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Biomedical subjects

M Hirata

Publications and source records attributed to M Hirata.

At least 595 records · Page 33Linked to original sources
PubMed1985

[Multiple primary cancers observed after surgery of lung cancer, and their countermeasures].

Multiple primary cancers were found after surgery in 80 (2.5%) of 3,154 patients with lung cancer. Patients with squamous cell carcinoma most frequently suffered from multiple primary cancers. The period up to discovery of the second primary cancers was within two years in 78.8% of the patients. Second primary cancers were most frequently observed in the lung, followed by the stomach, colon and rectum. Second primary cancers were found in the lung in 26 patients, 14 of these (53.8%) having squamous cell carcinoma. Multiple primary cancers were noted in 2.8% of 1,210 lung cancer patients who underwent stage I curative operation and 2.4% of the remaining 1,944 cases. As to prognosis, 14 patients survived for more than three years after the second primary cancers were found.

Adenocarcinoma↗
PubMed1985

Role of macrophages in atherosclerosis. Sequential observations of cholesterol-induced rabbit aortic lesion by the immunoperoxidase technique using monoclonal antimacrophage antibody.

To elucidate the role of macrophages in atherosclerosis, sequential observations were carried out on cholesterol-induced aortic lesions of the rabbit with the immunoperoxidase technique by use of monoclonal antimacrophage antibody. Animals on cholesterol diets for 8 weeks or longer showed increased accumulations of lipid-filled macrophages in the intima. At a very early stage, when no grossly visible alterations were observed, macrophages were seen clinging to the endothelial surface with apparent penetration of the endothelium. A single line of three or four vacuolated macrophages were found in otherwise normal subendothelial spaces. In flat lesions consisting of a few layers of foam cells, lipid-laden macrophages were the cells that predominated. In advanced plaque lesions, negatively staining, most presumably, smooth muscle foam cells became noticeable and increased in number. At this stage, macrophage foam cells predominated in the superficial layer of the lesion, whereas negatively staining foam cells were prevalent in deeper areas. Macrophages were also spotted within areas of necrosis, and they were occasionally observed near the necrotic core of the atheroma. During 24 to 74 weeks after termination of the cholesterol diet, the number of cells with specific macrophage staining markedly diminished. The results support the concept that circulating monocytes are the prime source of foam cells in the initial phase of atherogenesis. It seems likely that the major role of macrophages in atherogenesis is to remove lipids from areas of lesion formation. The failure of macrophages to perform their scavenger role successfully may be a major factor in the accumulation of lipid-rich debris in advanced lesions. Relative paucity of macrophages may also be an important factor explaining why regression of atherosclerosis occurs rarely in the rabbits.

Animals↗
PubMed1985

Abnormal lactate dehydrogenase isoenzyme in serum and tumor tissue of a patient with neuroblastoma.

Serum and tumor tissue of a patient with neuroblastoma contained an abnormal isoenzyme of lactate dehydrogenase (LDH; EC 1.1.1.27), which, on agarose gel electrophoresis, migrated between LDH-2 and LDH-3 with a mobility the same as that of the extra LDH isoenzyme found in normal human erythrocytes. On surgical removal of the tumor, the high total LDH activity (775 U/L) in the serum of the patient rapidly decreased to normal (70-220 U/L), and the abnormal LDH isoenzyme was no longer detected. The total LDH activity of the abnormal LDH isoenzyme per gram of hemoglobin in the tumor tissue was 26 times that of erythrocytes, suggesting that the abnormal isoenzyme originated mainly from the tumor cells themselves rather than the erythrocytes contained in the tumor tissue. This first report on the appearance of the abnormal LDH isoenzyme in a patient with neuroblastoma suggests that this abnormal LDH isoenzyme may have some significance as a marker enzyme for neurogenic tumors.

Abdominal Neoplasms↗
PubMed1985

[Early invasive squamous cell carcinoma of the tongue--report of a case].

A 65-year-old woman with early invasive squamous cell carcinoma of the tongue is reported. Atypical but not definitely malignant epithelium was detected by cytology, although the gross appearance of the glossal lesion looked like early invasive squamous cell carcinoma. On the surgical material, the basal and para-basal cell layers were occupied by cancer, but the upper portion of the epidermis from the prickle cell layer through the surface of the mucosa was histologically benign. In such cases, to obtain the correct diagnosis on cytology, repeated examinations as well as using a sharp instrument like a curatte are necessary.

Aged↗
PubMed1984

Release of Ca2+ from a non-mitochondrial store site in peritoneal macrophages treated with saponin by inositol 1,4,5-trisphosphate.

