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Biomedical subjects

M Matsunaga

Publications and source records attributed to M Matsunaga.

At least 91 records · Page 5Linked to original sources
PubMed1993

[Rapid recovery of chronic inflammatory demyelinating polyneuropathy induced by steroid pulse therapy--changes in nerve conduction].

A 47-year-old female patient with chronic inflammatory demyelinating polyneuropathy started to recover from her numbness and weakness within a few hours following the commencement of intravenous methylprednisolone 1,000 mg. In parallel with the recovery of muscle strength, a prolonged latency time of the M-wave was normalized within a day by a revival of the new motor units with a normal latency. In many cases with CIDP, it has been recognized that the gradual decrease in latency time over weeks is a later phenomenon following early increase in amplitude of the M-wave during recovery of weakness, which is explained by remyelinating process. On the other hand, the revival of motor units with a normal latency time from demyelinating conduction block is difficult to explain by remyelinating process, because remyelinating fibers usually have a very slow conduction velocity. Some minor morphological changes of paranodes or humoral factors may be partly responsible for development conduction block in CIDP.

Chronic Disease↗
PubMed1993

[Chronic inflammatory demyelinating polyneuropathy in childhood].

Clinical, electrophysiological and histopathological findings in 6 children with steroid-responsive acquired demyelinating neuropathy are presented. The clinical features and nerve conduction findings are basically similar to those of chronic inflammatory demyelinating neuropathy (CIDP) in adults, although early-onset cases had prominent pes cavus deformity and thickened nerves, which are rare findings in acquired neuropathies in adults. The diagnostic criteria of adult CIDP can be adopted for most of the cases, however, repeated electrophysiological tests may be required to identify multifocality of the nerve lesion, especially when conduction block is not apparent before treatment. The biopsied sural nerves showed many thinly-myelinated fibers, subperineurial and endoneurial edema, and cellular infiltrations. Varied fascicular involvements were common. Two cases with almost complete or considerable loss of myelinated fibers in the biopsied sural nerve revealed good clinical response to steroid therapy. The degree of nerve degeneration in the sural nerve thus, may not be helpful to estimate the prognosis and the responsiveness to treatment. Therapeutic trials should be employed when the main conduction findings are those of demyelinating neuropathies, even if genetically-determined neuropathy is suggested from the clinical pictures.

Adolescent↗
PubMed1993

[Chronic inflammatory demyelinating polyneuropathy in childhood--a case with markedly hypertrophic nerves and pes cavus].

We describe a 9-year-old boy with chronic inflammatory demyelinating polyneuropathy (CIDP), whose distal dominant, slowly progressive motor sensory involvement developed since infancy. Thickened peripheral nerves were visible in his neck and palpable in the extremities. The hand muscles were atrophic and both feet showed pes cavus deformity. He was unable to walk. Nerve conduction study revealed no sensory potentials. Compound muscle potential (CMP) was absent in the legs. In the arms, CMP showed markedly low amplitude and temporal dispersion. Motor conduction velocities were 1.7 to 2.7 m/sec, showing extremely high threshold to electrical stimuli. Conduction block was not convincing, nevertheless the asymmetric conduction abnormalities strongly suggested multifocality of the lesion. In the biopsied sural nerve no myelinated fibers were found. Considerable improvements in muscle power and electrophysiological findings were brought about by corticosteroid therapy. CIDP in childhood may masquerade hereditary neuropathies presenting hypertrophic peripheral nerves and pes cavus deformity. A careful nerve conduction study is thus desirable to find out electrophysiological multifocality.

Child↗
PubMed1993

[Influences of anesthetic method on post-cholecystectomy pain--a comparison between epidural and general anesthesia].

This study was designed to compare the influence of epidural anesthesia with that of general anesthesia on postoperative pain state and management. We studied 16 patients who underwent elective laparotomy-cholecystectomy with epidural anesthesia without general anesthesia or with general anesthesia (nitrous oxide-isoflurane). Following bolus epidural injection with 3 micrograms.kg-1 of buprenorphine in 0.25% bupivacaine 4-7 ml at the end of surgery, all patients received continuous epidural buprenorphine administration at the rate of 12 micrograms.h-1 for 48 hours. Pain relief was assessed for 72 hours after surgery using visual analogue scale. Postoperative rest pain of the epidural group remained at a lower state of pain than that of the general anesthesia group not only for 48 hours (P < 0.005) but also until 72 hours (P < 0.005) after surgery. We concluded that the epidural anesthesia produces a greater postoperative pain relief than general anesthesia.

Anesthesia, Epidural↗
PubMed1992

Enhancement of the uptake of 1-methyl-4-phenylpyridinium ion (MPP+) in mitochondria by tetraphenylboron.

