Endoscopic characteristics and Helicobacter pylori infection in NSAID-associated gastric ulcer

Background and Aim: Helicobacter pylori infection and non‐steroidal anti‐inflammatory drugs (NSAIDs) are deeply involved in the etiology of gastric ulcers. The aim of our study was to clarify the endoscopic characteristics and H. pylori infection status of NSAID‐associated gastric ulcers. Methods: The study group comprised 50 patients (23 men, 27 women; mean age 66.5 years) with NSAID‐associated gastric ulcers and 100 sex‐ and age‐matched patients with gastric ulcer associated with other factors (control group). Ulcer morphology, size and number of lesions, onset site and incidence of hemorrhagic ulcers were investigated endoscopically in both groups. H. pylori infection was diagnosed by serology, histology and ¹³C‐urea breath test. Results: Multiple lesions (68% vs 20%, P < 0.001), occurrence in the antrum (56% vs 6%, P < 0.001), and hemorrhagic ulcer (34% vs 4%, P < 0.001) were significantly more prevalent in patients with NSAID‐associated gastric ulcers than in patients with non‐NSAID‐associated gastric ulcer. The H. pylori infection rate was significantly lower in NSAID‐associated gastric ulcer patients than in non‐NSAID‐associated gastric ulcer patients (48% vs 96%, P < 0.001). In the NSAID‐associated gastric ulcer group, the prevalence of H. pylori infection was significantly lower in patients with ulcers in the antrum than in those with ulcers in the angulus or corpus (25% vs 77.3%, P < 0.001). Conclusions: In contrast to non‐NSAID‐associated gastric ulcers, NSAID‐associated gastric ulcers frequently occur in the antrum with bleeding. The rate of H. pylori infection in NSAID‐associated gastric ulcers is significantly lower than that in non‐NSAID‐associated gastric ulcers.     

Analysis of Atrioventricular Nodal Reentrant Tachycardia with Variable Ventriculoatrial Block: Characteristics of the Upper Common Pathway

Background: The precise nature of the upper turnaround part of atrioventricular nodal reentrant tachycardia (AVNRT) is not entirely understood.
Methods: In nine patients with AVNRT accompanied by variable ventriculoatrial (VA) conduction block, we examined the electrophysiologic characteristics of its upper common pathway.
Results: Tachycardia was induced by atrial burst and/or extrastimulus followed by atrial-His jump, and the earliest atrial electrogram was observed at the His bundle site in all patients. Twelve incidents of VA block: Wenckebach VA block (n = 7), 2:1 VA block (n = 4), and intermittent (n = 1) were observed. In two of seven Wenckebach VA block, the retrograde earliest atrial activation site shifted from the His bundle site to coronary sinus ostium just before VA block. Prolongation of His-His interval occurred during VA block in 11 of 12 incidents. After isoproterenol administration, 1:1 VA conduction resumed in all patients. Catheter ablation at the right inferoparaseptum eliminated antegrade slow pathway conduction and rendered AVNRT noninducible in all patients.
Conclusion: Selective elimination of the slow pathway conduction at the inferoparaseptal right atrium may suggest that the subatrial tissue linking the retrograde fast and antegrade slow pathways forms the upper common pathway in AVNRT with VA block.     

Effect of Catheter Tip‐Tissue Surface Contact on Three‐Dimensional Left Atrial and Pulmonary Vein Geometries: Potential Anatomic Distortion of 3D Ultrasound,Fast Anatomical Mapping,and Merged 3D CT‐Derived Images

Anatomic Distortion of 3D Mapping . Background: Although catheter tip‐tissue contact is known as a reliable basis for mapping and ablation of atrial fibrillation (AF), the effects of different mapping methods on 3‐dimensional (3D) map configuration remain unknown. Methods and Results: Twenty AF patients underwent Carto ‐based 3D ultrasound (US) evaluation. Left atrium (LA)/pulmonary vein (PV) geometry was constructed with the 3D US system. The resulting geometry was compared to geometries created with a fast electroanatomical mapping (FAM) algorithm and 3D US merged with computed tomography (merged 3D US‐CT). The 3D US‐derived LA volumes were smaller than the FAM‐ and merged 3D US‐CT‐derived volumes (75 ± 21 cm³ vs 120 ± 20 cm³ and 125 ± 25 cm³, P < 0.0001 for both). Differences in anatomic PV orifice fiducials between 3D US‐ and FAM‐ and merged 3D US‐CT‐derived geometries were 6.0 (interquartile range 0–9.3) mm and 4.1 (0–7.0) mm, respectively. Extensive encircling PV isolation guided by 3D US images with real‐time 2D intracardiac echocardiography‐based visualization of catheter tip‐tissue contact generated ablation point (n = 983) drop‐out at 1.9 ± 3.8 mm beyond the surface of the 3D US‐derived LA/PV geometry. However, these same points were located 1.5 ± 5.4 and 0.4 ± 4.1 mm below the FAM‐ and merged 3D US‐CT‐derived surfaces. Conclusions: Different mapping methods yield different 3D geometries. When AF ablation is guided by 3D US‐derived images, ablation points fall beyond the 3D US surface but below the FAM‐ or merged 3D US‐CT‐derived surface. Our data reveal anatomic distortion of 3D images, providing important information for improving the safety and efficacy of 3D mapping‐guided AF ablation. (J Cardiovasc Electrophysiol, Vol. 24, pp. 259‐266, March 2013)     

