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Biomedical subjects

K Saida

Publications and source records attributed to K Saida.

At least 19 recordsLinked to original sources
PubMed1992

Involvement of rho p21 in the GTP-enhanced calcium ion sensitivity of smooth muscle contraction.

In the rabbit mesenteric arterial smooth muscle skinned by saponin, Ca2+ induced contraction in a concentration-dependent manner. Guanosine 5'-(3-O-thio)triphosphate (GTP gamma S), a non-hydrolyzable GTP analogue, lowered the Ca2+ concentrations required for this contraction and increased the Ca2+ sensitivity of the skinned smooth muscle contraction. GTP gamma S alone did not induce the contraction in the absence of Ca2+. This GTP gamma S-enhanced Ca2+ sensitivity was completely abolished by an exoenzyme of Staphylococcus aureus, named EDIN, and an exoenzyme of Clostridium botulinum, named C3, both of which are known to ADP-ribosylate the rho p21 family that belongs to the ras p21-like small GTP-binding protein superfamily. The GTP gamma S-bound form of rhoA p21 overcame the inhibitory action of EDIN. smg p21B, another small GTP-binding protein, was inactive. EDIN ADP-ribosylated a protein, which was most likely to be rho p21, in the skinned smooth muscle. The GTP gamma S-bound form of rhoA p21, but not the GDP-bound form, substituted for GTP gamma S and enhanced the Ca2+ sensitivity of the skinned smooth muscle contraction. smg p21B was inactive. These results indicate that rhoA p21 is involved in the GTP gamma S-enhanced Ca2+ sensitivity of the smooth muscle contraction.

Adenosine Diphosphate Ribose↗
PubMed1991

cDNA cloning, sequence analysis and tissue distribution of a precursor for vasoactive intestinal contractor (VIC).

A full-length cDNA encoding preprovasoactive intestinal contractor (PPVIC) has been cloned. From the deduced 160 amino acid PPVIC, the mature VIC is predicted to be produced via a 37 residue intermediate, big VIC. The PPVIC also contains a VIC-like peptide of 16 amino acids structurally related to to the amino-terminal residues of VIC and flanked by pairs of dibasic amino acids, putative processing sites. RNA blot hybridization with PPVIC cDNA confirmed the PPVIC gene to be expressed in the small and large intestinal tract in a tissue specific manner.

Amino Acid Sequence↗
PubMed1991

Structure of the precursor for vasoactive intestinal contractor (VIC): its comparison with those of endothelin-1 and endothelin-3.

Vasoactive intestinal contractor (VIC) is a member of the endothelin (ET) peptide family, which evokes a strong contractile response in the ileum, its gene being expressed only in the intestine. Using dot blot analysis, we carried out an interspecies comparison of the nucleotide and deduced amino acid sequences of the precursor for VIC with those of ET-1 and ET-3 to investigate the physiological significance of processing of the precursor for VIC. The highly conserved amino acid sequence was observed between the big form region (big VIC, big ET-1, and big ET-3) of about 40 amino acids and the like peptide region (VIC-like peptide, ET-1-like peptide, and ET-3-like peptide) of 15 amino acids downstream from the big form region. Sequence identity of amino acids of the precursors of ET-1 and ET-3 with that of VIC was 29 and 28%, respectively. Thus, the precursors for the three peptides might have arisen from a common progenitor gene. However, apparent cleavage sites of the like peptide regions are rather unique in the VIC-like peptide, i.e., it had dibasic amino acids at the amino and carboxy termini. Therefore, we suggest that the VIC-like peptide might be liberated from its precursor protein and play some role in the intestine in vivo.

Amino Acid Sequence↗
PubMed1991

Non-Menkes-type copper deficiency with regression, lactic acidosis, and granulocytopenia.

A 2-year-old girl with granulocytopenia developed fever followed by truncal ataxia and progressive neurologic regression. CT demonstrated symmetric low-density areas in the cerebral white matter. Sural nerve biopsy revealed axonal degeneration. Blood lactate levels were high, and serum levels of copper and ceruloplasmin and urinary excretion of copper were low. Cultured skin fibroblasts showed normal copper uptake. Treatment with oral copper administration normalized serum copper and ceruloplasmin levels, blood lactate levels, and granulocyte count. However, copper levels in the CSF were still low, and the patient showed no clinical improvement. We speculated that copper transport across the intestinal wall and across the blood-brain barrier was impaired.

