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Biomedical subjects

T Yoshimi

Publications and source records attributed to T Yoshimi.

At least 19 recordsLinked to original sources
PubMed1992

Blood serotonergic mechanisms in type 2 (non-insulin-dependent) diabetes mellitus.

Serotonin (5-hydroxytryptamine, 5HT) is believed to play a role in vasospasm and increased platelet aggregability that in turn could contribute to atherosclerosis. The present study was designed to evaluate a possible participation of serotonin in the development of vascular complications in diabetes mellitus. Whole blood and plasma serotonin, the platelet uptake and release of the amine and serotonin- induced platelet aggregation were studied in 32 patients with Type 2 diabetes. The patients were divided into three groups according to the presence and advancement of retinopathy. Mean levels of blood serotonin content were significantly lower in diabetic patients. The concentration of the amine in the plasma was markedly increased in diabetes. It was correlated with vascular changes of the retina. We established that platelets from diabetic patients took up less serotonin when compared to the control group. Concomitantly enhanced spontaneous release of 5HT from platelets was observed. The platelets of diabetic patients showed increased response to serotonin. There was a relation between serotonin-induced aggregation and the presence of retinopathy. These results suggest that serotonin may be involved in the pathogenesis of diabetic vasculopathy.

Adult↗
PubMed1992

Increased level of atrial natriuretic peptide messenger RNA in the hypothalamus and brainstem of spontaneously hypertensive rats.

OBJECTIVE: The aim of this study was to investigate atrial natriuretic peptide (ANP) gene expression in the central nervous system (CNS) during hypertension. METHODS: We measured and compared immunoreactive atrial natriuretic peptide (irANP) and ANP messenger RNA (mRNA) in the hypothalamus and brainstem of 17-week-old spontaneously hypertensive rats (SHR) with those of age-matched Wistar-Kyoto (WKY) rats using ribonuclease (RNase) protection assay for ANP mRNA and a specific radioimmunoassay for irANP. RESULTS: RNase protection assay revealed that the concentrations of ANP mRNA in the hypothalamus and brainstem of SHR were higher than those of WKY rats. IrANP concentrations in the hypothalamus and brainstem of SHR were determined by a specific radioimmunoassay and found to be higher than those of WKY rats. Elevated mRNA levels in the hypothalamus and brainstem of SHR indicated that increased level of irANP in the CNS resulted from increased synthesis of ANP. CONCLUSION: We propose that increased synthesis of brain ANP in SHR may reflect a compensatory mechanism induced by hypertension.

Animals↗
PubMed1992

Plasma free fatty acids, inhibitor of extrathyroidal conversion of T4 to T3 and thyroid hormone binding inhibitor in patients with various nonthyroidal illnesses.

In order to clarify the role of free fatty acid (FFA) in thyroid hormone abnormalities in patients with nonthyroidal illness, thyroid function, FFA, inhibitor of extrathyroidal conversion of T4 to T3 (IEC) and thyroid hormone binding inhibitor (THBI) were studied in 99 patients with various nonthyroidal illnesses including diabetes mellitus (DM) (n = 35), liver cirrhosis (LC) (n = 33), chronic obstructive pulmonary disease (COPD) (n = 17) and chronic heart failure (CHF) (n = 14). Patients were divided into three groups based on the level of serum T3: Group I (T3 < 50 ng/dl), Group II (50 < or = T3 < 80) and Group III (80 < or = T3). Serum T4, FT3 and the T3/T4 ratio decreased significantly in the order Group III, Group II and Group I (Group III > II > I). The plasma FFA level was 0.91 +/- 0.12 mmol/l in Group I (P < 0.05, vs. Group III), 0.65 +/- 0.06 in Group II and 0.54 +/- 0.04 in Group III, respectively. The incidence of positive IEC was 80.0% in Group I (P < 0.05, vs. Group III), 53.7% in Group II (P < 0.05, vs. Group III) and 34.2% in Group III. However, IEC was not correlated with the serum T3 concentration. The incidence of positive THBI was 80% in Group I (P < 0.05, vs. Group III), 68.3% in Group II and 47.4% in Group III, but THBI was not correlated with the serum T4 level. Positive correlations were observed among FFA, IEC and THBI (P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1992

Lactate dehydrogenase (LDH)-linked immunoglobulin in a patient with Graves' disease treated with methimazole.

