Predominance of mother-to-child transmission of Helicobacter pylori infection detected by random amplified polymorphic DNA fingerprinting analysis in Japanese families

BACKGROUND: Helicobacter pylori (H. pylori) is one of the most common bacterial pathogens in humans but the route of transmission remains unclear. We investigated transmission by DNA fingerprinting analysis of cultured H. pylori from pediatric patients and their family members. METHODS: Forty-two index patients with a mean age of 11.7 years (range, 4-19) were diagnosed as having H. pylori gastritis with or without duodenal/gastric ulcer disease. A total of 66 family members for whom the results of the H. pylori stool antigen test and/or serum H. pylori IgG test were positive underwent endoscopic examination and biopsy or aspiration of gastric juice for H. pylori culture. The extraction of H. pylori genomic DNA and PCR-based RAPD analysis were performed. RESULTS: Thirty-two (76%) of the 42 patients showed DNA fingerprint patterns identical to those of at least one of the respective family members. The patterns of 29 (69%) of the analyses of the H. pylori infected patients were identical to those of their mothers. The patterns for 7 patients were identical to those of their fathers, and those for 6 of the latter patients were also identical to those of their mothers. The rate of fingerprint patterns identical to those of the index patients was significantly higher in those of mothers compared with those of fathers (P < 0.01). CONCLUSIONS: Mother-to-child transmission is the predominant route of H. pylori infection in Japan.     

Complete remission of pancreatic cancer after multiple resections of locally pancreatic recurrent sites and liver metastasis: Report of a case

Pancreatic cancer has the most dismal prognosis of all gastrointestinal cancers. We herein report a case of complete remission from pancreatic cancer by multire-sections of locally pancreatic recurrent sites and liver metastasis over a 14-year period. A 60-year-old man was admitted to our hospital because of a neoplasm of the tail of the pancreas in April 1992. A distal pancreatectomy was curatively performed on this patient. At 1 year after surgery a solitary liver metastasis appeared, and we thus performed a partial hepatectomy. Thereafter, local recurrences appeared twice and we performed a pancreatectomy each time. Finally, we performed a total pancreatectomy. The histopathological findings of specimens of the pancreas showed papillary adenocarcinoma, although the original pancreatic tumor also demonstrated areas of tubular adenocarcinoma. Metastatic liver tumor showed tubular adenocarcinoma. The patient has survived for 14 years since the first operation. This is a rare case of a long survival of a patient with pancreatic cancer due to its histopathology and biologic characteristics.     

Involvement of phosphorylation of Tyr-31 and Tyr-118 of paxillin in MM1 cancer cell migration.

We demonstrated previously that rat ascites hepatoma MM1 cells require both lysophosphatidic acid (LPA) and fibronectin (FN) for phagokinetic motility and transcellular migration and that these events are regulated through the RhoA-ROCK pathway. It remains to be elucidated, however, how the signals from both LPA and FN are integrated into cell migration. To examine this, total cellular lysates after stimulation with LPA or FN were subjected to time-course immunoblot analysis with anti-phosphotyrosine antibodies (Abs). Consequently, tyrosine-phosphorylation of paxillin was obviously persistent after stimulation with FN + LPA as compared to after stimulation with either alone. Tyrosine-phosphorylated paxillin comprised 2 components; slowly and fast migrating ones. Immunoblotting of anti-paxillin immunoprecipitates with phosphorylation site-specific Abs revealed the following: tyrosine-phosphorylation was enhanced preferentially on a slowly migrating component after stimulation with FN + LPA; this component contained phosphorylation at both tyrosine residue (Y) 31 and Y118; and phosphorylation of paxillin at Y181 was constitutive and not augmented by stimulation with either FN or LPA. Amiloride, an inhibitor of the Na+/H+ antiporter downstream of ROCK, suppressed cell motility and correspondingly paxillin tyrosine-phosphorylation at both Y31 and Y118. Paxillin phosphorylation weakly induced by FN alone, insufficient for cell migration, was not inhibited by amiloride. These results demonstrate that LPA collaborates with FN for persistent tyrosine phosphorylation of paxillin at both Y31 and Y118, regulated by the Na+/H+ antiporter downstream of ROCK and that this phosphorylated paxillin is essential for MM1 cancer cell migration.     

