crohn's colitis in his 30s and who presented with post-prandial lower abdominal pain in January, 20XX. Colonoscopy and abdominal contrast-enhanced computed tomography revealed abscesses around the sigmoid colon. Although his response to antibiotics was poor, treatment with a combination of antibiotics and adalimumab resolved the abscesses. Nine months later, however, the abscesses around the sigmoid colon recurred. Treatment comprising bowel rest and antibiotics led to immediate improvement of the symptoms. We report a case of effective anti-tumor necrosis factor-α therapy in Crohn's colitis with abscesses around the sigmoid colon.

A 62-year-old man was referred to our hospital with dysphagia. Blood examination revealed significantly elevated serum CA19-9 levels but normal CEA and SCC levels. Imaging uncovered thoracic esophageal cancer with lung and bone metastasis, and subsequent endoscopic biopsy specimens of the primary esophageal tumor showed poorly differentiated squamous cell carcinoma. The patient underwent palliative chemoradiotherapy, but died due to progression of multiple metastases and increasing serum CA19-9 levels. Autopsy revealed adenocarcinoma in multiple metastatic foci, although the squamous component had disappeared in the primary and metastatic lesions. Therefore, we concluded that the adenocarcinoma component of adenosquamous cell carcinoma was refractory to chemoradiotherapy.

We examined the psychometric properties of the Japanese version of the Autism Spectrum Screening Questionnaire (ASSQ) and developed a short-form. This study included 157 children with autism spectrum disorders (ASD, ages 7-18, 128 boys) and 4,101 healthy controls (ages 7-15, 3,344 boys) from a general population with a controlled male-female ratio. Four factors (Unusual Interests, Sociality, Peer Relations, and Repetitive Behaviors) were extracted by exploratory factor analysis of control group data. Confirmatory factor analysis revealed that the 4-factor model fit well with data for another sample of the control and ASD groups. Logistic analysis showed that the former 3 factors could significantly predict ASD diagnosis. Thus, a short form of the ASSQ was developed, consisting of 11 items for these 3 factors. This short form showed sufficient internal consistency and high discrimination power for ASD diagnosis that was comparable to that of the 22-item version. Receiver operating characteristic analysis indicated an optimal cut-off of 7 for the 22-item version (sensitivity .949, specificity .801) and 5 for the short-form (sensitivity .936, specificity .818).

A woman in her 60s was referred to our department with advanced rectal cancer and multiple unresectable metastases of the liver and peritoneum. She had been diagnosed with idiopathic thrombocytopenic purpura (ITP) in her 20s, with a platelet count maintained at approximately 1.0×10(4)/μL by prednisolone; on admission, her platelet count was 0.9×10(4)/μL. Romiplostim, a thrombopoietin receptor agonist, was administered prior to chemotherapy. Her platelet count increased to approximately 10.0×10(4)/μL during chemotherapy with oxaliplatin plus capecitabine, and she developed deep venous thrombosis requiring inferior vena cava filter placement and anticoagulation. No other severe adverse events occurred. There is no standard regimen for the treatment of solid tumors in patients with ITP. This is the first reported case of the concomitant use of romiplostim and chemotherapy for advanced rectal cancer. We believe that romiplostim can effectively salvage the platelet count in emergency situations such as during chemotherapy.

Cancer stem cells (CSCs) represent a subpopulation of tumour cells endowed with self-renewal and multi-lineage differentiation capacity. Clinically, drug resistance is the most important feature, because CSCs resist conventional cancer therapies and are involved in relapse. Therefore, major clinical challenges towards the complete eradication of minimal residual cancer are likely to target CSCs. Several molecules have been investigated as a target: specific signal transduction, cell surface marker, and microenviromental factors. Several drugs (salinomycin, metformin) have been also identified by chemical screening. For clinical use, however, more precise molecular mechanisms remain to be clarified.

