Application of solid low residue diets consisting mainly of elemental diet in colorectal diseases.
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Biomedical subjects
Publications and source records attributed to M Ohta.
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Antitumor therapies using polyamine antimetabolites combined with 1-(4-amino-2-methyl-5-pyrimidyl)methyl-3(2-chloroethyl)-3-nitrosourea (ACNU) or fluorinated pyrimidines for human gastric cancer xenotransplanted into nude mice were studied to determine inhibiting post-therapeutic regrowth of the tumor after cessation of antitumor treatments with polyamine antimetabolites alone. ACNU 20 mg/kg, fluorinated pyrimidine, 5-FU 52.8 mg/kg and 5'-deoxy-5-fluorouridine (5'-DFUR) 100 mg/kg as well as polyamine antimetabolites, alpha-difluoromethylornithine (DFMO) 1000 mg/kg and methylglyoxal-bis-guanylhydrazone (MGBG) 50 mg/kg were given intraperitoneally for 5 successive days. When DFMO and MGBG were combined with ACNU, the post-therapeutic regrowth was definitely inhibited, while combined treatments with 5-FU or 5'-DFUR did not inhibit the regrowth. Post-therapeutic DNA biosynthesis was suppressed in mice given DFMO, MGBG plus ACNU. On the contrary, in mice treated with DFMO, MGBG plus 5-FU or 5'-DFUR, suppression of DNA biosynthesis was not observed. Tumor tissue spermine levels in the DFMO, MGBG plus 5-FU or 5'-DFUR group remained unchanged, compared to those in the DFMO + MGBG group. In mice given DFMO, MGBG plus ACNU, however, spermine levels were markedly depressed; and the ACNU alone depressed also the tissue spermine levels. These different results between nitrosourea and fluorinated pyrimidines may relate to mechanisms of action of these antitumor drugs.
Occlusion of the right coronary artery (RCA) in the dog is associated with spontaneous sustained ventricular tachycardia (VT) during the 18 to 26 hours post occlusion period. Electrophysiologic studies suggest that these tachycardias are caused mainly by an automatic mechanism. In the present study we evaluated in 16 conscious dogs with VT 1 day after RCA occlusion the efficacy of (1) lidocaine (L), which depresses primarily the mechanism of enhanced normal automaticity; (2) verapamil (V), which depresses the mechanism of abnormal and triggered automaticity; and (3) combination of both L and V on these VTs. The RCA was occluded in 16 anesthetized closed-chest dogs by intracoronary balloon inflation. All 16 dogs had spontaneous VT while in the conscious state during the 18 to 26 hours post occlusion study period. L (5 mg/kg intravenously) bolus restored within 1 minute normal sinus rhythm (NSR), with a mean rate of 118 +/- 14 bpm, in dogs (n = 7) which had their VTs overdrive suppressed and had a mean rate of 145 +/- 14 bpm (range 110 to 150 bpm). L was ineffective in dogs (n = 9) which did not have their VTs overdrive suppressed and had a mean VT rate of 192 +/- 24 bpm (range 175 to 250 bpm). In contrast, however, V (0.15 mg/kg intravenously) was ineffective in all seven dogs with the slower VT rates, but was effective in restoring NSR with a mean rate of 140 +/- 14 bpm in six out of nine dogs with the faster VT rates.(ABSTRACT TRUNCATED AT 250 WORDS)
The efficacy of intravenous cibenzoline (3 mg/kg), propafenone (4 mg/kg), and procainamide (20 mg/kg) against inducible sustained and nonsustained ventricular tachycardias (VT) was evaluated in 12 conscious dogs with chronic isolated right ventricular (RV) infarction. RV infarct was caused by permanent occlusion of the right coronary artery in the closed-chest dog by intracoronary balloon inflation. Three to 10 days following the occlusion period, programmed electrical stimulation reproducibly induced sustained and/or nonsustained VT, allowing evaluation of antiarrhythmic drug efficacy. Propafenone was effective in preventing the induction of sustained VT in only one out of six dogs tested, but caused a significant (p less than 0.05) slowing of VT rate (269 +/- 13 to 230 +/- 10 bpm). Procainamide had effects similar to those seen with propafenone. Propafenone and procainamide were ineffective against nonsustained VT, and on established sustained VT once induced. Cibenzoline was effective in preventing the induction of sustained VT in two out of seven dogs, an effect which was not significantly different from either propafenone or procainamide. However, cibenzoline was significantly (p less than 0.05) more effective than either procainamide or propafenone in terminating an established induced sustained VT (four out of six dogs). Furthermore, cibenzoline converted nonsustained to sustained VT in four out of seven dogs tested. Histopathologic studies have shown infarction of the basal two thirds of the RV (38.5 +/- 7.8% of the RV) with no left ventricular involvement. It is concluded that the isolated RV infarction model is highly suitable for serial drug testing against inducible VT in conscious dogs, and this model of VT appears to be fairly resistant to standard and newer antiarrhythmic drug therapy.
