[Ruptured bronchial artery aneurysm; report of a case].

A 74-year-old man who went into shock following an acute hemomediastinum and left hemothorax was operated on. Postoperative angiographies revealed a saccular aneurysm of the left bronchial artery of 2.0 cm in diameter. Sixty days after the initial operation, the aneurysm was resected under F-F bypass. A saccular aneurysm was found at the root of the left bronchial artery, which had a very short segment between the aneurysm and the aorta. Pathological study of aneurysm revealed thinning of the wall and lack of tunica media.

Effect of postural change on blood volume in long-term hemodialysis patients.

In healthy subjects, the blood volume (BV) increases rapidly after postural change from standing to the supine position. However, little is known about the effect of postural change on BV in long-term hemodialysis (HD) patients. Therefore, we have examined the BV change caused by adopting the supine position from standing by continuous hematocrit monitoring, using the CRIT-LINE instrument, in 8 anuric HD patients. The hematocrit was monitored for 25 min with the patient in the supine position just before HD. The percentage change in the BV (% Delta BV) was calculated from the hematocrit and approximated using the equation: % Delta BV = b - [1 - exp(-c x time (min)] -a x time (min). Coefficient a was the slope of the linear part in the % Delta BV, b was the magnitude of BV increase and c was the rate of BV increase. Then we examined the relationship between the coefficients (a, b and c) and clinical parameters. In all patients, % Delta BV increased quickly after adopting the supine position. The mean increases were 2.8 +/- 0.6% after 5 min and 4.8 +/- 0.5% after 25 min. There was a significant correlation between the value of % Delta BV calculated from the hematocrit and the value calculated using above equation (0.92 < r < 0.99, p < 0.001). Although coefficient a did not correlate with a clinical parameter, coefficient b showed a significant positive linear correlation with the serum albumin level (r = 0.816, p < 0.05) and coefficient c showed a significant positive linear correlation with the percentage change in interdialytic weight gain (r = 0.736, p < 0.05). Furthermore, based on the % Delta BV, we calculated the change in total BV, which had increased by 181.5 +/- 21.9 ml after 25 min in the supine position. In conclusion, the change in the BV with time by continuous hematocrit monitoring using the CRIT-LINE instrument can be approximated by a modified monoexponential equation. BV increased quickly in HD patients after postural change from standing to the supine position.

Parenchymal echo patterns of cirrhotic liver analysed with a neural network for risk of hepatocellular carcinoma.

BACKGROUND: To objectively evaluate the parenchymal echo patterns of the liver in cirrhosis, an image analysing system in which a neural network is used has been found capable of numerically calculating coarse score (CS). Using this system, we analysed whether or not CS can serve as a predictive factor for the development of hepatocellular carcinoma (HCC). METHODS: The risk factors for HCC were evaluated in 95 patients with liver cirrhosis with an average follow-up period of 2041 +/- 823 days. We used a three-layer feed-forward neural network and a back-propagation algorithm to calculate CS. RESULTS: There were strong correlations between CS, alanine aminotransferase (ALT) and alpha-fetoprotein (AFP) and the average cumulative incidence rate of HCC evaluated by the Cox's proportional hazards model. The adjusted rate ratios were estimated to be 3.00, 2.80 and 2.01, respectively. The cumulative risks of HCC were significantly higher with an initial CS > or = 1.5 than with an initial CS < 1.5, with ALT > or = 80 IU/L than with initial ALT < 80 IU/L and with AFP > or = 20 ng/mL than with initial AFP < 20 ng/mL, all analysed by the log-rank test. CONCLUSIONS: Coarse score is a useful predictor for development of HCC.

An image analyzing system using an artificial neural network for evaluating the parenchymal echo pattern of cirrhotic liver and chronic hepatitis.

To objectively evaluate the parenchymal echo pattern of cirrhotic liver and chronic hepatitis, we applied an image analyzing system (IAS) using a neural network. Autopsy specimens in a water tank (n = 13) were used to examine the relationship between the diameter of the regenerative nodule and the coarse score (CS) calculated by IAS. CS was significantly correlated with the diameter of the regenerative nodule (p < 0.0001, r = 0.966). CS is considered to be useful for evaluating the coarseness of the parenchymal echo pattern.

[Clinical results of left ventricular free wall rupture following acute myocardial infarction].