The uptake of 1-methyl-4-phenylpyridinium (MPP+) by intact mitochondria was measured by an electrode sensitive to MPP+. The electrode was constructed with a polyvinyl chloride membrane that contained tetraphenylboron (TPB) as an ion-exchange. MPP+ was taken up by mitochondria in an energy-dependent process. TPB rapidly enhanced MPP+ uptake by mitochondria, and then induced release of MPP+ from mitochondria in medium containing glutamate and malate. No release of MPP+ from mitochondria after addition of TPB could be observed in medium containing succinate, the oxidation of which is not inhibited by MPP+. The release of MPP+ was caused by respiratory inhibition by MPP+ taken up in mitochondria. Since the release of MPP+ did not increased O2 uptake in mitochondria, the major part of MPP+ released from the matrix, where no respiratory enzyme inhibited by MPP+ exists. We concluded the following effect of TPB on MPP+ uptake from the results: (1) The increase of MPP+ concentration in matrix by addition of TPB increased the amount of bound to the inner membranes of mitochondria. (2) The increase of the amount of MPP+ in the inner membranes enhanced the respiratory inhibition. (3) The respiratory inhibition induced to release MPP+ from the matrix. The relation between MPP+ distribution in the membrane of mitochondria and the respiratory inhibition by MPP+ are discussed.

1-Methyl-4-phenylpyridinium↗
PubMed1992

Therapeutic and prognostic value of modal number of chromosomes at the blastic phase of Philadelphia-chromosome-positive chronic myeloid leukemia: comparison based on the same criteria between Nagasaki University and Roswell Park Memorial Institute.

In a comparison of 47 patients with Philadelphia-chromosome (Ph)-positive chronic myeloid leukemia (CML) in the Nagasaki University School of Medicine and 64 patients with the same disease in the Roswell Park Memorial Institute, the correlation between the modal number of chromosomes and the therapeutic response and/or survival after the onset of the blastic phase (BP) was evaluated. The patients were divided into four groups on the basis of the modal number of chromosomes of the cells in the bone marrow: those with hypodiploidy (group 1), those with pseudodiploidy carrying a Ph chromosome (group 2), those with 47 chromosomes (group 3), and those with 48 or more chromosomes (group 4). The results revealed similar trends in the two institutes. Namely, the therapeutic response and the survival after the onset of the BP in groups 1 and 4 were more unfavorable and shorter than those in groups 2 and 3, although the former (group 2) had a better prognosis than the latter (group 3). Thus, the statistical analysis revealed that the numerical chromosome findings at the BP are useful parameters for assessing the therapeutic response and survival after the onset of the BP of CML.

Adolescent↗
PubMed1992

Behavioral study on the gracile axonal dystrophy (GAD) mutant mouse.

We investigated motor function and pain sensation in the gracile axonal dystrophy (GAD) mutant mouse, using the tail-flick test and the rotarod test. GAD (gad/gad) and normal sib mice (gad/+ or +/+) were used between 5 and 11 weeks of age, during which time the behavioral signs of GAD mice shifted from sensory ataxia (about 4 to 8 weeks of age) to paresis (after about 9 weeks of age). In the tail-flick test, significant shortening of latency was observed at 6 and 8 weeks of age in female GAD mice, in comparison with normal female mice. This may be related to dysfunction or degeneration of axons in the fasiculus gracilis, whose collaterals are thought to control the transmission of nociceptive information. In the rotarod test, a cumulative chi 2 test showed significant reduction in the performance times of GAD mice beginning at 5 and 6 weeks of age in males and females, respectively, indicating that the rotarod test can detect the development of motor incoordination as early as these ages. The performance times of GAD mice dropped sharply from 9 weeks of age onwards, and this is believed to reflect the progression of paresis. The rotarod test therefore appears to be a good method of quantifying behavioral changes in GAD mice and to be applicable both to objective selection of GAD mice before 8 weeks of age and to evaluation of drugs to treat ataxia or paresis.

Age Factors↗
PubMed1992

Persistent hemichorea associated with thyrotoxicosis.

We describe a case with unilateral chorea associated with thyrotoxicosis. A 23-year-old female with no family history of neurological diseases acutely developed choreic movements of the left extremities during gross thyrotoxicosis. CT scan and MRI study demonstrated no abnormality. Single-photon emission CT with technetium Tc 99m-labeled hexamethylpropyleneamine oxime revealed normal cerebral perfusion. Although the choreic movements were partially improved by dopamine antagonist, they persisted for two months until successful treatment of the thyrotoxicosis finally abolished these movements. Increased sensitivity of dopamine receptors may be responsible for persistent choreic movements in thyrotoxicosis.

Adult↗
PubMed1992

[High-dose intravenous immunoglobulin treatment in chronic inflammatory demyelinating polyneuropathy].

