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Biomedical subjects

K Takano

Publications and source records attributed to K Takano.

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

Hypercoagulability in acute ischemic stroke: analysis of the extrinsic coagulation reactions in plasma by a highly sensitive automated method.

The coagulability of plasmas from 63 patients with acute ischemic stroke (cerebral thrombosis and cerebral embolism) was analyzed by an automated method for prothrombin time using a fluorogenic peptide substrate. The fluorogenic prothrombin time (FPT) of patients' plasmas collected within 48 hr after onset, as expressed as percent of control plasma, was significantly higher in cerebral thrombosis than in an age-matched control group (p less than 0.01). The high values of FPT in cerebral thrombosis patients were observed until the 30th day after onset. On the other hand, FPT values in cerebral embolism patients were not significantly different than that of the control group. Factor VII activity levels in cerebral thrombosis patients were significantly higher than those of the control group and cerebral embolism patients, while levels of factor X activity were not significantly different among these groups. Although FPT and factor VII activity in these stroke patients did not significantly correlate, factor VII activity did correlate well with factor VII antigen. Decreased levels of antithrombin III and elevated levels of FDP and alpha 2-antiplasmin-plasmin complexes were observed only in cerebral embolism patients. Our findings strongly suggest that patients with cerebral thrombosis have been in a hypercoagulable state before the onset of symptoms, which was caused in part by an increase of factor VII activity/antigen, and in part by other unknown mechanisms. In contrast, patients with cerebral embolism were in a low grade consumptive coagulopathy.

Adult↗
PubMed1990

Ischemic flow threshold for striatal dopamine release in rats.

To determine the level of cerebral blood flow reduction which causes striatal dopamine release, extracellular dopamine and cerebral blood flow was simultaneously determined using in vivo brain dialysis and a hydrogen clearance method, respectively, in the striatum of spontaneously hypertensive rats before and during experimental cerebral ischemia. The ischemic flow threshold for neurotransmitter dopamine release was found to be 20% of the resting value or 8-10 ml/100g/min of cerebral blood flow, being similar to those for energy and membrane failures.

Animals↗
PubMed1990

Effects of short-term growth hormone therapy in short children without growth hormone deficiency.

Evaluation of 24-hour endogenous growth hormone (GH) secretion was carried out in 62 children, aged 7-16 years, who did not have classic GH deficiency (GHD). The mean 24-hour GH concentration, determined at 20-minute intervals over 24 hours, was variable, ranging from 1.28 to 11.39 micrograms/l with a mean of 4.95 +/- 2.55 micrograms/l (+/- SD). There was a positive correlation between mean 24-hour GH concentration and plasma insulin-like growth factor I (IGF-I) values (r = 0.54; p less than 0.01). Recombinant human GH, 0.1 IU/kg/day was administered to 30 of the 62 children for 6 months followed by 6 months' observation without treatment. Thereafter, GH was administered at the same dose for a further 6 months to 16 children. The mean height velocities before, during, and after the first treatment period were 4.3 +/- 0.9, 7.3 +/- 1.9 and 4.9 +/- 2.0 cm/year (mean +/- SD), respectively. The height velocity during treatment was greater than pre- and post-treatment values (p less than 0.001). The height velocity increased again during the second treatment period to a mean of 8.5 +/- 2.0 cm/year (p less than 0.001). Nine other children were treated continuously in a similar manner for 1 year and their height velocity increased significantly from 4.1 +/- 1.4 to 6.0 +/- 1.9 cm/year (p less than 0.001). According to our criteria, 29 of the 39 children (74.4%) who were treated for 6-12 months showed a GH-dependent height increase during therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

Effects of sc administration of recombinant human insulin-like growth factor I (IGF-I) on normal human subjects.