We studied 19 cases of Left Ventricular Free Wall Rupture (LVFWR) following acute myocardial infarction, admitted to our CCU between 1987 and 1996. We were able to treat 15 patients and diagnosed 4 cases as LVFWR at postmortem after sudden deaths. Of the treated 15 patients, 11 survived: 1 out of 2 repaired under cardiopulmonary bypass (CPB), 5 out of 7 repaired without CPB, and 5 out of 6 non-surgically treated. Although the survival rate for those able to be treated was 73%, overall rate was 58%. There were 7 cases of blow-out type: 4 of which were sudden deaths, and 3 were operated. Thoracotomy and direct closure of rupture without CPB was done at bed-side in 2 cases. Even though hemostasis was successful, they did not survive. The 3rd case survived with the patch closure under CPB. In this case, the circulation was maintained pre-operatively with the pericardial-central venous bypass drainage method. This method seems to be extremely effective in saving blow-out cases. There were 12 subacute patients. Although 2 cases were lost, total of 10 patients were saved, including 2 direct suture closures of rupture without CPB, 3 median sternotomy and fibrin-glue fixations, 1 where only pericardial drainage was done, and 4 in whom percutaneous intrapericardial fibrin-glue fixation therapy was utilized. Since the risk of secondary damage to the fragile infarcted are from direct suturing of ruptured myocardium exists in LVFWR, we changed to the Infarction Exclusion Technique under CPB during surgical repair, based on our experiences with ruptured intraventricular septum. In general, the only treatment believed to be available for LVFWR has been surgical. However, our experiences suggest that other treatments may also be effective. If the best suitable method could be chosen from various therapies, it may contribute to improving outcome statistics. The reduction of left ventricular pressure in the treatment is extremely important, being the key to improving survival rate.

The significance of right ventricular ischemia in reflex bradycardia in humans.

Heart rates (HR) were measured before (control HR) and after (ischemic HR) balloon inflation during percutaneous transluminal coronary angioplasty in 96 patients with effort angina pectoris. The delta HR, defined as (ischemic HR-control HR), in the right coronary artery occlusion was significantly smaller than that in the left anterior descending artery or left circumflex artery occlusion. Among right coronary artery occlusions the delta HR in segment 1 occlusion was significantly smaller than that in segment 2 or segment 3 occlusion. It is suggested that the ischemia of the right ventricle plays an important role in producing a reflex bradycardic response in humans.

[Partial anomalous pulmonary venous connection to inferior vena cava (incomplete type of scimitar syndrome) in an elderly patient].

A 71-year-old woman presented with recent onset of dyspnea and fatigue on moderate exertion. She had been well during her entire life and had had three pregnancies and deliveries. Cardiomegaly was noted at the age of 30. On physical examination, systolic murmur was detected at the lower left sternal border. The chest X-ray showed cardiomegaly, increased pulmonary vascular markings and elevated right diaphragm. The electrocardiogram showed left ventricular hypertrophy. The echocardiography showed enlargement of right ventricle and atrium, massive tricuspid regurgitation and anomalous venous flow connected to the inferior vena cava from its right-posterior side. Cardiac catheterization demonstrated mild pulmonary hypertension and O2 step-up at the level of the anomalous venous connection to the inferior vena cava. On pulmonary arteriography, left pulmonary venous flow return to the left atrium and atrial septal defect was not found. Veins from the right lung met to form one vessel, went downward, and connected to the inferior vena cava at the level of Th12. L-R shunt was 45% and Qp/Qs was 1.83. Isolated partial anomalous pulmonary venous connection is a rare finding, and it is thought that the natural prognosis is good. The existence of our case, diagnosed at the age of 71, supported this concept.

Isolation and characterization of major urinary oligosaccharides excreted by a patient with type 3 GM1 gangliosidosis.