A 26-year-old woman who received methimazole treatment for Graves' disease is discussed. Two months following treatment, her serum GOT level rose to 45 K.U, her GPT to 60 K.U, and her lactate dehydrogenase (LDH) to 645 W.U; a hepatic disorder was then suspected. Later, the serum GOT and GPT concentrations decreased to a normal range, but her serum LDH continued to maintain a high level. An LDH isoenzyme analysis showed an abnormally broad LDH. The IgG that was linked to the LDH is suspected to have been the result of her underlying autoimmunity, the methimazole treatment, and the development of her hepatic disorder. Thus, this IgG was thought to be the autoantibody to LDH.

Adult↗
PubMed1992

[Acid-base balance disorder in various diseases--diabetes mellitus].

Metabolic acidosis is the serious acid-base balance disorder complicated in diabetes mellitus. The pathogenesis and treatment of various type of metabolic acidosis (Keto-acidosis, lactic acidosis, hyperchloremic acidosis and type IV renal tubular acidosis) are discussed. Metabolic acidosis in the diabetic patient is associated with an increased anion-gap caused by the presence of organic anion (beta-hydroxybutyrate, acetoacetate, and lactate). The rise in anion-gap usually equals the fall in plasma bicarbonate. With appropriate therapy, progressive decline in the anion-gap is one of the best indications of successful treatment. If hyperchloremic acidosis is established, appropriate infusion of hypochloremic rehydration fluid may be useful.

Acidosis, Lactic↗
PubMed1991

Atrial natriuretic peptide and brain natriuretic peptide coexist in the secretory granules of human cardiac myocytes.

To elucidate the intracellular localization of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in human cardiac myocytes, an immunocytochemical study was carried out by a double immunogold technique using antisera highly specific for ANP and BNP. Surgical and autoptic tissue specimens of human heart were studied. In the atrial myocytes, ANP was localized in almost all of the secretory granules, whereas BNP was colocalized with ANP in some of the granules. Although very few secretory granules were observed in ventricular myocytes, colocalization of ANP and BNP was basically the same as in atrial myocytes. No immunoreactive products were found in the control studies. These results suggest that secretion of BNP is under a regulatory mechanism similar to that of ANP.

Atrial Natriuretic Factor↗
PubMed1990

[Radioimmunoassay for dexamethasone and its plasma levels after oral administration in patients with liver disease].

Dexamethasone (DXM), one of the strong synthetic glucocorticoids, has been used widely for therapeutic purposes and for evaluation of the hypothalamic-pituitary-adrenal axis. However, information concerning the plasma concentrations of DXM and its metabolism in various liver diseases is limited. In this study, plasma DXM levels were examined in patients with chronic inactive hepatitis (CH), patients with liver cirrhosis (LC) and normal subjects (NR) after oral administration of one milligram DXM. Plasma DXM levels were measured directly in plasma extract, using reliable and sensitive radioimmunoassay (RIA). The antiserum was obtained by immunizing rabbits with DXM-3-oxime-bovine serum albumin conjugate. Standard curves for DXM were obtained over the range 10-5000 pg. The cross reactivity of endogenous steroids with DXM antiserum was less than 0.1%. In the group of NR, the peak of plasma DXM was 20.9 +/- 2.9 ng/ml within 1.3 +/- 0.4 hours after administration. Half time of its disappearance was 3.3 +/- 1.1 hours, and plasma DXM disappeared in 24 hours, remaining less than 1 ng/ml. In patients with CH and those with LC, the peak levels of DXM were 10.8 +/- 1.0 ng/ml and 10.5 +/- 0.5 ng/ml, respectively, and those values were significantly lower than those of NR. Half time of DXM disappearance in patients with CH and in those with LC were 6.2 +/- 0.6 and 6.3 +/- 0.6 hours, respectively, significantly prolonged compared with that of NR. Although DXM metabolism was impaired in CH as well as in LC, the retention rate of indocyanine green (ICG) at 15 minutes in CH was found within the normal range, 10.0 +/- 1.1%, respectively. These results might suggest that the impaired DXM metabolism in patients with chronic liver disease may be affected not only by the decreased hepatic blood flow but also by some other factors.

Administration, Oral↗
PubMed1990

Stimulation of platelet-derived growth factor-induced DNA synthesis by angiotensin II in rabbit vascular smooth muscle cells.

