Search PubMed⌕ Search

Biomedical subjects

H Ueyama

Publications and source records attributed to H Ueyama.

At least 127 records · Page 7Linked to original sources
PubMed1990

Studies on the anti-tumor-promoting activity of naturally occurring substances. IV. Pd-II [(+)anomalin, (+)praeruptorin B], a seselin-type coumarin, inhibits the promotion of skin tumor formation by 12-O-tetradecanoylphorbol-13-acetate in 7,12-dimethylbenz[a]anthracene-initiated mice.

Since Pd-II [(+)anomalin, (+)praeruptorin B], a seselin-type coumarin, was found to inhibit tumor promoter induced phenomenon in vitro, the effect of Pd-II on the in vivo tumor-promoting action of 12-O-tetradecanoylphorbol-13-acetate (TPA) in 7,12-dimethylbenz[a]anthracene-initiated mouse skin was investigated. Pd-II, applied 40 min before the TPA treatment, at a dose of 10 mumol/painting, completely suppressed tumor formation up to 20 weeks of tumor promotion, without any toxicity. Besides Pd-II, various anti-tumor-promoter coumarins were found in the traditional Chinese medicine Qian-Hu, from which Pd-II was obtained. These coumarins may be useful for the development of an effective method to prevent cancer.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1990

Increase of 63 kDa protein kinase in the nuclear matrix of HL-60 cells during differentiation by retinoic acid.

The changes of protein kinases (PKs) in the nuclear matrix of HL-60 cells during the differentiation by retinoic acid (RA) were examined by in situ assay after sodium dodecyl sulfate-polyacrylamide gel electrophoresis. In the nuclear matrix of HL-60, at least seven species of PKs (83, 63, 58, 46, 42, 38, and 31 kDa) were always detected. Among these PKs, 63 kDa PK was increased dramatically during differentiation by RA. Two-dimensional electrophoresis revealed that two species of 63 kDa PKs (pI 5.0 and 5.4) were presented in the nuclear matrix and increased similarly during the differentiation. This increase of 63 kDa PKs may be related to the lobulation of the nucleus and the nuclear matrix accompanying the differentiation by RA.

Cell Nucleus↗
PubMed1989

Homozygous variant of antithrombin III that lacks affinity for heparin, AT III Kumamoto.

Abnormal antithrombin III (AT III) was found in the plasma of a 31-year-old female who suffered from recurrent thrombotic episodes. Heparin cofactor activity was 28% of normal and undetectable when measured by inhibition of thrombin and factor Xa (F.Xa), while both progressive antithrombin and antifactor Xa activities were normal. The concentration of plasma AT III antigen was 37 mg/dl. Analysis by crossed-immunoelectrophoresis (CIE) in the presence of heparin and affinity chromatography on heparin-Sepharose revealed that the propositus' AT III did not bind to heparin. When heparin cofactor II (HC II) was removed from propositus' plasma, heparin cofactor activity of AT III was not detected. Thus, HC II seemed to account for the plasma heparin cofactor activity found in the presence of thrombin. The patient's parents and three of her brothers demonstrated qualitative abnormality of AT III; heparin cofactor activity was 30-50% of normal levels in the presence of both thrombin and F.Xa. These findings indicate that the propositus' AT III lacks affinity for heparin and the mode of its inheritance seems to be autosomal dominant and, hence, the propositus would be a homozygote. For this variant, the name of AT III Kumamoto is proposed.

Adult↗
PubMed1989

Restriction fragment length polymorphisms on the q24-q28 region of X chromosome among Japanese population.

Restriction fragment length polymorphisms were studied among the Japanese population using 12 polymorphic DNA probes on the q24-q28 region of X chromosome. The frequency distribution for probes p22-33, p482.6a, p43-15, 52A, pPM101, cX33.2 and cpx234, was the same as that for Caucasians, and that for probes 4D-8 and St14-1 (MspI) was slightly different (p less than 0.05). However, it was quite different (p less than 0.01) for probes p114.12, St14-1 (TaqI), 36B-2 and MN12. Probe p114.12 showed no HindIII polymorphism for the Japanese people. On the contrary, probe MN12, which has a low PIC value (0.15) for Caucasians, was found to be useful for Japanese (PIC value = 0.50). These results suggest that 7 DNA probes (p482.6a, p43-15, 52A, St14-1, p114.12 (BclI), 36B-2 and MN12) are useful (PIC greater than 0.42) for linkage analysis of X-linked disease in Japan.