Two major oligosaccharides were isolated from the urine of a patient with type 3 GM1 gangliosidosis. From structural studies including compositional sugar analysis, fast-atom bombardment mass spectrometry, direct-inlet chemical ionization mass spectrometry, methylation analysis, chromium trioxide oxidation, and proton magnetic resonance spectroscopy, their structures were deduced to be as follows: [formula: see text] Both oligosaccharides have beta-linked galactose at the non-reducing ends. Oligosaccharide 1 is one of the most common urinary oligosaccharides found in type 1 and type 2 GM1 gangliosidosis. Oligosaccharide 2, lacto-N-difucohexaose II, has not been described in the urine of GM1 gangliosidosis patients. Excretion of oligosaccharide 1 in the type 3 patient was much less than that of a type 2 patient. Thin-layer chromatographic analysis revealed that the excretion of oligosaccharides with higher molecular weight than that of oligosaccharide 1 (octasaccharide) in the type 3 patient was much less than that of a type 2 patient, raising the possibility that the mutant beta-galactosidase of type 3 GM1 gangliosidosis can still act to some extent on higher molecular weight oligosaccharides containing beta-linked galactose at the non-reducing end.

[Sudden cardiac death in the emergency hospital].

We investigated 303 (men: women = 2:1) cases who suffered sudden heart arrest in Yamagata city since 1984 to 1987. The incidence rate was 41.0/100,000/year, and increased markedly with increasing age. There was a tendency for sudden death to occur in the winter season, evening and early morning. Two major causes were cardiac disease (especially ischemic heart disease) (46.4%) and intracranial hemorrhages (18.6%). 20% of all the heart-arrest cases were able to be saved, but, depending on the kind of heart disease the survival rate varied greatly (18.8% in acute myocardial infarction and 71.4% in vasospastic angina), (40.0% in ventricular fibrillation and 13.3% in the bradycardic arrhythmias). Survival rate was also effected by the time interval from the onset till the beginning of cardio-pulmonary resuscitation. About one half of the cases had histories of cardiac disease. Premonitory symptoms were observed in at least one third of the cases.

Type 3 (adult) GM1 gangliosidosis: case report.

GM1 gangliosidosis is usually a pediatric disease caused by hereditary acid beta-galactosidase deficiency. There have been a few cases in adults. We saw a 51-year-old Japanese man with type 3 GM1 gangliosidosis who was manifesting dementia, dysarthria, gait disturbance, and limb rigidity. Radiologic studies showed platyspondylia, acetabular hypoplasia, and flattened femoral heads. Biochemical analysis revealed generalized acid beta-galactosidase deficiency.

Interspecies comparison of muscle gangliosides by two-dimensional thin-layer chromatography.

Skeletal muscle gangliosides prepared from ten species of animals (human, monkey, bovine, hog, dog, cat, rabbit, guinea pig, mouse, and chicken) were studied by two-dimensional thin-layer chromatography. Densitometric quantification of spots on the chromatograms was carried out with an image analysis system equipped with a computer system. In about thirty-five resorcinol-positive spots, sixteen components could be identified by comparison with authentic standards we had previously obtained. GM3 ganglioside was found as a major component in all examined animals, but there were remarkable species variations in the minor gangliosides. In bovine and hog muscle gangliosides, more than fifteen minor components were detected owing to the presence of N-glycolyl neuraminic acid species. In contrast to this, muscle gangliosides of human, dog, cat, rabbit, and chicken showed relatively simple patterns because of the absence or the small amounts of N-glycolyl type gangliosides. The presence of lactosamine containing gangliosides was characteristic of muscle gangliosides of the examined species.

Comutagenic effect of norharman with aminopyridine derivatives.

The mutagenicities of 3 monoaminopyridines, 4 methyl-substituted monoaminopyridines and 3 diaminopyridines were tested with or without norharman in the Salmonella assay system. None of the compounds was mutagenic without norharman. However, 3-aminopyridine and 2-amino-3-methylpyridine were mutagenic in the presence of norharman and S9 mix; 3-aminopyridine was mutagenic to TA98, but not to TA100, while 2-amino-3-methylpyridine was mutagenic to both TA98 and TA100, although its mutagenicity was much stronger in TA98.

Mutagenicities of 61 flavonoids and 11 related compounds.

