Diffusion field around a dendrite growing under microgravity.
Explore the source record for details and available documents.
Journal Article↗
Biomedical subjects
K Shigematsu
Publications and source records attributed to K Shigematsu.
Adrenocorticotropic hormone-independent bilateral macronodular adrenocortical hyperplasia associated with Cushing's syndrome.
A case of adrenocorticotropic hormone independent bilateral adrenocortical macronodular hyperplasia (AIMAH) is reported. A 59 year old male was admitted to hospital because of hypertension. Subsequently, hypercortisolism, low plasma adrenocorticotropic hormone (ACTH), loss of diurnal rhythm of ACTH, lack of suppression with high dose dexamethasone were found and bilateral adrenal enlargement was detected by abdominal computerized tomography and adrenal scintigraphy. Bilateral total adrenalectomy was performed under a diagnosis of bilateral adrenal hyperplasia associated with Cushing's syndrome. Both adrenal glands were enlarged in size and weight. Bulging nodules were found at the cut section. Microscopically, a variegated histologic pattern including trabecular, adenoid and zona glomerulosa-like (ZG-like) structures was revealed in the nodules. Immunohistochemical examination disclosed positive staining of cytochrome P-450 17 alpha, negative of 3 beta-HSD in the ZG-like structure. Ultrastructurally, the cells composing the ZG-like structure were similar to those of the ZG in normal adrenal cortex. The authors agree that AIMAH is one of the entities causing Cushing's syndrome, and advise pathologists to keep this disorder in mind when they examine the adrenals in Cushing's syndrome.
17-Ketosteroids↗
Accumulation of proteinase K-resistant prion protein (PrP) is restricted by the expression level of normal PrP in mice inoculated with a mouse-adapted strain of the Creutzfeldt-Jakob disease agent.
Creutzfeldt-Jakob disease (CJD) is a transmissible neurodegenerative disease of humans caused by an unidentified infectious agent, the prion. To determine whether there was an involvement of the host-encoded prion protein (PrPc) in CJD development and prion propagation, mice heterozygous (PrP+/-) or homozygous (PrP-/-) for a disrupted PrP gene were established and inoculated with the mouse-adapted CJD agent. In keeping with findings of previous studies using other lines of PrP-less mice inoculated with scrapie agents, no PrP-/- mice showed any sign of the disease for 460 days after inoculation, while all of the PrP+/- and control PrP+/+ mice developed CJD-like symptoms and died. The incubation period for PrP+/- mice, 259 +/- 27 days, was much longer than that for PrP+/+ mice, 138 +/- 12 days. Propagation of the prion was barely detectable in the brains of PrP-/- mice and was estimated to be at a level at least 4 orders of magnitude lower than that in PrP+/+ mice. These findings indicate that PrPc is necessary for both the development of the disease and propagation of the prion in the inoculated mice. The proteinase-resistant PrP (PrPres) was undetectable in the brain tissues of the inoculated PrP-/- mice, while it accumulated in the affected brains of PrP+/+ and PrP+/- mice. Interestingly, the maximum level of PrPres in the brains of PrP+/- mice was about half of the level in the similarly affected brains of PrP+/+ mice, indicating that PrPres accumulation is restricted by the level of PrPc.
Animals↗
Endothelin-3 stimulates inositol 1,4,5-trisphosphate production and Ca2+ influx to produce biphasic dopamine release from rat striatal slices.
1. Real-time monitoring of dopamine (DA) release from rat striatal slices demonstrated that endothelin (ET)-3 (0.1-10 microM) produced a biphasic DA release consisting of transient and sustained components. When extracellular Ca2+ was removed, the sustained but not transient response remarkably decreased. 2. ET-3 (1-10 microM) stimulated an increase in the intracellular Ca2+ concentration ([Ca(2+)]i), which also consisted of two components. The external Ca2+ depletion inhibited primarily the sustained component of the Ca2+ response to ET-3. 3. ET-3 increased inositol 1,4,5-trisphosphate (IP3) concentrations in striatal slices. This response peaked at 10 to 20 sec and returned to the basal level 2 min after stimulation, an event which was in good accord with a prompt and transient phase of both cytosolic Ca2+ activity and DA release evoked by ET-3. 4. Thus, ET-3 produces a transient and a sustained release of DA from striatal slices by stimulating intracellular Ca2+ mobilization via IP3 formation and extracellular Ca2+ influx, respectively.
Animals↗
Microglia with an endothelin ETB receptor aggregate in rat hippocampus CA1 subfields following transient forebrain ischemia.