When fresh liver is smeared on slides and incubated in Krebs-Henseleit Ringer solution containing 1 mM H2O2 at 37 degrees C, a yellowish-green autofluorescence develops in the hepatocyte plasma membrane. Indirect evidence shows that this peroxide-induced autofluorescence (PIAF) is due most probably to chemical reactions between proteins and the malondialdehyde produced by the membrane lipid peroxidation. Although the chemical nature of the PIAF has not been clarified yet, it is suitable under certain conditions for the measurement of the average lateral diffusion constant of the membrane proteins by means of the fluorescence recovery after photobleaching (FRAP) technique without the addition of any external fluorescent label. Analysis of four age groups for both sexes of Fischer 344 rats (3-5 rats per group, total 32) from 2 to 31 months of age revealed a significant negative linear correlation of the lateral diffusion constant of proteins with age in both sexes, with the slope of the females being somewhat smaller. Young males showed a diffusion constant about 2.8 X 10(-10) decreasing to 1.7 X 10(-10) cm2 X s-1 by 31 months of age at 37 degrees C, whereas the respective values in females were 2.7 X 10(-10) and 1.9 X 10(-10). The results are consistent with the predictions of the membrane hypothesis of aging, according to which an age-dependent loss of the passive permeability of the cell membrane for potassium (and probably for water) is the crucial point of the cellular aging.
Stimulation of the supratrigeminal area (STA) of the rat induced a monosynaptic EPSP in most mylohyoid-digastric motoneurons and a monosynaptic IPSP or EPSP in the majority of masseteric ones, contralaterally. Stimulation of the central amygdaloid nucleus induced the ipsilateral STA activity immediately followed by the contralateral mylohyoid nerve activities. The same amygdaloid stimulated excited 19 of 46 STA neurons, which were antidromically identified to project to the contralateral trigeminal motor nucleus. Nine of these were monosynaptically excited. The mean of the antidromic and monosynaptic latencies of these neurons explains the mean onset latencies of the amygdaloid influences on the contralateral trigeminal motoneurons. Therefore, the shortest crossing amygdalo-motoneuronal pathway is probably disynaptic and mediated by commissural STA neurons.
A method has been developed recently for measuring the average lateral diffusion constant of the proteins (D) in the cell membrane of hepatocytes in liver smears by fluorescence recovery after photobleaching (FRAP). A peroxide-induced autofluorescence (PIAF) of the membrane proteins was used as a fluorescent label. It has been established that D displays a significant negative linear correlation with age. The present paper describes age-estimations carried out on 12 male Fischer 344 rats (7-29 months of age) in so-called "blind experiments": the operator knew only the sex of the rat, determined D from a small piece of the freshly removed liver, and estimated the age of the rat from the age-dependent regression line for D established previously on 16 other Fischer 344 male rats of various ages. There was a strong correlation of the estimated age with the actual one (r = 0.92), the slope of the regression line was 0.98 and its intercept differed from 0 by only 0.5 months. These results indicate that D may play a decisive role in the determination of membrane functions as predicted by the membrane hypothesis of aging.
