AbstractBackground: The direct contribution of bile to gastric inhibitory polypeptide (GIP) release and the role of bile in regulating GIP secretion in response to fat ingestion are still obscure. The present study was aimed to clarify the influence of bile on GIP release. Methods: Seven patients with obstruction of the common bile duct and nine volunteers participated in the study. Fifty milliliters of Lipomul® was ingested, and GIP was measured serially for 180 min. After intraduodenal instillation of pooled autologous bile for 2 days, the same study was carried out. Results: The fat-stimulated GIP response was significantly lower in the patients than in the controls. The basal GIP level did not change on bile instillation, but the GIP response to fat ingestion was significantly increased on bile instillation compared with that in the absence of bile. Conclusions: Intraluminal bile alone does not stimulate the secretion of GIP, but it promotes GIP secretion in response to fat ingestion.Key Words: Bilebile duct obstructiongastric inhibitory polypeptideperiampullary tumor
We investigated the reduction in the accuracy of DNA replication and repair (i.e. genetic instability) in urinary tract malignancy using microsatellite regions. The subjects were 17 patients with renal cell carcinoma and 14 with bladder tumors. After polymerase chain reaction (PCR) was performed with FITC-labeled primers, CA repeats were analyzed. The primers used were D2S123, D3S1067, and TP53. Tissue positive for all 3 primers was considered to show a replication error (RER). Genetic instability was found in 5 out of 17 patients with renal cell carcinoma (29%) and 3 out of 14 patients with bladder tumors (21%). Among the bladder tumor patients, 2 were positive for only TP53 and 1 was considered to have RER. Among the patients with renal cell carcinoma, one was positive only for D3S1067 and the other 4 were considered to have RER.
Scrutinization of data on 56 patients of primary esophageal squamous cell carcinoma and not given preoperative irradiation therapy disclosed 36 areas (64.1%) of intra-epithelial carcinoma contiguous to the main lesion, and in 16 (28.7%) there was a multiple occurrence of squamous cell carcinoma, in which 13 were double and 3 were triple carcinomas. A total of 96 junctions between intra-epithelial carcinoma and non-cancerous epithelium were histologically investigated. These junctions could be grouped into two types: well-demarcated (29 areas, 30.2%) and ill-demarcated (67 areas, 69.8%) types. The latter was separable into 12 (12.5%) of whole layer, 33 (34.4%) of basal layer and 22 (22.9%) of irregular patterns. Epithelial dysplasia occurred in one (3.4%) of well-demarcated and ten (14.9%) of ill-demarcated junctions, and almost all lesions of dysplasia were moderate or severe. Thus, most carcinomatous transformation had occurred at the site of junction (in-situ carcinogenesis) and epithelial dysplasia may be a carcinoma rather than pre-cancerous lesion, per se.
The analysis of peripheral blood lymphocytic subpopulations was conducted with 16 bladder tumor patients. Lymphocytes were collected centrifugally from the peripheral blood of preoperative patients with bladder tumors, and measured by means of flow cytometry. Among the stages of the bladder tumor patients, there were no clear relationships in the ratio between T cells and B cells. However, with the progression in stages a rise in OKT 8, as well as the lowering of the OKT 4/OKT 8 ratio were discerned. In relation to pTis, Leu 7 showed a higher value than that in other groups with advanced invasion. This suggests that in measurements of lymphocyte subsets in peripheral blood, it will to a certain extent be possible to estimate the preoperative immunological competence of bladder tumor patients.
Background In the clinical situation, the saddle-back (S-B) type is more frequently detected than the coved type. In the present study, the discrimination of Brugada syndrome from the S-B type individuals using a marker of the standard 12-lead electrocardiography (ECG) was attempted. Methods and Results The study group consisted of 55 individuals with the S-B type in whom pilsicainide provocation test (PLC test) was carried out. The time from the onset of the QRS wave in lead V2 (IV 2) to the peak of the late R-like wave in the QRS wave (PV2), and the time from IV2 to the offset of the QRS wave in lead V5 (EV5) were measured. The coved type was induced by the PLC test in 29 cases (N-C group), but not in the remaining 26 cases (N-N group). The (IV2 -PV2) - (IV2 - EV5) value before the PLS test was greater in the N-C group than in the N-N group. The negative predictive value of `(IV2 - PV2) - (IV2 - EV5) ≥0' was 76.4% for the prediction of a positive PLC test. Conclusions A `(IV2 - PV2) - (IV2 - EV5) ≥0' is a useful ECG marker for the discrimination of Brugada syndrome in the S-B type individuals. (Circ J 2007; 71: 546 - 549)
There is no agreement at present as to which is the optimal site for artery cannulation for cardiopulmonary bypass in repair of acute aortic dissection (AAD). We have employed right axillary artery cannulation (RAAC) in combination with femoral artery cannulation to overcome the drawbacks of single cannulation. From January 2000 to August 2006, 88 patients underwent emergency surgical repair of the aortic arch (mean age 65+/-13 years, 37 men) for AAD. All operations were performed under hypothermic circulatory arrest with antegrade selective cerebral perfusion. Preoperatively, nine patients were in shock and 18 patients showed malperfusion. The average duration of circulatory arrest was 52+/-17 min and that of myocardial ischemia was 135+/-53 min. Total aortic arch replacement was done in 47 patients and hemiarch aortic replacement in 41. The hospital mortality rate was 2.3% (2 of 88); the fatal cases were among those who were in shock preoperatively. The perioperative stroke rate was 5.7% (5 of 88). The hospital mortality rate of the 25 patients with preoperative malperfusion was 4.0% (1 of 25); the fatal case had coronary malperfusion. Our approach for AAD was associated with a low mortality even in patients with malperfusion.
