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Biomedical subjects

K Minakata

Publications and source records attributed to K Minakata.

At least 55 records · Page 3Linked to original sources
PubMed1987

Enhancement of testicular cysteine proteinase inhibitor level in vitamin E-deficient rats.

The effect of vitamin E deficiency on levels of proteinase inhibitors in sex glands of male rats was studied. Inhibitor levels against cysteine proteinases, such as ficin and cathepsin H, and against serine proteinase such as trypsin were examined. Vitamin E deficiency for 4 mo after weaning induced a fivefold increase in cysteine proteinase inhibitor level in testis, a two- to fourfold increase in prostate and epididymis and no change in seminal vesicle. No appreciable change was observed in trypsin inhibitor level in testis, epididymis or seminal vesicle. Therefore, vitamin E deficiency was reflected most sensitively by the cysteine proteinase inhibitor level in testis. These observations agree with our previous findings that alpha-cysteine proteinase inhibitors in serum increased greatly whereas trypsin inhibitor in serum did not change in vitamin E-deficient rats. Major histological changes were observed in the testes of rats fed a vitamin E-deficient diet for 4 mo, although testis weight was not significantly affected by vitamin E deficiency.

Animals↗
PubMed1987

Cysteine proteinase inhibitors in human and rat male sex glands.

The testis and prostate of men had two types of cysteine proteinase inhibitors of different isoelectric point (pI = 4.5 and 6.3) and molecular masses (90,000 and 12,000). The seminal vesicle contained not only these two inhibitors but also a basic inhibitor with a pI = 9.5 and Mr 11,000. In rats, the inhibitors in the testis and prostate consisted of two types with pI values of 4.3 and 4.8 and Mr 90,000 for both. In addition to these two inhibitors, the seminal vesicle contained large amounts of two basic inhibitors with pI values of 7.5 and 8.3 and Mr of 11,000 for both. We suggest that the basic cysteine proteinase inhibitor found in semen might be excreted from or be modified in the seminal vesicle.

Animals↗
PubMed1986

Cysteine proteinase inhibitor levels in semen.

New proteinase inhibitors have recently been found in seminal plasma which specifically inhibit cysteine proteinases such as ficin, papain, cathepsin H and cathepsin B. The inhibitors consist of two components, In-A and In-B, both of which are effective in native semen. In the present work, a method of assay is devised to determine activities of both components separately. Under conditions in which In-B is denatured completely while In-A is not, inhibitory activity of In-A alone is determined. The mean In-A inhibitory level is 1.52 +/- 0.28 inhibitor unit/mL and the level is independent of the number of spermatozoa. In-B level is calculated by subtracting In-A level from the total ficin inhibition level of the semen. The mean In-B level is 1.47 +/- 0.52 inhibitor unit/ml. In-B level has a tendency to increase with increasing number of spermatozoa. The correlation coefficient is 0.307 and statistical significance p less than 0.005.

Clinical Enzyme Tests↗
PubMed1985

Acidic cysteine proteinase inhibitor in seminal plasma.

A cysteine proteinase inhibitor with acidic isoelectric point (pI = 4.7-5.0) was found in human seminal plasma. Its apparent molecular mass is 16 kDa. It inhibits cysteine proteinases like ficin, cathepsin H, cathepsin B and papain. The inhibitory activity of seminal plasma against ficin is almost the same as that of human serum.

Cysteine Proteinase Inhibitors↗
PubMed1984

New protein inhibitors of cysteine proteinases in human saliva and salivary glands.

New protein inhibitors of cysteine proteinases were found in human saliva and salivary glands. The inhibitory potency present in saliva against ficin is about 30% of that in serum: 1 ml of saliva gives 100% inhibition of 1 nmol of ficin. The same amount of saliva causes no inhibition of 1 nmol of trypsin. The salivary inhibitors occur as multiple forms with different isoelectric points (pI of 4.5-4.7, 5.8, 6.8, 7.8 and 8.2) and different molecular masses of approximately 16, 11, 10, 9.5 and 9 kDa. The inhibitor forms having molecular masses of less than 11 kDa have not yet been described by other authors. The salivary inhibitors have a high thermal stability and a high stability both in alkaline and acidic solutions.