In cultured rabbit vascular smooth muscle cells (VSMCs), angiotensin II by itself had little mitogenic effect even in the presence of cell-free plasma-derived serum (PDS), but markedly stimulated the platelet-derived growth factor (PDGF)-induced DNA synthesis in the presence of PDS. The maximal extent of DNA synthesis induced by PDGF plus angiotensin II was about twice that induced by PDGF alone. The stimulatory effect of angiotensin II was dose-dependent with the maximal response seen at 1 microM and was inhibited by the specific angiotensin II receptor antagonist, [Sar1, Ile8]angiotensin II. In VSMCs, both PDGF and angiotensin II induced expression of the c-fos gene in dose-dependent manners. In contrast to the synergistic effect of angiotensin II and PDGF on DNA synthesis, they induced expression of the c-fos gene in an additive manner. These results suggest that angiotensin II may act as a growth regulator for VSMCs in addition to acting as a vasoconstrictor.

Angiotensin II↗
PubMed1989

Effect of atrial natriuretic peptide on the release of beta-endorphin from rat hypothalamo-neurohypophysial complex.

The aim of this study was to determine whether atrial natriuretic peptide (ANP) alters beta-endorphin (beta-END) secretion from rat intermediate pituitary and whether this effect is a direct action on the intermediate pituitary or an indirect one mediated by hypothalamic factor(s). We studied the release of beta-END from rat neuro-intermediate lobes of the pituitary (NIL) and from the hypothalamo-neurohypophysial complex (HNC), which consists of the hypothalamus, pituitary stalk, intermediate and posterior lobes of the pituitary, by means of an in vitro perifusion system. NIL and HNC were prepared from male Wistar rats and individually perifused for 30 min with perifusion medium followed by 20 min perifusion with medium containing alpha-rat ANP and/or dopamine (DA). Samples of perifusion medium were collected every 5 min and subjected to RIA for beta-END. The basal release of beta-END from NIL was 180% of that from HNC (p less than 0.01), which provides further support for the presence of hypothalamic factors that inhibit beta-END release from the intermediate pituitary. The perifusion of HNC with ANP at 10(-7) and 10(-6) M increased the beta-END concentration by 25 and 50%, respectively (p less than 0.01). In contrast, ANP (10(-8) to 10(-6) M) had no effect on beta-END release from NIL. The inhibitory effect of DA (10(6) M) on beta-END release from NIL and HNC (51% and 50% of the basal release, respectively, p less than 0.01) was confirmed. However, this inhibitory effect was not reversed by ANP.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Effect of sodium valproate on the secretion of proopiomelanocortin derived peptides from cultured rat anterior pituitary cells.

We examined effects of sodium valproate, a gamma amino butyric acid (GABA)-transaminase inhibitor, on the secretion of immunoreactive (IR)-ACTH and IR-beta-endorphin/LPH from cultured rat anterior pituitary cells to determine whether sodium valproate has a direct action on the secretion of ACTH and its related peptides from the cultured rat anterior pituitary gland. During the 3 h incubation, the basal secretion of IR-ACTH and IR-beta-endorphin/LPH decreased to 50.8% and 58.3%, respectively, of the control concentration after adding 10(-7) M sodium valproate into the incubation media and to 67.7% and 69.3%, respectively, of the control levels with 10(-8) M sodium valproate. However, sodium valproate at a concentration of 10(-6) M or 10(-9) M did not affect the basal concentration of IR-ACTH and IR-beta-endorphin/LPH. Sodium valproate at a concentration of 10(-7) M significantly attenuated the stimulated release of IR-ACTH and IR-beta-endorphin/LPH by 10(-9) or 10(-10) M of ovine corticotrophin releasing factor. These results indicate that sodium valproate could directly effect rat anterior pituitary cells to suppress both basal and stimulated release of proopiomelanocortin derived peptides and this supports the hypothesis that sodium valproate has a direct effect at the pituitary corticotroph in reducing plasma ACTH.

Adrenocorticotropic Hormone↗
PubMed1988

[An inhibitor of extrathyroidal conversion of thyroxine to 3,5,3'-triiodothyronine (IEC) in plasma of patients with various nonthyroidal illnesses].

