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Biomedical subjects

N Takasu

Publications and source records attributed to N Takasu.

At least 91 records · Page 5Linked to original sources
PubMed1985

Ontogeny of the visual system in the cuttlefish, Sepiella japonica. II. Intramembrane particles, histofluorescence, and electrical responses in the developing retina.

To study molecular and functional differentiation of photoreceptive membranes, the development of the retina in embryos of the cuttlefish, Sepiella japonica, was examined by the freeze-fracture technique, by histo-fluorescence of retinal-related protein, and by electrical responses to photic stimulation. P-face particles in the microvillar plasma membrane of the receptor cell increased in density from about 2,000/micron2 to about 6,000/micron2 during the early stages of rhabdomere formation (from stage 31 to stage 36). The size distribution of P-face particles in the microvillar and the cell body plasma membranes showed a similar monomodal pattern with a peak at 8 nm in diameter from stage 31 to 33. In the cell body plasma membrane, the size distribution pattern hardly changed throughout later stages, but in the microvillar membrane, the peak shifted progressively to 9 nm (stages 35 and 36) and then to 10 nm (stage 37). The histofluorescence of reduced rhodopsin was first visible at stage 36 in the layer of growing apical processes. The fluorescence of reduced retinochrome first appeared faintly at stage 40 on both sides of the basal lamina. Electroretinograms (ERGs) were first obtained at stage 34 when many microvilli appeared from the apical processes, increasing rapidly in amplitude with increase in regularity of the microvillar arrangement from stage 35 to 36. Early receptor potentials (ERPs) elicited by a bright light flash were first recorded at the earliest stage of the apical process formation (stage 30), increasing gradually in amplitude during development. The increase was correlated with an increase in the total number of P-face particles in the microvillar membrane within the retina. These findings suggest that the P-face particles in the microvillar membrane are associated with rhodopsin, that the receptor cells have a small amount of rhodopsin before rhabdomere formation, and that differentiation of the apical plasma membrane of the receptor cells into the functional photoreceptive membrane occurs in conjunction with its morphological differentiation into rhabdomeres.

Animals↗
PubMed1985

Effects of iodide on thyroid follicle structure and electrophysiological potentials of cultured thyroid cells.

In cultured porcine thyroid cells, exposure to iodide induces morphological and electrophysiological changes in the cells and suppresses the iodine uptake and organification activities of the cells. NaI affects thyroid structures: after exposure to 10(-7), 10(-6), and 10(-5) M NaI, the follicles first lose their typical roundness, and then the numbers of microvilli decrease. NaI (10(-6) and 10(-5) M) decreases the thyroid electrical membrane potentials. NaI induces suppression of iodine uptake and organification: exposure to 10(-6) and 10(-5) M NaI suppresses subsequently determined iodine uptake and organification. This iodide-induced suppression of iodine uptake and organification may be related to the iodide-induced morphological and electrophysiological changes. The iodide-induced changes and suppression of iodide uptake and organification are reversible. They are observed when thyroid cells are cultured in the presence of TSH.

Animals↗
PubMed1985

Black (or brown) adrenal cortical adenoma: its characteristic features on computed tomography and endocrine data.

Seventeen patients with adrenal adenoma causing Cushing's syndrome, eight patients with Cushing's disease due to hypersecretion of ACTH, and five patients with primary aldosteronism due to an aldosteronoma were studied for their computed tomographic (CT) patterns, hormonal profiles, and macroscopic and microscopic findings of the adrenal gland. Black (or brown) adrenal adenomas were found in 71% of the patients with Cushing's syndrome, but not in patients with aldosteronoma. The adrenal tissue of patients with Cushing's disease was predominantly yellow. The number of compact cells was larger in black or brown adenomas than in yellow tumors or hyperplastic adrenal tissue. In patients with Cushing's syndrome, urinary excretion of 17-ketosteroids (17-KS) and serum aldosterone concentrations were lower in those with black or brown adenomas than in those with yellow adenomas (P less than 0.05). Patients with Cushing's disease had even higher 17-KS and serum aldosterone levels. No difference was found in serum cortisol concentrations and dexamethasone suppressibility in two types of adenomas causing Cushing's syndrome. Visual estimation of radiological density of the adrenal tissue relative to the kidney on CT scan and quantitative measurement of it by CT number revealed a difference between the two types of adrenal tumors causing Cushing's syndrome. Adrenal tumors with decreased density on CT scan were yellow adenomas with predominantly clear cells, and those with equal or increased density were black or brown adenomas with predominantly compact cells. All aldosteronomas had decreased density and consisted of clear cells. It is suggested that black or brown adenomas of the adrenal gland have higher radiological density and accompanying lower serum aldosterone and urinary 17-KS levels than ordinary yellow tumors. The abundance of compact cells may have some significance for the development of this particular type of adrenal tumor.

