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Biomedical subjects

Y Nishida

Publications and source records attributed to Y Nishida.

At least 325 records · Page 18Linked to original sources
PubMed1990

[Management with antithrombin III concentrate in a pregnant woman with hereditary antithrombin III deficiency].

Pregnant women with hereditary antithrombin III (AT-III) deficiency are frequently associated with thromboembolic disorders. We have treated a pregnant woman with hereditary AT-III deficiency, who had suffered from thromboembolic disorders at her past three gestations, with AT-III concentrate. Dosage of AT-III concentrate to maintain plasma AT-III activity over 80% was 3,500 units per week during second and third trimesters, but more frequent administration was necessary around delivery. In recent reports, pregnant women with hereditary AT-III deficiency had been treated with heparin or warfarin except for during abortion and delivery, in which time AT-III concentrate was widely utilized. But the use of heparin or warfarin during gestation is occasionally harmful, AT-III concentrate should be chosen for management in pregnancy in women with hereditary AT-III deficiency.

Adult↗
PubMed1990

[Prognosis of gastric carcinoma sited in the cardiac part determined by the type of esophageal invasion].

A study has been made of type and prognosis of esophageal invasions exhibited by gastric carcinomas sited in the cardiac part of the stomach. Examined were 14 such cases of an adenocarcinoma with an esophageal invasion. Histopathologically, the invasions into the esophagus were classified into 4 types of severity, from 1 to 4, according to the depth of the invasion into the esophago-gastric junction (EGJ) and the pattern of the invasion to the oral side (thoracic side). The prognosis was found to be good for EGJ invasion that had penetrated to the pm and/or sm layer only, whereas it was very bad if the invasion had penetrated the entire EGJ wall (the pm, sm, mp, and the sa) and the infiltrative pattern had reached the oral side (thoracic side). Almost all patients given a type 4 classification soon had a recurrence after surgery and did not live beyond two years. Thus, a close relationship has been noted between the type of invasion into the esophagus and the prognosis.

Adenocarcinoma↗
PubMed1989

Increased replication of HTLV-I in HTLV-I-associated myelopathy.

To estimate the replication of the human T-cell leukemia virus type I (HTLV-I) in patients with HTLV-I-associated myelopathy (HAM), or tropical spastic paraparesis (TSP), HTLV-I DNA integrated into lymphocyte genomes was analyzed by Southern blot hybridization. HTLV-I DNA was detected in 125 (82%) of 153 patients and most showed random integration. This incidence was much higher than the 29% found in asymptomatic carriers. Therefore, HAM/TSP development is associated with a high level of HTLV-I replication. In addition, lymphocytes from 3 patients with HAM/TSP showed monoclonal integration of HTLV-I DNA, indicating adult T-cell leukemia.

Adult↗
PubMed1989

Erythrocyte adenine PRPP availability in two types of APRT deficiency using silicon oil method.

Erythrocyte phosphoribosylpyrophosphate availability for adenine was measured by silicon oil method previously described. The homozygotes of Japanese type APRT deficiency (n = 6, from 4 families) showed 4.3 +/- 2.7% (mean +/- standard deviation) of adenine PRPP availability and the heterozygotes (n = 5) showed 86.0 +/- 6.0% of adenine PRPP availability. All homozygotes of Japanese type APRT deficiency from 4 unrelated families show the equally decreased adenine PRPP availability and it supports the presumption of the presence of the similar defect of APRT in all families. In a Japanese family of complete APRT deficiency, adenine PRPP availability of the homozygote was undetectable and that of the heterozygote was normal low (54.3% of normal mean activity). The adenine PRPP availability of the heterozygote of complete APRT deficiency was diagnostically different from that of the homozygotes of Japanese type APRT deficiency, despite, these two conditions showed almost the same erythrocyte APRT activity. These results prove that the silicon oil method previously written is the rapid and useful method for differential diagnosis between two types of APRT deficiency.