A 48-year-old man with locally advanced pancreatic cancer underwent combined treatment with gemcitabine and proton radiation therapy. Because of subsequent obstruction of the common bile duct, a metallic biliary stent was placed and he received further gemcitabine chemotherapy. During chemotherapy, he developed an acute abdomen with a sudden-onset of tarry stool and jaundice. Gastroduodenoscopy revealed hemobilia from the biliary metallic stent. Contrast-enhanced abdominal computed tomography revealed the presence of a pseudoaneurysm arising from the right hepatic artery adjacent to the top of the stent. Hemostasis of the right hepatic artery pseudoaneurysm was achieved via transcatheter arterial embolization using cyanoacrylate.

The present study examines the relationship among inattentive, and hyperactive-impulsive behavior, aggression, and depression in elementary school and junior high school students. The participants were 3,885 children and their teachers and caregivers. Children's inattentive and hyperactive-impulsive behavior was rated by their teachers and caregivers (ADHD-RS). Children rated aggression (HAQ-C) and depression (DSRS-C) themselves. Inattentive and hyperactive-impulsive behavior rated by teachers and caregivers were positively related to aggression and depression. Inattention predicted higher levels of aggression and depression. Inattentive and hyperactive-impulsive behavior as rated by teachers was more highly related to depression than those behaviors as rated by caregivers. The relationships among inattentive, and hyperactive-impulsive behavior, aggression, and depression were almost the same for both elementary school and junior high school students. This study suggests the importance of assessing inattentive and hyperactive-impulsive behavior from multiple views to examine the relationship between inattentive and hyperactive-impulsive behavior and mental health problems.

Tobacco smoking directly or hematogenously acts on digestive organ and induces benign and malignant alimentary diseases. Nicotine, nitrosamines, and polycyclic aromatic hydrocarbons included in tobacco smoke are major causative agents of tobacco smoking-related alimentary diseases. These agents have harmful effects on digestive organ through compromised blood circulation, impaired neural regulation, and cell dysfunction. These malfunctions cause tissue destruction, such as chronic inflammation and ulcer formation. Besides forming DNA adducts, they also act on endogenous signal transduction, leading to gene mutation and abnormal cell death and growth. Interestingly, in inflammatory diseases, smoking improves symptoms of ulcerative colitis, while it worsens the condition of Crohn diseases. Smoking is also involved in lately increasing Barrette's esophagus. Future studies are needed.

Bone mineral density is decreased in inflammatory bowel diseases, which are intractable inflammation in the digestive tract. The causes of decreased bone mineral density are multifactorial including steroid use, insufficiency of nutritional intake, malabsorption in the gastrointestinal tract and activation of mucosal immune system. Insufficient levels of vitamins D and K are reported in patients with inflammatory bowel diseases and are also suggested to be involved in acceleration of intestinal inflammation.

Serologic and fecal biomarkers can be used in the diagnosis and management of inflammatory bowel disease (IBD). Antibodies against Saccharomyces cerevisiae and perinuclear antineutrophil cytoplasmic proteins have been used in diagnosis of IBD, to distinguish Crohn's disease from ulcerative colitis, and to predict the risk of complications of Crohn's disease. C-reactive protein has been used to assess inflammatory processes and predict the course of IBD progression. Fecal markers have been studied for their ability to identify patients with IBD, assess disease activity, and predict relapse. We recently reported that oligosaccharides in IgG and leucin rich alpha 2-glycoprotein are potential biomarkers of IBD. This review addresses the potential for biomarkers to improve treatment strategies and challenges to their use.

This study developed a Japanese version of the Child Social Preference Scale, which measures children's social withdrawal. In addition, we examined developmental changes of children's withdrawal and the relationships between withdrawal and problematic behaviors. The participants were 7 012 mothers of preschool, elementary school, and middle school children. A factor analysis revealed a two-factor solution of shyness and social disinterest, which is consistent with previous studies. Shyness decreased as children's grade level increased. Social disinterest changed in a quadratic manner. The shyness score was lowest in the lower grades of elementary school. Shyness was related to more emotional symptoms, more peer relationship problems, and less prosocial behavior. Social disinterest was related to peer relationship problems. The importance of the distinction between shyness and social disinterest is discussed.

