Primary cardiac chondrosarcoma--a case report.
We report a case of chondrosarcoma of the heart that was managed surgically. As chondrosarcoma of cardiac origin is extremely rare, this case is described with a brief comment.
Chondrosarcoma↗
Biomedical subjects
K Minakata
Publications and source records attributed to K Minakata.
[A case of scheduled mitral valve replacement for mitral regurgitation caused by papillary muscle rupture after acute myocardial infarction].
Mitral regurgitation caused by papillary muscle rupture after acute myocardial infarction has poor prognosis, and it is the usual course for such cases in cardiogenic shock to be performed early mitral valve replacement. However, we recently experienced a case of successful scheduled mitral valve replacement for mitral regurgitation caused by rupture of the posterior papillary muscle after acute inferior myocardial infarction. The patient was a 63-year-old woman who admitted to a hospital with back pain and dyspnea and was diagnosed as pulmonary edema due to mitral regurgitation after acute myocardial infarction. She was treated with dopamine and diuretic agents effectively, but not weaned from these drugs. Then, she was transferred to our hospital. At the admission, she was in the NYHA class II due to mitral regurgitation and inferior myocardial infarction with papillary muscle rupture revealed by transesophageal echocardiography. Cardiac catheterization demonstrated total occlusion of the proximal right coronary artery (segment #2) and mitral regurgitation in Sellers III. The patient underwent a successful scheduled mitral valve replacement with SJM 27M concomitant with coronary artery bypass grafting 47 days after the onset of acute mitral regurgitation. There are few reports that successful surgical treatment for papillary muscle rupture was done more than 4 weeks after the onset of mitral regurgitation in Japan.
Female↗
[Surgical treatment of infective endocarditis associated with cerebral mycotic aneurysm].
We experienced two cases of infective endocarditis associated with cerebral mycotic aneurysm. Case 1: 58 year-old man underwent emergency aortic and mitral valve replacement due to active infective endocarditis and congestive heart failure diagnosed by transesophageal echocardiography. After the operation, he did not wake up and his bilateral pupils were dilated. Computed tomography demonstrated massive intracranial hemorrhage and severe brain edema. He died from multiple organ failure 22th postoperative day. Rupture of cerebral mycotic aneurysm was strongly suspected. Case 2: 56 year-old man was admitted with severe headache and high grade fever. Computed tomography demonstrated intracranial hemorrhage. Cerebral mycotic aneurysm was detected at left distal middle cerebral artery by cerebral angiography. Infective endocarditis and mitral regurgitation were also diagnosed by echocardiography. He underwent cerebral mycotic aneurysmectomy after intensive antibiotics therapy, followed by successful mitral valve replacement. We review the literatures and discuss the problems of surgical management of infective endocarditis with cerebral mycotic aneurysm.
Aneurysm, Infected↗
Effect of dietary paraquat on a rat mutant unable to synthesize ascorbic acid.
To obtain some insight into the toxicity of paraquat (PQ) in humans, PQ dichloride at 250 ppm in the diet was administered to both normal (NO) rats and ODS-od/od (OD) rats which are unable to synthesize ascorbic acid (AsA). Firstly, OD rats and NO rats treated with PQ were compared with untreated NO rats (CO). Only OD rats displayed several symptoms of PQ poisoning such as anorexia, hypokinesia, diarrhea, epistaxis, tremor and their pili became rough about 9 days after. Their cysteine proteinase inhibitor level in plasma and lung increased to 2- and 6-fold, respectively, of CO. In contrast, NO rats treated with PQ resembled CO rats, and their cysteine proteinase inhibitor levels were unchanged until 11 days. After this period they began to display symptoms. Secondly, OD rats fed with different amounts of AsA were compared. Excess AsA delayed the onset of symptoms by only 1 day. Thirdly, the day of onset of symptoms was found to be influenced with the weight of rats.
Animals↗
[Paternity probability in the cases of incest].
To calculate the paternity probability in the cases of incest where the alleged father was either the father or the brother of the plaintiff's mother, some algebraic expressions applicable to a simple codominant diallelic genetic marker system were derived by modifying the formulas of Essen-Möller and Komatsu (the both formulas gave the same result). The paternity probability in the incest case is generally lower than that in usual case, because in the former case an allele present in the mother is sometimes found in both the alleged father and the child (plaintiff), even if the alleged father is not true father. The paternity probability in the incest case, however, becomes higher than that in usual case when an allele is common to both the alleged father and the child but not to the mother. The mean value of paternity probability becomes lower, as the relationship becomes closer between the alleged father and the mother.
Alleles↗
[A method to calculate the probability of paternity between relatives--a paternity case where the putative father was a deceased granduncle].
