[Pick's disease in two brothers].
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Biomedical subjects
Publications and source records attributed to N Yamaguchi.
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The plasma thyrotropin (TSH) and prolactin (PRL) responses to thyrotropin releasing hormone (TRH) were studied before and during lithium treatment for 3-4 weeks in 6 patients with manic states and 8 control subjects. The plasma TSH responses to TRH were not different between the two groups before lithium treatment. Lithium administration did not alter non-stimulated secretion of TSH in any groups, but resulted in exaggerated responses of plasma TSH to TRH in both groups. No difference between two groups was observed in plasma TSH responses to TRH. The basal plasma PRL concentration did not differ between the two groups and was not affected by lithium administration to either group. The plasma PRL responses to TRH in female subjects were greater than those in male subjects. In females, the plasma PRL responses to TRH in manic patients were significantly higher than those in control subjects before the treatment. Lithium administration caused enhanced responses to TRH in patients when compared to pretreatment levels, but not in control subjects. Although the small number of male subjects limits conclusions, pretreatment plasma PRL responses to TRH in male manic patients were apparently greater than those in control subjects. However, lithium administration appeared not to affect the responses of plasma PRL to TRH in manic patients when compared to pretreatment levels. The augmented responses of plasma PRL to TRH in patients with manic states suggest the existence of some abnormality in the hypothalamo-pituitary axis. Thus, the effect of the anti-manic agent on PRL secretion in manic patients may suggest the mechanism by which the drug affects manic symptoms.
Phasing of nucleosomes on SV40 DNA was studied by the reconstitution of chromatin from SV40 DNA form I and core histones. The reconstituted chromatin sedimented with increasing S values as the histone : DNA ratios increased, and the buoyant densities in CsCl decreased concomitantly. The average repeat lengths of nucleosomes in the chromatin reconstituted at ratios of 1.0 and 1.5 were estimated to be 168 and 143 base pairs, respectively, by electrophoretic analysis of DNA fragments generated by micrococcal nuclease digestion. The chromatin generated a series of DNA bands that differed in size by about 10 nucleotides upon DNase I digestion followed by heat-denaturation. Phasing of nucleosomes was probed by the use of single-site restriction endonucleases, EcoRI, BamH1, BglI, and HpaII: the latter two cleave DNA at and near the origin of DNA replication and transcription. The form I DNA in the chromatin reconstituted at ratios of 0.5, 1.0, and 1.5 was cleaved up to 60 to 80%, 20 to 60%, and 0 to 10%, respectively. Although the frequency of cleavage by these enzymes was not very different at the ratio 0.5, the BglI site became relatively more susceptible than the other sites at the ratio 1.0. At the ratio 1.5, the DNA was almost resistant to these enzymes, though a significant amount (10%) was cleaved by BglI. These results suggest that the origin is the site unfavorable for nucleosome phasing although the region can be almost completely covered with nucleosomes at higher histone : DNA ratios. The fraction of chromatin immunoprecipitated with anti-T serum after in vitro T antigen binding also decreased with increase in the histone : DNA ratios. The results suggest that T antigen binds preferentially to the internucleosomal region. T antigen preferentially bound to the chromatin reconstituted with the DNA fragment containing the origin. Inefficient phasing of nucleosomes at the origin of DNA replication may facilitate the binding of T antigen to the origin.
Serum gamma-glutamyl transpeptidase (gamma-GT) activity was significantly (p less than 0.001) elevated in 85 (49.7%) out of 171 epileptics receiving anticonvulsant therapy. The effects of phenytoin, phenobarbital, carbamazepine, and valproate sodium on gamma-GT activity were analyzed statistically. Among these anticonvulsants, only phenytoin seemed to be responsible for the elevation of gamma-GT activity, since its daily dose and serum level were significantly (p less than 0.05) related to the gamma-GT value. Fifteen out of 17 epileptics with abnormal serum glutamic pyruvic and/or oxaloacetic transaminase levels also showed considerable elevations of gamma-GT values. The possible relationships between the enzyme induction of liver microsomes or chronic hepatic toxicity and the elevation of serum gamma-GT activity in epileptics under treatment are also discussed.