The mutagenicities of 61 flavonoids (naturally occurring flavonoid aglycones and flavonal glycosides and synthetic flavonoids) and those of 11 compounds structurally related to flavonoids were tested with Salmonella typhimurium strains TA100 and TA98. Among the 22 flavone derivatives tested, only wogonin was strongly mutagenic, while five derivatives, apigenin triacetate, acacetin, chrysoeriol, pedalitin, and pedalitin tetraacetate, were only weakly mutagenic. Two bisflavonyl derivatives, neither of which has a 3-hydroxyl group, were not mutagenic. Of the 16 flavonol derivatives tested, all except 3-hydroxyflavone and the tetra- and penta-methyl ethers of quercetin were mutagenic. Of the five flavanone derivatives tested, only 7,4-dihydroxyflavanone was mutagenic, showing weak activity. Of the four flavanolol derivatives tested, hydrorobinetin and taxifolin were weakly mutagenic. Of the six isoflavone derivatives tested, tectorigenin was weakly mutagenic. Of the 11 compounds in the miscellaneous group structurally related to flavonoids, only isoliquiritigenin was mutagenic, showing weak activity. For the emergence of strong mutagenicity, the double bond between positions 2 and 3 and the hydroxyl group at position 3 are required, except in wogonin, which does not have a hydroxyl group at position 3 but is strongly mutagenic to TA100. The 3-O-acetyl ester of flavonol, quercetin, was mutagenic with S9 mix, but 3-O-methyl ethers were not. Six flavonol glycosides, three quercetin glycosides and three kaempferol glycosides were mutagenic after preincubation with "hesperidinase," a crude extract of Aspergillus niger. Of 66 flavonoid agylcones and compounds structurally related to flavonoids, quercetin was the strongest mutagen. The carcinogenicity of this compound should be clarified because it is ubiquitously found in vegetables.

Pyrolysis products from amino acids and protein: highest mutagenicity requires cytochrome P1-450.

Pyrolysis products of proteins and amino acids are highly mutagenic, but metabolism of these chemicals by rat liver subcellular fractions is known to be required for production of the mutagenic intermediates. We examined the mutagenesis of seven purified pyrolysis products from tryptophan, lysine, glutamic acid, and soybean globulin with Salmonella typhimurium strain TA98 in the presence of liver fractions from genetically "responsive" C57BL/6N and Ah(b)/Ah(d) or "nonresponsive" DBA/2N and Ah(d)/Ah(d) mice that had been pretreated in vivo with benzo[a]pyrene. For all pyrolysis products tested, mutagenesis is 2-fold to more than 1000-fold greater with C57BL/6N and Ah(b)/Ah(d) than with DBA/2N or Ah(d)/Ah(d) liver fractions. A sucrose density gradient assay for detecting the Ah regulatory gene product, the receptor, was studied with C57BL/6N hepatic cytosol. At levels 100 times in excess of [1,6-(3)H]2,3,7,8-tetrachlorodibenzo-p-dioxin, nonlabeled 2,3,7,8-tetrachlorodibenzo-p-dioxin, 3-methylcholanthrene, and beta-naphthoflavone (inducers of cytochrome P(1)-450) are able to displace the radioligand from its hepatic cytosolic receptor; four pyrolysates from tryptophan, glutamic acid, and soybean globulin did not have this capacity. These data indicate that the pyrolysis products tested, although not effective as inducers of cytochrome P(1)-450, are most mutagenic when metabolized by P(1)-450. Potent P(1)-450 inducers-present in pyrolysates during the combustion process-might be present in quantities insufficient to initiate mutagenesis or carcinogenesis but might have a synergistic action, or act as "comutagens" or "cocarcinogens," with the N-containing heterocyclic pyrolysis products. A quantitative relationship between mutagenic and carcinogenic potency of these pyrolysis products remains, however, to be demonstrated.

The effect of norharman on the metabolism of benzo[alpha]pyrene by rat-liver microsomes in vitro in relation to its enhancement of the mutagenicity of benzo[alpha]pyrene.

The effect of norharman on the metabolism of benzo[alpha]pyrene by rat-liver microsomes was studied. Separation of the metabolites into hydrophilic and hydrophobic fractions showed that norharman inhibited the conversion of hydrophobic metabolites to hydrophilic ones. Analysis of the hydrophobic metabolites by high-pressure liquid chromatography showed that norharman also inhibited the disappearance of benzo[alpha]pyrene itself. However, large amounts of hydrophobic metabolites, such as phenol, quinones and diols, were formed in the presence of norharman, and formation of the strong mutagen 7,8-dihydroxybenzo[alpha]pyrene was increased 10-fold by norharman. The increase in formation of this compound may be one of the chief reasons why norharman enhances the mutagenicity of benzo[alpha]pyrene on Salmonella typhimurium.