A man in his thirties with epigastric pain was referred to our hospital for detailed examinations. Abdominal computed tomography showed an abdominal cystic lesion with a longest dimension of 7 cm, located behind the stomach. Endoscopic ultrasonography through the stomach showed a cystic lesion and the wall of the lesion revealed continuity to the proper muscle layer of the gastric wall. Therefore, gastric duplication was suspected and the cystic lesion was resected because of the possibility of malignancy and also for a definitive diagnosis. The cystic lesion consisted of columnar ciliated epithelium, seromucous glands, smooth muscle and cartilage and was diagnosed as a bronchogenic cyst. Bronchogenic cysts are sometimes encountered in the thoracic or mediastinal area, but abdominal bronchogenic cysts, such as the present case, are extremely rare.

A man in his seventies visited our hospital due to positive a fecal occult blood test. Colonoscopy showed a submucosal tumor in the rectum covered with reddish and irregular mucosa. Pathological examination of the biopsy specimen revealed well differentiated adenocarcinoma. The tumor was resected, and pathological examination showed carcinoid and adenocarcinoma components coexisting and mixed with each other. Because a previous colonoscopy had shown a submucosal tumor with a smooth surface, this case was diagnosed as a collision tumor of adenocarcinoma which developed on a carcinoid.

A 47-year-old man who was diagnosed as Crohn's disease at the age of 27 became aware of a mass on the forehead. CT and PET scan revealed many scattered tumors in his body. The CEA level was 4424 ng/ml. Primary lesion was not detected by the surveillance of whole gastro-intestinal tract. Liver tumor biopsy samples were histologicaly analyzed and were diagnosed as adenocarcinoma. Further immunohistochemical analysis revealed that the biopsy material had colonic character determined by positive CK20 and negative CK7 staining. Therefore, we performed 12 cycles of mFOLFOX6 chemotherapy. It was effective with the reduced size of tumors and the decreased level of CEA.

Non-steroidal anti-inflammatory drugs(NSAIDs) have a potential to cause mucosal injury in the gastrointestinal tract. Inhibitions of cyclooxygenase, one of the targets of NSAIDs and direct cytotoxic effects of NSAIDs, are reported to be involved in NSAIDs-related mucosal damage. It is estimated that 15-30% of patients taking NSAIDs develop gastroduodenal ulcers, 2% of patients have life-threatening complications. Normal gastroduodenal mucosa expresses only COX-1, and it is reported that NSAIDs are more strongly inhibiting COX-1 are more harmful to gastroduodenal mucosa. Therefore, selective COX-2 inhibitors have been developed as safer NSAIDs than non-selective NSAIDs. Recent reports have, however, shown that COX-2 is expressing in gastroduodenal ulcers and H. pylori infection, suggesting that COX-2 plays an important role in mucosal healing. In this article, we discuss whether COX-2 selective inhibitors are able to prevent NSAIDs-associated ulceration.

It is suggested that nonsteroidal antiinflammatory inhibitors alter the biology of colorectal carcinogenesis. Cyclooxygenase-2, one of target molecules of these drugs, is reported to be upregulated in cancer tissues. Cultured cells which were derived from intestinal epithelium and programmed to express COX-2 showed several phenotypic changes in favor of carcinogenesis, including resistance to apoptosis and enhancement of cell proliferation, angiogenesis, and invasion. Tumor growth implanted in COX-2 null mice was significantly attenuated, but not in COX-1 null or wild type mice, suggesting that COX-2 in stroma also has an important role in tumor growth. Moreover, PGE2, one of COX-2 metabolites, reversed these antitumor effects, indicating that inhibition of PGE2 production has a pivotal role in tumor suppression. However, NSAIDs show antitumor effects in cancer cells lacking COX-1 or COX-2 expression, and some derivatives lacking the ability to suppress COX activity show antitumor effects. These results suggest that COX independent pathway might be involved in antitumor effects of NSAIDs. For the development of novel and effective therapies, it is required to elucidate mechanisms underlying antitumor effects of NSAIDs.