17-Hydroxycorticosteroids↗
PubMed1985

Hyperthyroidism caused by a pituitary thyrotrophin-secreting tumour with excessive secretion of thyrotrophin-releasing hormone and subsequently followed by Graves' disease in a middle-aged woman.

A 46-year-old woman had signs of thyrotoxicosis and galactorrhoea. Serum immunoreactive TSH and its alpha-subunit increased in the presence of high serum triiodothyronine (T3), thyroxine (T4), and free T4 concentrations, whereas beta-subunit TSH was undetectable. Exogenous TRH failed to increase serum TSH. Serum TSH was markedly suppressed by glucocorticoid, but was increased by antithyroid drug. L-Dopa or bromocriptine partially suppressed, but nomifensine had no influence on serum TSH. Serum prolactin (Prl) was above normal and markedly increased by TRH, but depressed by bromocriptine and not suppressed by nomifensine. Plasma TRH was normal in the hyperthyroid state, but was increased by glucocorticoid and antithyroid drug. Excess thyroid hormone depressed plasma TRH concentrations. Basal serum GH levels were constantly low. Transsphenoidal removal of the tumour normalized serum hormones (T3, T4 free T4, TSH, alpha-subunit and Prl), and eradicated the clinical signs of hyperthyroidism and galactorrhoea. Histological study of the tumour tissue demonstrated both thyrotrophes and somatotrophes. A reciprocal relationship between serum TSH and T4 concentrations shifted to a higher level before but was normalized after removal of the tumour. Ten months later, the clinical signs of thyrotoxicosis and the increase in serum thyroid hormone recurred without a concomitant increase in serum TSH and its alpha-subunit. Thyroidal auto-antibodies were slightly positive, but thyrotrophin-binding inhibitor immunoglobulin (TBII) was negative. Administration of antithyroid drug produced a euthyroid state, but 3 years later, discontinuation of the treatment resulted in recurrent hyperthyroidism without suppressed plasma TRH and with no evidence of regrowth of the pituitary tumour. It is suggested that the patient initially had hyperthyroidism owing to excessive TSH secretion from the tumour caused by abnormal TRH secretion, and subsequently had hyperthyroidism owing to Graves' disease.

Adenoma↗
PubMed1985

Visualization of the cerebrospinal fluid drainage into the Galen's vein.

Arachnoid granulations are not always present in lower mammals and primate newborns. In order to visualize the route for the cerebrospinal fluid (CSF) to drain into the venous system, horseradish peroxidase (HRP) was injected into the lateral ventricle or cisterna cerebellomedullaris of the mouse and rat. From 30 to 60 min after the commencing of a slow infusion for 15-30 min of 0.05-0.1 ml solution containing 10-20 mg HRP, the mouse, whose skull had been exposed, was dropped into cold acetone at dry ice temperature; other animals were fixed by perfusion with aldehyde solution. The frozen head was dissected in a cryostat kept at -18 degrees C to remove the skull, but leave the dura mater and the falx cerebri. The brain with meninges was cut into 30-45 microns sagittal sections in the cryostat, and processed for peroxidase reaction. The perfusion-fixed brains were used for scanning electron microscopy and for electron microscope observation of the tracer. The reaction product was found within fenestrated venous capillaries of the choroid plexus. The route for the HRP in the CSF to drain into the sinus rectus via the vena choroidea and vena cerebri magna was directly visualized in the mouse.

Animals↗
PubMed1984

Modulation of prostaglandin E2, F2 alpha, I2 content and synthesis by thyrotropin in cultured porcine thyroid cells and intact rat thyroid glands.

