PubMed Health⌕ Search

Biomedical subjects

T Hashizume

Publications and source records attributed to T Hashizume.

At least 109 records · Page 6Linked to original sources
PubMed1995

[Changes of liver function measured by 99mTc-GSA scintigraphy after hepatectomy].

In 14 patients with hepatic tumors, liver volume and liver function indices were studied by 99mTc-GSA liver scintigraphy before and after hepatectomy. The liver volume measured by 99mTc-GSA SPECT was significantly decreased after surgery in all 14 patients (p < 0.001). Postsurgically, 7 patients showed an increase of greater than 10% in the LU15 value, while 3 showed a decrease of 10% in the LU15 value, while 3 showed a decrease of 10%. Two patients showed a decrease of greater than 10% in the HH15 value after surgery. The changes in LU15 after surgery were inversely correlated with those in HH15. The present findings clarified that in several cases of surgically treated hepatic tumors, 99mTc-GSA indices of liver function generally thought to indicate the size of the functioning liver cell mass were distinctly improved after surgery in comparison with those before surgery, despite the postoperative decrease in the liver volume. Furthermore, the results of a 99mTc-GSA SPECT study separately measuring the volume of the unilateral hepatic lobe and its radioactivity uptake, indicated that regeneration of the functioning liver cells often occurred in the entire liver. 99mTc-GSA scintigraphy appears to be a valuable method for evaluating changes in both the liver volume and the liver function indices after hepatectomy.

Aged↗
PubMed1994

Arachidonic acid liberation induced by phosphatidic acid endogenously generated from membrane phospholipids in rabbit platelets.

The action of phosphatidic acid generated from membrane phospholipids on phospholipase A2 activation in rabbit platelets was investigated. When [3H]arachidonic acid-labelled platelets were treated with phorbol 12-myristate 13-acetate (PMA) and the membranes isolated from the cells incubated at 37 degrees C with 50 microM CaCl2 and 50 microM guanosine 5'-O-(3-thiotriphosphate) (GTP gamma S), both phosphatidic acid production and arachidonic acid liberation increased in PMA- and GTP gamma S-concentration-dependent manners. Ethanol dose-dependently inhibited these responses, accompanied by the formation of phosphatidylethanol. Since propranolol, an inhibitor of phosphatidic acid phosphohydrolase, had no influence on the production of phosphatidic acid, the arachidonic acid liberated does not appear to be derived from diacylglycerol which may be produced from phosphatidic acid through the action of this enzyme. In another approach, treatment of [3H]arachidonic acid-labelled membranes with phospholipase D from Streptomyces chromofuscus induced arachidonic acid liberation as well as phosphatidic acid formation in time- and dose-dependent manners. The former response was suppressed by p-bromophenacyl bromide, a phospholipase A2 inhibitor. These results suggest that phosphatidic acid derived from membrane phospholipids potentiates phospholipase A2 activation and contributes to the amplification of platelet activation.

Animals↗
PubMed1994

A novel modified nucleoside found at the first position of the anticodon of methionine tRNA from bovine liver mitochondria.

Methionine tRNA was purified from bovine liver mitochondria, and its nucleotide sequence was determined. The tRNA possesses only three posttranscriptionally modified nucleosides, two pseudouridines in the anticodon and T stems and a previously unknown nucleoside specified by the gene sequence as cytidine, in the first position of the anticodon. Structure analysis of the anticodon nucleoside by mass spectrometry revealed a molecular mass 28 Da greater than that of cytidine, and unmodified ribose, with substitution at C-5 implied by hydrogen-deuterium exchange experiments. Proton NMR of the intact tRNA showed presence of a formyl moiety, thus leading to the candidate structure 5-formylcytidine (f5C), not a previously known compound. The structure assignment was confirmed by chemical synthesis and comparison of data from combined HPLC/mass spectrometry and proton NMR for the natural and synthetic nucleosides. The potential function of f5C in the tRNA(Met) anticodon is discussed with regard to codon-anticodon interactions.

Animals↗
PubMed1994

Effects of pituitary adenylate cyclase-activating polypeptide (PACAP), prostaglandin E2 (PGE2) and growth hormone releasing factor (GRF) on the release of growth hormone from cultured bovine anterior pituitary cells in vitro.