The effects of inositol 1,4,5-trisphosphate, prepared from human erythrocyte ghosts, on Ca2+ release from intracellular store sites were studied in saponin-treated guinea pig peritoneal macrophages. Micromolar concentrations of inositol 1,4,5-trisphosphate released Ca2+ within 1 min from store sites which had accumulated Ca2+ in the presence of 10 mM-NaN3. In the presence of 10 mM-NaN3, the Ca2+ accumulated in the presence of oxalate was seen in the endoplasmic reticulum of saponin-treated macrophages by electron microscopy, indicating that the site of Ca2+ released by inositol 1,4,5-trisphosphate may be endoplasmic reticulum-like membranes. When the concentrations of free Ca2+ were over 3.5 X 10(-6) M, the release of Ca2+ by this agent was inhibited. This inhibition may be due to either the higher concentration of extra-vesicular free Ca2+ or the larger accumulation of Ca2+ into the store site or perhaps both effects. MgCl2 also had an inhibitory effect on the Ca2+ release. Inositol 1,4,5-trisphosphate also released Ca2+ from cardiac sarcoplasmic reticulum, but not from erythrocyte inside-out vesicles.

Animals↗
PubMed1984

Prostacyclin release from the coronary vascular wall by vasoactive substances.

Which vasoactive substances that are synthesized in vivo could induce the release of a sufficient amount of prostacyclin (PGI2) to inhibit platelet aggregation from the vascular wall was investigated in the isolated dog heart perfused by a modified method of Langendorff. Infusion of 5 microM bradykinin or 25 u/ml crude thrombin into the heart for 30 sec resulted in the transient appearance of inhibitory activity of platelet aggregation. The inhibitory activity was stable at alkaline pH but unstable at acidic pH and thermolabile. The appearance of the inhibitory activity was prevented by treatment of the coronary vessel with 30 microM indomethacin or 1 mM tranylcypromine. These results indicated that the inhibitory activity was caused by PGI2. When 25 microM acetylcholine, 25 microM noradrenaline, 25 microM isoproterenol, 10 microM adenosine triphosphate (ATP), 5 microM adenosine, 1 microM angiotensin II, 25 microM histamine or 1 microM serotonin was infused for 30 sec, no inhibitory activity of platelet aggregation was observed. Bradykinin (5 X 10(-9) approximately 5 X 10(-6) M) and purified thrombin (1 X 10(-9) approximately 1 X 10(-7) M) induced a dose-dependent release of PGI2 which was assayed using a radioimmunoassay for 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha).

Adenosine↗
PubMed1984

Effect of cAMP-elevating drugs on Ca2+ efflux and actin polymerization in peritoneal macrophages stimulated with N-formyl chemotactic peptide.

To investigate intracellular cAMP inhibitory mechanisms related to migration of guinea-pig peritoneal macrophages, we examined the effects of cAMP-elevating drugs on the Ca2+ efflux and actin polymerization in macrophages stimulated with fMet-Leu-Phe, a chemotactic peptide. The stimulation with 1 X 10(-8) M fMet-Leu-Phe enhanced the Ca2+ efflux, and induced actin polymerization. Dibutyryl cAMP, theophylline and papaverine, which continuously increased the levels of intracellular cAMP, inhibited the enhancement of Ca2+ efflux and induction of actin polymerization by fMet-Leu-Phe. On the other hand, isoproterenol, which transiently increased the cAMP level, inhibited only the early phase of Ca2+ efflux and not the actin polymerization. As additions of both cAMP and cAMP-dependent protein kinase did not modify the Ca2+ uptake of phagocytic vesicles, the inhibition of Ca2+ efflux by these drugs may be due to the inhibition of the Ca2+ release from the intracellular store site(s). The cAMP-elevating drugs increased the monomeric actin content without change in the total actin content, indicating an induction of the depolymerization of filamentous actin. From these findings, we conclude that the inhibition of macrophage migration induced by cAMP may be due to the inhibition of both the increase of intracellular Ca2+ concentration and actin polymerization. Furthermore, the intracellular levels of cAMP probably play a role in regulating actin states in the macrophages.

Actins↗
PubMed1984

Effects of cAMP- and cGMP-dependent protein kinases, and calmodulin on Ca2+ uptake by highly purified sarcolemmal vesicles of vascular smooth muscle.