Inhibition of in vitro Tumor Cell Invasion by Transmethylation Inhibitors

Three inhibitors of S -adenosylmethionine-mediated transmethylation, 5'-methylthioadenosine (MTA), 2'-deoxyadenosine and sinefungin, inhibited in vitro invasion by a highly invasive clone (Cl-30) of rat ascites hepatoma cells, AH 130 (AH cells). Difluoromethylthioadenosine (DFMTA), a non-metabolizable derivative of MTA, also caused strong inhibition of invasion at concentrations that did not suppress the growth of the tumor cells. Cl-30 cells precultured in methionine-depleted medium showed decreased invasiveness. DFMTA was also effective on the invasion by fibrosarcoma, B16 melanoma and human lung carcinoma cell lines.     

IGFBP3 Promoter Methylation in Colorectal Cancer: Relationship with Microsatellite Instability,CpG Island Methylator Phenotype,and p53

Insulin-like growth factor binding protein 3 (IGFBP3), which is induced by wild-type p53, regulates IGF and interacts with the TGF-β pathway. IGFBP3 promoter methylation may occur in colorectal cancer with or without the CpG island methylator phenotype (CIMP), which is associated with microsatellite instability (MSI) and TGFBR2 mutation. We examined the relationship between IGFBP3 methylation, p53 expression, CIMP and MSI in 902 population-based colorectal cancers. Utilizing real-time PCR (MethyLight), we quantified promoter methylation in IGFBP3 and eight other CIMP-high-specific promoters (CACNA1G, CDKN2A, CRABP1, IGF2, MLH1, NEUROG1, RUNX3, and SOCS1). IGFBP3 methylation was far more frequent in non-MSI-high CIMP-high tumors (85% = 35/41) than in MSI-high CIMP-high (49% = 44/90, P < .0001), MSI-high non-CIMP-high (17% = 6/36, P < .0001), and non-MSI-high non-CIMP-high tumors (22% = 152/680, P < .0001). Among CIMP-high tumors, the inverse relationship between MSI and IGFBP3 methylation persisted in p53-negative tumors (P < .0001), but not in p53-positive tumors. IGFBP3 methylation was associated inversely with TGFBR2 mutation in MSI-high non-CIMP-high tumors (P = .02). In conclusion, IGFBP3 methylation is inversely associated with MSI in CIMP-high colorectal cancers, and this relationship is limited to p53-negative tumors. Our data suggest complex relationship between global genomic/epigenomic phenomena (such as MSI/CIMP), single molecular events (e.g., IGFBP3 methylation, TP53 mutation, and TGFBR2 mutation), and the related pathways.     

Barrett’s Esophageal Adenocarcinoma with CREST Syndrome

Scleroderma is a systemic and connective tissue disease. Gastrointestinal manifestations including esophageal dysmotility are common in scleroderma patients. The relationship between esophageal reflux and scleroderma has been well described; however, the complication of Barrett’s esophagus and adenocarcinoma due to chronic esophagitis is rare. In addition, there are no detailed reports on the treatment of esophageal adenocarcinoma or the pathological findings in patients with scleroderma. We report the case of a 55-year-old woman who presented with chronic cough and a dilated esophagus. The patient was diagnosed with Barrett’s adenocarcinoma and CREST syndrome, which is a form of scleroderma. Subtotal esophagectomy was performed, and the patient’s chronic cough was relieved. A surgical specimen revealed histological changes at the dilated parts of the esophagus that showed the thinning of the muscular layer with fibrotic changes.     

Evaluation of methods for calculating maximum allowable standing height in amputees competing in Paralympic athletics

The International Paralympic Committee has a maximum allowable standing height (MASH) rule that limits stature to a pre‐trauma estimation. The MASH rule reduces the probability that bilateral lower limb amputees use disproportionately long prostheses in competition. Although there are several methods for estimating stature, the validity of these methods has not been compared. To identify the most appropriate method for the MASH rule, this study aimed to compare the criterion validity of estimations resulting from the current method, the Contini method, and four Canda methods (Canda‐1, Canda‐2, Canda‐3, and Canda‐4). Stature, ulna length, demispan, sitting height, thigh length, upper arm length, and forearm length measurements in 31 males and 30 females were used to calculate the respective estimation for each method. Results showed that Canda‐1 (based on four anthropometric variables) produced the smallest error and best fitted the data in males and females. The current method was associated with the largest error of those tests because it increasingly overestimated height in people with smaller stature. The results suggest that the set of Canda equations provide a more valid MASH estimation in people with a range of upper limb and bilateral lower limb amputations compared with the current method.