Porcine thyroid gland contains prostaglandin E2, prostaglandin F2 alpha and prostacyclin (prostaglandin I2) (measured as an end metabolite, 6-keto prostaglandin F1 alpha) and it contains more prostaglandin I2 than prostaglandin E2 or F2 alpha. Cultured porcine thyroid cells contain prostaglandin E2, F2 alpha and I2. When cultured in the presence of thyroid stimulating hormone (TSH), thyroid cells contain more prostaglandin I2 than prostaglandin E2 or F2 alpha but when cultured in its absence, they contain more prostaglandin E2 or F2 alpha than prostaglandin I2. Thyroid cells synthesize prostaglandin E2, F2 alpha and I2; when cultured in the presence of TSH, they synthesize more prostaglandin I2 than prostaglandin E2 or F2 alpha but when cultured in its absence, they synthesize more prostaglandin E2 or F2 alpha than prostaglandin I2. When cultured in the presence of TSH, thyroid cells take up iodide and organify it but when cultured in its absence, they do not take up iodide. When cultured in the presence of TSH, thyroid cells synthesize prostaglandin I2 and take up iodide, indicating that in the physiological conditions, prostaglandin I2 plays a more important role than prostaglandin E2 or F2 alpha. Rat thyroid gland contains prostaglandin E2, F2 alpha and I2. Endogenous increase in serum TSH through goitrogen treatment and exogenous TSH administration augment prostaglandin I2 contents and depress prostaglandin E2 and F2 alpha contents. Suppression of endogenous TSH by thyroxine treatment depresses prostaglandin I2 contents and augments prostaglandin E2 and F2 alpha contents. Chronic exposure to TSH augments prostaglandin I2 synthesis and depresses prostaglandin E2 and F2 alpha syntheses but chronic nonexposure to TSH depresses prostaglandin I2 synthesis and augments prostaglandin E2 and F2 alpha synthesis in in vivo rat thyroid glands and in vitro cultured porcine thyroid cells.

Animals↗
PubMed1984

Membrane particles and gap junctions in the retinas of two species of cephalopods, Octopus ocellatus and Sepiella japonica.

To study correlation between membrane structure and photoreceptor function, we compared the size and density of intramembrane particles (IMPs) in various membrane compartments of freeze-fractured retinas in a cuttle-fish, Sepiella japonica, and an octopus, Octopus ocellatus. Distribution of gap junctions in the retinas was also examined. Similar results were obtained in the two species. P-faces of both rhabdomeric microvillar membrane and non-rhabdomeric plasma membrane of the apical process were characterized by a random distribution of dense IMPs (ca. 5500-6500/microns2), which showed a unimodal size distribution with a mean diameter of ca. 10 nm. Unlike other invertebrate ocelli, the plasma membrane of the cell body in both the outer and inner segments had significantly denser P-face particles (ca. 7500-8000/microns2) than the rhabdomeric microvillar membrane. The size distribution of IMPs in each part of the membrane was also unimodal, but with a mean diameter of ca. 8 nm. In tangential fractures, each lamella of the myeloid body showed a patchwork of P-faces with irregularly arranged, dense particles and E-faces with orderly patterened granulation. Density and size distribution of the P-face particles in the myeloid membrane resembled those in the rhabdomeric microvillar membrane. The plasma membranes of the supporting cell and the gial cell had relatively sparse P-face particles (ca. 1500-3000/microns2). In addition to the previously reported gap junctions, which connected visual cell inner segments with each other, directly or via collaterals, small gap junctions were found between the visual cell axons and presumed efferent nerve fibres in the plexiform layer. Large-sized gap junctions provided mutual connections for both supporting cells and glial cells. In conclusion, IMPs of 10 nm in mean diameter in the microvillar and non-microvillar parts of the apical process plasma membrane and in the myeloid membrane represent the molecules or their clusters of two photopigments in the cephalopod visual cell, rhodopsin and retinochrome, respectively, and electrical transmission plays a role in visual cell-efferent nerve interactions.

Animals↗
PubMed1984

A unique photoreceptive structure in the arrowworms Sagitta crassa and Spadella schizoptera (Chaetognatha).

The ultrastructure of photoreceptors in two species of chaetognaths, Sagitta crassa and Spadella schizoptera, was studied by electron microscopy using a goniometer specimen stage as well as by freeze-fracture techniques. In contrast to earlier descriptions, the photoreceptor is made up of a stack of lamellae with pores. The lamellae, each 30-45 nm in thickness, are piled one on top one another at intervals of 10-20 nm. The lamellar surface is often perpendicular to the incident light. The pores are 35-55 nm in diameter and arranged in an orderly square lattice with a center-to-center distance of 80-95 nm. These perforated lamellar structures, resembling annulate lamellae, are entirely new as photoreceptive structures.

Animals↗
PubMed1984

Two types of thyroid function-blocking antibodies in autoimmune atrophic thyroiditis and transient neonatal hypothyroidism due to maternal IgG.

We examined the effects of IgG from four patients with autoimmune atrophic thyroiditis on cAMP responses and iodine metabolism (post-receptor processes), using cultured thyroid cells. We found two types of thyroid function-blocking antibodies: (1) one blocks TSH binding to its receptors and inhibits TSH-stimulated cAMP responses but does not block cAMP-stimulated iodine uptake and organification; (2) the other blocks TSH binding to its receptors, inhibits TSH-stimulated cAMP responses and does block cAMP-stimulated iodine uptake and organification (post-receptor processes). Among the four patients with autoimmune atrophic thyroiditis, three had TSH binding blocking antibodies only and one had antibodies which block post-receptor processes. These antibodies might be responsible for thyroid dysfunction in autoimmune atrophic thyroiditis. The daughter of one of the women with autoimmune atrophic thyroiditis had transient neonatal hypothyroidism and recovered spontaneously from the hypothyroid state with the disappearance of the maternal blocking antibodies.