Sarcolemmal fractions of vascular smooth muscles were prepared from porcine thoracic aortae by differential and sucrose density gradient centrifugation. In these fractions, there was a high activity of 5'-nucleotidase, a putative marker enzyme of plasma membrane, and a low activity of rotenone insensitive NADH-cytochrome c reductase a marker of sarcoplasmic reticulum. In these fractions, the Ca2+ uptake was ATP-dependent. A low concentration of saponin which inhibited Ca2+ uptake by the plasma membrane but not by the sarcoplasmic reticulum, inhibited 65% of the Ca2+ uptake of this fraction. The Ca2+ uptake of this fraction was enhanced by cAMP- and cGMP-dependent protein kinases, and by calmodulin. The cAMP-dependent protein kinase enhanced the phosphorylation of 28 and 22 kDa proteins, while the cGMP-dependent protein kinase phosphorylated the 35 kDa protein. The phosphorylation of 100, 75, 65, 41 and 22 kDa proteins was enhanced by Ca2+ and calmodulin. These results indicate that cAMP- and cGMP-dependent protein kinases as well as calmodulin play important roles in Ca2+ transport in the sarcolemma, and that the phosphorylated proteins may be associated with an enhancement of Ca2+ transport in the sarcolemma.

Animals↗
PubMed1984

Inositol 1,4,5-trisphosphate releases Ca2+ from intracellular store sites in skinned single cells of porcine coronary artery.

Effects of inositol 1,4,5- trisphosphate , extracted from human erythrocyte ghosts, on Ca2+ release from intracellular store sites were studied in saponin-treated single muscle cells of the porcine coronary artery. Application of micromolar concentrations of inositol 1,4,5- trisphosphate released Ca2+ from the intracellular non-mitochondrial store sites, within 1 min. However, when the concentrations of free Ca2+ were over 1.5 X 10(-6) M, the release of Ca2+ by this agent was inhibited. The Ca2+ releasing mechanism differed from that seen with A23187, therefore this release of Ca2+ from store sites was not due to Ca2+ ionophore actions. This agent may play the role of messenger in increasing the cytosolic Ca2+, provoking pharmaco-mechanical coupling, and thus producing the contraction.

Animals↗
PubMed1984

Drug interactions in biotransformation of 1-phthalidyl 5-fluorouracil to 5-fluorouracil in rat liver.

Two rat liver hydrolases were found to be involved in the metabolism of 1-phthalidyl 5-fluorouracil (PH-FU) to 5-fluorouracil (5-FU), one of which was induced by phenobarbital (PB) treatment of rats. Both inducible and constitutive enzyme were soluble and showed different characteristics in gel filtration and response to inhibitors. Further study showed that the blood level of PH-FU could be modulated by PB-pretreatment or coadministration of enzyme inhibitors to rats.

Animals↗
PubMed1984

Precipitates found around Schistosoma haematobium eggs from human urine prior to circumoval precipitin test.

Schistosoma haematobium eggs were recovered in urine from schoolchildren in Mwachinga Village, Kwale District, Kenya. The surface of the eggs showed a pattern similar to that observed in a circumoval precipitin (COP) test. Observed precipitates were removed by treatment of the eggs with pepsin, but were not affected by trypsin. Similar precipitates occurred after incubating the pepsin-treated eggs with urine supernatants from the same children. Attempts were made to identify the components that might contribute to observed bleb (precipitate) formation. The fluorescent antibody test revealed both IgG and IgM in the precipitate, while urine examination by immunodiffusion revealed IgG, IgM, IgA and C3. These components probably participated in the bleb formation. This possibility seemed more likely because of the presence of anti-egg antibodies in the immunoglobulins identified in the urine, and agrees well with the expected activity of pepsin on these immunoglobulins. These results, therefore, suggest that S. haematobium eggs recovered in urine contain precipitates formed mainly by immunoglobulins; it is necessary to treat such eggs with pepsin before carrying out a COP test. The relevance of these findings to the immunodiagnosis of Schistosomiasis haematobium in man is discussed.

Adolescent↗
PubMed1984

An inhibitor of lipoxygenase, nordihydroguaiaretic acid, shortens actin filaments.

An inhibitor of lipoxygenase of arachidonic acid, nordihydroguaiaretic acid, shortens actin filaments, as judged by electron microscopic observation of negatively stained actin filaments, actin sedimentability and measurement of specific viscosity, at concentrations that inhibit the migration of phagocytic cells. At higher concentrations (more than 10 microM) nordihydroguaiaretic acid strikingly inhibits myosin ATPase activity. Thus nordihydroguaiaretic acid has a severe side effect on the cytoskeleton.

Actins↗