Evaluation of T colony-stimulating factor in patients with lipoid nephrosis.
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Biomedical subjects
Publications and source records attributed to K Okano.
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Human placental microsomal aminopeptidase (microsomal PAP) was purified 3,880-fold from human placenta and characterized. The enzyme was solubilized from membrane fractions with Triton X-100 and also trypsin digestion, and subjected to zinc sulfate fractionation, chromatographies with DE-52, hydroxylapatite, Sephacryl S-300 and lentil lectin-Sepharose 4B, and finally affinity chromatography with bestatin-Sepharose 4B. Microsomal PAP was separated from aminopeptidase A (AAP) by affinity chromatography. The apparent relative molecular mass (Mr) of the enzyme was estimated to be 220,000 by high-performance liquid chromatography with an aqueous gel column. The purified enzyme gave almost a single band with a molecular mass of 140,000 by sodium dodecyl sulfate (SDS) gel electrophoresis. The isoelectric point of the enzyme was 5.2. The purified enzyme was most active at pH 8.0 with L-leucine-p-nitroanilide as substrate; the Km value for this substrate was 1.1 mmol/l. The microsomal PAP was immunologically different from the pregnancy serum cystyl aminopeptidase (serum PAP).
The serum bone Gla-protein (BGP) and urinary gamma-carboxyglutamic acid (gamma-Gla) levels were determined in patients with primary hyperparathyroidism (PHP). The mean serum BGP and urinary gamma-Gla levels were 18.6 +/- 2.34 ng/ml and 65.5 +/- 4.62 nmoles/mgCr, respectively, for the 11 patients with the skeletal type of PHP, 5.13 +/- 0.85 ng/ml and 45.2 +/- 1.33 nmoles/mgCr for the 4 with the chemical type, and 7.91 +/- 2.43 ng/ml and 43.2 +/- 3.47 nmoles/mgCr for the 5 with the renal type. Thus, patients with skeletal-type PHP had significantly higher serum BGP and urinary gamma-Gla levels than those with the other type of PHP. Serum BGP levels had significant positive correlations with serum Ca (r = 0.64, P less than 0.005), serum A1-p (r = 0.77, P less than 0.001) and serum PTH (r = 0.45, P less than 0.005). Urinary gamma-Gla levels also had significant positive correlations with serum Ca (r = 0.50, P less than 0.05), serum A1-p (r = 0.67, P less than 0.005), serum 1,25(OH)2D (r = 0.62, P less than 0.02), and serum BGP (r = 0.72, P less than 0.001). Mineral content in the left radius had significant negative correlations with serum BGP levels (r = -0.73, P less than 0.001) and urinary gamma-Gla levels (r = -0.59, P less than 0.01). As these data show, serum BGP and urinary gamma-Gla levels clearly reflect the abnormal bone metabolism and can therefore be useful biochemical markers in PHP.
To examine the functional differences in primate motor cortex (MC), premotor cortex (PM) and supplementary motor area (SMA), single cell activities in these areas were recorded from monkeys performing either visually triggered or self paced key press movement. EMG recordings made clear that activities in finger and hand flexor muscles preceding the triggered or self paced movement were identical and no limb and body muscles were active during performing the task. Neuronal activity changes preceding movement onsets were classified into two categories; a short lead type with the preceding time of less than 300 ms, a long lead type with longer preceding times. In MC, a majority of movement-related neurons (86%) was active phasically and therefore belonged to a short lead type. They exhibited similar activity changes regardless of whether triggered or self paced. In PM, 87% of movement-related neurons were of short lead type. About one third of them were triggered movement specific and another one third were triggered movement predominant. These preferential relation to triggered movement were characteristic in PM. Neurons of SMA were different from MC and PM cells in that as much as a half of them showed the long lead type of activity changes and almost all of these cells were classified into self paced movement dominant or specific. These results suggest that each of these areas have different functional characteristics. PM has more preferential relation to the triggered movement and SMA has more preferential relation to the self paced movement, whereas MC is involved equally in both.