The effect of pituitary adenylate cyclase-activating polypeptide (PACAP) on growth hormone (GH) release was compared with that of prostaglandin E2 (PGE2) and growth hormone releasing factor (GRF) from cultured bovine anterior pituitary cells in vitro. Both PACAP and PGE2 stimulated GH release at concentrations as low as 10(-9) and 10(-8) M, respectively, (P < 0.01). However, GRF released GH at a concentration as low as 10(-13) M (P < 0.01). Percent increases of GH compared with controls were not significantly different among GRF, PACAP, and PGE2 at 10(-7) M; however, the increases of GH by the 10(-8) M GRF, PACAP and PGE2 were 196, 118, and 27%, respectively, (P < 0.01), and 124, 65, and 1% in the 10(-9) M media, respectively, (P < 0.01). When GRF and somatostatin (SS) were added together, the GH releasing effect of GRF was blunted (P < 0.01). Similar bluntness were observed in PACAP and PGE2, when SS was added. The stimulatory effects of GRF and PGE2 together were similar to that by either GRF or PGE2 alone. When GRF and PACAP were added together, the GH released by both secretagogues was greater than that by PACAP alone (P < 0.01); however, a synergistic effect was not clear when compared with GRF alone. These findings suggest that PACAP and PGE2 may modulate the release of GH in cattle.

Animals↗
PubMed1994

Transforming growth factor beta 1 as a prognostic factor in pulmonary adenocarcinoma.

AIMS: To evaluate the efficacy of transforming growth factor beta (TGF-beta) for the prognosis of pulmonary adenocarcinoma. METHODS: TGF-beta was detected immunohistochemically using the avidin-biotin-peroxidase complex technique in resected pulmonary adenocarcinomas from 88 patients. RESULTS: Of the 88 patients, 39 were TGF-beta negative and 45 TGF-beta positive. The five year survival rate was 56% for the TGF-beta negative and 16% for the TGF-beta positive group. CONCLUSIONS: TGF-beta can be used as a prognostic factor in pulmonary adenocarcinoma.

Adenocarcinoma↗
PubMed1994

Effect of growth hormone (GH)-releasing peptide (GHRP) on the release of GH from cultured anterior pituitary cells in cattle.

The effect of His-D-Trp-Ala-Trp-D-Phe-Lys-NH2 (GHRP) on growth hormone (GH) release from cultured bovine anterior pituitary (AP) cells was studied in vitro with the interactive effects of GH-releasing factor (GRF: hpGRF (1-29)-NH2) and somatostatin (SRIF). The AP cells (5 x 10(4) cells per well) were incubated with media, and the media were changed 3 days after plating. After 3.5 days in culture, cells were incubated for 2 h with the peptides. GHRP stimulated GH release from cultured cells in a dose-related manner. At doses from 10(-11) to 10(-7) M GHRP, the amount of GH released was significantly greater than the controls (P < 0.05 to P < 0.001). The amounts of GH released at lower doses of GHRP (10(-14) to 10(-12) M) were not significantly different from the controls. GH concentrations after treatment with 10(-11) and 10(-7) M GHRP were 3.98 +/- 0.27 and 4.81 +/- 0.16 ng/ml, respectively. In experiments performed similarly, the 10(-7) M GHRH, GHRP, and combined treatment with GHRP plus GHRH increased GH 126, 57, and 139%, respectively (P < 0.001). The GH releasing effects of either GHRH alone or GHRP plus GHRH were significantly more potent than that of GHRP alone (P < 0.001). The additive effect was not significant when compared with GHRH alone. GH release induced by either GHRH or GHRP was significantly inhibited by SRIF (P < 0.01) compared with the untreated control. The inhibitory effect of SRIF in combined treatment with GHRP plus GHRH was significantly less than that of SRIF with GHRH or with GHRP (P < 0.01). The present study suggests that GH-releasing peptide (GHRP) induced GH release in cattle via a direct action on anterior pituitary cells in vitro.

Animals↗
PubMed1994

Intracerebral methionine-enkephalin, serum cortisol, and serum beta-endorphin during acute exposure of sheep to physical or isolation stress.

In vivo microdialysis was used to estimate extracellular concentrations of methionine-enkephalin in 19 brain sites for 5 h on each of three consecutive days (trials) in six conscious ewes. Following control procedures on d 1, ewes were completely isolated from other sheep for 60 min on d 2 (psychological stress). Physical stress was imposed on d 3 and consisted of continuous pinching of the skin for 60 min during the middle of the 5-h experimental period. Imposition of both physical and psychological stress rapidly increased serum concentrations of cortisol, and the induced increase persisted for at least 30 min after termination of the stress. Psychological stress of isolation initially increased cortisol to a greater extent than the physical stress of skin pinch, but this difference disappeared after 30 min of stress exposure. Psychological stress also transiently increased serum concentrations of beta-endorphin/beta-lipotropin, whereas physical stress did not. Average concentrations of methionine-enkephalin in dialysate ranged between 1.52 and 1.85 ng/mL when the intracerebral probes were placed into the caudate nucleus, the preoptic area of the hypothalamus, or the thalamus. The concentration of methionine-enkephalin was consistently less than 1.0 ng/mL when probes were placed into major fiber tracts of the brain (corpus callosum, internal capsule). Potassium-induced depolarization around the probe tip located in the caudate nucleus increased dialysate concentrations of methionine-enkephalin by 2.7-fold. Imposition of physical or psychological stress did not consistently increase or decrease dialysate concentrations of methionine-enkephalin in any of the brain sites studied.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Pharmacokinetics of the H1-receptor antagonist ebastine and its active metabolite carebastine in healthy subjects.