Acidosis, Lactic↗
PubMed1991

Establishment of vascular endothelial cell lines in a serum-free culture and the discovery of endothelin and a vasoactive intestinal contractor (VIC).

Immortal vascular endothelial cell lines were established and utilized for the production of an endothelium-derived contraction factor (EDCF) in a serum-free medium. After the discovery of Endothelin (21 amino acid peptide, ET) as an EDCF, a prepro ET cDNA isolated from human tissue was used to examine the expression of ET and its regulation in human endothelial cells. A gene family of ET was shown in mouse by using prepro ET cDNA as a probe. Thus, a novel peptide, Vasoactive Intestinal Contractor (VIC) homologous to ET was deduced from the sequence of one of these genes. VIC was confirmed to induce vasocontraction as well as intestinal contraction. Northern blot analysis indicated that this gene was expressed in the intestine but not in endothelial cells. A cloning and sequencing of prepro VIC cDNA from mouse intestine suggest that a VIC-like peptide, as well as VIC, are co-synthesized by cleavage from prepro VIC with 160 amino acids.

Amino Acid Sequence↗
PubMed1991

[Two brother cases of late-onset familial amyloidotic polyneuropathy in Kyoto].

Measurement of variant Met30 transthyretin is diagnostic for a patients with familial amyloidotic polyneuropathy (FAP) type I. The elder brother first noticed numbness of the feet at 64 years of age, and developed weakness of the legs. A few years later, he noticed numbness of the hands, and he was admitted to the hospital at 67 years of age. He was emaciated and had hoarseness and macroglossia. He had moderate muscle atrophy and weakness of all extremities with distal predominance. Deep tendon reflexes were hypoactive in the upper limbs and absent in the lower limbs. There was marked sensory loss of pain and temperature in all 4 limbs distally, and position sense was also impaired. He had mild orthostatic hypotension, severe cardiomegaly and arrhythmia. The younger brother noticed cold sensation of the feet and sexual impotence at 59 years of age. Two years later, he had numbness of the feet and developed weakness of the legs. At 65 years of age, he was admitted to the hospital because of the micturition syncope. He was emaciated and had macroglossia. He had moderate muscle atrophy and weakness of all extremities with distal predominance. Deep tendon reflexes were absent. There was marked sensory loss in the extremities which was predominant in pain and temperature. He had severe orthostatic hypotension (112/70 mmHg in supine position, 50/30 mmHg on standing). Plasma NE value was low and showed poor response to standing. He had neither cardiomegaly nor arrhythmia. Their parents were supposed to have no neurological symptom and were not related with any other Japanese foci of FAP.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1991

[Mitral valve replacement in idiopathic hypereosinophilic syndrome].

Idiopathic hypereosinophilic syndrome (IHES) is a rare systemic manifestation of eosinophilia that may cause endocardial fibrosis and thrombus formation. We presented a 48-year-old man with rapid onset of intractable congestive heart failure during the course of chemotherapy for IHES. After the urgent operation, which included left ventricular thrombectomy and mitral valve replacement the patient was asymptomatic, but died 1 month after operation because of development of IHES. Atrioventricular valve replacement may be beneficial to selected patients with congestive heart failure associated with the cardiac process of the IHES and review of the literature led us to prefer porcine heterograft prostheses in patients with IHES.

Eosinophilia↗
PubMed1991

[Evaluation of treatment of lung cancer combined with the disease which has needed a semi-emergency operation].

Six cases of lung cancer combined with the disease which has needed semi-emergency operation, two cases of unstable angina, two of ileus due to colon cancer, one of impending rupture of abdominal aortic aneurysm and one of purulent cholecystitis with cholelithiasis, were discussed. Mean age was 62.0 years (range, 36 to 73); four were male and two were female. Case 1 and 2 were admitted with anterior chest pain, Case 3 with lumbago and abdominal pain, Case 4 and 5 with an abnormal shadow on chest x-ray film and Case 6 with abdominal pain. Of the two with unstable angina, one was operated on with right upper lobectomy during the first months after aorto-coronary bypass. Of the two with colon cancer, one was operated on with right upper lobectomy during about 5 weeks after right hemi-colectomy. Case 3 with abdominal aortic aneurysm operated on with left upper lobectomy during 4 weeks after replacement of abdominal aorta. Case 4 with cholecystitis was operated on with left pneumonectomy during about 3 weeks after cholecystectomy. The postoperative course of 4 cases and the post-chemotherapy condition of 2 cases were uneventful.