A mitogenic substance, which stimulates murine and human B lymphocytes, has been isolated from the seeds of Ulex europeus. The m.w. of this mitogen was estimated to be approximately 100,000 by sodium dodecyl sulfate disc gel electrophoresis. Under physiologic conditions Ulex mitogen was in the form of a polymer. The isolated mitogen was found to contain 80% carbohydrate, in which glucose, galactose, and rhamnose were the predominant sugars. The carbohydrate portion of the mitogen could be responsible for the mitogenic activity, since the activity was destroyed by periodate treatment but not by protease digestion. It is unlikely that the mitogenic activity is due to the contamination by lipopolysaccharide (LPS), because Ulex mitogen strongly activated spleen cells from C3H/HeJ mice and did not contain a detectable amount of fatty acid. Spleen cells from nude mice, T-depleted spleen cells from conventional mice, or T-depleted spleen cells from conventional mice, or T-depleted lymphocytes from human peripheral blood responded as strongly as lymphocytes (T + B) from normal origin as measured by 3H-thymidine incorporation. It seems that the mitogenic effect is primarily on B cells. Ulex mitogen also induced the increase of immunoglobulin synthesis in murine and human B cells.
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New techniques have been devised for the cytochemical demonstration of purine nucleoside phosphorylase (PNP) and adenosine deaminase (ADA) activities in unfixed human lymphocytes. A suspension of living lymphocytes is mixed with agarose sol containing the reagents for the detection of PNP or ADA activity on a glass slide. The mixture solidifies, is incubated, and then dried for lightmicroscopic observation. Reactive cells are recognized by the diffusely deposited granules of formazan, the end-product of the cytochemical reaction, and are divided into three groups of the cell with the low, middle, and high enzyme activity by the number of the granule. In healthy adults, the mean percentages of PNP- and ADA-positive cells were more than 90% in unfractionated lymphocytes, T-cell fractions, and complement-receptor cell fractions and cells with middle PNP and ADA activities were predominant. The PNP and ADA staining was observed in lymphoid cells of patients with lymphoproliferative disorders. A decrease in the percentage of PNP-positive cells concomitant with a relative increase of cells with the low enzyme activity was observed in the lymphocytes of nine patients with chronic lymphocytic leukemia (CLL). Similar findings were obtained in the ADA staining of the lymphocytes of five patients with B-cell CLL.
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In order to establish the relationship between renin-angiotensin-aldosterone (R-A-ALDO), water and electrolyte balance in fetuses and neonates, a series of their plasma levels were evaluated concurrently and the following results were obtained. Neonates at delivery with birth weights in excess of 3.0 kg, consistently showed high umbilical plasma levels of ALDO, deoxycorticosterone (DOC), plasma renin activity (PRA) and angiotensin-II (A-II). Potassium (K+), sodium (Na+) and chloride (Cl-) levels were roughly equivalent in both maternal and fetal compartments. In umbilical arteries (UA), ALDO showed a definite relationship with 18OH-B and ACTH, however, did not for DOC, A-II, Na+ or K+. A comparison between umbilical vein (UV) and UA, revealed a relationship between ALDO, 18OH-B and PRA. Neonatal DOC, PRA, A-II and ACTH decreased significantly during the 1st post partum day in the presence of a rapid increase of 18OH-B and ALDO to levels in excess of that found in UA, these conditions persist up to the 3rd post partum day. Neonates with birth weights of less than 2.5 kg showed high ALDO, PRA, A-II ad K+ levels in the umbilical plasma, especially the UA. Comparing these neonates with those exceeding 3.0 kg birth weight revealed that in the UA, ALDO and K+ were at high levels. Neonatal PRA, A-II, Na+ and K+ showed no demonstrable variations up to the 8th post partum day and DOC after day 1 increased in the presence of a decrease in ALDO levels during day 1 and 18OH-B during day 3. Comparison of findings between the R-A-ALDO, water and electrolyte balance in fetuses and neonates are discussed.
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A simple method for quantifying lysozyme in serum and urine has been established by modifying the procedures of sample application in the lysoplate method reported by Osserman and Lawlor [1]. A strip of filter paper is partially immersed in a liquid sample, dried at room temperature and cut into discs which are later placed on the surface of an agarose gel containing Micrococcus lysodeikticus. The follow-ng procedures for determination are carried out as described in the lysoplate method. There was no statistically significant loss of enzyme activity during the sample preparation. Lysozyme dried on filter paper is so stable that it can be stored at room temperature for at least 13 weeks and can be mailed. The sensitivity of the method is increased by pretreatment of the filter paper with Triton X-100 and consequently corresponds to that of the lysoplate method. The reproducibility of our method is practically good since the variation coefficient of the diameters of lytic zones within assays is around 1%. There is a very close correlation between lysozyme levels determined by this method and by the lysoplate method with serum samples obtained from patients with various hematological diseases (r = +0.994). The method can be utilized for routine clinical determinations of lysozyme.
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