Adult↗
PubMed1984

Reappraisal of the 3,5,3'-triiodothyronine-suppression test in the prediction of long term outcome of antithyroid drug therapy in patients with hyperthyroid Graves' disease.

Thyroidal suppressibility by exogenous T3 in terms of both radioiodine uptake (RAIU) and serum T4 was evaluated in 115 hyperthyroid patients treated with methimazole for 2 yr and followed for an additional 2 yr to study the rate of recurrence. Various other serum parameters including serum thyroglobulin concentrations, thyroid autoantibody, and TSH receptor antibody titers, and thyroidal responses to TRH-induced TSH elevation were also determined. After 2 yr of methimazole therapy, thyroidal RAIU was not suppressible (RAIU less than 12%/4 h was defined as suppressible) in 50 of 115 patients (group I). Of 65 patients with suppressible thyroid RAIU, serum T4 was significantly reduced (less than 60% of pre-T3 level) by T3 administration in only 43 patients (group III) but not in the remainder (group II). Antithyroid drug therapy was discontinued in the group II and III patients, and 7 of the patients had recurrence of hyperthyroidism within 2 yr of follow-up. All of them were from group II. The thyroidal response to TSH was greater in group III patients than in group II patients. During antithyroid drug therapy, decrease of microsomal antibody titer was more likely to occur in group III patients than in those of group II. Serum thyroglobulin concentrations were uniformly normal in treated patients irrespective of T3 suppressibility. TSH receptor antibody was positive in all 13 untreated patients with Graves' disease but was negative in treated patients regardless of their T3 suppressibility. Measurement of both thyroidal RAIU and serum T4 after administration of T3 improves the reliability of T3-suppression testing as a predictor of the remission of Graves' disease.

Adolescent↗
PubMed1984

Transient neonatal hypothyroidism due to maternal immunoglobulins that inhibit thyrotropin-binding and post-receptor processes.

Transient neonatal hypothyroidism was found in a daughter of a 25-yr-old mother, who was receiving treatment for primary hypothyroidism due to Hashimoto's thyroiditis. During the neonatal period the infant had antithyroid microsomal and antithyroglobulin antibodies and TSH-receptor antibodies. The daughter recovered spontaneously from the hypothyroid state and the antithyroid antibodies disappeared from her serum. The mother's serum contained the same antibodies, and immunoglobulin G (IgG) from maternal serum blocked TSH binding to its receptors, TSH-stimulated cAMP responses, and cAMP-stimulated iodine uptake and organification in cultured thyroid cells. The latter finding suggests that the IgG had a postreceptor locus of action as well as inhibiting TSH binding to its receptor. The presence of such IgGs might have induced hypothyroidism both in the mother and in the daughter.

Adult↗
PubMed1984

Effects of long-term treatment with thyroxine on pituitary TSH secretion and heart action in patients with hypothyroidism.

The effects of thyroxine (T4) treatment on pituitary thyrotroph cells and on the heart were studied in 68 female patients with hypothyroidism. During the initial 12 months of T4 treatment, relatively small doses of T4 (1.3 micrograms/kg) normalized serum T4, triiodothyronine (T3), TSH and lipid concentrations in mild hypothyroidism, while moderate doses of T4 (1.7-2.0 micrograms/kg) normalized serum T4, T3 and lipid concentrations but not serum TSH levels or the volume of sella turcica in moderate and severe hypothyroidism; however, serum TSH levels and the volume of sella turcica returned to normal with continuation of these doses of T4. Systolic time intervals (ET/PEP) can discriminate between euthyroid and hyperthyroid states and agree well with serum TSH levels. However, ET/PEP was unequivocally elevated in about 40% of treated hypothyroid patients with normal serum T3, T4 and TSH levels which had been maintained over 48-54 months. Since the reciprocal relationship between free T4 and TSH levels was maintained in all treated patients, elevated ET/PEP with normal TSH levels indicates that the heart is more sensitive to thyroid hormones than the pituitary thyrotroph in 40% of treated hypothyroid patients. During T4 treatment in patients with hypothyroidism, ET/PEP should be followed and T4 doses adjusted to maintain normal ET/PEP rather than normal serum TSH levels, especially in older patients in whom T4 may aggravate angina pectoris or provoke myocardial infarction.

