[Structure and function of glomerular mesangium--vulnerability of juxtamedullary glomeruli].
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Biomedical subjects
Publications and source records attributed to J Maeda.
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A case of prolymphocytic leukemia with IgM hypogammaglobulinemia in a 47-year-old man was presented. The leukemic cells possessed Ia-like antigen and receptors for the third component of complement but lacked surface immunoglobulins, cytoplasmic IgM, receptors for sheep red blood cells, or terminal deoxynucleotidyl transferase activity. In vitro immunoglobulin production experiments demonstrated that the leukemic cells did not have the capacity to produce IgM, while patient's T cells were shown to possess helper function on normal B cells to produce immunoglobulins. By these findings, together with the presence of selective IgM hypogammaglobulinemia, it was suggested that the leukemic cells were derived from a B-cell clone of a stage in differentiation and maturation of IgM-forming B-cell spectrum.
The effect of gliclazide, a hypoglycemic sulfonylurea, on the formation of prostaglandin (PG) I2 by the aortic rings of normal and streptozotocin-induced diabetic animals was studied. In in vitro experiments, gliclazide (100-300 micrograms/ml) enhanced the spontaneous PGI2 formation by the guinea-pig and rat aorta. Gliclazide also enhanced the transformation of both arachidonic acid and PGH2 to PGI2 in guinea-pig aorta, indicating that one of the main enhancing sites is the step of converting PGH2 to PGI2. In ex vivo experiments, the formation of PGI2 in the aorta of streptozotocin-diabetic rats was markedly reduced as compared with that of normal rats. An oral administration of gliclazide (100-300 mg/kg) significantly restored this reduced formation of PGI2 without any effect on blood glucose level. This enhancing effect of gliclazide may be favorable to the treatment of diabetic microangiopathy.
Synaptic inputs of rubrospinal (RN) neurons from the cerebral cortex, pretectal area (PRT), and medial lemniscus (ML) were investigated electrophysiologically in the cat. Stimulation of the ipsilateral parietal association cortex (PASC) and secondary sensory area (SII) produced slow-rising about 3 msec rise time monosynaptic EPSPs which were, in some cases, followed by hyperpolarizations, similar to the sensorimotor cortex (SM)-induced PSPs previously observed. Stimulation of the contralateral cerebral cortex never produced detectable PSPs. Topographical arrangement of PASC-rubral projection was found. Stimulation of the lateral part of PASC induced EPSPs predominantly in RN cells innervating the cervicothoracic spinal segments, while stimulation of the medial part of PASC produced EPSPs predominantly in RN cells innervating the lumbosacral cord. Furthermore, PASC-induced EPSPs were more frequently recorded at the rostral half of RN than at the caudal half. Monosynaptic EPSPs and multisynaptic IPSPs were induced by stimulation of the ipsilateral PRT and ML. PRT- and ML-induced EPSPs had times-to-peak of 1.0 +/- 0.4 msec (mean +/- S.D.) and 1.6 +/- 0.5 msec, respectively, which were intermediate to those of the cerebral peduncle (CP)- and nucleus interpositus of the cerebellum (IP)-induced EPSPs. Furthermore, sensitivity of amplitudes of PRT-induced EPSPs to membrane hyperpolarization was intermediate to those of CP- and IP-EPSPs, and that of ML-induced EPSPs was lower than that of IP-EPSPs. Therefore, it is likely that synapses of PRT and ML fibers are formed between the distal dendrites where CP-rubral synapses terminate and soma where IP-rubral synapses terminate. PASC-induced EPSPs after chronic IP and SM lesions had a new fast-rising component and the effectiveness of ML stimulation to induce the unit spike of RN cells was clearly increased in IP and SM lesioned cats. It was suggested that PASC-rubral fibers sprouted and formed new synapses at the proximal portions of soma-dendritic membranes of RN cells after IP and SM destructions. Collateral fibers to RN cells of the pyramidal tract were also shown to sprout new synapses following IP and ML lesions.
A case of adult T-cell leukemia (ATL) in a 23-yr-old Japanese man without immunoglobulin (Ig)G antibody to ATL-associated antigen (ATLA) (anti-ATLA) is presented. Comparative studies revealed that there were no differences between the present case and the anti-ATLA-positive ATL cases, except for the onset of the former at a younger age. Serologic and epidemiologic studies were performed to determine whether in this case the disease was still dependent on ATLA. As serum IgE and IgA had been persistently elevated, the serum was examined for these antibodies to ATLA. Furthermore, after the patient's serum was treated with glycine buffer to dissociate possibly existing immune complexes, it was assayed for antibodies (IgG, IgE and IgA) to ATLA. However, no antibody activity could be demonstrated. Sero-epidemiologic studies revealed that there were no anti-ATLA-positive healthy adults (ATLA-HA) in either his family or among the residents of his birthplace, whereas some ATLA-HA have been found among the residents of the birthplaces of other ATL patients. Although further investigation is necessary, it seems reasonable for the present to consider that a minor group of ATL patients independent of ATL virus may exist.