Adenine↗
PubMed1989

Congenital myopathy with myasthenic features and congenital cataract in two siblings.

Two siblings with congenital myopathy showing myasthenic manifestations together with congenital cataract are reported. Their muscle weakness fluctuated and was alleviated by edrophonium chloride. Their serum creatine kinase activity was elevated, and the waning phenomenon was observed on repetitive nerve stimulation. Biopsied muscle showed degenerative changes with type 1 fibre predominance and abnormal morphology of neuromuscular junctions.

Adult↗
PubMed1989

Loss in transformed cells of cell cycle regulation of expression of a nuclear protein recognized by SLE patient antisera.

The identification of cellular proteins involved in the control of cell proliferation in normal cells is essential for understanding the mechanism underlying growth regulation and cellular transformation. A nuclear protein termed Ki antigen with a relative mobility of 32,000 (Mr 32K) and which is recognized by SLE patient antisera has been identified in cells of human, bovine, and murine origin. Recently, cDNA clones for the bovine and human Ki antigens have been isolated using SLE patient antisera (T. Nikaido, et al., in preparation). The nucleotide sequence predicted a protein of 239 amino acids with a possible nuclear localization signal resembling that identified in SV40 T antigen and other nuclear proteins. Here we show that the expression of Ki antigen is regulated in the normal cell, but not in the transformed cell. Furthermore, in the K-ras temperature-sensitive mutant cell line, ts 371 normal rat kidney (NRK), Ki antigen expression increases several-fold at the permissive temperature relative to the nonpermissive temperature. These results suggest that expression of Ki antigen might be correlated with cellular transformation as well as with cell growth regulation.

Animals↗
PubMed1989

Structure and activity of artificial mutant variants of human growth hormone.

Four artificial mutant variants of human growth hormone (hGH) with the following characteristics were prepared in Escherichia coli by in vitro mutagenesis: (i) replacement of Trp86 with Tyr (W86Y hGH); (ii) deletion of Trp86 (delta W86 hGH); (iii) deletion of residues 32-46 (20-kd-hGH); and (iv) deletion of residues 32-71 (17.5-kd-hGH). Both W86Y hGH and delta W86 hGH have a point mutation at Trp86 which is the only Trp residue in hGH and is conserved among members of the growth hormone family. 20-kd-hGH is a minor component of hGH in the pituitary gland and plasma and is the result of an alternative splicing of the primary gene transcript, while only the corresponding mRNA and not the protein has been found in the case of 17.5-kd-hGH. The biological activities (adipogenic activity and potentiation of gain in body weight) and structures (as analyzed by circular dichroism) were mostly retained by the W86Y, delta W86 and 20-kd-hGH variants but not by 17.5-kd-hGH.

Adipose Tissue↗
PubMed1989

Alpha-agonist modifies baroreflex vasoconstriction by a postjunctional mechanism in dogs.

1. We examined whether or not circulating alpha-agonist modified baroreflex vasoconstriction of the hindlimb, using anaesthetized dogs in which the limb was vascularly isolated and perfused with blood from a donor dog using a pulsatile pump. 2. The open-loop gain (G) of the baroreflex was estimated from changes in mean arterial pressure following mild quick haemorrhage from the aorta of the recipient dog. 3. The hindlimb perfusion pressure increased after haemorrhage due to neurogenic vasoconstriction. 4. An overall gain (Gh) of the baroreflex hindlimb vascular bed control system was estimated from the ratio of the increase in hindlimb perfusion pressure to the change in systemic arterial pressure of the recipient dog. 5. Administration of a relatively selective alpha 1-agonist with no prejunctional beta 2 stimulating action (phenylephrine) or a selective alpha 2-agonist (clonidine) to the donor dog increased its systemic arterial pressure and augmented Gh. 6. Since both drugs were administered to the donor dog and could not enter into the recipient dog, these drugs did not affect the recipient's sympathetic nervous system, including the central nervous system and afferent limb of the baroreflex system. Therefore, these drugs could modify baroreflex vasoconstriction of the hindlimb only at the junction of the efferent sympathetic nerve and the vascular smooth muscle. 7. It was concluded that postjunctional alpha-adrenoceptor stimulation augments neurogenic vasoconstriction.