To evaluate the role of a circulating inhibitor of extrathyroidal conversion of T4 to T3 (IEC) in the causation of low T3 states in patients with various nonthyroidal illnesses (NTI), we measured the in vitro T3 production in the presence of ether extract of plasma. Blood samples were obtained from 22 normal subjects and 140 patients with various NTI; liver cirrhosis (LC) 37, diabetes mellitus (DM) 48, respiratory failure (RF) 15, chronic renal failure (CRF) 10 and others 30. The assay procedure of in vitro T3 production was as follows. Rat liver homogenate was incubated with 2.5 microM T4 in the presence of evaporated ether extract of plasma and the amount of T3 produced was quantified by RIA. In each assay, control plasma extracts taken from the two normal subjects were used. The results were expressed as a percentage of the control value (%T3 production), and estimated as positive IEC when %T3 production was under 72.7%, that was 2SD below the mean value of normal controls. Patients were divided into three groups; Group I (T3 greater than or equal to 80 ng/dl), Group II (80 greater than T3 greater than or equal to 50) and Group III (50 greater than T3). The %T3 productions were 88.5 +/- 22.0 in Group I, 84.9 +/- 31.5 in Group II and 78.9 +/- 34.0 in Group III respectively. The %T3 productions of each group were significantly lower than that of normal control, 101.9 +/- 14.6. IEC was positive 23.4% in Group I, 41.9% in Group II and 43.8% in Group III. There were eight nonsurvivors, and they all belonged to Group III, in which both serum T3 and T4 were subnormal. In nonsurvivors, serum concentrations of T3 (20 +/- 11 ng/dl) and TSH (1.2 +/- 1.1 microU/ml) were significantly lower than that of survivors in Group III (T3; 38 +/- 10 ng/dl p less than 0.005, TSH; 2.8 +/- 1.4 microU/ml p less than 0.05). The %T3 productions were 83.8 +/- 32.1 in survivors and 64.8 +/- 37.9 in nonsurvivors, and the incidences of positive IEC were 37.5% in survivors and 62.5% in nonsurvivors. From the standpoint of the underlying illnesses, serum concentrations of T3 (mean +/- SD ng/dl) were 49 +/- 21 in LC, 64 +/- 11 in DM, 40 +/- 22 in RF and 63 +/- 15 in CRF, and %T3 productions were 60.6 +/- 26.5 in LC, 82.5 +/- 25.8 in DM, 109.6 +/- 32.1 in RF and 97.6 +/- 24.3 in CRF.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1988

[Autonomic neuropathy in diabetics--autonomic function and plasma catecholamines].

Autonomic neuropathy is one of the complications of diabetes. Recently, several authors reported that measuring R-R interval variation of ECG is a noninvasive and useful method for testing parasympathetic function. However, there were few reports about sympathetic function in diabetics. In order to evaluate sympathetic function in diabetics quantitatively, we studied the responses of plasma norepinephrine (NE), epinephrine (E) and related factors after 60 min bed rest and sequentially during 10 min of upright posture and 5 min handgrip while still upright. We also studied the responses of NE and E during 5 min smoking in supine position. Subjects were divided into four age-matched groups. These were 15 normal subjects (Group I), 20 diabetics without complications (Group II), 20 diabetics with peripheral neuropathy but no autonomic symptoms (Group III) and 15 diabetics with autonomic symptoms (Group IV). We also studied R-R interval variation (CV: Coefficient of Variation) as a parameter of parasympathetic function and compared this with sympathetic function. Upon standing, blood pressure (BP) dropped precipitously in Group IV, whereas no significant changes were observed in the other three groups. Heart rate (HR) increased in Groups I and II, but not in Groups III and IV. During handgrip, BP and HR did not change significantly in all groups. Basal NE levels in Group IV were significantly smaller than those in Group I. NE responses to both standing and handgrip stimuli were markedly reduced in Group IV and, even in Group III, increments were significantly smaller than those in Groups I and II. Basal E levels did not differ, and significant changes were not observed after standing and handgrip in all groups. Both plasma renin activity (PRA) and plasma aldosterone concentrations (PAC) in Groups III and IV were lower than those in Groups I and II at rest and standing. After smoking, both BP and HR increased significantly in Groups I, II and III, whereas no changes were observed in Group IV. Both NE and E responses were markedly reduced in Group IV and, even in Group III, responses were significantly smaller than those in Groups I and II. CV in Groups III and IV were significantly smaller than those in Groups I and II. In diabetics, CV was strongly correlated with NE increments after standing (r = 0.78, p less than 0.01). Also, CV was correlated with both NE and E increments after smoking (r = 0.71 (NE), r = 0.82 (E), p less than 0.01).(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