The susceptibility of infarcted right ventricular myocardium to inducible ventricular tachyarrhythmias was serially evaluated in 18 conscious dogs during the first 2 weeks after permanent right coronary artery occlusion. Properly timed double premature stimuli applied to the right ventricular outflow tract induced sustained (longer than 1 minute) ventricular tachycardia at rates of 190 to 400 beats/min in nine dogs, and ventricular fibrillation in six dogs. No ventricular arrhythmias could be induced in the remaining three dogs. The zone of premature coupling intervals within which ventricular tachyarrhythmias could be induced decreased in each dog as the infarct aged, and by day 12 after occlusion, no ventricular arrhythmias could be induced in any of the dogs studied. Both the size and the degree of patchiness (graded from 0 for no patchiness to +4 for patchiness throughout the infarct) of the infarct appear to be related to the nature of the induced rhythm. Infarcts with greater heterogeneity and those that were larger than 8% of the right ventricular volume were associated with a higher incidence of ventricular fibrillation, and infarcts with a lesser degree of patchiness were more suitable for sustained ventricular tachycardia (3.4 +/- 1.2 versus 1.4 +/- 0.4, p less than 0.05). These findings indicate that the infarcted right ventricular myocardium, independent of left ventricular involvement, can be associated with malignant ventricular tachyarrhythmias, ventricular tachyarrhythmias can be induced only during a well defined postinfarction period; and both the size and geometry of the right ventricular infarct determine the nature of the induced ventricular rhythm.
The efficacy of retrograde coronary venous delivery of procainamide for the management of spontaneous and inducible sustained ventricular tachycardia was evaluated and compared with systemic intravenous procainamide administration in 22 conscious dogs with permanent left anterior descending coronary artery occlusion. Selective retrograde injection of procainamide was achieved through an autoinflatable balloon catheter placed in the great cardiac vein, with the tip positioned in the vicinity of the site of left anterior descending coronary occlusion. Great cardiac vein retroinfusion of procainamide was significantly (p less than 0.05) more effective than systemic intravenous injection against spontaneous ventricular tachycardia 1 day after coronary artery occlusion (13 dogs) and against electrically induced sustained ventricular tachycardia in the 3 to 12 day postocclusion period (9 dogs). Significantly lower doses of procainamide were used with retroinfusion as compared with systemic administration, that is, 19.6 +/- 8.8 versus 35 +/- 0 mg/kg body weight during spontaneous tachycardia and 13.4 +/- 4.1 versus 32.1 +/- 2 mg/kg during induced tachycardia (p less than 0.01). Retroinfusion of saline solution through the great cardiac vein had no effect on either type of tachycardia. Myocardial tissue procainamide levels measured in infarcted and ischemic zones of the left anterior ventricular wall were 9 to 100 times higher after great cardiac vein retroinfusion than after systemic injection. Great cardiac vein dye injection studies demonstrated a preferential distribution in left ventricular regions supplied by the occluded coronary artery. It is concluded that regional coronary venous procainamide retroinfusion in dogs with myocardial infarction is more effective than systemic intravenous injection against both spontaneous and inducible sustained ventricular tachycardia. The greater efficacy of great cardiac vein treatment appears to be primarily related to selectively increased delivery of procainamide to ischemic myocardial sites.