Adrenergic alpha-Agonists↗
PubMed1989

Molecular analysis of hypoxanthine-guanine phosphoribosyltransferase mutations in five unrelated Japanese patients.

The isoenzyme of hypoxanthine-guanine phosphoribosyltransferase (HPRT, E.C.2.4.2.8) functions in the metabolic salvage of purines. Partial HPRT deficiency is associated with gouty arthritis, while absence of activity results in Lesch-Nyhan (LN) syndrome. We characterized five unrelated patients with HPRT deficiency to understand the spectrum of molecular defects using Southern and Northern blot, polymerase chain amplification of HPRT mRNA and DNA sequencing, and oligonucleotide hybridization analysis of the HPRT gene. Southern blot analysis of DNA indicated that mutations leading to HPRT deficiency in our five patients were not the result of major chromosomal rearrangements or deletions. Sequencing analysis of the amplified DNA from three different patients with HPRT deficiency implied three unique molecular abnormalities: 1) one single-base substitution at codon 54 (from ATG to CTG) resulting in the replacement of methionine with leucine in an LN patient, 2) two single-base substitutions at codon 179 (from GTT to GGT) and at codon 180 (from GGA to AGA) resulting in the replacement of valine with glycine and glycine with arginine in a gouty patient, and 3) 51 nucleotide deletion between nucleotides 747 and 797 resulting in the formation of shorter sized HPRT mRNA and putative two amino-acid deleted HPRT protein in another gouty patient. These results are the direct molecular evidence of genetic heterogeneity in mutant HPRT.

Amino Acid Sequence↗
PubMed1989

Effects of brain natriuretic peptide on renal nerve activity in conscious rabbits.

Responses of renal nerve activity (RNA) to intravenous infusion of brain natriuretic peptide (BNP) were examined in chronically instrumented conscious rabbits with all baroreflexes intact, sinoaortic baroreceptor denervation (SAD), and SAD plus vagotomy. In intact rabbits, an infusion of BNP at a rate of 0.3 microgram.kg-1.min-1 for 30 min decreased mean arterial pressure (MAP) by 8 +/- 1 mmHg and increased RNA by 48 +/- 4% but did not alter heart rate (HR). The decrease in MAP in SAD rabbits (20 +/- 3 mmHg) was greater than in intact rabbits, whereas RNA increased less (21 +/- 7%). After SAD plus vagotomy, BNP lowered MAP by 25 +/- 4 mmHg, whereas RNA was not altered significantly. To further examine the effects of BNP on baroreflex control of HR and RNA, the baroreceptors were stimulated or unloaded by raising or lowering MAP by injections of phenylephrine or glyceryl trinitrate, respectively. The maximum change in each HR or RNA response to phenylephrine or glyceryl trinitrate was plotted against the maximum change in each MAP response and a logistic function curve was fitted to the MAP-HR and MAP-RNA relationship. BNP did not alter the slope of either curve but shifted both curves to the left. These results indicate that 1) in intact rabbits, BNP increases RNA due to sinoaortic and cardiopulmonary baroreflexes and 2) BNP resets the baroreflex control of HR and RNA to a lower arterial pressure.

Animals↗
PubMed1989

HTLV-I-associated myelopathy with adult T-cell leukemia.

We report a 42-year-old Japanese woman with HTLV-I-associated myelopathy (HAM) combined with adult T-cell leukemia (ATL). Combination of the 2 diseases has been extremely rare. The infrequency is explained by HLA types unique to each disease. Our patient suggests that the HAM-associated HLA haplotype does not prevent the development of ATL.

Adult↗
PubMed1989

Injection and sampling methods for drug residue study in calf muscle.