Adenocarcinoma↗
PubMed1991

[Combined valvular and coronary artery surgery].

We report 14 consecutive patients who have undergone myocardial revascularization combined with valve surgery during 7 years (1983-1989). There were 7 males and 7 females with a mean age of 53.8 years. All patients had congestive heart failure and 7 had angina pectoris. Coronary angiography revealed single-vessel disease in 6 patients, double-vessel disease in 5, triple-vessel disease in 3. Mitral regurgitation was predominant in 5, aortic regurgitation in 5, mitral stenosis in 3 and aortic stenosis in 1. The indicated operations were: valve replacement in 12 and mitral anuloplasty in 2 with coronary artery bypass grafting (mean 1.6). One operative and 1 late death were seen in our series, however, NYHA functional class was improved from 3.4 to 1.7 postoperative. Postoperative evaluation by UCG showed good recovery of cardiac function (EF, MVcf, LVEDV, CI). No angina pectoris was evident in surviving patients, the quality of life was significantly improved.

Aged↗
PubMed1991

[A case of esophageal duplication cyst associated with a total left pericardial defect].

Esophageal duplication cyst associated with pericardial defect in a 57-year-old man is reported. Differential diagnosis was very difficult in the preoperative examination. The tumor was a cyst and its wall was a perfect replica of normal esophagus e.g. esophageal duplication, and total left pericardial defect also was found at the operation. There was no malignant or inflammation findings in the excised specimens. The association of esophageal duplication cyst associated with pericardial defect is very rare.

Esophageal Cyst↗
PubMed1990

[Effector mechanisms of PNS demyelination in Gal-C induced-EAN].

Myelin in PNS is multi-layered membranes formed by Schwann cells, and surrounds axon. Destruction of myelin sheath results in demyelination and disturbance of nerve conduction. In PNS, Charcot-Marie-Tooth disease, certain lipidoses, Guillain-Barré syndrome, lead poisoning, compression and some metabolic neuropathies can produce demyelination. In these diseases, GBS is thought to be resulted from abnormalities of immune mechanism. Recently, autoantibodies against Gal-C, P2 and GM1, and complement fixing antibodies against PNS myelin are found in some of GBS patient sera. Here, I present studies on effector mechanism of PNS demyelination using models produced by application of Galactocerebroside (Gal-C) antibodies to PNS. Mainly, three types of effector mechanisms are involved in Gal-C antibody-induced demyelination. In abundance of antibodies, complement-mediated demyelination is at work. When complements are absent, antibody dependent macrophage-mediated demyelination can be involved. Thirdly, myelin once damaged by oxidants and etc can be opsonized by antibodies and C3b, and phagocytized by macrophages. These processes may be operating in such diseases like GBS and CIDP.

Animals↗
PubMed1979

Experimental allergic neuritis induced by sensitization with galactocerebroside.

Thirteen of 31 rabbits immunized repeatedly with bovine brain galactocerebroside developed experimental allergic neuritis, manifested by flaccid paresis and hypesthesia of four limbs, 2 to 11 months after the initial inoculation. Electrophysiological studies revealed multifocal conduction block of peripheral nerves. Perivenular demyelinative lesions associated with phagocytic mononuclear cells occurred in spinal ganglia, roots, and less frequently in distal nerves.

Animals↗
PubMed1979

Demyelination produced by experimental allergic neuritis serum and anti-galactocerebroside antiserum in CNS cultures. An ultrastructural study.

