Biomedical subjects
Publications and source records attributed to N Takasu.
This is the first report to show that polypeptide hormone increases cellular calmodulin contents. In cultured porcine thyroid cells, 6 days' exposure to TSH (above 0.02 mU/ml) increased cellular calmodulin contents. Six days' exposure to TSH also increased calcium uptake in thyroid cells. This TSH-stimulated increase in calcium uptake was partly due to the increase in cellular calmodulin contents.
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To examine the effects of severe burns on preload and left ventricular (LV) contractility, we continuously measured LV pressures and dimensions in severely burned dogs throughout the early part of the postburn period. Hemodynamic parameters, including cardiac output (CO), mean aortic pressure (MAP), heart rate (HR), LV pressures and their first derivatives (dP/dt), and the LV regional dimension, were measured and compared before and every 30 min after burns were produced (up to 360 min) in four groups: group A (n = 7), dogs with sham burns; group B (n = 5), dogs with nonresuscitated full-thickness burns involving 50% of the total body surface area; group C (n = 6), dogs with burns resuscitated with lactated Ringer's solution at 4 ml X kg X % burn/24 h; and group D (n = 6), dogs with burns resuscitated with 1.5% dextran in lactated Ringer's solution at 2 ml X kg X % burn/24 h. From these measurements, we obtained the LV end-diastolic segment length (EDL) as an index of preload and three indices of cardiac contractility, i.e., peak dP/dt, the percentage of shortening (% delta L), and mean Vcf. Our results showed that CO, MAP, and preload (i.e., EDL) decreased significantly more in the three burn groups (groups B, C, and D) than in the sham burn group, but that there were no significant differences in CO, MAP, and EDL among the three burn groups. The three indices of contractility also decreased significantly more in the three burn groups than in the sham burn group.(ABSTRACT TRUNCATED AT 250 WORDS)
One hundred and twenty-one patients with hyperthyroidism of Graves' disease were treated with antithyroid drugs for 3 years and thyroidal response to an increase or decrease of TSH and the serum thyroid stimulating immunoglobulin (TSI) activity were studied in relation to the presence or absence of TSH binding inhibiting immunoglobulin (TBII). TBII activity was positive in 83% of untreated patients but decreased gradually with time during antithyroid drug therapy. Thyroidal radioactive iodine uptake (RAIU) was suppressed by T3 in 86 of 121 treated patients but 16% of suppressible patients had TBII activity. Thyroidal RAIU was not suppressed by T3 in 35 treated patients, and 19 of 35 unsuppressible patients had TBII activity but other 16 patients did not. When suppressible and unsuppressible patients were combined, suppression of serum T4 and thyroidal RAIU by T3 tended to be less in the presence of TBII activity. TSI activity was detected in the sera of untreated patients but did not correlate with TBII activity. TSI activity was undetectable after treatment for 3 years irrespective of presence or absence of TBII activity and T3-suppressibility. TSH, T4 and T3 elevation in response to 500 micrograms thyrotropin releasing hormone (TRH) was normal in all treated patients irrespective of presence or absence of TBII activity and T3-suppressibility. It is suggested that in vivo thyroidal responsiveness to an increase or decrease of endogenous TSH did not correlate with the presence or absence of TBII activity after long-term therapy with antithyroid drugs.
Calcinosis universalis associated with dermatomyositis occurred in a 58-year-old woman. Tissues removed from the sublingual region in the patient were studied by ordinary microscopy, electron microscopy, and an electron-microanalytic method. The calcified materials were distributed on collagen fibers and seemed to have a relationship with foci of fibrinoid degeneration. Moreover, globular and/or membranous structures, considered to originate from the degenerate cells of the stroma, were observed in these calcified zones. Some of them contained electron-dense materials. Therefore, the globular and/or membranous structures were thought to be concerned with initial calcification in this case. Furthermore, irregular bone tissue was formed adjacent to the calcified masses. In addition, the calcified materials were identified by X-ray diffraction examination and electron microscopy as hydroxyapatite.
This report demonstrates TSH-stimulated electrical excitation in the thyroid and its refractoriness after exposure to TSH. TSH depolarizes the membrane potentials and causes action potentials. TSH-induced electrical activity is characterized by a latent period, rapid depolarization, action potentials (usually two spikes were observed), and then repolarization to the potential level of the silent phase. This TSH-induced electrical excitation is associated with iodide discharge. Previous exposure to TSH induces refractoriness of electrophysiological excitation and iodide discharge to further TSH stimulation.
The high mortality rate of patients with acute mesenteric ischemia may be mainly due to the difficulty of making an early diagnosis. Many clinical and experimental studies have been attempted to make an early diagnosis in the view of history, physical examination, laboratory data, X-rays and angiographies. This study was undertaken to estimate the diagnostic value of twenty one laboratory parameters and three clinical parameters measured after superior mesenteric artery occlusion (SMAO) in the mongrel dogs. Consequently, the valuable diagnostic indicators of SMAO that statistically had significant difference were serum CPK isoenzyme-BB, serum CPK isoenzyme-MB, serum inorganic phosphate, serum calcium and base excess of arterial blood gas analysis. In these indicators, serum CPK isoenzyme-BB, serum inorganic phosphate and serum calcium were especially valuable indicators of its early diagnosis, because they showed significant change in the early phase after SMAO. However, other indicators showed significant change within eighteen hours after SMAO. Therefore, if these indicators are able to be examined in a case of abdominal emergency, they are considered to play a valuable role in the diagnosis of acute mesenteric ischemia.
Recurrent intestinal obstruction for which no underlying cause can be found has been termed "chronic idiopathic intestinal pseudoobstruction (CIIP)" by Maldonado et al. Some clinical features of CIIP have been pointed out in literatures. More often than not, CIIP often shows hereditary occurrence. The authors have summed up twenty-one cases of CIIP reported till 1984 in Japan, In these cases, only one familial occurrence has been reported excluding our own. Our cases were a young woman and her father and they showed clinical features of CIIP and they might have hereditary factors.
This report demonstrates TSH-stimulated electrical excitation in cultured porcine thyroid cells. TSH depolarizes the thyroid cell membrane potentials and causes the appearance of action potentials, which occur in a burst. The burst is preceded by depolarization and after the burst, during which usually 2 spikes are seen, a repolarization occurs. This TSH-induced electrical excitation is associated with iodide discharge.
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.
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.
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.
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.
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.
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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.
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.