The R-form lipopolysaccharide (LPS) from Klebsiella strain LEN-111 (O3-:K1-) forms a hexagonal lattice structure with a lattice constant of 14 to 15 nm when it is precipitated by addition of two volumes of 10 mM MgCl2-ethanol. When the LPS was suspended in various buffers (50 mM) at pH 2 to 12 for 24 hr at 4 C, at pH 2 and 3 pits of the hexagonal lattice structure markedly disappeared, at pH 4 to 8.5 the lattice structure was stable, and at pH 9 to 12 it tended to loosen somewhat. The LPS from which cations were removed by electrodialysis retained the ability of hexagonal assembly, although the lattice constant of the hexagonal lattice of the electrodialyzed LPS was large. The lattice structure of the electrodialyzed LPS was much more labile than that of the non-electrodialyzed LPS at alkaline pH levels and the former was completely disintegrated into ribbon-like structures when the LPS was suspended in 50 mM Tris buffer at pH 7.7 or higher. However, the electrodialyzed LPS formed a hexagonal lattice structure in Tris buffer at pH 8.5 containing 0.1 to 100 mM MgCl2. The lattice constants of the hexagonal lattice formed by the electrodialyzed LPS at 10 or 100 mM MgCl2 were very similar to that of the lattice of the non-electrodialyzed LPS. From these results it is concluded that the lability of the hexagonal lattice structure of the electrodialyzed LPS at alkaline conditions is due to removal of Mg2+ by electrodialysis.
The R-form lipopolysaccharide (LPS) from Klebsiella strain LEN-111 (O3-:K1-) forms a hexagonal lattice structure with a lattice constant of 14 to 15 nm when it is precipitated by addition of two volumes of 10 mM MgCl2-ethanol. The stability of this hexagonal lattice structure in long-term incubation at 4 C was investigated. The hexagonal lattice structure was stable for at least 220 days when the LPS was suspended in distilled water, but it had been disintegrated into a rough mesh-like structure when the LPS was suspended in 50 mM tris(hydroxymethyl)aminomethane (Tris) buffer, pH 8.5, at 4 C for 60 days. Half of the Mg bound to the LPS was released when the LPS was suspended in Tris buffer for 60 days, whereas Mg was not released when it was suspended in distilled water even for 220 days. By contrast, it was stable for at least 220 days in Tris buffer containing 5 mM MgCl2. The LPS suspended in Tris buffer for 60 days, at which time the structure had been disintegrated, could be restored to the original hexagonal lattice structure within 24 hr by addition of 5 mM MgCl2. From these results it is concluded that the hexagonal lattice structure of the LPS retains long-range stability if Mg bound to the LPS is not released from the LPS.
S-form lipopolysaccharides (LPS) from Klebsiella strain LEN-1 (O3: K1-) and from Salmonella minnesota strain 1114 were positively stained with ruthenium red, whereas R-form LPS from Klebsiella strain LEN-111 (O3-: K1-) and Ra, Rb1, RcP+, Rd1P-, and Re LPS from the respective mutant strains of S. minnesota were not or only faintly stained by such treatment. From these results it was concluded that ruthenium red stains the O-specific polysaccharide chains of LPS. The appearance of stained preparations of S-form LPS suggested that the material responsible for this positive staining corresponded to the surface projections which were seen by the negative staining technique as attached to the ribbon-like structures and spherules of the LPS.
We examined Escherichia coli K-12 lipopolysaccharide (LPS), which is known to be an R-form LPS, for its ability to form a hexagonal lattice structure in vitro. The LPS from E. coli K-12 strain JE1011 did not form a hexagonal lattice structure when it was precipitated by addition of two volumes of 10 mM MgCl2-ethanol, but it did form such a structure when it was electrodialyzed and then converted to the magnesium or calcium salt form. The lattice constant of the magnesium salt form was 15.2 +/- 0.3 nm and that of the calcium salt form 18.5 +/- 0.3 nm. Since prior treatment of the LPS with proteinase K in the presence of sodium dodecyl sulfate did not affect its capability of hexagonal assembly, the lattice formation by the LPS does not require the presence of proteins.
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A 73-year-old female with a calcified splenic mass received exploratory laparotomy and subsequent splenectomy. The histologic diagnosis of the splenic tumor was hamartoma associated with secondary cystic degeneration and calcification of the cyst wall. The tumor was composed of red pulp-like and white pulp-like areas. The former contained many plasma cells and hyalinized trabecular vessels, while the main component in the latter was lymphocytes. Splenic hamartoma was first described by ROKITANSKY in 1861 under the name of "splenoma". Usually, this rare tumor is asymptomatic and represents an incidental finding at autopsy. To the best of our knowledge, this is the second case report of splenic hamartoma in Japan. The clinicopathological features of splenic hamartoma are briefly reviewed.