We examined endothelin (ET) receptors in the hippocampus CA1 subfields of stroke-prone spontaneously hypertensive rats subjected to a 10-min bilateral carotid occlusion and reperfusion. When delayed neuronal death had occurred in the pyramidal cell layer at 7 days after transient forebrain ischemia, the quantitative receptor autoradiographic method we used revealed a dramatic increase in number of 125I-ET-1 binding sites in the hippocampus CA1 subfields. The highest number of de novo binding sites appeared in the area corresponding anatomically to the pyramidal cell layer with neuronal death. These binding sites were characteristically the ETB receptor. The de novo 125I-ET-1 binding was mainly present on microglia aggregating with a high density in the damaged pyramidal cell layer. As ET-1- and ET-3-like immunoreactivities were highly expressed within astrocytes in damaged neural tissue, the possibility that microglia with the ETB receptor are activated to participate in the pathophysiology of ischemia-related neural tissue damage by astrocytic ET-1 and ET-3 produced in response to transient forebrain ischemia would have to be considered.
Amino Acid Sequence↗
Intrapulmonary lymph nodes.
We report two cases of intrapulmonary lymph nodes detected by a chest roentgenogram or CT scan. The first patient was a 61-year-old fisherman referred complaining of cough and hemosputum. Chest roentgenogram showed a subpleural small nodular shadow at the superior segment of the right lower lobe. Thoracotomy showed a small anthracotic lymph node. The other case was a 68-year-old female patient admitted for further examination of a subpleural small nodular shadow at the latero-basal segment of the left lower lobe detected on a chest CT scan. Thoracoscopic surgery revealed that the black nodule was an anthracotic lymph node. The appearance of an intrapulmonary lymph node on radiological examination is rare, however, it should be considered in the differential diagnosis of a solitary or multiple peripheral pulmonary nodules in adults. A small nodular shadow should be resected if malignancy is suspected though not proven. Subpleural intrapulmonary lymph node warrants thoracoscopic surgery.
Aged↗
Periventricular nucleus lesioning modulates specific somatostatin binding in various brain regions and anterior pituitary.
The effects of periventricular nucleus (Pe) lesioning on the plasma growth hormone (GH) levels and the anterior pituitary (A.P.) and brain somatostatin (SRIF) receptors were studied. A transient significant increase in plasma GH level in lesioned rats was detected 1 day after the operation. This elevated level of plasma GH started to decrease 3 days after lesioning. These changes were paralleled by an increase in binding of 125I-Tyr11-SRIF-14 to the A.P. 1 day after lesioning. This result could further confirm that the SRIF inhibitory action on GH release takes place at the A.P. level. Also, a transient increase in binding of the radioligand was detected in some brain areas 1 and 4 days after the lesion. However, the mechanism by which this increase takes place remains to be elucidated.
Animals↗
Localization of angiotensin AT1 receptors in the rat heart conduction system.
We characterized angiotensin II receptor subtypes in the conduction system of the rat heart using quantitative autoradiography. In both the sinoatrial and atrioventricular nodes, binding could be totally displaced by losartan, and was insensitive to PD 123177, indicating that angiotensin II receptors in the conduction system of the rat heart belong to the AT1 subtype. Angiotensin AT1 receptors could play a direct role in the regulation of the heart chronotropic properties.
Angiotensin II↗
Increased production of endothelins in the hippocampus of stroke-prone spontaneously hypertensive rats following transient forebrain ischemia: histochemical evidence.
1. The effect of transient forebrain ischemia on endothelin-1 (ET-1) and endothelin-3 (ET-3) production in the hippocampus of stroke-prone spontaneously hypertensive rats (SHRSPs) was investigated using immunohistochemical techniques. 2. In SHRSPs subjected to 10-min bilateral carotid occlusion, neuronal degeneration in the CA1 pyramidal cell layer of the hippocampus was detectable at 4 days and remarkable at 7 days after reperfusion. 3. Coinciding with neuronal degeneration, ET-1- and ET-3-like immunoreactivities were intense in the CA1 pyramidal-cell layer, the stratum lacunosum moleculare, and the CA4 subfield of the hippocampus. Almost all of the immunostained cells had morphological characteristics of astrocytes. 4. The possibility that ET has a role in the development of neuronal cell death following transient forebrain ischemia warrants further attention.
Animals↗
Reproductive hormones modulate angiotensin II AT1 receptors in the dorsomedial arcuate nucleus of the female rat.