Recombinant human insulin-like growth factor I (IGF-I) was administered subcutaneously to each of 5 normal human subjects at doses of 0 mg/kg (control), 0.06 mg/kg, or 0.12 mg/kg successively at one week intervals. After 0.06 mg/kg or 0.12 mg/kg IGF-I injections, plasma IGF-I levels increased from 185 +/- 17 ng/ml (mean +/- SEM) to maximal levels of 396 +/- 21 ng/ml at 3 hours and from 169 +/- 14 ng/ml to 480 +/- 27 ng/ml at 4 hours, respectively. These two peak values were statistically different (p less than 0.05). After 0.06 mg/kg and 0.12 mg/kg IGF-I administration, blood glucose levels decreased from 85 +/- 2 mg/dl to minimal levels of 73 +/- 3 mg/dl at 3 hours and from 83 +/- 1 mg/dl to 50 +/- 4 mg/dl at 2 hours, respectively. These two minimal values were statistically different (p less than 0.001). Serum insulin and C-peptide levels were decreased in a dose dependent manner after IGF-I administration. There were no changes between blood urea nitrogen levels before and 4 hours after IGF-I administration. The urinary GH concentration decreased after 0.06 mg/kg IGF-I administration, but increased and maintained normal values after 0.12 mg/kg IGF-I administration.

Adult↗
PubMed1990

Radioimmunoassay for insulin-like growth factor II (IGF-II).

Insulin-like growth factor II (IGF-II) levels in human plasma were measured in physiological and pathological conditions by radioimmunoassay (RIA) with biosynthetic IGF-II. This RIA was specific for IGF-II and cross-reactivity with IGF-I was 1%. The sensitivity was 15 pg/tube with 50% displacement at 50 pg/tube. The intra- and inter-assay coefficients of variation for IGF-II were 6.3 and 9.3%, respectively. The plasma IGF-II levels in normal adults, patients with hypopituitarism and patients with active acromegaly were 589.6 +/- 15.8, 800.9 +/- 45.6 and 330.3 +/- 24.3 ng/ml, respectively. After human growth hormone (hGH) treatment in hypopituitarism, IGF-II slightly increased, but not significantly. After adenomectomy in patients with acromegaly, IGF-II significantly decreased. These data indicate that IGF-II concentrations in plasma were partially GH dependent. This GH dependency was less than that of IGF-I. IGF-II was low in patients with anorexia nervosa and with liver cirrhosis and high in patients with renal failure. In two cases with extrapancreatic tumor-associated hypoglycemia, plasma IGF-II was increased to 1123.8 and 843.5 ng/ml, and returned to normal after tumor resection. These data showed that IGF-II was partly dependent on GH and nutritional conditions and that IGF-II was the most likely cause of some cases of hypoglycemia with extrapancreatic tumor. This specific and sensitive RIA of IGF-II would be useful in evaluating its physiological and pathological role in plasma and tissue.

Acromegaly↗
PubMed1990

Effects of insulin-like growth factor-I on insulin and glucagon release from isolated perfused rat pancreas.

The infusion of recombinant insulin-like growth factor I (IGF-I) causes a decrease in plasma glucose and insulin. In this study we examined whether or not IGF-I directly affects islet hormone release by means of a rat pancreas perfusion system. A superphysiologic concentration of IGF-I (2 nM) elicited a slight but significant decrease in insulin release under the perfusate glucose concentration of 120 mg/dl. A pharmacological concentration of IGF-I (200 nM) significantly suppressed the increase in insulin release in response to an increase in the perfusate glucose concentration (from 4.5 mM to 12.8 mM), but did not affect the decrease in insulin release in response to a decrease in the perfusate glucose concentration (from 6.9 mM to 2.8 mM). Glucagon release was not influenced by IGF-I in these experiments. These results suggest that IGF-I potentially inhibits the insulin release from islet B-cells directly, but its pathophysiological significance may be slight considering its partial inhibition at superphysiologic concentrations and its stable plasma level.

Animals↗
PubMed1990

[Basic research on measurement of mental work load utilizing physiological information].