1 alpha,25-Dihydroxyvitamin D3, the active form of vitamin D3, induced maturation of circulating monocytes to form macrophage-epithelioid cells and multinucleated giant cells in vitro. Calcitriol not only promoted the differentiation of monocytes, as shown by the marked morphological changes and enhanced secretion of lysozyme, but also induced their prominent proliferation, as exhibited by enhanced DNA synthesis and the increased number of monocyte cell nuclei. The proliferation of monocytes was observed after the addition of physiological concentrations of calcitriol. Multinucleated giant cells were frequently observed among the monocytes. These marked morphological changes and the proliferation of monocytes were not observed in control cultures, which did not include calcitriol. These results indicate that calcitriol plays a critical role in the formation of the sarcoid granuloma and give an explanation of some of the clinical findings on sarcoidosis. In view of the evidence that sarcoid macrophages convert 25(OH)D3 to calcitriol, our results raise the possibility that the active metabolite of vitamin D3, which may be produced by macrophage-epithelioid cells, induces the differentiation and proliferation of circulating monocytes into macrophage-epithelioid cells, which in turn form sarcoidosis granulomas. This autostimulation mechanism of sarcoid granuloma formation may provide a model for future studies.
This article describes a new attempt at the design of a general digital filter for the state estimation of a nonstationary nonlinear stochastic sound system. A recursive algorithm for estimating the higher-order statistics of arbitrary-function type, mean, and variance is obtained by introducing a new expansion form of Bayes' theorem. Further, the state probability density function (PDF) can also be estimated in a unified form of orthogonal or nonorthogonal series expansions by using these estimates. This method is widely applicable for cases where the random-noise fluctuation is non-Gaussian. The estimation algorithm proposed in this article agrees completely with a well-known Kalman filtering theory [J. Basic Eng. 82, 35-45 (1960); Kalman and Buchy, J. Basic Eng. 83, 95-108 (1961)], as a simplified special case when the stochastic system is of linear type with Gaussian random excitation. The validity and effectiveness of the proposed theory were confirmed experimentally by applying it to actually observed room acoustic data and road-traffic noise data.
It was recently suggested that the apparent biliary transport maximum (Tm, secretory maximum) for bile salts is primarily determined by their degree of cytotoxicity (the cytotoxicity hypothesis), based on experiments on male rats [Hardison, W. G., D. E. Hatoff, K. Miyai, and R. G. Weiner. Am. J. Physiol. 241 (Gastrointest. Liver Physiol. 4): G337-G343, 1981]. To confirm this hypothesis, we determined the Tm of three different bile salts, taurocholate (TC), taurochenodeoxycholate (TCDC), and tauroursodeoxycholate (TUDC) in female rats and hamsters. The order of Tm values in female rats was the same as that reported for male rats (TUDC greater than TC greater than TCDC), whereas in female hamsters it was TC greater than TCDC greater than TUDC. On the other hand, in hamsters, the order of cytotoxicity, evaluated in vivo by the biliary excretion of hepatocyte enzymes such as lactate dehydrogenase and alkaline-phosphatase and an increase in plasma lactate dehydrogenase, aspartate aminotransferase and alanine aminotransferase levels under a fixed rate infusion (0.6 and 1.2 mumol X min-1 X 100 g body wt-1) of bile salts, was inverse to the order of Tm values (TCDC greater than TC greater than TUDC) in rats, but in hamsters, too, TCDC was most cytotoxic. The order of Tm value in hamsters thus does not correspond to the order of cytotoxicity of these bile salts, suggesting that the cytotoxicity of bile salts may not be the sole determinant of bile salt Tm.