To test paternity in a case where the putative father was a deceased uncle of mother (plaintiff's granduncle), we designed a new method to calculate the probability of paternity likelihood. The putative father's genotypes of red cell antigens, HLA and short tandem repeat (STR) polymorphism were estimated from those of mother and sister of the plaintiff. When the probability was calculated from the frequencies in the unrelated individuals (the standard method), a significant bias might be introduced since the putative father and the plaintiff were likely to have the same alleles come from their common ancestry. Therefore, we designed a new method to calculate the likelihood ratio from the frequencies in the group of mother's uncles estimated from mother's genotypes. The probability (0.9299) calculated with our method was found to be lower than that (0.9992) done with the standard method indicating that the new method could remove the bias introduced from the incest.
Adult↗
[Right ventricular function in patients with poor left ventricular function: studies in patients undergoing coronary artery bypass surgery].
In many patients, right ventricular (RV) dysfunction is due to RV infarction. In some patients, however, RV dysfunction may be secondary to the left ventricular (LV) dysfunction. In order to clarify the influence of poor LV function on RV function, RV ejection fraction (EF) was evaluated serially by thermodilution techniques (REF-1, Edwards Laboratories) in patients with LVEF less than 40% who underwent aorto-coronary bypass surgery with uneventful postoperative course. The patients were divided into four groups depending on the site of LV infarction; anterior (n = 13), inferior (n = 8), anterior + inferior (n = 16), and no infarction (n = 4). Control (n = 11) consisted of the patients with LVEF more than 60% and with no significant stenosis of the right coronary artery. Cardiac index, intracardiac pressures and amount of catecholamine used during postoperative course showed no significant differences among the groups including control. However, the groups except for the group of anterior infarction showed significantly low pre- and postoperative RVEF compared with control. Only the group of anterior infarction had almost normal RVEF. These results mean that RV dysfunction associated with inferior infarction remain long afterwards and that low LVEF due to anterior infarction caused little effect on RV function.
Aged↗
Diquat increases cysteine proteinase inhibitors greatly in rat plasma and tissues.
Biochemical and gross pathological effects of diquat were studied with special attention to cysteine proteinase inhibitor level which was often increased in acute and chronic disorder. Diquat was fed continuously to rats at the dose of 1000 ppm in the diet. After 10 days, anorexia and severe diarrhea were observed but epistaxis and hypokinesia were not apparent. The rats were killed after feeding the diet for 13.5 days and plasma components such as acute phase reactant proteins and some vitamins which act as antioxidants were examined. The results showed that alpha-cysteine proteinase inhibitor (alpha-CPI) increased to 9-fold and vitamin C radical increased to 1.6-fold, whereas alpha 1 proteinase inhibitor (alpha 1-PI) decreased to 0.9-fold and vitamins C and E were the same as the control. Among three components of alpha-CPI, the T kininogen level in intoxicated rat plasma was about 20-fold, whereas the high molecular weight kininogen level was about 2-fold of the control. Diquat also enhanced the cysteine proteinase inhibitor (CPI) level to 20-fold in kidney and to 7- to 10-fold in the other organs. The large increment of T kininogen in these organs was also confirmed immunologically. The kidney showed a granular degeneration and its weight increased to 1.2-fold of control. The other organs showed neither gross pathological alteration nor weight change, compared with the control. The diquat distribution was highest in spleen and next highest in kidney among several organs. These results were compared with those caused by paraquat.
Animals↗
Acute-phase reactant proteins and antioxidants in rats intoxicated chronically with paraquat.
Paraquat dichloride at 250 ppm in the diet was fed continuously to rats. Though no apparent effect of paraquat was observed until 10 d, some rats then began to show several symptoms such as diarrhea, anorexia, epistaxis, and hypokinesia, and in some cases rats died after this period. The biochemical examination of plasma components revealed appreciable changes in the concentrations of an acute-phase reactant protein and some vitamins that act as antioxidants. alpha-Cysteine proteinase inhibitor increased by 5-fold, and vitamin C and its radical increased by 1.5- and 1.7-fold, respectively, whereas alpha 1 proteinase inhibitor decreased slightly. Paraquat enhanced the cysteine proteinase inhibitor levels in lung, liver, and kidney by 6.2-, 6.0-, and 4.5-fold of control, respectively. Among three components of alpha-cysteine proteinase inhibitor, the T kininogen level of treated rat plasma was about eight-fold higher than control, whereas the high-molecular-weight kininogen level was unchanged. The large increment of T kininogen was also seen in lungs of the treated rats.
Acute-Phase Proteins↗
Ascorbate radical levels in human sera and rat plasma intoxicated with paraquat and diquat.