Cysteine Proteinase Inhibitors↗
PubMed1983

Computer analysis of parentage in relation to maternity and paternity.

General formulas for statistical calculations of parentage by means of blood group analysis are presented in relation to those of maternity and paternity. Based on these formulas, a computer program has been devised to calculate plausibilities, exclusion probabilities, and distributions of log (Y/X) of parentage for any blood groups. The program also gives numerical values of these quantities of maternity and paternity. The values of plausibility and exclusion probability are highest for parentage, and decrease in the order of paternity and maternity. Concerning the distribution of log (Y/X) for true families, a simple relation holds for the ratio of the mean value of log (Y/X) in parentage ap, to that in paternity af, and to that in maternity am as, ap: af: am = 1: 0.6: (0.6)2 This relation holds for all 14 blood groups examined.

Adult↗
PubMed1983

Serum alpha-cysteine proteinase inhibitor levels in pregnancy.

Variation in alpha-cysteine proteinase inhibitor levels in human sera were investigated with special attention to the effect of pregnancy and diseases. The inhibitor level in 111 pregnant women, examined by our previous method, increased as the pregnancy advanced. The correlation coefficient between the level and the duration, r, was 0.578 with the level of significance p less than 0.001. The mean value for 50 pregnant women in the third trimester of gestation was 0.49 +/- 0.04 unit/mL, which was 47% higher than the control value, 0.33 +/- 0.04 unit/mL (p less than 0.001). However, the levels in patients with myoma of uterus, endometritis, cervical cancer, ovarian cyst and ovarian cancer were not significantly different from the control value. From these results, it was concluded that pregnancy enhanced appreciably the alpha-cysteine proteinase inhibitor level in serum.

Adult↗
PubMed1982

Assay of alpha-cysteine proteinase inhibitor in serum or plasma.

A new proteinase inhibitor has recently been found in human serum or plasma which specifically inhibits cysteine proteinases such as ficin, papain, bromelain and cathepsin B. However, serum contains alpha 2-macroglobulin which also inhibits these cysteine proteinases and, consequently, interferes with the assay of the new alpha-cysteine proteinase inhibitor. Therefore, assay of the inhibitor in serum has not been established previously. In the present method, the alpha 2-macroglobulin is inactivated by preincubating the serum in methylamine solution at 55 degrees C, while the alpha-cysteine proteinase inhibitor retains its activity. The inhibitory power against cysteine proteinases is found to be due mainly to this protein in human serum. This inhibitor is also found in mammals such as cows, pigs and rats. Vitamin E deficient rats show a very high inhibitor level. Therefore, the present method will enable us to investigate the relation between diseases and the activity of the alpha-cysteine proteinase inhibitor. Also, this method is simple and inexpensive. The necessary amount of serum is only 10 microliter.

Animals↗
PubMed1980

General formulas of the estimated likelihood ratio Y/X in the diagnosis of paternity of a deceased putative father.

When the putative father is dead his probable genotype, essential for estimate of likelihood ratio in the diagnosis of paternity, should be deduced from his relatives. In the present paper are described the general method for such deduction of probable genotype and the derivation of the formula of likelihood ratio. 10(4) examples of the diagnosis of paternity of deceased father are examined using a Monte Carlo method and the distributions of relative frequencies of log(Y/X) are calculated for the true father and non-father. These results indicate that the present method of estimation of Y/X from relatives is quite useful for the diagnosis of paternity of a deceased putative father.

Blood Group Antigens↗
PubMed1980

Diagnosis of paternity for cases without mother and without both mother and putative father based on blood group findings from the relatives.

