Supporting the resolution of inconsistencies in specifications based on mathematical argumentation theory (Model theoretic aspects of the notion of independence and dimension)

In this paper, we propose a method to support for resolving “inconsistencies” in a requirement specification document which is written in a natural language. We also develop a tool based on the method. We use mathematical argumentation theory and natural language processing to realize the method. Based on mathematical argumentation theory, we can formulate various “inconsistencies” including logical contradiction as an attack relation R in an argumentation framework (A, R). Then an extension S in (A, R) represents a set of acceptable descriptions of a requirement specification document. Moreover, an extension S suggests an engineer the set of descriptions which should be corrected to resolve “inconsistencies” by referring R. Our method consists of the following methods. First, we adopt the method in [1], which is based on natural language processing, to generate an argumentation framework (A, R) from a requirement specification document. Second, we use the method in [2] to define an extension S of (A, R) in an extension of first-order logic, and then we use the method in [3] to enumerate extensions from (A, R) by solving a Partial Maximal Satisfiable Subsets Enumeration problem that is an extension of a Maximal Satisfiable Subsets Enumeration problem. Finally we visualize the (A, R) and S's to support for resolving “inconsistencies” in a requirement specification document

Distribution and Endocrine Morphology of Polypeptide YY (PYY) Containing Cells in the Human Gut

Using human materials, the distribution of PYY containing cells was determined by immunocytochemical methods and discussion was made on their morphological endocrinology. PYY cells were fairly numerous in the lower gastrointestinal tract of man, particularly in the colon and rectum. The cells were also present in the pancreas and duodenum but quite rarely. PYY cells were not observed at all in the lower part of the esophagus, stomach and gall bladder. Their peculiar and characteristic shapes as well as distribution suggest that PYY may have some action (probably specific) on the function of the distal gastrointestinal tract

Preventive Effect of Proglumide on Erosive Gastritis in the Rat

The purpose of this study is to determine whether or not proglumide has a preventive effect on the erosive gastritis induced by sodium salt of taurocholic acid (TCA) in the rat. Its effect on the formation of gastric erosions, serum gastrin levels and secretion of acid and pepsin were also studied. The rats were given standard feed containing 0.25% proglumide and water containing 5mM TCA (experimental E group). The control rats were given standard feed and water containing 5mM TCA (TCA group). All rats were killed at the end of the 3 months. The tissue specimens of the resected gastric mucosa were stained with hematoxylin eosin for histopathology and with azan for evaluation of fibrous ploriferation. From microscopic observation of the stained specimens, the following results were obtained. TCA-group showed long mucosal surface injury (erosion), inflammatory cell infiltration, a reduction in the number of parietal cells, a decrease of mucosal thickness, and proliferation of collagenous fiber. In contrast, in the E group, these morphological and morphoquantitative changes were significantly small. The length of erosion and inflammatory cell infiltration were significantly reduced in the E group when compared with the TCA group. Furthermore, mucosal thickness was almost normal and fibrous proliferation was significantly scarce in the E group. Proglumide had an insignificant effect on pH on the mucosa, volume and pH of gastric juice, serum gastrin levels and tetragastrin-induced secretion of acid and pepsin. It is, thus, evident that proglumide has a preventive effect on the induction of erosive gastritis caused by TCA in the rats. Since it is difficult to explain its mechanism for the prevention of gastritis from only the already known facts that it has protective action on gastric mucosa and an inhibitory effect on secretion of acid and pepsin, unknown mechanisms are suspected to be involved

Endocrine Profile in Rats with Postgastrectomy Malabsorption: a Pilot Study

Abnormal endocrine profile, especially in the enteropancreatic axis, was described in rats with malnutrition caused by malabsorption after total gastrectomy. Insulin, substance P and motilin concentrations at the fasting condition were significantly elevated in malnutritious rats after total gastrectomy when compared to those in control rats. A significant elevation of pancreatic glucagon and motilin was noted after intraduodenal fat administration in malnutritious rats. These data suggest that these peptides of many humoral factors may thus cause abnormal enteropancreatic axis and consequent malnutrition