Unusual Mechanism in the Initiation of the Paroxysmal Supraventricular Tachycardia in a Patient with WPW Syndrome

A heretofore unreported unusual mechanism in the initiation of the paroxysmal supraventricular tachycardia (PSVT) in a patient with WPW (Wolff-Parkinson-White) syndrome was observed using His bundle recordings. The patient initially had some degree of AV conduction disturbance at the level of the AV node. A premature atrial impulse initially activated the ventricle exclusively through the accessory pathway and the same impulse re-excited the ventricle via the AV nodal-His axis after finishing the pure pre-excitation with marked prolongation of the AH and the HV intervals. After finishing this double ventricular response it traversed to the atrium to produce the PSVT.     

CONCURRENT GASTRIC AND COLONIC LOW‐GRADE MUCOSA‐ASSOCIATED LYMPHOID TISSUE LYMPHOMATA IN A PATIENT WITHOUT HELICOBACTER PYLORI INFECTION

Mucosa‐associated lymphoid tissue (MALT) lymphomata observed simultaneously in the stomach and colon are rare. We report concurrent gastric and colonic low‐grade MALT lymphomata that originated from the same clone in a 58‐year‐old Japanese man without Helicobacter pylori infection. Endoscopy showed multiple erosive lesions in the gastric body and antrum, and a single flat elevation with an irregular margin in the sigmoid colon. Histopathological findings of both lesions suggested low‐grade MALT lymphoma. Lymphoepithelial lesions were evident in the gastric lesions, but not in the colonic lesion. Southern blot analysis of lymphoma cells revealed the same immunoglobulin heavy‐chain rearrangement pattern. The chromosomal translocation t(11;18)(q21;q21) was also observed. After six courses of cyclophosphamide, doxorubicin, vincristine and predonisolone, the gastric lesions disappeared endoscopically, while the colonic lesion persisted. A sigmoidectomy was consequently performed. The chromosomal translocation may be related to the pathogenesis of the present MALT lymphoma case without H. pylori infection. It is interesting that the gastric and colonic lesions differed in response to treatment and in their endoscopic and histologic features, despite having the same origin.     

Molecular epidemiology of hepatitis B virus in Indonesia

The S-gene sequences of hepatitis B virus (HBV) from 22 carriers in several islands of Indonesia were amplified by polymerase chain reaction, and XbaI-SpeI fragments corresponding to nucleotides 93-529 (437 base pairs) in the S gene were sequenced. The 22 sequences, along with the 5 reported sequences from Indonesia, were compared with each other, and with the corresponding sequences of 20 clones from other countries including China, France, Great Britain, Japan, Kenya, Papua New Guinea, Philippines, USA and USSR. When the 27 HBV DNA clones of various subtypes from Indonesia were classified by the homology in the nucleotide sequence into the five genotypes, twelve belonged to genotype B (subtype adw 7 and ayw 5), 13 to genotype C (adw 1, adr 10, ayr 1 and ar 1), and 2 to genotype D (ayw); none belonged to genotype A or E. Different subtypes of clones in the same genotype indicated that point mutations inducing d-to-y or w-to-r phenotypic changes would be common among Indonesian carriers. Comparison of the translation products of XbaI-SpeI fragments, now available for 47 HBV DNA clones of different genotypes (A 4; B 14; C 21; D 7; E 1), identified several amino acids characteristic to or influenced by the five genotypes as well as those highly conserved by clones of different genotypes.     

Hepatocellular carcinoma not associated with cirrhosis. A clinicopathological study in 41 patients including 29 resected cases

Abstract Clinicopathological features were studied in 41 patients with histology-proven hepatocellular carcinoma without cirrhosis. Of these, 13 (31.7%) were positive for hepatitis B virus surface antigen (HBsAg) and 28 were negative. Twenty-six of 28 (92.9%) HBsAg negative cases had anticore antibody (anti-HBc) of low titres. The age of patients at the time of diagnosis of hepatocellular carcinoma was significantly younger in the HBsAg positive cases compared with the negative. The initial diagnostic clue was either abdominal mass or abdominal pain in 18 (43.9%) patients. However, the number of patients in whom hepatocellular carcinoma was detected by imaging in the absence of such clinical signs has increased recently. The tumour was encapsulated in 31 cases (75.6%) and most solitary encapsulated tumours were growing expansively. Tumours were resectable in 29 (70.7%) cases, and the prognosis of resected cases was much better than that of 12 non-operated cases. Twenty-one out of 29 (72.4%) resected tumours were solitary and encapsulated. However, recurrence of tumour occurred in 12 out of 28 (42.9%) cases, and it was within 2 years of resection in 11 cases. These observations and data seem to indicate that early detection and resection of tumour is very important in management, but tumour recurrence is inevitable in a considerable proportion of the patients with non-cirrhotic hepatocellular carcinoma.     