We treated two patients with chronic inflammatory demyelinating polyneuropathy (CIDP) with high-dose intravenous immunoglobulin (HIG). The patients received 400 mg/kg of immunoglobulin a day for five days. One patient, who had failed to respond to prednisolone before, was treated with HIG, 18 months after the onset. His motor symptoms resolved immediately after the commencement of HIG. Electrophysiologically, the compound muscle action potentials increased in amplitude in all nerves examined and F wave reappeared in the left median nerve. The electrophysiological changes were compatible with improvement of conduction blocks. This patient had headache and exanthema during the HIG therapy, but they settled after cessation of the infusion. The other patient was administered HIG as an initial treatment, four months after the onset. HIG was of no effect in this case, but he showed remarkable recovery during the following prednisolone therapy. Although corticosteroid therapy is the first choice for CIDP, there are CIDP patients who do not respond to steroid or can not complete the steroid therapy because of adverse effects. HIG is an expectative and recommendable treatment for the steroid resistant CIDP patients.

Adolescent↗
PubMed1992

[Chronic inflammatory demyelinating polyneuropathy--an electrophysiological and histological study of the ulnar nerve from a case with intractable persistent conduction block].

We report a 71-year-old male with CIDP, in whom complete motor conduction block persisted for more than several years. Corticosteroid and plasma therapy showed little effect to his weakness. He died of pneumonia. The ulnar nerve in which complete conduction block had persisted was taken out immediately after death and studied with conventional histological and morphometrical techniques. In the transverse section, many thinly-myelinated fibers and some cluster formations were confirmed. Active axonal degeneration was scarce. Myelinated fiber density was 7,417/sgmm. Fiber diameter histogram showed a two-peaked normal distribution. It is thus concluded that demyelination with little axonal degeneration can be the main pathological process causing intractable weakness and poor prognosis of CIDP. Low CMAPs should not lead to therapeutic nihilism, because it may simply be caused by demyelination without exonal degeneration in CIDP.

Aged↗
PubMed1991

(BALB/c x C57BL/6)F1 mice are tolerant to undetectable mixed haplotype A beta dA alpha b and mixed isotype A beta dE alpha d self class II molecules.

The existence of mixed haplotype A beta dA alpha b and mixed isotype A beta dE alpha d molecules was demonstrated in A beta d gene introduced C57BL/6 (B6) transgenic and in A beta dE alpha d double gene introduced B6 transgenic mice, respectively. Using alloreactive and antigen reactive T-cell clones, these mixed class II molecules were shown to function as mixed lymphocyte culture reaction (MLR) stimulating determinants and restriction elements for antigen recognition by T cells. The amounts of expression of these mixed class II molecules were sufficient for the stimulation of alloreactive T cells in primary MLR culture. (BALB/c x B6)F1 (CBF1) mice were shown not to express functional mixed haplotype and mixed isotype class II molecules using alloreactive and antigen reactive T-cell clones. Interestingly, however, CBF1 mice did not respond to such mixed haplotype and mixed isotype class II molecules. These results show that CBF1 mice do not respond to undetectably-expressed class II molecule and suggest that they are tolerant to undetectable self class II molecules. The possible interpretations for this are discussed.

Animals↗
PubMed1991

Enhancing effect of a choline-deficient diet on alterations of hepatic drug-metabolizing enzymes in hepatitis- and hepatoma-predisposed rats (LEC rats).

Marked alterations of hepatic drug-metabolizing enzymes were observed in hepatitis- and hepatoma-predisposed rats (LEC rats) fed a choline-deficient diet. The diet enhanced the development of hepatitis with severe jaundice. The levels of two major classes of cytochrome P-450, P-450PB and P-450MC, were markedly decreased. GST-Yp was dramatically increased, whereas GST-Ya, Yb1 and Yb2 were decreased. LEA rats (the control rats to LEC) fed a choline-deficient diet mimicked LEC rats fed a normal diet in terms of the above enzyme alterations, indicating that hypomethylation is involved in the pathogenesis of hepatitis and hepatoma in LEC rats. Such hypomethylation may initiate the hepatocytes that spontaneously develop hepatitis and hepatoma.

Animals↗
PubMed1991

Does heparin inhibit renin activity?

Although heparin was reported in the 1960s to inhibit renin activity, this has not always been confirmed by other investigators. Hence, we re-examined whether heparin really inhibits renin or not. Renin activities were determined by radioimmunoassay of angiotensin I generated at pH 7.4. (i) No significant difference was found between the two kinds of plasma samples obtained with heparin and with EDTA as anticoagulant, in ARC (renin activity with addition of sheep renin substrate), TRC (ARC after activation of inactive renin by trypsin), or PRA (plasma renin activity without additional substrate). (ii) Even in higher concentrations of heparin up to 500 U/mL, neither PRA, ARC, nor TRC of plasma was affected significantly. (iii) Heparin, in concentrations up to 500 U/mL, exerted no significant effect on TRC of the media of human vascular smooth muscle cell culture. In conclusion, heparin does not exert any significant inhibitory effect on human renin nor does it affect activation of inactive renin by trypsin in the range of concentration of practical use, under the conditions employed in this study.

Edetic Acid↗