Induction of Experimental Atrophic Gastritis by N-Methyl-N'-Nitro-N-Nitrosoguanidine or Taurocholic Acid in Donryu Rats

The morphology of the rat (Donryu) gastric mucosa was examined by light microscopy after administration of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) or taurocholic acid (TCA), a component of bile acids. MNNG was given to rats ad libitum from light-sealed bottles for 5 months and deionized water was given freely for 6 months thereafter. TCA was administered to rats freely for 11 months. Deionized water was given to rats as control (non-treated rats). Rats treated with MNNG or TCA and control rats were killed at 11 months after the beginning of the experiment. Using 3 micron tissue samples taken from the area of the gastric mucosa designated before the experiment, hematoxylin and eosin and azan stain were made for histopathological evaluation and fibrosis. Marked atrophic changes, such as reduction in the number of parietal cells, shortened mucosa! length, inflammaotry cell infiltration, and proliferation of fibrosis, were present in the gastric mucosa of rats treated with MNNG as well as TCA. These findings were typical for atrophic gastritis. Such atrophic changes were slight in the gastric mucosa of the control rats. The frequency of tumourous lesions was very low in MNNG-treated rats. We have concluded on the basis of the present data that MNNG as well as TCA can induce atrophic gastritis in Donryu rats

Existence of VIP and PHI-Like Immunoreactivities in the Amphibian Gut

The present paper provides the first definitive evidence on the presence and possible co-existence of VIP- and PHI-like peptides in the peripheral nervous system of the amphibian (bullfrog) gut wall. The possibility of co-existence of the peptides suggests that VIP- and PHI-like peptide may be synthesized from the same precursor protein in the amphibian

Gastrin and Somatostatin in Patients with Hyperchlorhydric Duodenal Ulcer

Hormonal and morphological studies were conducted to ascertain the role played by gastrin and somatostatin in the pathophysiology of duodenal ulcer, in particular hyperchlorhydric duodenal ulcer, using 35 patients with duodenal ulcer, of whom 15 were hyperchlorhydric and 20 were normochlorhydric. Twenty normal subjects with normochlorhydria were used as a control. In patients with hyperchlorhydric duodenal ulcer following significant findings were observed: 1. Basal and stimulated hyperchlorhydria, 2. Parietal cell hyperplasia, 3. Basal hypergastrinemia, 4. Increased concentration of gastrin and large number of G cells (G cell hyperplasia) in the antral mucosa. 5. Mucosal concentration of somatostatin and D cells in the antrum was reduced, but the former in patients with hyperchlorhydric duodenal ulcer was not different from that in patients with normoacidic duodenal ulcer. 6. A significant correlation in mucosal concentration was demonstrated between gastrin and somatostatin in control subjects but not in patients with duodenal ulcer. 7. There was a significant correlation in maximal acidity in gastric secretion and mucosal concentration of antral somatostatin in control subjects but not in patients with duodenal ulcer. 8. Concentration of plasma somatostatin in patients with duodenal ulcer was not different from that in control subjects. These findings indicate that gastrin and somatostatin may participate in the pathophysiology of duodenal ulcer, at least in the subgroup of duodenal ulcer associated with hyperchlorhydria, and the subgroup of duodenal ulcer may be an endocrine disorder