Second Malignancy in Stomach Cancer Patients and Its Possible Risk Factors

To identify possible risk factors of multiple primary cancersin stomach cancer patients, a case-control analysis based ondata from medical records was conducted on 73 patients (54 malesand 19 females) with stomach cancer who were affected by oneor more other primary cancers subsequently or concurrently (cases)and 146 patients with stomach cancer alone (controls), by matchingsex, age, time of the operation for stomach cancer and survivalperiod. The relative risks (RR) for cancer history in the father(RR = 3.21), for family history of stomach cancer (RR = 2.52)and for history of hemorrhoids (RR = 3.15) were significantlyincreased in both sexes. The proportion of professionals inmales was significantly higher in cases than in controls. Ina conditional multiple logistic regression analysis for males,the adjusted relative risk (aRR) for family history of cancerin two or more members (aRR = 3.54) was statistically significant.Smoking tended to increase the risk of multiple primary cancersin males, especially in the cases with smoking-related secondmalignancy (RR =4.83). These data suggest the possibility thatboth genetic and environmental factors are involved in the multiplicityof cancer in stomach cancer patients.     

Antitumor effect of reduction of 150-kDa oxygen-regulated protein expression on human prostate cancer cells

BACKGROUND: The 150-kDa oxygen-regulated protein ORP150, a new member of the heat shock protein family that functions as a molecular chaperone in the endoplasmic reticulum, was found to increase in infiltrating cancer cells. Since enhancement of ORP150 expression and the presence of vascular endothelial growth factor (VEGF) in human prostate cancer glands were immunohistochemically demonstrated, we examined whether transduced antisense ORP150 cDNA can reduce angiogenicity and tumorigenicity through suppression of VEGF secretion. METHODS: Human prostate cancer specimens were immunohistochemically stained with fluorescein isothiocyanate (FITC) for ORP150 or vascular endothelial growth factor (VEGF). An adenovirus vector (Ad) carrying antisense ORP150 cDNA (AdCA-Antisense ORP150) was constructed and infected to prostate cancer DU145 cells. Expression of ORP150 in the cells was analyzed with western blotting and secretion of VEGF into the supernatant with an enzyme-linked immunoabsorbent assay (ELISA). Angiogenicity was evaluated by chorioallantoic membrane (CAM) assay. A nude mouse xenograft model was used to examine tumorigenicity. RESULTS: Immunohistochemical study proved that the expression of ORP150 and VEGF was enhanced in the cytoplasm of prostate cancer cells. The Ad showed 100% transduction efficiency and minimum cytotoxicity when the cells were infected at a multiplicity of infection (MOI) of 20 for 24 h. Expression of ORP150 was substantially reduced by the antisense treatment. Secretion of VEGF into the culture supernatant was reduced to 30%. Consequently, the CAM assay showed relatively low angiogenicity, while marked suppression of tumor formation was observed in the xenograft model. CONCLUSION: Adenoviral-mediated antisense ORP150 cDNA transfer is well worth considering as an option for prostate cancer gene therapy.     

Potentiated Toxicity of 2-sec-Butylphenyl Methylcarbamate (BPMC) by O,O-Dimethyl O-(3-Methyl-4-nitrophenyl)phosphorothioate (Fenitrothion) in Mice; Relationship between Acute Toxicity and Metabolism of BPMC

Potentiated Toxicity of 2-sec-Butytpbenyl Methylcarbamate (BPMC)by O,O-Dimethyl O-(3-Methyl-4-nitrophenyl)phosphorothioate (Fenitrothion)in Mice; Relationship between Acute Toxicity and Metabolismof BPMC. TAKAHASHI, H., MIYAOKA, T., TSUDA, S., AND SHIRASU,Y. (1984). Fundam. Appl. Toxicol. 4, 718–723. Fenitrothionof oral subtoxic dose (100 mg/kg; 4 hr pretreatment) decreasedacute oral LD50 of BPMC from 360 to 66 mg/kg in male mice. Thetreatment prolonged the hexobarbital sleeping time and increasedthe plasma BPMC concentrations. The BPMC toxicity and its plasmaconcentrations were significantly reduced by phenobarbital treatment(80 mg/kg/day, 2 days, ip). This treatment diminished the effectsof fenitrothion on BPMC toxicity and plasma BPMC concentrations.BPMC was metabolized by mixed-function oxidases of the liverin vitro. The metabolism of BPMC was competitively inhibitedby the addition of fenitrothion (5 µg/ml). Fenitrothionremained in the liver (7 µg/g liver). These results suggestthat competitive inhibition of BPMC metabolism by fenitrothionmay, at least in part, play a role in inhibition of BPMC detoxication,resulting in potentiation of its toxicity.