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This paper describes the embryotoxicity and teratogenic effects of (2"R)-4'-O-Tetrahydropyranyladriamycin (THP). The drug was administered intravenously to female rats at 0.01, 0.03, 0.1 or 0.3 mg/kg daily from day 7 to day 17 of pregnancy and to female rabbits at 0.01, 0.05 or 0.1 mg/kg daily from day 6 to day 18 of pregnancy. Results were summarized as follows. Rats THP, at the highest dose of 0.3 mg/kg, decreased body weight gains of pregnant females. This dose caused a decrease in body weights of fetuses, tendencies to increase the rate of death of fetuses or of resorption, an increase in the number of lumbar vertebrae and a delayed ossification of forelimbs of fetuses. Other parameters were not affected by THP at any dose levels. At any dose levels, THP did not produce external, visceral or skeletal malformations in the offspring (F1), nor did it affect the development, physiological functions, behavior, mating, fertility or pregnancy of the offspring. However, at the highest dose level, THP decreased the weight of testes of the offspring. The results suggest that the maximum "no effect" dose level of THP to pregnant females and offspring is 0.1 mg/kg/day intravenously. Rabbits The highest dose of THP, 0.1 mg/kg, decreased the consumption of food and water by pregnant females, but at any dose levels, it did not affect their body weight gain. THP did not cause teratological effects such as external malformation or visceral and skeletal anomalies in the fetuses at any dose levels tested. The results suggest that the maximum "no effect" dose of THP is 0.05 mg/kg/day intravenously to pregnant females and above 0.1 mg/kg/day intravenously to fetuses.
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The medial surface of the rostral part of frontal agranular cortex, largely corresponding to the supplementary motor area, was rapidly and reversibly cooled while a monkey was performing a trained motor task requiring a premovement selection process of determining sensory signals as movement triggering or non-triggering. During cooling, the motor task was poorly performed with grossly altered reaction times and variable amount of force, along with erroneous responses. Neuronal activity in the precentral motor cortex in response to sensory signals was also found to be altered.
Single cell recordings were made from the premotor cortex (lateral part of area 6) of a monkey trained to perform either a distal hindlimb or forelimb movement separately. Out of 175 movement-related neurons, 59 neurons showed modulation of activity only prior to the hindlimb movement, and the majority of them was distributed in a focal region around the superior precentral sulcus, several mm posteromedial to the genu of the arcuate sulcus. The hindlimb focus was separate from a focal region for forelimb movement-related neurons, which lay immediately posterior to the genu of the arcuate sulcus.
Adechlorin exhibiting a potent inhibitory activity against calf intestinal adenosine deaminase was isolated from the cultured broth of Actinomadura sp. OMR-37. The molecular formula was C11H15N4O4Cl. The aglycone of adechlorin was identical with that of the known adenosine deaminase inhibitors coformycin and 2'-deoxycoformycin. Adechlorin did not exhibit inhibitory activity against various bacteria and fungi at 1.0 mg/ml. The Ki values for adechlorin, coformycin and 2'-deoxycoformycin against adenosine deaminase were determined to be 5.3 X 10(-10) M, 2.1 X 10(-10) M and 7.6 X 10(-11) M, respectively. Adechlorin as well as coformycin and 2'-deoxycoformycin enhanced the antiviral activity of Ara-A. The acute toxicity of adechlorin in mice was less than those of coformycin and 2'-deoxycoformycin.
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The T-colony-forming capacity was examined in 13 normal subjects and 14 patients with biopsy-proven lipoid nephrosis (LN). Eighteen additional patients with other well-defined forms of glomerulonephritis were studied as a disease control. Significantly fewer T lymphocyte colonies were found in LN patients and the nephrotic syndrome (NS) than in normal controls. A similar change could be observed in the groups with other types of NS. LN patients with NS had the lowest values of T-colony-forming cells (TCFC), but there was no statistically significant difference between the groups of nephrotic subjects. It was also of interest that peripheral blood lymphocytes (PBL) from 3 patients with lupus nephritis (SLE) produced significantly low levels of TCFC. The lower levels of TCFC in LN could be enhanced when exogenous interleukin 2 (IL 2) was added to the system. We also examined the production of T-colony-stimulating factor (TCSF). The TCSF production by stimulated PBL from LN patients was lower than in normal subjects. To explain our observations, we presumed that the T colony dysfunction seen in LN patients with NS might in part be due to the decreased TCSF activity.
A 59 years old male with abdominal aortic aneurysm ruptured into the left common iliac vein was transferred to us with symptoms resembling deep vein thrombosis of the left lower extremity, such as leg pain, swelling and dilatation of the superficial veins. At operation, a Fogarty's occlusion catheter was inserted through the right greater saphenous vein into the inferior vena cava and inflated concomitantly during aortic clamp to prevent pulmonary embolism which may be caused by the dislodged thrombi from the aneurysm, and as well as to control back-flow-bleeding from the central. The fistula (3.0 X 1.0cm) was closed from inside of the aneurysm using the inferior wall of the aneurysm. The blood from the fistula was collected by the Cell Saver and re-transfused to the patient. The abdominal aorta was replaced with a Dacron Y-shaped prosthesis. The postoperative course was uneventful. CTR on chest X-ray subsided from 51% to 42%, cardiac output normalized from 11l/min to 6l/min, and symptoms resembling the deep vein thrombosis disappeared.
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