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Aim: To investigate the efficacy and tolerability of second-line metronidazole triple therapy with vonoprazan (VPZ) for Helicobacter pylori (H. pylori). Methods: We retrospectively reviewed medical records of patients who experienced clarithromycin triple therapy failure and were treated with second-line (20 mg VPZ (n = 274)/30 mg lansoprazole (n = 323) or 10 mg rabeprazole (n = 141) twice daily, 750 mg amoxicillin twice daily, 250 mg metronidazole twice daily for 7 days) eradication therapies. Successful eradication rates were compared between two groups: those receiving VPZ and those receiving a proton pump inhibitor (PPI). Adverse events were also investigated. Results: Successful second-line eradication rates according to ITT analysis and PP analysis, respectively, were 79.9% and 92.4% for VPZ therapy and 83.6% and 93.3% for PPI therapy. There were no significant differences between treatment groups. The eradication rates in those who had received first-line VPZ therapy previously according to ITT and PP analysis were 75.2% and 88.1%, respectively; in contrast, values were 82.5% and 95.4%, respectively, for those who had received first-line PPI therapy previously. In second-line therapy, the overall adverse event rate for VPZ therapy was the same as for PPI therapy. Conclusions: The efficacy and tolerability of metronidazole-containing second-line triple therapy with VPZ or a PPI were equivalent.

Foods reducing postprandial hyperglycemia could suppress the postprandial blood glucose response after the next meal (a "second-meal" effect). However, the second-meal effect of refined barley flour bread has not been evaluated. The aim of this study is to determine whether consumption of refined barley flour bread reduces postprandial glucose concentrations after this and the subsequent meal.We enrolled 23 healthy young Japanese adults and conducted a randomized, double-blind, placebo-controlled, crossover study. The participants consumed refined barley flour bread containing 2.5 g β-glucan or refined wheat flour bread in a first meal, then consumed three rice balls as a second meal. Their postprandial blood glucose concentrations were measured 0, 15, 30, 45, 60, 90, and 120 min after both meals. Participants with fasting glucose concentrations above the diagnostic threshold for diabetes were excluded.The blood glucose concentration 30 min after the first meal was significantly lower (P0.05) if refined barley flour bread (7.1 ± 1.0 mmol/L) rather than refined wheat flour bread (7.7 ± 1.2 mmol/L) was consumed. Significantly lower glucose concentrations after the second meal measured at 60 (P0.05, barley flour bread: 8.7 ± 1.8 mmol/L, wheat flour bread: 9.3 ± 1.7 mmol/L) and 90 min (P0.01, barley flour bread: 7.8 ± 1.4 mmol/L, wheat flour bread: 8.8 ± 2.1 mmol/L) were lower in participants who had previously consumed the refined barley flour bread.Consumption of bread made with refined barley flour lowers postprandial blood glucose concentration after this and a subsequent meal compared with the consumption of refined wheat flour bread in healthy young Japanese adults.

The LZ test "Eiken" for H. pylori antibody (LZ test) was examined. In patients with an antibody titer of ≥3.0U/mL and10.0U/mL among 698 patients who underwent breath tests, the status of H. pylori infection was assessed from the results of the

Using cDNA microarray analysis that displays a total of 8734 mouse genes, we have identified 21 known and novel transcripts, including mouse expressed sequence tags (ESTs) that were consistently up- or downregulated in the fundus of wild-type mice and W/W(V) mice, where intramuscular interstitial cells of Cajal (ICC; IC-IM) are lost.By using these tags as part of the full-length mRNA sequence of the murine genes, we screened a mouse-brain cDNA library and the FASTA database (http://www.ebi.ac.uk/fasta33/).Three of the queries were identified as novel mouse genes, whereas six transcripts had their human counterparts that were known to encode functional proteins. Four transcripts, DRIM (downregulated in metastasis), SLP8 (tumor antigen), PTK7/CCK4 (receptor protein tyrosine kinase-like molecule-7/colon carcinoma kinase-4), and a novel gene AWMS2 were increased in W/W(V) mice. Expression of another five genes was decreased in W/W(V) mice: BB1 (overexpressed in bladder and breast carcinoma), HTATIP/CPLA2 (HIV-1 TAT interactive protein/cytosolic phospholipase A2), Tenascin-receptor like (Hexabrachion, Cytotactin, Neuronectin, Myotendinous antigen), and two novel transcripts: DRWMS1 and DRWMS2. Molecular profiling generated by cDNA microarray analysis from the fundus of W/W(V) mice and its complete list of full-length cDNAs will be shown on our web site (http://www.yamanashi.ac.jp/).Differential gene comparisons between control and mutant animals with losses in specific populations of ICCs will contribute significantly to our understanding of motility disorders associated with the loss of these cells and electrical slow waves in the gastrointestinal tract.