SUMMARY 1. This study has pharmacologically characterized endothelin (ET) receptor subtype(s) mediating contraction and enhancement of adrenergic contraction in guinea‐pig pulmonary artery. Isometric tension of the isolated endothelium‐denuded ring preparations was measured in the presence of indomethacin (10 −5 mol/L) and N G ‐nitro‐L‐arginine methyl ester ( l ‐NAME; 3X10 −4 mol/L) to exclude a mechanism via endothelium, cyclo‐oxygenase‐generated eicosanoids and nitric oxide. 2. In the additional presence of tetrodotoxin (TTX; 3X10 −7 mol/L), ET‐1 (10 −11 ‐10 −7 mol/L) concentration‐dependently contracted the preparations. The rank order of potency to contract the preparations among ET receptor agonists was ET‐1, sarafotoxin (STX) 6b>ET‐3>IRL 1620, STX 6c. BQ‐123 (7X10 −7 ‐7X10 −6 mol/L) concentration‐dependently shifted the concentration‐contraction curve for ET‐1 to the right in a parallel manner. Pretreatment with STX 6c (3X10 −7 mol/L for 30 min) did not significantly desensitize contractions to ET‐1, ET‐3 or IRL 1620 (P>0.05; t ‐test, 10 d. f.). 3. ET‐1 (10 −10 ‐10 −9 mol/L) and STX 6b (10 −9 ‐10 −8 mol/L) significantly enhanced the electrical field stimulation‐induced contraction in a BQ‐123‐sensitive manner (P<0.05; t ‐test, 24–38 d.f.), while ET‐3 (10 −11 ‐10 −8 mol/L) and STX 6c (10 −11 ‐10 −7 mol/L) did not affect contractions. ET‐1 (10 −11 mol/L) significantly enhanced contractions to exogenous nor‐adrenaline in the presence of TTX (3X10 −7 mol/L) (P<0.05; t ‐test, 16 d.f.). 4. These data indicate that the BQ‐123‐sensitive ET A receptor mediates both contraction and enhancement of adrenergic contractions in the guinea‐pig pulmonary artery.
Aims: Pulmonary vein triggers play an important role in the initiation of atrial flutter (AFL) and atrial fibrillation (AF) explaining the high incidence of AF after cavotricuspid isthmus ablation (CTI).We present the long-term results of a prospective randomized trial including a stand-alone pulmonary vein isolation (PVI) for the treatment of AFL.Methods and Results: 74 patients with AFL without a history of AF were randomly assigned to three groups: 1) antiarrhythmic drugs (AAD), 2) CTI ablation, 3) circumferential PVI.The primary end-point was defined as the recurrence of any atrial arrhythmia, the secondary endpoint was recurrence of AFL.After arrhythmia recurrence in the PVI group a second procedure was performed to close gaps.During follow-up of 2.77 + 1.28 years 19 of 23 patients in the AAD group (82.6%), 19 of 25 patients in the CTI group (76%) and 14 of 26 patients in the PVI group (53.8%) reached the primary endpoint ( p .0.05).AFL reoccurred in 13 patients in the AAD group (56.5%) and after a single ablation in 2 patients in the CTI group (8%) and in 5 patients in the PVI group (19.2%) ( p , 0.05).After a second PVI in 13 of 14 patients 21 patients (80.8%) remained free of any atrial arrhythmia ( p , 0.001) and 24 patients remained free of AFL ( p , 0.001 PVI vs. AAD, p , 0.001 PVI vs. CTI ablation).
'%3e%3cpath fill='%23012169' d='M0 0v30h60V0z'/%3e%3cpath stroke='%23fff' stroke-width='6' d='m0 0 60 30m0-30L0 30'/%3e%3cpath stroke='%23C8102E' stroke-width='4' d='m0 0 60 30m0-30L0 30' clip-path='url(%23b)'/%3e%3cpath stroke='%23fff' stroke-width='10' d='M30 0v30M0 15h60'/%3e%3cpath stroke='%23C8102E' stroke-width='6' d='M30 0v30M0 15h60'/%3e%3c/g%3e%3c/svg%3e)