Formulas of the estimated likelihood ratio Y/X are derived for cases without mother as well as those without both mother and putative father, by using blood group findings of their relatives. The distribution curves of the relative frequencies of log(Y/X) for these cases are calculated with respect to 10(4) families which are created by a Monte Carlo simulation. The extent of success in the paternity diagnosis is clarified by the statistical analysis based on these distribution curves. According to the above analysis, fairly high chance of success can be obtained in the diagnosis of such ambiguous cases without the plaintive mother and/or the putative father, if there relatives are alive. It is also concluded that the genetic information as to the parents of the deceased person increases the exclusion probability, whereas that as to the spouse and children increases the fraction of log(Y/X) greater than 1 for non-father, corresponding to the fraction where the Essen-Möller value is less than 9%.

Blood Group Antigens↗
PubMed1980

Distribution of likelihood ratio in relation to the exclusion probability.

The relation between the exclusion probability (E) and the paternity probability is derived by assuming the distributions of logarithm of paternity likelihood ratio, log(Y/X) for true fathers and unexcluded non-fathers as the normal distributions. Under this assumption the value log(1-E) is equal to the mean of the mean value for true fathers (a) and that for unexcluded non-fathers (b), i.e., log(1-E)=(a+b)/2. This relation holds quite well for the various actual distributions of log(Y/X) of father-child combinations and those of father-mother-child combinations using 14 blood group systems. Therefore, the derived relation is found to be a convenient way to deduce one of the three quantities (E, a, b) from the remaining two quantities in the actual distributions.

Blood Group Antigens↗
PubMed1980

A new approach to the computation of indices of paternity.

This paper describes an algorithm to calculate several indices of paternity (combination frequency, paternity likelihood (Y/X) and paternity exclusion probability (E) for father-mother-child combination (trio) as well as father-child combination (duo). This program is written in FORTRAN IV and applicable to any kinds of blood group systems such as Rh and HLA. The characteristic points of the present method are as follows: First, the relation between genotypes and phenotypes is given in a straightforward way by introducing a translational matrix. Secondly, by a unit run on a computer, several indices of paternity are tabulated for all kinds of combinations of trio as well as duo. Finally, the efficiency of diagnosis of a certain system is listed by calculating the distribution of log (Y/X).

Child↗
PubMed1979

Spin-label studies of membrane-associated denatured hemoglobin in normal and sickle cells.

A maleimide spin label (N-(1-oxyl-2,2,5,5-tetramethylpyrrolidinyl)-maleimide) was reacted with oxyhemoglobin-free cell stromata of normal and sickle cells. The EPR spectrum of spin-labeled red cell membranes showed that the spin labels are attached to at least two different binding sites. There was a major signal, A, which characterized a strongly immobilized environment and a minor signal, B, which characterized a weakly immobilized environment. Quantitative EPR measurements using equal amounts of Hb AA and Hb SS red blood cells demonstrated that Hb SS red cell membranes had an approximately four times higher EPR signal intensity than Hb AA red cell membranes ((7.98 +/- 1.14 . 10(5) and (2.2 +/- 1.2) . 10(5) spin labels/cell, respectively). Moreover, the ratio of signal intensities A and B are different in these cells. Comparative spectrophotometric studies of membrane-associated denatured hemoglobins of Hb AA and Hb SS red cell membranes suggested that the EPR signal A is derived from spin labels attached to membrane-associated denatured hemoglobin, while signal B is mainly from spin labels attached to membranes. The combination of EPR spectrum of Hb AA membranes pretreated with N-ethylmaleimide and that of spin-labeled precipitated hemoglobin further strengthened this conclusion.

Anemia, Sickle Cell↗
PubMed1979

Calculation of likelihood ratio y/x in diagnosis of paternity using computer methods.

A new computational method using a Monte Carlo technique is described for the calculation of plausibility of paternity in blood group systems. In this study gene frequencies of a blood group system are simulated by the range of the seven digit random numbers. By using a Monte Carlo method, four random numbers are generated and converted into paternal and maternal genotypes. Then the genotype of the child is determined according to the law of inheritance, and finally genotypes of the father, mother and child are converted into phenotypes. Repeating this process more than one hundred thousand times, the phenotypic frequencies of child-mother-father combinations (trio) and the likelihood ratio of paternity in any blood group system are calculated for all phenotypic combinations of the trios. This method is much easier than methods reported previously, and is sufficiently accurate.

Blood Group Antigens↗