To clarify the toxicological mechanism of action of paraquat and diquat, the level of ascorbate radical, an oxidized product of ascorbic acid, was examined using the electron spin resonance (ESR) method. The ascorbate radical level increased to twice the normal level in sera from humans acutely intoxicated with a 1:1 mixture of paraquat and diquat, and to more than 1.5 times the normal level in rat plasma containing moderate levels of paraquat. The dosage level for rats was 0.025% paraquat dichloride in the diet. The ascorbate radical in both intoxicated human sera and rat plasma decayed much faster than that in normal samples.
Aged↗
Correlation between plasma alpha-cysteine proteinase inhibitor level and pyruvate kinase activity in vitamin E-deficient rats.
Weaning rats were divided into two groups, one group being fed a vitamin E-deficient diet, and the other an alpha-tocopherol-containing (50 mg/kg) control diet. Rats were killed at 1, 2, 3 and 4 months of feeding. The following results were obtained. 1. Both plasma and liver alpha-tocopherol levels decreased greatly by feeding vitamin E-deficient diet for 1 month, and thereafter decreased gradually by continued feeding. 2. Somehow different results were obtained concerning liver peroxidation value by the method of analysis. In the case of chemiluminescence, the value increased by vitamin E deficiency during the first 2 months, but thereafter, the value was almost unchanged. On the contrary, in the case of TBA-RS, the value increased gradually throughout the entire 4 months of feeding period. 3. Both plasma alpha-CPI level and pyruvate kinase activity increased by vitamin E deficiency, showing similar pattern of change with feeding period. Especially, marked increase of these values was observed in vitamin E-deficient rats fed for longer than 2 months, and differences from control groups were highly significant (in both cases, at 2 months, p < 0.005, and at 3 and 4 months, p < 0.001). And, in vitamin E-deficient group, including all the rats fed on test diet for 1 to 4 months, correlation between both values was very high, and was highly significant (r = 0.9060, p < 0.001).
Animals↗
Quantitative analysis of chlorpromazine by electron spin resonance (ESR) spectroscopy.
A simple and sensitive method is described for quantitative analysis of chlorpromazine in blood, serum, urine and tissue homogenate. The chlorpromazine cation radical produced by adding perchloric acid and 2,3-dichloro-5,6-dicyano-p-benzoquinone to the sample can be detected by the ESR method at room temperature. The sensitivity limit is 10 ng, that is, 20 microliters of the solution containing 0.5 microgram chlorpromazine/ml. The time needed for the measurement is within 10 min. The chlorpromazine radical thus produced is very stable; for example, 95% of the radical was observed after 24 h. The advantage of this method is discussed by comparing with the ordinary spectrophotometry which requires the purification of the sample.
Chlorpromazine↗
Identification of full-sized forms of salivary (S-type) cystatins (cystatin SN, cystatin SA, cystatin S, and two phosphorylated forms of cystatin S) in human whole saliva and determination of phosphorylation sites of cystatin S.
Our recent work on the gene structures for human salivary (S-type) cystatins [Saitoh, E. et al. (1987) Gene 61, 329-338] has suggested that the structures of cystatins which we determined previously at the protein level lack N-terminal peptide portions of the full-sized intact forms. In the present study, attempts were made to isolate full-sized S-type cystatins by introducing methanol fractionation into the purification steps to suppress the enzymatic activity present in saliva. Full-sized cystatin SN and two phosphorylated forms of full-sized cystatin S were thus isolated. Analysis of one fraction indicated that this was a mixture of full-sized cystatin SA and non-phosphorylated cystatin S. The phosphorylation sites of cystatin S were determined to be Ser-Ser-Ser1(P)-Lys-Glu-Glu- for monophosphorylated cystatin S and Ser1(P)-Ser-Ser3(P)-Lys-Glu-Glu- for diphosphorylated cystatin S. Immunoblotting analysis with anti-cystatin S antiserum revealed that tears and seminal plasma also contained S-type cystatins, but diphosphorylated cystatin S was detected neither in tears nor in seminal plasma and no cystatin SN was found in seminal plasma. These data indicate that S-type cystatins are secreted into the oral cavity without significant degradation in salivary glands or ducts and that they are expressed tissue specifically.
Amino Acid Sequence↗
Effects of vitamin E on toxicity by minute amounts of paraquat fed continuously to rats.