Angiotensin II AT1 receptors are highly localized in the dorsomedial arcuate nucleus. AT1 receptor number is very low during proestrus and in ovariectomized and male rats, and is high only during the estrus phase of the estrous cycle and after ovariectomized rats receive a sequential estrogen-progesterone treatment. Our results suggest that the mechanism of the estrogen-progesterone inhibition of the prolactin surge may involve the selective stimulation of dorsomedial arcuate AT1 receptors.
Animals↗
[A case of bronchial lipoma treated by Nd-YAG laser surgery].
A 59-year-old man was referred to our hospital with complaint of cough. On physical examination the patient was 159 cm tall and weighted 68 kg. Chest X-ray showed an infiltrative shadow in the left lower lung field. Bronchoscopic findings revealed a polypoid tumor with smooth surface, located at the lower part of the left main bronchus and occupying over two-thirds of the left basal bronchus. A hamartoma was suspected as the result of bronchial biopsy. Endoscopic Nd-YAG laser surgery was performed. The left basal bronchus was opened. Histologically the tumor consisted mainly of mature fat tissue with collagen fibers and was diagnosed as a bronchial lipoma. Bronchial lipoma arising from the submucosal tissue of a large bronchus, occurs mainly in obese and middle-aged men. It is a rare benign tumor of the lung and only 38 cases have been reported in Japan.
Bronchial Neoplasms↗
Functional-morphological effect of the synthetic atrial natriuretic factor (ANF 101-126) on the zona glomerulosa cells of adrenal cortex.
The effects of atrial natriuretic factor (ANF) on the adrenal steroidogenesis were examined in the zona glomerulosa of rats in vivo. ANF administration provoked a significant decrease in the width of zona glomerulosa (P < 0.01) and a significant enlargement of nuclei of zona glomerulosa cells (P < 0.01). Ultrastructurally conspicuous change was observed in mitochondria of the cells of the zona glomerulosa treated with ANF, representing elongated mitochondria with "parallel arrays" of tubules with pipe-like structure. In vitro autoradiography 125I-labelled ANF binding displayed a significant decrease of a specific receptor site in the zona glomerulosa treated with ANF. A significant lowering in plasma levels of aldosterone was observed in ANF-treated rats. These findings could be interpreted as an inhibitory effect of ANF on adrenal steroidogenesis of the glomerular zone by action through a specific ANF-receptor.
Aldosterone↗
Accumulation of amyloid precursor protein in damaged neuronal processes and microglia following intracerebral administration of aluminum salts.
Alzheimer's disease is characterized by neurofibrillary tangles and amyloid deposits, with the latter probably occurring because of abnormal accumulation and/or processing of amyloid precursor protein (APP). Aluminum salts are known to be neurotoxic and to be capable of inducing neurofibrillary tangles. We explored the effects of intraventricular or intrastriatal injections of AlCl3 on the immunodistribution of APP in rat brain. There was a striking and long-lasting accumulation of APP in affected neurites, as well as in activated microglia/macrophages. Abnormal neurites also showed argentophilic changes, neurofilament accumulation, and Alz50 immunoreactivity. However, no extracellular amyloid fibrils were seen. The results, taken together with previous studies on colchicine, are consistent with the hypothesis that interruption of axoplasmic flow can lead to both APP accumulation and cytoskeletal changes.
Aluminum↗
Localization of amyloid precursor protein in selective postsynaptic densities of rat cortical neurons.
One of the hallmarks of Alzheimer pathology is extracellular deposition of beta-amyloid protein (BAP) which is derived from a larger glycoprotein called amyloid precursor protein (APP). Although APP has often been described as a surface membrane protein, such a localization has not previously been demonstrated at the light or electron microscopic level. We now report the results of immunoelectron microscopy using three specific antibodies against different synthetic fragments of APP. All three antibodies demonstrated a major localization to organelles such as the Golgi apparatus, endoplasmic reticulum and vesicular-like structures. A minor proportion of staining with all three was on selective postsynaptic membranes of asymmetrical synapses, whereas staining of presynaptic membranes was not observed. The morphological evidence suggests that one role of APP may be in association with the function of selective synapses.
Amyloid beta-Protein Precursor↗
Specific binding sites for 125I-endothelin-1 in the porcine and human spinal cord.