Blotting, Southern↗
PubMed1989

Restriction fragment length polymorphisms of X chromosome among Japanese population.

Restriction fragment length polymorphisms were studied among the Japanese using 13 polymorphic DNA probes on the X chromosome. For 6 probes (pPA4B, cpX203, p58-1, pHPGK-7e, cpX289 and 7b) the allelic frequencies were the same as those for Caucasians, but they were quite different (p less than 0.01) for 4 probes (dic56, pOTC (MspI), pTAK8B and pXG-16 (HindIII)). No polymorphisms were observed for 4 probes (pG95 alpha 1-7dIII/RI (n (chromosome number studied) = 54), pXG-16 (TaqI) (n = 50, p8 (n = 108), and pXG-17 (n = 76). These results suggest that not a small number of DNA probes currently available are useless for linkage analysis in Japan.

DNA Probes↗
PubMed1989

Progressing ischemic stroke in a homozygote with variant antithrombin III.

A 31-year-old woman developed disturbance of consciousness and left hemiparesis. Cerebral computed tomograms showed a low-density area in the right temporal lobe that extended to the right parietal and left frontal lobes as her clinical symptoms worsened. The diagnosis of familial variant of antithrombin III (AT-III) was based on decreased biologic activity and a normal immunologic level of AT-III in this patient and in her family members. Transfusion of normal AT-III concentrate led to a striking clinical recovery. Blood coagulation studies revealed that nine of 13 family members had decreased biologic AT-III activity and that the patient herself was the only homozygote with variant AT-III. We conclude that variant AT-III, especially in a homozygote, seems to be one cause of ischemic stroke in young adults and that simultaneous measurement of both the biologic and immunologic activities of AT-III is necessary to detect it.

Adult↗
PubMed1989

[A case of ischemic oculopathy followed by border zone infarction].

We reported a 72-year-old male with ischemic oculopathy due to ophthalmic artery stenosis followed by ipsilateral border zone infarction due to internal carotid artery stenosis. The patient had history of hypertension and diabetes mellitus. He had severe headache and visual disturbance of the right eye. He was diagnosed right neovascular glaucoma and left diabetic retinopathy (simple type), and received diuretics, beta-blockade and other anti-hypertensive drugs. One month later, he noticed left mild hemiparesis in a morning, and he experienced progression of left hemiparesis over a week. He was admitted to our hospital on the 11th day. He showed left complete hemiplegia, left sensory disturbance, anosognosia and left unilateral spatial neglect. His right eye was diagnosed neovascular glaucoma but left eye was normal. The 5th days CT showed low density area in the right terminal zone and bilateral periventricular lucency. At the same area, the 46th days MRI showed high intensity area in the T2-weighted image and low intensity area in the T1-weighted image. Cerebral angiography performed on the 33rd day, disclosed severe kinking at the cervical segment and 50% stenosis at the intracavernous segment in the right internal carotid artery, and 90% stenosis and post-stenotic dilatation of the right ophthalmic artery. Left internal carotid artery had each 60% stenosis at the cervical segment and the intracavernous segment. Left ophthalmic artery had severe stenosis from its beginning to distal part. This infarction was considered berder zone infarction by it's localization (terminal zone) and internal carotid artery stenosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1989

[Familial antithrombin III abnormality accompanied with progressing ischemic stroke].

We report a case of familial antithrombin III (AT-III) abnormality accompanied with progressing ischemic stroke. The patient was a 31-year-old female who developed consciousness disturbance and left hemiparesis on December 1 in 1987. She had a history of two transient ischemic attacks and three episodes of thrombophlebitis of the extremities. Cerebral CT scan showed a low density area on the right temporal lobe that had extended to the right parietal and on the left frontal lobe as clinical symptoms worsened. Cerebral angiogram revealed branch occlusions of the right middle cerebral artery and showed no cerebral venous and sinus obstruction. When her symptoms had been progressing to show semi-comatose state, left hemiplegia and transient Cheyne-Stokes respiration, we found her decreased biological activity and normal immunological level of AT-III. The diagnosis of familial AT-III abnormality had been made by familial investigation. As the treatment of AT-III concentrates transfusion was started from the third day, her symptoms gradually recovered and the low density area stopped extending. Further examinations revealed that she was a homozygote of AT-III abnormality presenting no affinity for heparin and that her parents were heterozygotes. It was suggested that the homozygous AT-III abnormality was the main cause of her progressing ischemic stroke.