The effects of vitamin E on toxicity by minute amounts of paraquat fed continuously for some period to rats were investigated. Two experiments were carried out as experiments 1 and 2. In both experiments, weaning rats were divided at first into two groups; one group was given a vitamin E-deficient diet, and the other a vitamin E-supplemented control diet (50 mg alpha-tocopherol/kg of diet). They were fed on these diets for 40 days. After that, in both experiments, the rats that had been fed the vitamin E-deficient diet were further divided into two groups, which were either given a paraquat-added diet (+PQ-E) or continuously fed the same vitamin E-deficient diet (-E). The amount of paraquat added was 250 mg of methyl viologen per kg of diet. After the addition of paraquat, these two groups were pair-fed. In experiment 1, paraquat was given to all the rats fed the vitamin E-supplemented control diet (+PQ+E). In experiment 2, rats fed the control diet were divided into paraquat-added (+PQ+E) and non-paraquat-added (+E) groups, similar to those of vitamin E-deficient rats. These two groups were also pair-fed thereafter. In both experiments, about 35 days after paraquat addition, they were sacrificed. Plasma and liver alpha-tocopherol contents were measured by HPLC, and liver peroxidation value was measured by chemiluminescence and the TBA method. And, as parameters of vitamin E deficiency, plasma pyruvate kinase and GOT activities and alpha-cysteine proteinase inhibitor (alpha-CPI) level were measured. When the analyzed values were compared between paraquat-added and the corresponding not-added control groups (+PQ-E vs. -E, +PQ+E vs. +E), the following results were obtained. In experiment 1, the values of plasma and liver alpha-tocopherol levels were significantly lower in the +PQ-E group than those of the -E group; however, liver peroxidation values and values of the three parameters of vitamin E deficiency were not different significantly. In experiment 2, the value of liver alpha-tocopherol level was significantly lower in the +PQ+E group than that of the +E group.(ABSTRACT TRUNCATED AT 400 WORDS)
Animals↗
Determination of diquat in biological materials by electron spin resonance spectroscopy.
An electron spin resonance (ESR) method already in use for the quantitative analysis of paraquat was applied to the analysis of diquat in blood, serum, urine, tissue homogenates and several drinks without purification of the samples. The diquat radical produced with ascorbic acid at alkaline pH was much more stable than that produced with the commonly used sodium dithionite. Radical decay in solutions covered with n-hexane was less than 5% after 60 min over a wide range of ascorbic acid concentrations. In 0.2 N NaOH solution 85% of the radicals was present even after 24 h. The limit of detection was 0.3 micrograms/ml and the required amount of sample was 0.1 ml. When both diquat and paraquat were present in a sample the diquat was first extracted with 1-butanol prior to the ESR measurement, because both species were converted to the radicals.
Diquat↗
Extraction of diquat with 1-butanol from biological materials.
Diquat can be extracted with 1-butanol from high pH solution in the presence of several moderate reductants. The red colored reduced compound of diquat in water turns to a purple compound in 1-butanol. The absorption of the purple compound is 0.105 at 383 nm and 0.119 at 520 nm in 1 microgram diquat/ml 1-butanol. The latter value is a little higher than that of the red compound at 495 nm in water. The purple compound is much more stable than the red compound in water. More than 80% of 10 ppm diquat added can be extracted from serum, blood, tissues, urine and some drinks. The extraction with 1-butanol is useful for concentration of diquat contained in large volume. The lower limit of detection is 0.1 microgram/ml 1-butanol. Paraquat is insoluble in 1-butanol under the same condition. Therefore, this method is applicable for the determination of diquat when paraquat is also contained in the solution.
1-Butanol↗
Determination of paraquat in raw and formalin-fixed tissues by electron spin resonance (ESR) spectroscopy.
ESR method was applied to determine paraquat levels in fresh and formalin-fixed tissues. Paraquat was converted to paraquat radical by adding sodium dithionite to tissue homogenates and detected by ESR. Paraquat levels of more than 0.2 micrograms/ml homogenate could be quantified with 0.1 ml of the homogenate. The use of manganese ions for standardization of paraquat signal enabled much more accurate ESR measurements because this ion was quite stable and its signal did not overlap that of paraquat. Even with tissues fixed in formalin, tissues paraquat levels were measureable after removing formalin from the tissue extract. This fact was verified by studying two cases; the tissues were kept in formalin for 1.5 years in case 1 and for 6.5 years in case 2. In both cases, the paraquat contents in tissues were 0.02-0.08 micrograms/g. In this way ESR is one of the most suitable methods in determining low levels of paraquat in tissues even after they were preserved in formalin for a long time.
Adult↗
Rapid quantitative analysis of paraquat by electron spin resonance spectroscopy.
A very simple and sensitive method for quantitative measurement of paraquat in plasma, urine and some drinks is described. The paraquat radical formed by its reduction can be detected by electron spin resonance spectroscopy (ESR) at room temperature without clean-up or concentration process of samples. The sensitivity limit is 0.1 microgram paraquat/ml and the required amount of sample is 100 microliter. The time needed for the measurement is within 10 min.
Beverages↗