Background and Aims: A division of labor exists between different classes of interstitial cells of Cajal (ICC) in the gastrointestinal tract. In the stomach and small intestine, ICC at the level of the myenteric plexus (IC-MY) act as slow wave pacemaker cells, whereas intramuscular ICC (IC-IM) in the stomach act as intermediaries in enteric motor neurotransmission. The muscle layers of the gastric fundus do not have IC-MY, therefore electric slow waves are not generated. Intramuscular ICC are absent in the gastric fundus of W/WV mutant mice, and excitatory and inhibitory motor nerve responses are reduced in these tissues. The absence of IC-IM in W/WV mutants in the fundus provides a unique opportunity to study the molecular changes that are associated with the loss of these cells. Methods: The tissue gene expression of wild-type and W/WV mice from gastric fundus was assayed using a murine microarray chip analysis displaying a total of 8734 elements. Results: Twenty-one queries were differentially expressed in wild-type and W/WV mice. One candidate gene, encoding a novel protein homologous to rat Shank-interacting protein (Sharpin) was significantly upregulated in fed and starved W/WV mice. The full-length clone of the murine gene and its human counterpart were isolated and designated as Shank-interacting protein-like 1 (SIPL1). Human SIPL1 complementary DNA encodes a protein of 345 amino acids. This gene was localized to chromosome 8. SIPL1 was abundantly expressed in human stomach and small intestine, and scarcely expressed in cecum and rectum. Conclusions: Gene analysis showed that SIPL1 differentially express in the gastric fundus of normal and W/WV mice. The upregulation of SIPL1 in the fundus of W/WV mice, and expression in the upper gastrointestinal tract suggest that the SIPL1 gene could be associated with ICC function in mice and humans. © 2003 Blackwell Publishing Asia Pty Ltd

We examined the effect of a cholesterol derivative, poly (ethylene glycol) cholesteryl ether on the structure/function of clathrin-coated pits and caveolae. Addition of the compound to cultured cells induced progressive smoothening of the surface. Markedly, when the incorporated amount exceeded 10% equivalent of the surface area, fluid pinocytosis, but not endocytosis of transferrin, became inhibited in K562 cells. In A431 cells, both clathrin-independent fluid phase uptake and the internalization of fluorescent cholera-toxin B through caveolae were inhibited with concomitant flattening of caveolae. In contrast, clathrin-mediated internalization of transferrin was not affected until the incorporated poly (ethylene glycol) cholesteryl ether exceeded 20% equivalent of the plasma membrane surface area, at which point opened clathrin-coated pits accumulated. The cells were ruptured upon further addition of poly (ethylene glycol) cholesteryl ether. We propose that the primary reason for the differential effect of poly (ethylene glycol) cholesteryl ether is that the bulk membrane phase and caveolae are both more elastic than the rigid clathrin-coated pits. We analyzed the results with the current mechanical model (Rauch and Farge, Biophys J 2000;78:3036-3047) and suggest here that the functional clathrin-lattice is much stiffer than typical phospholipid bilayers.

Interstitial cells of Cajal (ICC) are responsible for generating electrical slow waves in the gastrointestinal (GI) tract. Slow waves regulate the frequency of contractions of the tunica muscularis, and therefore ICC are critical for normal motility in the small intestine. ICC express Kit, the gene product of c-kit, a protooncogene that encodes a receptor tyrosine kinase. Physiological evidence demonstrating that ICC are pacemakers has come from experiments on W-mutant mice which have few Kit-positive cells at the level of the myenteric plexus (IC-MY) and also lack electrical slow waves. In the past identification of ICC required the use of electron microscopy, however the discovery that ICC express Kit has facilitated studies of the distribution of ICC in several species. Immunoelectron microscopy to relate ultrastructure to Kit expression has only been performed in a limited number of studies of mice. We examined the ultrastructure of Kit-expressing cells in the rat using immunoelectron microscopy and an anti-Kit antibody. We compared the presence and appearance of Kit-expressing ICC in wildtype and Ws/Ws rats, which carry a mutation in the white spotting locus and have a phenotype similar to W/Wv mutant mice. Kit-expressing cells could be detected in the myenteric plexus (MY) and deep muscular plexus (DMP) regions of the small intestine of wildtype animals. In Ws/Ws rats, Kit-expressing cells were not observed in the region of MY, but were observed in the DMP. The density of Kit-positive cells in the DMP of Ws/Ws rats was similar to those in wildtype rats. Electron microscopy showed that Kit-expressing cells at the level of the MY of the rat had similar ultrastructural features as IC-MY in wildtype mice. IC-DMP in the rat of both wildtype and Ws/Ws mutants were similar in structure to IC-DMP of the mouse. We conclude that wildtype rats have IC-MY and IC-DMP in the tunica muscularis of the jejunum. ICC express Kit-like immunoreactivity (Kit-LI) in the rat as in the mouse. IC-MY are absent in the small intestine of Ws/Ws rats, and this corresponds to the lack of Kit-labeling in this region. Ws/Ws rats, however, possess IC-DMP with normal ultrastructural features and Kit-LI. The absence of IC-MY of Ws/Ws rats is likely to account for the abnormal contractile activity of the GI tract observed in these mutants. The present study suggests that Ws/Ws rats could provide an interesting model to investigate the physiological significance of pacemaker activity because they manifest a defect in IC-MY.