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We investigated the effects of cross-innervating the peripheral forelimb flexor and extensor nerves of adult cats on the time course of corticorubral EPSPs. Red nucleus neurons were identified by antidromic invasion from C1 or L1 spinal segments as innervating the upper spinal segments (C-cells) or sending axons to the lumbosacral cord (L-cells). In C-cells, a fast-rising component, superimposed on the slow-rising corticorubral EPSPs induced by the cerebral sensorimotor cortex or the cerebral peduncle (CP) stimulation, was noted. The mean time-to-peak of this component in cross-innervated cats operated more than two months earlier was 1.9 +/- 0.9 ms (n = 160), shorter than in normal cats (3.6 +/- 1.4 ms, n = 100). The same value in cats cross-innervated less than two months before was 2.7 +/- 1.0 ms (n = 53). The mean time-to-peak of CP-EPSPs from L-cells was 2.9 +/- 0.9 ms (n = 115). The fast-rising component had a latency of 0.96 +/- 0.19 ms (n = 122), and it was mediated by fibers with conduction velocities of less than 20 m/s. The projective area of the fast-rising component is organized somatotopically. Since it is more sensitive to membrane hyperpolarization than slow rising corticorubral EPSPs, it is mediated by synapses located more proximally than the corticorubral synapses of normal cats. The time course of facilitation by preceding cerebral peduncle stimulation of the nucleus interpositus (IP)-induced RN population responses was measured. It was characterized by a rapid, followed by a slower, rise time in the RN region where C-cells are concentrated. In contrast, the L-cell region was characterized by a slow rise time. In cats subjected to self-union of the peripheral flexor and extensor nerves, the majority of C-cells had CP-EPSPs with a time-to-peak within the normal range. Our results suggest that after cross-innervation sprouting and formation of functional synapses occur on the proximal portion of the soma-dendritic membrane of red nucleus neurons.
We have developed a new method for hemoglobin determinations using sodium lauryl sulfate (SLS), a surfactant. The detailed action of SLS is still unknown, but presumably SLS will convert hemoglobin into methemoglobin in the order of oxyhemoglobin, hemochrome and methemoglobin, and its oxidative activity. Therefore, unlike others, this method does not need oxidative reagents and does not generate toxic wastes such as KCN and NaN3 which cause environmental pollution. The proposed method is applicable for the manual and Hemalog-8/90 procedures often used in clinical laboratories. Tentatively we have designated it as the "SLS-methemoglobin (SLS-Hb) method."
A case of a patient with needle-shaped inclusions in plasma cells was reported. Some of the inclusions were positively stained for acid phosphatase and beta-glucuronidase. Ultrastructurally, each inclusion was surrounded by a single limiting membrane without any relation to rough-surfaced endoplasmic reticulum and composed of numerous fine fibrous bundles. By the enzyme-labeled antibody technic, the inclusions were found as "stain defects" in IgG-forming plasma cells, but not in IgM-forming plasma cells. Although the exact nature of the inclusions could not be clarified, they were quite different from both amyloid fibrils and immunoglobulin-derived inclusions, and were thought to be synthesized by a clone of differentiated plasma cells. The patient showed moderate hypogammaglobulinemia but no evidence of a direct correlation between the inclusions and hypogammaglobulinemia was obtained. Though the possibility that the case was non-secretory myeloma could not be ruled out, it was unlikely judged by the findings of various examinations.
Effects of cholesterol-loading on platelet functions were studied. Guinea-pigs were fed on a diet containing 1% cholesterol for 1--5 months. Cholesterol-feeding caused an elevation of cholesterol content in the plasma and platelets, although the phospholipids increased only in the plasma. Enhanced platelet aggregation induced by ADP, collagen, and arachidonic acid was maintained for 5 months during cholesterol-feeding, concomitant with an increase in malondialdehyde production in platelets. Although basal levels of platelet cyclic AMP were not affected, PGE1-stimulated cyclic AMP levels were markedly decreased in platelets of cholesterol-fed animals. The same results were observed in platelets treated with theophylline. No change in the generation of PGI2-like substance by the aortic tissue occurred during 4 months of cholesterol-feeding, though a significant increase was seen after 5 months. These results suggest that the enhancement of platelet function by cholesterol-feeding is concerned with enhanced prostaglandin synthesis and suppressed adenylate cyclase activity in platelets.
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Single-unit discharges in the cat Clare-Bishop area were correlated with spontaneous accommodation responses. No appreciable change was found in accommodation responses evoked by stimulating the Clare-Bishop area, when cerebellar outflow was blocked reversibly by cooling the superior cerebellar peduncle. It is suggested, therefore, that the Clare-Bishop area plays an important role in the lens accommodation system through a pathway independent from that of the cerebellum.
In slice preparations from kitten striate cortex, long-term potentiation (up to 15 h) of field potentials was demonstrated after conditioning stimulation of white matter. Current source-density analysis and measurement of response latencies of cortical units indicated that the potentiation represented enhancement of both geniculo-cortical transmission in layer IV and intracortical transmission in layer II--III.
Thirty units were found in the midbrain of the anesthetized cat which discharged in correlation with spontaneously occurring lens accommodation. The frequency of spike potentials increased before the onset of the accommodation response. Increased discharges were followed by a silent period. These units were driven orthodromically by stimulating the interpositus nucleus of the cerebellum and the posterior commissure. Eleven of these units were identified antidromically as parasympathetic oculomotor neurons.