Various definitions and models have been proposed to evaluate mental work load, for example, task time analysis method and secondary task method based on single channel model. However, an evaluating method utilizing physiological information has been comparatively newly proposed. Therefore, this method has not been adequately examined with respect to its relation to be heretofore proposed methods and to its practical usefulness in evaluating mental work load. In this study comparison was made of various evaluating methods, i.e. task time analysis method, secondary task method, method utilizing physiological information, and subjective score method with emphasis on the method utilizing physiological information when a modeled experiment was conducted. In evaluating the regression by the experimental results, the adopted standard was time shared fraction (TSF), which was computed as the relative required time compared to actual permitted time based on the single channel model. The main results can be summarized as follows: (1) The evaluated TSF value is a useful index if it can be computed, because it reflects the individual ability of each subject, is proportional to the amount of given information, and is most faithful to the definition of single channel model. (2) The TSF value is significantly correlated to the value obtained by existing secondary task method and subjective score method. Thus, this result justifies the above mention. (3) In the adopted physiological indicators of this experiment, SRRP (skin resistance reflex pulse rate) has the strongest correlation to TSF value. Furthermore, this SRRP is relatively not affected by individual difference and is significantly correlated to subjective score and secondary task in the constant condition of atmospheric temperature and subject's arousal level and in the repetitive task.

Adult↗
PubMed1990

[Experiences in general anesthesia of patients with scoliosis presupposed to have difficulties in airway maintenance].

We experienced general anesthesia of two patients with cerebral palsy presupposed to have difficulties in tracheal intubation by reason of scoliosis. Case 1 is a 26-year-old woman. Chest X-ray photography and respiratory sounds in both pulmonary areas indicated neither airway stricture nor respiratory distress, but severe scoliosis presupposed difficult tracheal intubation. However, under the impression of possible intubation obtained by preoperative laryngoscopy, orotracheal intubation was tried with rapid induction. Epiglottis deviation to the left noted upon developing larynx made the glottis direct invisible, but some compression of cricoid from outside barely succeeded in intubation. The fixation of the endotracheal tube found much difficulties in its proper positioning so as to make stethoscopy uniform in both pulmonary areas, but trial rotations of the tube both in various directions and at various depths barely managed to find a position of uniform stethoscopy in both pulmonary areas, in which position the tube was fixed as proper positioning. Anesthesia was performed by nitrous oxide.oxygen.halothane; peroperative hemodynamics remained stable and arterial blood gas analysis presented no problems. Case II is a 16-year-old man. Resting respiration presented stridor and chest X-ray photography indicated scoliosis and laryngeal stricture. Patient's lack in the degree of cooperation made laryngoscopy impossible. Thus, in view of a high possibility of difficult tracheal intubation, orotracheal intubation was tried under the control of spontaneous respiration. While the intubation was being carried out by means of a stylet without developing larynx, severe bronchostriction was palpable at the point when the tube barely passed through the glottis, making the intubation impossible. However, the tube barely managed to be inserted while rotating with the stylet being extracted. Anesthesia was carried out by nitrous oxide.oxygen.halothane; peroperative hemodynamics underwent no remarkable change and arterial blood gas analysis presented no problems.

Adolescent↗
PubMed1990

[A metastatic Merkel cell carcinoma successfully treated with chemotherapy].

A 68-year-old man referred to the hospital because of a swelling of his bilateral cervical, left supraclavicular, and left axillary lymph nodes, and an ulcerated tumor in the right palatine tonsil. Three years previously, he had undergone a local excision in the left forearm of a skin tumor that had been pathologically diagnosed as a Merkel cell tumor. CT scan demonstrated an abdominal mass and his serum neurospecific-enolase (NSE) was found to be 20.3 ng/ml. Following biopsies of the lymph nodes and the tumor in the right tonsil, a metastatic Merkel cell carcinoma was diagnosed. Systemic chemotherapy thus was begun with doses of cyclophosphamide, doxorubicin and vincristine. After three cycles were completed, tumor were no longer present and his NSE returned to normal. Three months after the discontinuance of chemotherapy, he remains disease-free.

Aged↗
PubMed1989

A stimulatory effect of somatostatin: enhancement of activin A-mediated FSH secretion in rat pituitary cells.