Patients with long-standing diabetes commonly suffer from gastric neuromuscular dysfunction (gastropathy) causing symptoms ranging from postprandial bloating to recurrent vomiting. Autonomic neuropathy is generally believed to be responsible for diabetic gastropathy and the underlying impairments in gastric emptying (gastroparesis) and receptive relaxation, but the specific mechanisms have not been elucidated. Recently, it has been recognized that interstitial cells of Cajal generate electrical pacemaker activity and mediate motor neurotransmission in the stomach. Loss or defects in interstitial cells could contribute to the development of diabetic gastroparesis. Gastric motility was characterized in spontaneously diabetic NOD/LtJ mice by measuring gastric emptying and by monitoring spontaneous and induced electrical activity in circular smooth muscle cells. Interstitial cells of Cajal were studied by Kit immunofluorescence and transmission electron microscopy. Diabetic mice developed delayed gastric emptying, impaired electrical pacemaking, and reduced motor neurotransmission. Interstitial cells of Cajal were greatly reduced in the distal stomach, and the normally close associations between these cells and enteric nerve terminals were infrequent. Our observations suggest that damage to interstitial cells of Cajal may play a key role in the pathogenesis of diabetic gastropathy.

Dystrobrevin is a newly discovered dystrophin-associated protein that is classified as alpha- and beta-dystrobrevin. Previous studies reported that dystrophin, utrophin, syntrophin and beta-dystroglycan were expressed in the cerebellum. In the present study, we examined cellular and subcellular localization of dystrobrevin in the adult rat cerebellum immunohistochemically. Confocal microscopy showed that dystrobrevin was expressed around blood vessels and under the pia mater as dystrophin, utrophin and beta-dystroglycan were. Immunoelectron microscopy demonstrated that dystrobrevin was localized not only in the astrocytic endfeet around blood vessels and under the pia mater, but also in endothelial cells. Considering the fact that dystrobrevin possesses multiple phosphotyrosine kinase residues, these data suggest that dystrobrevin plays a role in blood-brain barrier functions as a component of the dystrophin complex.

In vitro studies on pacemaker-deficient W-mutants have revealed a disappearance of rhythmic contraction in their gastrointestinal tracts. Their contractile force has not been diminished, however. In contrast, W-mutants often present dysmoility-like symptoms with distension of the gastrointestinal tract in vivo. Gastrointestinal motility of W-mutant rats was examined in vivo by an extraluminal strain-gauge force transducer method. We examined a normal gastrointestinal motor pattern in the rats with two distinct motor phases, digestive and interdigestive. Moreover, we detected a failure to form an interdigestive contractile complex in pacemaker-deficient rats. The interdigestive motor activity of the gastrointestinal tract is important for cleaning gastrointestinal tract in preparation for the next meal. The impairment of the interdigestive contractile complex may be related to the dysmoility-like symptoms of W-mutant rats in vivo.