Cultures of mouse cerebellum were exposed to sera from rabbits with experimental allergic neuritis induced by whole peripheral nerve immunization (WN-EAN) and to rabbit anti-galactocerebroside (GC) antisera, and were studied by electron microscopy. Both antisera produced almost identical demyelinative patterns. These consisted of large intramyelinic splittings, "smudged" changes of myelin, degeneration of oligodendrocytes, and phagocytosis of myelin by astrocytes, changes similar to those described after application of whole spinal cord-induced experimental allergic encephalomyelitis (WM-EAE) sera. In addition, patterns which have been considered more characteristic of in vivo demyelinative lesions have been found, susch as vesicular disruption of myelin lamellae and peeling off and phagocytosis of myelin by phagocytic mononuclear cells with electron dense cytoplasm. The morphologic similarities between demyelinative patterns in central nervous system (CNS) cultures induced by anti-GC antiserum and WN-EAN serum and WM-EAE serum, and the fact that elevated antibody titers to GC are found in sera from rabbits with WN-EAN and WM-EAE (Saida, et al., 1977), support the concept that anti-GC antibody is the major factor in the production of CNS demyelination in vitro by sera from rabbits with WN-EAN and WN-EAE.

Animals↗
PubMed1979

Peripheral nerve demyelination induced by intraneural injection of experimental allergic encephalomyelitis serum.

Intraneural injection of sera from rabbits with experimental allergic encephalomyelitis, induced by sensitization with bovine brain white matter in complete Freund's adjuvant, produced focal primary demyelinative lesions in rat sciatic nerves. Demyelinating activity was removed by prior incubation of antisera with central (CNS) and peripheral nervous system (PNS) myelin but not with liver or kidney, and was heat-labile and complement-dependent. Recipient animals developed a sensorimotor disturbance of their toes and ankles on the side injected with antiserum. Twenty minutes after antiserum injection, Schwann cells showed focal cytoplasmic outpouching and their external mesaxons opened. Between 1 and 8 hours after injection vacuolation, splitting and vesiculation of myelin became increasingly prominent at Schmidt-Lanterman clefts and paranodal regions, with concomitant degenerative changes in Schwann cell cytoplasm. Polymorphonuclear cell infiltration and endoneurial edema were apparent at this time. Substantial demyelination occurred before the appearance of phagocytic cells. Between 8 hours and 3 days many nerve fibers were surrounded and attacked by invading macrophages. Axons became demyelinated progressively over several internodes by macrophage phagocytosis. Early signs of remyelination were observed by 5 days. These findings suggest that antibodies directed against antigens common to both CNS and PNS myelin can produce in vivo peripheral nerve demyelination.

Animals↗
PubMed1979

A case of the syndrome of inappropriate secretion of TSH.

A girl aged 4 years with goiter and accelerated physical and skeletal growth was found to be hyperthyroid on the basis of elevated serum thyroid hormone level, nevertheless both the basal TSH and TSH responsiveness to TRH were maintained within the normal range. Serum TSH was suppressed by exogenous T3 and dexamethasone administration, but not significantly changed after propylthiouracil (PTU) treatment. The diurnal rhythmicity of anterior pituitary hormones was preserved with the high nocturnal peak of TSH and prolactin. Clinically, neither thyrotoxic signs nor evidences of pituitary tumor were observed. Her accelerated growth and elevated thyroid hormone level appeared to be induced by inappropriate secretion of TSH. In view of the literature, this is the first case of the syndrome of inappropriate secretion of TSH excluding the neoplastic origin in Japan.

Adrenocorticotropic Hormone↗
PubMed1979

In vivo demyelination induced by intraneural injection of anti-galactocerebroside serum: a morphologic study.

Intraneural injection of rabbit anti-galactocerebroside (anti-GC) serum produced focaldemyelinative lesions in rat sciatic nerves. Recipient rats developed a sensory motordeficit of the toes and feet on the side injected with anti-GC serum. Schwann cellabnormalities in recipient nerves were apparent by 20 minutes, followed by myelinsplitting and vesiculation over the next 8 hours. Macrophages first appeared in moder-ate numbers by 15 hours, and degraded myelin was completely phagocvtized by 5 days.An acute inflammatory reaction consisting of endoneurial edema, polymorphonuclearcell infiltration, and fibrin extravasation also was prominent. In vivo demyelinativeactivity of rabbit anti-GC serums was removed by pre-incubation with GC or central orperipheral nervous system myelin and was also lost when the serums were heated at 56C for 30 minutes and injected into nerves of rats previously injected with cobra venomfactor. Anti-GC antibodies are present in the serum of rabbits with experimentalallergic neuritis (WNV-EAN) and encephalomyelitis (WM-EAE) produced, respectively,by immunization with whole peripheral nerve or brain white matter and may play arole in the pathogenesis of demyelination in GC-induced EAN, WN-EAN, or WM-EAE.

Animals↗