The interaction between somatostatin and activin A was studied in terms of FSH secretion in rat pituitary cells in primary culture. Incubation of pituitary cells with 1 nM activin A for 48 hrs resulted in an increase in FSH release into incubation medium. The effect of activin A was dependent on cell-density and the higher the density, the smaller the stimulatory action of activin A. Somatostatin, by itself, did not affect the FSH secretion. When 100 nM somatostatin was included together with activin A or the cells were pretreated with somatostatin for 2 hrs, the activin A-induced FSH secretion was enhanced. This potentiation effect of somatostatin was inversely dependent on the cell-density. These results indicate that somatostatin enhances, rather than inhibits, the activin A action in pituitary cells.

Activins↗
PubMed1989

Depression of liver microsomal vitamin K epoxide reductase activity associated with antibiotic-induced coagulopathy.

Hypoprothrombinemic changes in blood coagulation parameters, such as prolongation of prothrombin time, increase in the level of plasma protein induced by vitamin K absence, and decrease in plasma prothrombin level, were detected in rats fed a vitamin K-deficient diet. These changes were enhanced by the administration of beta-lactam antibiotics containing N-methyltetrazolethiol, thiadiazolethiol or methyl-thiadiazolethiol. Microsomal vitamin K epoxide reductase activity was suppressed with the maximum effect at 1-2 days after the treatment and with recovery, thereafter, gradually to the normal level after 5-7 days. Hypoprothrombinemic alterations in blood coagulation parameters following a single administration of antibiotic to vitamin K-deficient rats were somewhat delayed compared with the change in the epoxide reductase activity, but the effects of the antibiotic on both blood coagulation parameters and the enzyme activity disappeared completely 7 days after the antibiotic treatment. Antibiotic-induced depression of the epoxide reductase activity was observed even in the vitamin K sufficient rats, although the hypoprothrombinemic changes in the blood coagulation parameters did not develop. Vitamin K administration could normalize the blood coagulation parameters in the hypoprothrombinemic rats caused by treatment with the antibiotics but without recovery of the decreased epoxide reductase activity. These results suggest that some antibiotics inhibit liver microsomal vitamin K epoxide reductase, which causes hypoprothrombinemia to develop under vitamin K-deficient conditions.

Animals↗
PubMed1989

Growth hormone and insulin-like growth factor I stimulate Leydig cell steroidogenesis.

Leydig cells from 40 days old rats were incubated with or without human growth hormone (hGH) or insulin-like growth factor I (IGF-I) in the presence or absence of human chorionic gonadotropin (hCG), and testosterone and cyclic AMP (cAMP) levels in the medium were measured. Neither hGH nor IGF-I increased testosterone production in the absence of hCG in concentrations up to 1000 and 100 ng/ml, respectively. However, both peptides increased hCG-induced testosterone production in a dose-dependent manner. The maximal stimulatory concentrations of hGH and IGF-I were 100 and 50 ng/ml, respectively. Human GH did not further enhance the IGF-I-stimulated steroidogenesis. The hGH-augmented steroidogenesis was inhibited by anti-hGH IgG and anti-IGF-I IgG. hGH also enhanced hCG-stimulated cAMP production time dependently, suggesting that the stimulatory effect of hGH on steroidogenesis was due to an increased cAMP production. These data suggest that the effect of hGH might be mediated by locally produced IGF-I, which may act as a modulator on gonadal development in the presence of gonadotropin.

Animals↗
PubMed1989

Human growth hormone stimulates liver regeneration in rats.

To study the effect of human growth hormone (hGH) on liver regeneration in rats, 200 micrograms hGH was administered to partial hepatectomized rats twice a day for three days. The bw of hGH-treated rats was higher than that in untreated rats. After three day administration, the liver weight was 3.18 +/- 0.13 g, significant higher than that of untreated rats (2.68 +/- 0.17 g). Human GH also stimulated the mitosis in the liver. Serum insulin-like growth factor I (IGF-I) and albumin levels were significantly increased and urea nitrogen levels were significantly decreased in hGH-treated rats compared with those in untreated rats. When 120 micrograms/day IGF-I was continuously administered to partial hepatectomized rats for three days, the bw and the liver weight were not higher than those of controls. These data indicate that hGH directly stimulates liver regeneration and recover liver dysfunction in rats.

Animals↗