A quick-freezing and deep-etching (QF-DE) method was employed with whole-mount strips of rat duodenal muscle walls to exhibit the cytoskeletons of the myenteric plexus. Nerve fibers in the myenteric plexus, which contained fewer neurofilaments than other types of neurons examined, had many varicosed contours, and were bundled by enteroglial cells. Cytoskeleton arrays were rarely observed in the varicosed regions, where synaptic vesicles were often seen, although other nerve regions contained many neurofilaments running almost in parallel with the nerve fiber bundle. Enteroglial cells had short cytoskeletons predominantly across the cytoplasm, becoming thinner the around varicosed regions of the nerve bundles. Such enteroglial extruded areas were often in close association with neighboring nerve fibers, indicating intercommunications between the nerve fibers. In distal parts of enteric nerve processes, there were numerous synaptic vesicles, but few neurofilaments. Smooth muscle cells were closely associated with the enteric nerve processes. Fine network structures, responsible for the extracellular matrix, were present between the smooth muscle cells and the enteric nerve processes. These specific structures of the myenteric plexus could be important for signalling or for the transportation of neurotransmitters involved in gut motility.

Biopsy specimens obtained from the liver of a 32-year-old woman, diagnosed with acute fatty liver of pregnancy, were examined by light and electron microscopy. The patient had become pregnant after artificial insemination. At the 36th week of gestation, she suffered simultaneous fetal distress and liver dysfunction, and a cesarean operation was done immediately. Liver biopsies were performed on the 7th and 38th day after the cesarean operation. The first biopsy revealed enlarged hepatocytes in pericentral areas. Many transformed mitochondria with tubular cristae, which were often seen in steroid hormoneproducing cells and adrenal cortical cells, and microvesicular fatty droplets were detected in some swollen hepatocytes, as revealed by electron microscopy. At the second biopsy, almost all hepatocytes had recovered normal morphology as the result of appropriate treatment.

A novel "in vivo cryotechnique" with replica immunoelectron microscopy was developed for detecting caveolin localization on replica membranes prepared directly from living smooth muscle cells. After quick-freezing mouse duodenal walls by our "in vivo cryotechnique", the specimens were prepared for freeze-fracture and deep-etch replica membranes. Then they were treated with 5% SDS and 0.5% collagenase to keep some antigens on the replica membranes. The immunogold method could be used to clarify the localization of the caveolin antigen in relation to three-dimensional ultrastructures of living smooth muscle cells. Our new cryotechnique can provide native organization of functional molecules in living cells.

Background and Aim: Interstitial cells of Cajal (ICC) are pacemakers and mediators of neurotransmission in gastroenteric smooth muscles. Interstitial cells of Cajal require cellular signaling via KIT, a receptor tyrosine kinase, for development and maintenance of cellular phenotype. Much of the evidence demonstrating the functions of ICC comes from studies of W/W V mutant mice, which have reduced KIT function. The aim of the present study was to differentially examine gene expression in the small intestines of wild-type and W/W V mice. Methods: RNA from the jejunum of wild-type and W/W V mice was analyzed using a differential gene display method. Results: One candidate gene, encoding a novel small GTPase of the RAS superfamily, was significantly suppressed both in fed and starved W/WV mice. The full-length clone of the murine gene and its human and xenopus counterparts were designated GTP-binding protein, 28 kDa (G28K). Human G28K cDNA encodes a protein of 258 amino acids with homology to the human cell division cycle 42/G25K protein. This gene is located at 1q42.11–q42.3. G28K was abundantly expressed in the human stomach and the small intestine. Semi-quantitative reverse transcription–polymerase chain reaction analysis revealed expression of G28K mRNA within single isolated ICC. Conclusions: Gene analysis showed that G28K was differentially expressed in the small intestines of wild-type and W/W V mice. Interstitial cells of Cajal within the small intestine expressed mRNA for G28K. The specific downregulation of G28K in the jejunum of W/W V mice, and high expression in human intestinal tissue suggest that the G28K gene might be associated with ICC function in mice and in humans.

A case for primary gastrointestinal stromal tumor (GIST) is described with reference to its ultrastructural characteristics and mutation within the exon 11 of c-kit gene. A forty-seven years old woman complaining of dysphasia was examined by endoscopy, which depicted a submucosal tumor (70 mm in diameter) with ulcerations at the fundus of the stomach. Histopathologically, the tumor cells had large nuclei and eosinophilic cytoplasm and were frequently during mitosis phase. The tumor cells were immunopositive for KIT, CD 34 and vimentin, suggesting their fibroblast-like characteristics. In contrast, desmin and S-100, a smooth muscle and an enteroglial marker, were not immunopositive within the cells. At least 30 % of the tumor cells possessed MIB-I and 20 % of them possessed p53, which are compatible with fast development of the tumor. By electron microscopy, the tumor cells possessed large oval nuclei, abundant mitochondria, caveolae and smooth endoplasmic reticulums, while no gap junctions were seen on the cells: The tumor cells thus possessed interstitial cells-like characteristics at least in part. DNA mutation search for the tumor cells however realized no gain-of-function mutation within the exon 11 of the c-kit gene, suggesting existence of other mechanism for neoplasmic growth of the tumor cells classified as gastrointestinal stromal tumors.