Management of Acute Superior Mesenteric Artery Occlusion by Thrombolytic Therapy

Acute occlusion of the superior mesenteric artery (SMA) causes extensive bowel necrosis, resulting in a poor prognosis with an extremely high mortality rate. An 82-year-old woman was admitted to our hospital with the complaint of abdominal pain. She was diagnosed as having acute SMA occlusion by enhanced CT. Five hours from onset, the first thrombolytic therapy with urokinase was performed, but failed to complete thrombolysis and recanalization of peripheral blood flow. An exploratory laparotomy following the first thrombolytic therapy showed a mild ischemic change in the affected intestine and mesentery, but no sign of necrosis. After the laparotomy, local thrombolytic therapy with angiographic evaluation of blood flow at 24, 36 and 48 h from the first thrombolysis was performed. As a result, the residual thrombus disappeared and all branches of the SMA became well visualized. The patient was discharged well without a second-look operation or major bowel resection. Sequential intermittent thrombolytic therapy with meticulous angiographic evaluation of blood flow is effective for early-stage acute SMA occlusion

Attenuated response to liver injury in moesin-deficient mice: Impaired stellate cell migration and decreased fibrosis

AbstractHepatic stellate cells (HSCs) respond to injury with a coordinated set of events (termed activation), which includes migration and upregulation of matrix protein production. Cell migration requires an intact actin cytoskeleton that is linked to the plasma membrane by ezrin–radixin–moesin (ERM) proteins. We have previously found that the linker protein in HSCs is exclusively moesin. Here, we describe HSC migration and fibrogenesis in moesin-deficient mice. We developed an acute liver injury model that involved focal thermal denaturation and common bile duct ligation. HSC migration and collagen deposition were assessed by immunohistology and quantitative real-time PCR. Activated HSCs were isolated from wild-type or moesin-deficient mice for direct examination of migration. Activated HSCs from wild-type mice were positive for moesin. Migration of moesin-deficient HSCs was significantly reduced. In a culture assay, 22.1% of normal HSCs migrated across a filter in 36h. In contrast, only 1.3% of activated moesin-deficient HSCs migrated. Collagen deposition around the injury area similarly was reduced in moesin-deficient liver. The linker protein moesin is essential for HSC activation and migration in response to injury. Fibrogenesis is coupled to migration and reduced in moesin-deficient mice. Agents that target moesin may be beneficial for chronic progressive fibrosis

First-line pembrolizumab vs chemotherapy in metastatic non-small-cell lung cancer: KEYNOTE-024 Japan subset

This prespecified subanalysis of the global, randomized controlled phase Ill KEYNOTE-024 study of pembrolizumab vs chemotherapy in previously untreated metastatic non-small-cell lung cancer without EGFR/ALK alterations and a programmed death-ligand 1 (PD-L1) tumor proportion score of 50% or greater evaluated clinical outcomes among patients enrolled in Japan. Treatment consisted of pembrolizumab 200 mg every 3 weeks (35 cycles) or platinum-based chemotherapy (four to six cycles). The primary end-point was progression-free survival; secondary end-points included overall survival and safety. Of 305 patients randomized in KEYNOTE-024 overall, 40 patients were enrolled in Japan (all received treatment: pembrolizumab, n = 21; chemotherapy, n = 19). The hazard ratio (HR) for progression-free survival by independent central review (data cut-off date, 10 July 2017) was 0.25 (95% confidence interval [CI], 0.10-0.64; one-sided, nominal P = .001). The HR for overall survival (data cut-off date, 15 February 2019) was 0.39 (95% CI, 0.17-0.91; one-sided, nominal P = .012). Treatment-related adverse events occurred in 21/21 (100%) pembrolizumab-treated and 18/19 (95%) chemotherapy-treated patients; eight patients (38%) and nine patients (47%), respectively, had grade 3-5 events. Immune-mediated adverse events and infusion reactions occurred in 11 patients (52%) and four patients (21%), respectively; four patients (19%) and one patient (5%), respectively, had grade 3-5 events. Consistent with results from KEYNOTE-024 overall, first-line pembrolizumab improved progression-free survival and overall survival vs chemotherapy with manageable safety among Japanese patients with metastatic non-small-cell lung cancer without EGFRIALK alterations and a PD-L1 tumor proportion score of 50% or greater