Specific binding sites for 125I-endothelin-1 (125I-ET-1) in the spinal cord were investigated using quantitative receptor autoradiographic and chemical cross-linking methods. The binding sites were highly concentrated in porcine and human spinal cord areas corresponding anatomically to the dorsal horn (Rexed's laminae I-III), an area around the central canal (lamina X) and the principal part of the intermediolateral nucleus (IMLp). The localization of the binding sites differed from those of 125I-omega-conotoxin GVIA (125I-CgTx) and 125I-Bolton-Hunter substance P (125I-BH-SP), with the exception that the IMLp shared 125I-ET-1 with 125I-CgTx and 125I-BH-SP binding sites. Specific 125I-ET-1 binding sites in the areas examined were characteristically single and of high affinity. There were no differences between the potencies of unlabeled ET family peptides, ET-1, ET-2, ET-3 and sarafotoxin S6b at inhibiting 125I-ET-1 binding to the areas. Chemical cross-linking studies showed that 125I-ET-1 and 125I-ET-3 mainly bound to a protein with molecular mass of 43 kDa in the porcine and human thoracic spinal cord membranes. The present finding shows the neuronal significance of this newly discovered peptide in the spinal cord.
Aged↗
Reactive microglia/macrophages phagocytose amyloid precursor protein produced by neurons following neural damage.
Kainic acid lesions of rat striatum caused an elevation of amyloid precursor protein (APP) immunoreactivity in neurons and neurites, some of which were then phagocytosed by reactive microglia/macrophages. Immunoexpression of APP was observed in neurites and neurons 1 day after the kainic injection. Four days after lesioning, immunoreactivity was still concentrated in thick and distorted neurites, but it began to appear in microglia/macrophages and in the tissue matrix. The cells were identified as microglia/macrophages by the phenotypic markers Ia (OX6), leukocyte common antigen (OX1), C3bi receptor (OX42), and macrophage marker (ED1). They were negative for the astrocytic marker glial fibrillary acidic protein (GFAP). APP immunoreactivity in these phagocytic cells was most prominent between 1 week and 1 month postlesioning. No extracellular amyloid fibrils were detectable. These results suggest that APP production is rapidly upregulated in damaged neurons and accumulates in degenerating axons. However, phagocytosis of APP by reactive microglia/macrophages in this rat model does not result in production of Alzheimer type amyloid deposits.
Amino Acid Sequence↗
Accumulation of amyloid precursor protein in neurons after intraventricular injection of colchicine.
To study a possible relationship between inhibition of axonal flow and amyloidogenesis, the authors examined amyloid precursor protein (APP) immunoreactivity in rat brain treated with colchicine. After intraventricular injection of colchicine, the proximal axons of exposed neurons became swollen and showed a large increase in APP immunoreactivity, whereas the cytoplasm and dendritic processes showed lesser increases. These changes were seen in ipsilateral neurons of the hippocampus, lateral septal nucleus, amygdala, and entorhinal, parietal and temporal cortices, as well as bilaterally in the periventricular hypothalamic nucleus. The increase of APP immunoreactivity appeared as early as 3 hours after the injection. It peaked at around 24 hours, and began to clear after about 4 days. A few strongly APP-positive dystrophic neurons remained. In serial sections at these later time periods, some strongly argentophilic neurons and Alz-50 positive neurons, each with abnormal neurities, could be demonstrated. The result suggests that APP may undergo fast axoplasmic flow in rat brain and that argentophilic changes of Alz-50 immunoproduction may follow APP accumulation caused by inhibition of axoplasmic flow.
Amyloid beta-Protein Precursor↗
Immunoreactivity and receptor expression of insulinlike growth factor I and insulin in human adrenal tumors. An immunohistochemical study of 94 cases.
Using immunoperoxidase methods, 94 human adrenal tumors were examined for evidence of immunoreactivity and receptor expression of insulinlike growth factor I (IGF-I) and insulin. The frequency of IGF-I in adrenocortical carcinomas was significantly higher than that in adenomas of the adrenal glands. The adrenocortical carcinomas showed strong intensity of staining for IGF-I, IGF-I receptors, and insulin receptors. A significant correlation between immunoreactivity and receptor expression of both IGF-I and insulin was found only in the adrenocortical carcinomas. The adrenocortical adenomas with Cushing's syndrome and pheochromocytomas, more than adrenocortical adenomas with Conn's syndrome, also stained strongly for insulin receptors. Thus the IGF-I and insulin probably play a role in the growth of adrenocortical carcinoma tissues, possibly through autocrine mechanisms. The expression of insulin receptors in adrenocortical adenomas in the presence of Cushing's syndrome and pheochromocytomas may be associated with functions.
Adenoma↗