Background The muscle layers of murine gastric fundus have no interstitial cells of Cajal at the level of the myenteric plexus and only possess intramuscular interstitial cells and this tissue does not generate electric slow waves. The absence of intramuscular interstitial cells in W/WV mutants provides a unique opportunity to study the molecular changes that are associated with the loss of these intercalating cells. Method The gene expression profile of the gastric fundus of wild type and W/WV mice was assayed by murine microarray analysis displaying a total of 8734 elements. Queried genes from the microarray analysis were confirmed by semi-quantitative reverse transcription-polymerase chain reaction. Results Twenty-one genes were differentially expressed in wild type and W/WV mice. Eleven transcripts had 2.0–2.5 fold higher mRNA expression in W/WV gastric fundus when compared to wild type tissues. Ten transcripts had 2.1–3.9 fold lower expression in W/WV mutants in comparison with wild type animals. None of these genes have ever been implicated in any bowel motility function. Conclusions These data provides evidence that several important genes have significantly changed in the murine fundus of W/WV mutants that lack intramuscular interstitial cells of Cajal and have reduced enteric motor neurotransmission.

In spite of a claim by Kobayashi (1990) that they do not correspond to the cells originally depicted by CAJAL, a particular category of fibroblast-like cells have been identified in the gut by electron microscopy (Faussone-Pellegrini, 1977; Thuneberg, 1980) and by immunohistochemistry for Kit protein (Maeda et al., 1992) under the term of the "interstitial cells of Cajal (ICC)". Generating electrical slow waves, the ICC are intercalated between the intramural neurons and the effector smooth muscular cells, to form a gastroenteric pacemaker system. ICC at the level of the myenteric plexus (IC-MY) are multipolar cells forming a reticular network. The network of IC-MY which is believed to be the origin of electrical slow waves is morphologically independent from but associated with the myenteric plexus. On the other hand, intramuscular ICC (IC-IM) usually have spindle-shaped contours arranged in parallel with the bulk smooth muscle cells. Associated with nerve bundles and blood vessels, the IC-IM possess receptors for neurotransmitters and such circulating hormones as cholecystokinin, suggesting their roles in neuromuscular and hormone-muscular transmissions. In addition, gap junctions connect the IC-MY and IC-IM, thereby realizing the electrically synchronized integrity of ICC as a pacemaker system in the gut. The smooth muscle cells are also coupled with ICC via gap junctions, and the functional unit thus formed enables rhythmically synchronized contractions and relaxations. It has recently been found that a lack of Kit-expressing cells may induce hyper-contractility of the tunica muscularis in vitro, whereas a decrease in Kit expression within the muscle wall causes dysmotility-like symptoms in vivo. The pacemaker system in the gut thus seems to play a critical role in the maintenance of both moderate and normal motility of the digestive tract. A loss of Kit positive cells has been detected in several diseases with an impaired motor activity, including diabetic gastroenteropathy. Pathogenesis of these diseases is thought to be accounted for by impaired slow waves and neuromuscular transmissions; a pacemaker disorder may possibly induce a dysmotility-like symptom called 'gastroenteric arrhythmia'. A knowledge of the structure and function of the ICC and the pacemaker system provides a basis for clarifying the normal mechanism and the pathophysiology of motility in the digestive tract.

1. Partial obstruction of the murine ileum led to changes in the gross morphology and ultrastructure of the tunica muscularis. Populations of interstitial cells of Cajal (ICC) decreased oral, but not aboral, to the site of obstruction. Since ICC generate and propagate electrical slow waves in gastrointestinal muscles, we investigated whether the loss of ICC leads to loss of function in partial bowel obstruction. 2. Changes in ICC networks and electrical activity were monitored in the obstructed murine intestine using immunohistochemistry, electron microscopy and intracellular electrophysiological techniques. 3. Two weeks following the onset of a partial obstruction, the bowel increased in diameter and hypertrophy of the tunica muscularis was observed oral to the obstruction site. ICC networks were disrupted oral to the obstruction, and this disruption was accompanied by the loss of electrical slow waves and responses to enteric nerve stimulation. These defects were not observed aboral to the obstruction. 4. Ultrastructural analysis revealed no evidence of cell death in regions where the lesion in ICC networks was developing. Cells with a morphology intermediate between smooth muscle cells and fibroblasts were found in locations that are typically populated by ICC. These cells may have been the redifferentiated remnants of ICC networks. 5. Removal of the obstruction led to the redevelopment of ICC networks and recovery of slow wave activity within 30 days. Neural responses were partially restored in 30 days. 6. These data describe the plasticity of ICC networks in response to partial obstruction. After obstruction the ICC phenotype was lost, but these cells regenerated when the obstruction was removed. This model may be an important tool for evaluating the cellular/molecular factors responsible for the regulation and maintenance of the ICC phenotype.