Adult↗
PubMed1989

[Rendu-Osler-Weber syndrome presented paramedian thalamic and midbrain infarcts and primary medullary hemorrhage: a case report].

We reported a 41-year-old male with paramedian thalamic and midbrain infarcts due to cerebral embolism from bilateral pulmonary arterio-venous fistula and primary medullary hemorrhage. The patient had an episode of sudden onset consciousness disturbance with left Weber's syndrome (right hemiplegia and left oculomotor palsy) and vertical gaze palsy at age of 23. He noticed numbness in the left hand and the left half body under clavicular when he had got up in a morning at age 41. He had headache and left tinnitus on second and third days, and on the 3rd and 4th days, he experienced nausea. He had severe hiccup persisting from the 6th to the 13th days. The 23rd days he was admitted to our hospital. He showed dysesthesia and paresthesia in left half body under clavicular, dysesthesia in left hand and vertical gaze palsy and convergence disturbance. MRI performed on the 18th and 24th days, disclosed hyperdense mass in T1 and T2-weighted images in dorsal site of medulla, but the 70th days MRI showed no abnormal lesions. Therefore we diagnosed the high intensity mass as primary medullary hemorrhage. Cerebral angiography showed no abnormal vasculature. Many members of his family had history of sever nasal bleeding. He had skin hemangioma and mucosal hemangioma in esophagus, stomach, colon and rectum, and bilateral pulmonary arterio-venous fistula which had been operated at age 39. His mother also had skin hemangioma and pulmonary arterio-venous fistula. Therefore this family was diagnosed Rendu-Osler-Weber syndrome (hereditary hemorrhagic telangiectasia). MRI also disclosed multiple cerebral infarctions in bilateral thalamus, left cerebral peduncle and left cerebellar hemisphere.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Nuclear actin and transport of RNA.

The role of nuclear actin filaments in the RNA transport was investigated. Mouse lymphoma cells, L5178Y, were labeled for 20 min with 3H-uridine, and the isolated nuclei were incubated in a medium consisting of 0.25 M sucrose, 10 mM Tris-HCl (pH 7.5), 2 mM CaCl2, 1 mM ATP and 1mM PMSF. Release of the rapidly labeled RNA from the nuclei was temperature-dependent and was stimulated by ATP. Phalloidin, an inhibitor of actin filament depolymerization, had no effect on the system at 10 or 100 micrograms/ml. Therefore, actin filament depolymerization may not be involved in the transport of RNA.

Actins↗
PubMed1987

Characterization of acidic actin in mouse sarcoma 180 cells.

Mouse sarcoma 180 cells have a polypeptide that has the same molecular weight as actin but it is more acidic than alpha-actin. Its tryptic peptide pattern on reversed-phase HPLC was very similar to that of beta + gamma-actin, an actin sample prepared by affinity chromatography on DNase I-Sepharose contained the acidic polypeptide, and monoclonal anti-actin antibody reacted with it; therefore, the polypeptide is considered an actin isoform. The mRNA for this variant actin was identified by analyzing the polypeptides translated in vitro, which indicated that the variant actin is not a post-translationally modified form of any known actin. The variant actin was not stained by polyclonal anti-gizzard actin antibody which reacts with gamma-cytoplasmic, alpha-smooth and gamma-smooth muscle actins, nor by polyclonal anti-skeletal muscle actin antibody which reacts with skeletal, cardiac and alpha-smooth muscle actins. These results suggest that this variant actin is related to beta-cytoplasmic actin or, is a novel species whose N-terminal amino acid sequence is not Glu-Glu-Glu.

Actins↗
PubMed1986

[Various problems concerning the treatment of benign prostatic hypertrophy--operative treatment; subcapsular prostatectomy].

We were quite puzzled to be asked to talk about open surgery for benign prostatic hypertrophy (BPH) at this symposium because transurethral resection prostatectomy (TUR-P) is now the usual procedure and open surgery is rarely performed. Problems arise when open surgery is performed rather than TUR-P as the main treatment for BPH under these circumstances and the criticism of negligence is inevitable. Cases in which open surgery was performed because the application of TUR-P seemed unsuitable are reviewed.

Aged↗