In this review, various aspects of gastrointestinal microcirculation were described. Endothelin-1, vasoconstrictor, is elevated in gastric mucosa, causes gastric ischemia and results in gastric ulceration in human and animals under physical stress. Vasodilators such as NO anticipate the alove actions of endothelin, and thereby protect mucosa from injury. Once ulcer is developed, angiogenesis plays a key role in its healing. Various growth factors, cyclooxygenases-1 and -2, and non-peptide angiogenic factors stimulate this phenomenon and participate in ulcer healing. However, acidic conditions, H. pylori and its product, ammonia, suppress angiogenesis in vitro and in vivo. These evidences may explain why ulcer heals so slowly in gastroduodenal mucosa.

Although many authors reported that proton pump inhibitor showed mucosal protective activity, the precise mechanism is still unclear. In this study, we investigated the effect of proton pump inhibit on gastric mucosal hemodynamics, using a reflectance spectrophotometry system. The proton pump inhibitors had no effect on the gastric mucosal hemodynamics prior to the state of hemorrhagic shock state. However, during the hemorrhagic shock, proton pump inhibitors significantly inhibited the decrease in tissue oxygenation and significantly reduced ulcer formation. In conclusion, proton pump inhibitors maintained tissue oxygenation resulting in reduction of ulcer formation.

Although acute gastric mucosal lesions (AGMLs) develop after the mucosal ischemia and reperfusion, precise intracellular mechanism for the development of AGMLs remains unclear. In the present paper, we investigated intracellular calcium level, lipid peroxidation, and gastric mucosal lesion in rat hemorrhagic shock model. We estimated intracellular calcium by measuring phosphorylase a activity in the gastric mucosa. The mucosal phosphorylase a increased during hemorrhagic shock, while it returned to be normal after the reinfusion of shed blood. Although mucosal lipid peroxide and area of AGMLs did not increase significantly during hemorrhagic shock, they increased significantly after the reinfusion. Diltiazem, a calcium antagonist, prohibited both of the increase in mucosal phosphorylase a activity during hemorrhagic shock and the increase in lipid peroxide content and area of AGMLs after the reinfusion of the shed blood. Organ reflectance spectrophotometry revealed that the gastric corpus suffered mucosal ischemia and hypoxia during the hemorrhagic shock. The are of AGMLs had a good correlation with a level of lipid peroxidation in the gastric mucosa. These results suggest 1) that intracellular free calcium in gastric mucosa increases during the mucosal ischemia; 2) that a calcium antagonist prohibits the increased intracellular free calcium during mucosal ischemia; and 3) that a calcium antagonist prohibits the increased mucosal lipid peroxide and the development of AGMLs after the mucosal reperfusion. Thus it is concluded that the increased intracellular free calcium during ischemia plays a key role in the mucosal tissue injury in the ischemia-reperfusion state.

While gastric mucosa contains prostaglandins and leukotrienes, the roles of these substances in the gastric mucosal protection and damage are not clarified. Using AA-861, a specific 5-lipoxygenase inhibitor, and indomethacin, a cyclooxygenase inhibitor, we investigated the roles of intrinsic prostaglandins and leukotrienes in the gastric circulatory change and the development of gastric lesion induced by ethanol. Rats were fasted for 48 hours and allowed free access to water. After light ether anesthesia, rats were orally given AA-861 (gift from Takeda Chem. Industry; 2.5, 10, 40 or 640 mg/kg), indomethacin (20 mg/kg), and the both or AA-861 (40 mg/kg) and indomethacin (20 mg/kg). Thirty min after the treatment, 2 ml of ethanol (30, 40, 70, 99.5%) was orally administered. Sixty min later, the rats were killed to measure the area of mucosal lesions. The gastric mucosa was damaged by ethanol (greater than or equal to 40%) in a dose-dependent manner. The treatment with AA-861 prohibited the gastric mucosal damage. However, the treatment with indomethacin did not show a significant influence to the mucosal damage. Combined treatment of AA-861 and indomethacin yielded no significant difference from that of single treatment with AA-861 in acute gastric mucosal ulceration. The mucosal blood flow velocity was monitored by laser doppler velocimetry before and after the ethanol administration in the groups treated with vehicle, AA-861 or indomethacin. The blood flow velocity decreased after the administration of 40% ethanol in the group treated with indomethacin, and in a group treated with vehicle.(ABSTRACT TRUNCATED AT 250 WORDS)