A morphological approach to cell dynamics is usually difficult, since routine preparative techniques for electron microscopy always induce artifacts due to cessation of the blood supply into organs. An in vivo cryotechnique followed by the freeze-substitution method probably reduces such problems. It was applied for examining the pulmonary alveoli of BALB/c mice in vivo. The following ultrastructural features were revealed. (1) A surfactant layer provided a continuous covering to the alveolar epithelium. (2) Pleural epithelial cells, alveolar cells and endothelial cells contained many small vesicles and pits. In the alveolar epithelium, they were often localised near microtubules. (3) Typical lamellar structures in large alveolar epithelial cells were rarely detected. (4) Circulating erythrocytes with various shapes were observed in branching blood capillaries. (5) A close association between erythrocytes and the endothelium was seen at the peripheral alveolar septum. Such ultrastructural arrangements may be appropriate for the physiological functions of the pulmonary alveoli, such as exchanges of gases or materials in vivo.

Changes of intracellular localization of serotonin in rat mast cells were examined by freeze-fracture immunocytochemistry, to prevent the translocation of the serotonin antigen. Rat peritoneal cells including mast cells were stimulated in vitro with compound 48/80, at 17 degrees C for 0, 30 or 60 s for exocytosis to occur. The mast cells were fixed, quickly frozen and freeze-fractured to expose the antigen on the fractured surface. They were immunostained with serotonin antibody, and the immunoreactions on the fractured surface were examined on ultrathin sections by electron microscopy. Unstimulated mast cells exhibited serotonin localization mostly in each intragranular matrix. In contrast, mast cells stimulated for 30 s exhibited increased serotonin in their intergranular cytoplasm. Mast cells showed more distinct immunoreactions in the cytoplasm where degranulation would be promoted after 60 s. It is suggested that intracellular release of serotonin occurred in the stimulated mast cells.

It is well known that hemodynamic factors, such as blood pressure and flow, exert an important influence on native morphology of various animal organs. However, information about the significance of ultrastructures which are revealed by conventional preparation methods has been limited, because routine chemical fixation of cells and tissues takes considerable time, during which their morphology could easily change. Therefore, morphological studies with routine immersion or perfusion fixation have not revealed real ultrastructures of functioning animal organs with normal blood circulation.2 The ultimate goal of morphological study is that all features to be examined should reflect the physiological meaning under investigation. For that purpose, the preservation of cells and tissues in functioning organs is necessary for studies to define their ultrastructures. Most cryotechniques have been based on the use of prior excised tissues. Such small specimens are commonly frozen within several seconds following the excision of the tissues.

Background We previously identified eight known and novel genes differentially expressed in the small intestines of wild type and W/WV mice, which have greatly reduced populations of the interstitial cells of Cajal, that are responsible for the generation of electrical slow waves, by using a differential gene display method. Methods By using the same method we isolated additional candidate genes that were specifically down- or up-regulated in W/WV mice. Novel transcripts were designated as DDWMEST. Results We isolated seven candidates that were specifically down- or up-regulated in W/WV mice. Two novel transcripts, DDWMEST 1 and -91 were increased in both fed and fasted W/WV mice. Expression of another five genes was suppressed in W/WV mice: ARG2 (Arginase II), ONZIN (encoding leukemia inhibitory factor regulated protein), and three novel transcripts: DDWMEST62, -84, and -100. Together with the previous report, we identified fifteen differentially expressed genes in total in the small intestines of W/WV mice. Eight of these genes were reduced in the jejunums of W/WV mice compared to age matched wild type mice, whereas the other seven genes showed an increase in expression. Differential expression was the same in fasted and fed animals, suggesting that the differences were independent of the dietetic state of the animal. Conclusions Several known and novel genes are differentially expressed in the small intestines of W/WV mice. Differential gene comparison might contribute to our understanding of motility disorders associated with the loss of the interstitial cells of Cajal.