Pharmacokinetics of ebastine (CAS 90729-43-4), a histamine H1-receptor antagonist, was evaluated in healthy male volunteers. The subjects were given single oral doses of 5, 10, 20 and 40 mg of ebastine (5 or 6 subjects) and repeated oral doses of 20 mg once daily for 7 days (6 subjects). Administration of ebastine resulted in a negligible level of the unchanged drug in plasma and urine. Mean plasma concentration of carebastine (CAS 90729-42-3), an active carboxylated metabolite, reached maximum levels of 40, 112, 195 and 388 ng/ml at 4-6 h after single oral administration of ebastine at doses of 5, 10, 20 and 40 mg, respectively. Plasma levels of carebastine showed a first-order decrease with apparent half-lives of 13.8 to 15.3 h. The Cmax and AUC of carebastine increased in proportion to the dose. Urinary excretion of carebastine during 72 h after single administration accounted for 1.3-1.8% of the dose. Food intake did not affect the pharmacokinetics and gastrointestinal absorption of ebastine. Repeated administrations of ebastine once daily for 7 days did not cause any change in the pharmacokinetics of ebastine and carebastine. Plasma concentration of carebastine reached the steady state on day 4. The Cmax (360-396 ng/ml) was 1.6- to 1.7-fold greater than that after the first administration (229 ng/ml). These results strongly suggest that carebastine is responsible for the antihistamine activity after administration of ebastine.

Adult↗
PubMed1993

Dietary selenium affects methylation of the wobble nucleoside in the anticodon of selenocysteine tRNA([Ser]Sec).

We reported previously that the presence of selenium in culture media of mammalian cells influences both the steady-state levels and distributions of two tRNA isoacceptors involved in the insertion of selenocysteine into protein in response to certain UGA codons. In this study, we demonstrate an increase in the levels of these isoacceptors in rats fed a selenium-adequate diet compared to animals fed a selenium-deficient diet, as well as a shift in the relative distribution toward the tRNA which elutes later from an RPC-5 column. These effects were found to occur in a tissue-specific manner. Both selenocysteine tRNAs were isolated from rat liver, sequenced, analyzed by mass spectrometry, and shown to differ only by ribose 2'-O-methylation of 5-methylcarboxymethyluridine that occurs in the wobble position of the anticodon. This modified nucleoside has been documented previously only in yeast tRNA while the corresponding 2'-O-methylribose derivative has not been observed. The structure of these nucleosides was established by mass spectrometry and confirmed by chemical synthesis. Although the role of methylation of the wobble nucleotide is not known, the differences in elution properties from RPC-5 columns are consistent with other experimental observations indicating that a change in tRNA conformation accompanies this methylation.

Animals↗
PubMed1993

Structure of the archaeal transfer RNA nucleoside G*-15 (2-amino-4,7-dihydro- 4-oxo-7-beta-D-ribofuranosyl-1H-pyrrolo[2,3-d]pyrimidine-5-carboximi dam ide (archaeosine)).

A number of post-transcriptional modifications in tRNA are phylogenetically characteristic of the bacterial, eukaryal, or archaeal domains, both with respect to sequence location and molecular structure at the nucleoside level. One of the most distinct such modifications is nucleoside G*, located in archaeal tRNA at position 15, which in bacterial and eukaryal tRNAs is a conserved site involved in maintenance of the dihydrouridine loop-T-loop tertiary interactions. G* occurs widely in nearly every branch of the archaeal phylogenetic domain, in contrast to its absence in all reported bacterial and eukaryal tRNA sequences. The structure of G*-15 is 2-amino-4,7-dihydro-4-oxo-7-beta-D-ribofuranosyl-1H- pyrrolo[2,3-d]pyrimidine-5-carboximidamide (7-formamidino-7-deazaguanosine), which is a non-purine, non-pyrimidine ribonucleoside; its structure thus reflects extensive modification beyond the guanine-15 specified by corresponding gene sequences. The structure was established by mass spectrometry, and in particular from collision-induced dissociation mass spectra of derivatives formed by microscale permethylation, and is confirmed by chemical synthesis.

Chromatography, High Pressure Liquid↗