Eight calves, weighing 50-150 kg, were given intramuscularly 5 ml of ampicillin (ABPC) aqueous suspensions (200 mg potency/ml) in their right and left gluteal and femoral regions. All calves were sacrificed one hour later to confirm the location of injected drug. The drug was found in a muscle layer when injected with a needle 15 mm long to the following positions, 1. the midpoint between the central position of the gluteal region (CG) and the tuber coxae (M-CTc), 2. the midpoint between CG and the tuber ossis ischii (M-CTo), 3. the central position of M. semimembranaceus in the femoral region (CF). Seven calves, weighing 130-150 kg, were given intramuscularly 5 ml of ABPC suspensions at M-CTo and CF and sacrificed one hour (4 calves) and 3 days (3 calves) later. ABPC diffused along the long axis of the muscle fibers but not to the radial direction. ABPC was detected only in the injected muscle layer even after 3 days indicating that the drug did not diffuse to the neighboring muscles. In the injected muscle layer, concentration of ABPC was remarkably different from part to part. From these results, sampling of the injected muscle for the drug residue study was proposed as follows: 1. isolate about 100 g of muscle just under the stick point marked on the skin considering the direction of drug diffusion, and 2. isolate separately about 200 g of the surrounding muscle to confirm if the sampling is appropriate.

Ampicillin↗
PubMed1989

Renal nerve blunts natriuretic and diuretic response to atrial natriuretic peptide in conscious rabbits.

The contribution of the renal nerve to the natriuretic and diuretic responses to rat atrial natriuretic peptide (rAMP) was investigated in conscious rabbits with unilateral renal denervation. Renal nerve activity (RNA) was measured at the contralateral innervated kidney. Catheters were bilaterally implanted into the ureters. Urine samples were collected from each kidney by gravity drainage at 10-min clearance intervals. In rabbits with all baroreflexes intact, infusion of rANP at 0.3 micrograms/(kg.min) for 30 min decreased mean arterial pressure by 8 +/- 4 mmHg and increased RNA by 53 +/- 13%. After sinoaortic baroreceptor denervation (SAD), hypotensive response to infusion of rANP was greater than that in intact rabbits, while RNA did not change. After SAD plus vagotomy, infusion of rANP lowered mean arterial pressure by 21 +/- 4 mmHg and RNA by 19 +/- 6%. In the denervated kidney, infusion of rANP increased Na+ excretion by 16.1 +/- 4.5 from 3.5 +/- 1.0 muEq/min and water excretion by 0.17 +/- 0.05 from 0.08 +/- 0.02 ml/min. In the contralateral innervated kidney, infusion of rANP increased the amount of Na+ and water excretion by 4.5 +/- 3.2 muEq/min and 0.07 +/- 0.04 ml/min, which were significantly less than those in the denervated kidney. These results indicate that infusion of rANP increases RNA, due to baroreceptor reflexes, and that this increase in RNA blunts natriuretic and diuretic action of rANP.

Animals↗
PubMed1989

Effects of endolymphatic mastoid shunt operation for patients with Menière's disease.

During the past 10 years, the endolymphatic mastoid shunt operation was carried out on 108 patients with Meniere's disease: 54 men and 54 women between 22 and 72 years old. According to criteria AAOO proposed in 1972, 86 cases (79.6%) belonged to class A, 19 cases (17.7%) to class B and 3 cases (2.7%) to class C. Forty patients took the body sway test before and after the operation. Four of the 40 patients were found to have Meniere's disease on the contralateral side within 12 months after the operation and one patient was found to have a complicating psychogenic disease. The abnormal body sway had recovered 2 to 9 months after the operation, but the medical treatment could not be stopped during this period. The average hearing gain after the operation was 21.3 +/- 14.4 dB; that for the patients with a short period of illness (within 23 months of the first onset to the operation) was 25.2 +/- 14.5 dB and that for the patients with a longer period of illness (over 24 months) was only 13.8 +/- 10.6 dB.

Adult↗