Female↗
PubMed1984

Age-related alterations of pituitary-thyroid function in normal female subjects and in female patients with simple goitre.

Age-related alterations in pituitary-thyroid function were studied in 173 female patients with simple goitre and in 70 normal female subjects. They were divided into 4 groups according to age: A group, less than 19 years; B group, 20 to 29 years; C group, 30 to 39 years; D group, 40 to 59 years. Serum triiodothyronine (T3) concentrations decreased progressively but insignificantly with age in female patients with simple goitre and in normal female subjects, whereas serum thyroxine (T4) concentrations remained constant throughout the studied age range. Only in female patients with simple goitre, did basal serum TSH concentrations show a tendency to increase with age. However, thyrotrophin-releasing hormone (TRH)-stimulated increase of serum TSH was progressively augmented with age both in female patients with simple goitre and in normal female subjects; the magnitude of change was greater in the former group. As reflected by acute increases of serum T3 and T4 concentrations, thyroidal responsiveness to endogenous TSH was progressively depressed with age in female patients with simple goitre and in normal female subjects. This age-related thyroidal refractoriness to TSH was more apparent when the changes were expressed as delta T3 (stimulated T3 - basal T3)/delta TSH (maximum TSH after TRH - basal TSH), and delta T4 (stimulated T4 - basal T4)/delta TSH. Delta T4/delta TSH was lower in female patients with simple goitre than in normal female subjects in all age groups. However, the difference was significant only for delta T4/delta TSH in group A. Thyroidal responsiveness to exogenous TSH also gradually declined with age in female patients with simple goitre.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Electrophysiological and morphological cell polarity and iodine metabolism in cultured porcine and human (normal and Graves') thyroid cells.

In cultured porcine and human thyroid cells, electrophysiological and morphological studies showed that cultivation in the presence of TSH, prostaglandin E2 (PGE2) or dibutyryl cyclic AMP (dbcAMP) maintained normal cell polarity with iodine incorporation and organification. Cells cultivated in the absence of these substances had inverted cell polarity and lacked iodide incorporation. In the presence of TSH, PGE2 or dbcAMP, the thyroid cells formed follicles with normal cell polarity and the microvilli pointed toward the follicle lumina. Intracellular resting potentials were -60mV and the electrical potentials in the follicle lumina were negative at -20mV. The transmembrane potential differences (p.d.) between the follicle lumina and the epithelial cells were -40mV and those between the epithelial cells and the culture media -60mV. In the absence of TSH, PGE2 or dbcAMP, the thyroid cells formed 'domes' or hollow spheres with inverted cell polarity and the microvilli pointed toward the culture media. Intracellular resting potentials were -40mV, being less negative than those in the presence of TSH, PGE2 or dbcAMP. The electrical potentials in the 'dome' or hollow sphere cavities were positive at +19mV. The transmembrane p.d. between the culture media and the epithelial cells was -40mV and that between the epithelial cells and the cavities -60mV, indicating that electrophysiologically the cell polarity was inverted in the absence of TSH, PGE2 or dbcAMP. No significant differences in electrophysiology and iodine metabolism were observed between normal and Graves' human thyroid cells in culture.

Animals↗
PubMed1983

Differences in prostaglandin E2, prostaglandin F2 alpha and prostacyclin contents and their response to thyrotrophin stimulation and in prostaglandin-stimulated cyclic AMP response in normal and Grave's thyroid slices.

The human thyroid contained prostaglandin (PG) E2, PGF2 alpha and 6-oxo-PGF1 alpha, an end-metabolite of prostacyclin (PGI2), the 6-oxo-PGF1 alpha content being the highest of these prostaglandins. Graves's thyroid contained a significantly higher amount of PGF2 alpha and lower amounts of PGE2 and 6-oxo-PGF1 alpha than the normal thyroid. Thyrotrophin acutely augmented the thyroid contents of PGE2, PGF2 alpha and 6-oxo-PGF1 alpha. The TSH-stimulated increases in PGE2 and 6-oxo-PGF1 alpha were lower but the TSH-stimulated increase in PGF2 alpha was significantly higher in Graves's thyroid than in the normal thyroid. Prostaglandin E2 and PGI2 stimulated human thyroid cyclic AMP synthesis, with the magnitudes of PGE2- and PGI2-stimulated increases in cyclic AMP being equal in normal and Graves's thyroid. Prostaglandin F2 alpha did not stimulate cyclic AMP synthesis significantly. These results provide evidence that prostaglandins play important roles in thyroid physiology and the pathophysiology of Graves's disease.

6-Ketoprostaglandin F1 alpha↗