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S Takashima

Publications and source records attributed to S Takashima.

At least 19 recordsLinked to original sources

Serial diffusion-weighted imaging in a patient with MELAS and presumed cytotoxic oedema.

A patient with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) was studied with serial diffusion-weighted MRI (DWI) after stroke-like episodes and the apparent diffusion coefficient (ADC) was measured in an infarct-like lesion. In the acute and subacute stages, the affected area gave high signal on DWI and its ADC was much lower than that in a normal control region. In the chronic stage, the ADC became higher than that in normal brain. We therefore suggest that the stroke-like episodes did not cause vasogenic oedema but were related to energy failure and cytotoxic oedema.

Brain Edema↗

Comparison of high-resolution contrast-enhanced 3D MRA with digital subtraction angiography in the evaluation of hepatic arterial anatomy.

AIM: To evaluate the validity of high-resolution contrast-enhanced three-dimensional magnetic resonance angiography (MRA) in defining hepatic arterial anatomy and to compare this with digital subtraction angiography (DSA). MATERIALS AND METHODS: MRA and DSA were performed in 30 patients. MRA was performed with breath-hold, gadolinium-enhanced, three-dimensional, fast low-angle shot sequence with a 512 pixel matrix. MRA was compared with DSA in terms of image quality and depiction of hepatic arterial anatomy. The agreement in image quality between MRA and DSA was determined with the kappa statistic. RESULTS: With respect to image quality, there was excellent or good correlation between MRA and DSA for the common hepatic artery (kappa=0.85), proper hepatic artery (kappa=0.72), gastroduodenal artery (kappa=0.70), left hepatic artery (kappa=0.49), left gastric artery (kappa=0.50), splenic artery (kappa=0.84), and superior mesenteric artery (kappa=0.88). Poor correlation was found for the right hepatic artery (kappa=0.18) and right gastric artery (kappa=0.38). With regard to hepatic arterial anatomy, MRA correlated correctly with DSA in 28 of the 29 cases, i.e. 97% of patients. CONCLUSION: MRA is a useful technique for the evaluation of the hepatic artery, and for the vast majority of patients, MRA can replace intra-arterial DSA.

Aged↗

Developmental neurotransmitter pathology in the brainstem of sudden infant death syndrome: a review and sleep position.

Developmental studies on neurotransmitters and their receptors in sudden infant death syndrome (SIDS) infants and controls are reviewed, including comparison between the prone and supine positions at death. In SIDS infants, there are an increase of glial fibrillary acidic protein (GFAP)-positive astrocytes in the brainstem, an increase of substance P (SP) in the medulla and pons, a decrease of tyrosine hydroxylase (TH)-positive catecholaminergic neurons in the ventrolateral medulla (VLM), and vagal nuclei in the medulla oblongata and basal ganglia, a decrease of tryptophan hydroxylase (TrH)-positive serotonergic neurons in the periaqueductal gray matter (PAG), and decreases of 5-hydroxytryptamine 1A (5-HT1A) and 5-HT2A receptor immunoreactivities in the VLM and vagal nuclei in the medulla oblongata. These findings may be the result of chronic or repeated hypoxia and at the same time suggest hypofunction or immaturity of cardiorespiratory regulation. In contrast, 5-HT1A and 5-HT2A receptor immunoreactivities are increased in the PAG of SIDS infants. These increased immunoreactivities may reflect delayed neuronal maturation or a developmental abnormality of the nocicetive reaction of cardiorespiratory and arousal control in SIDS. Also, there are no differences of brainstem gliosis and catecholaminergic neuron changes between the prone and supine positions. Therefore, these changes may be predisposing factors for SIDS.

Astrocytes↗

Molecular biology in cerebral cortex of sudden infant death syndrome.

Full-scale investigations of sudden infant death syndrome (SIDS) by methods of molecular pathology have been carried out. This paper reports the basic preliminary data of SIDS cerebral cortex analyzed by restriction landmark genomic scanning (RLGS) method, which is the second dimension electrophoresis of DNA recently developed in Japan. The RLGS method was carried out separately using the cerebral cortex of a 4-month-old infant with SIDS and using the cerebral cortex of a 3-month-old infant as a control to investigate SIDS-specific spots. As a result, the coincidence rate of spots between the infant with SIDS and the infant without SIDS was 98.12%. The average coincidence rate of spots in humans is usually 99.07%. Therefore, it was confirmed that the coincidence rate of spots by RLGS between the infant with SIDS and the infant without SIDS was lower than that in humans. In addition, the incidence of SIDS-specific spots was 1.19% and the incidence of non-SIDS-specific spots was 0.6%.

Case-Control Studies↗

Quantification of trace elements in the brain of SIDS victims.

In this report, the quantification and analysis of trace elements in the frontal lobes of the brains of sudden infant death syndrome (SIDS) cases were carried out. In all materials, V, Cr, Sn and Sb were not observed and Mg, Na, K, Fe, Zn and Br were observed. As for all of these trace elements, there was no significant difference between SIDS and non-SIDS. Only Ca was not observed in SIDS and observed only in non-SIDS. It is well known that Ca moves from outside of cells to inside of cells and induces cell damage by membrane disturbance in a hypoxic situation. The result in this report suggests that the deaths in SIDS cases are so sudden and are not sufficient for the kinetics of Ca into brain cells in the hypoxic situation.

Calcium↗

Concentric structure of thalamic lesions in acute necrotizing encephalopathy.

Acute necrotizing encephalopathy of childhood (ANE) is characterized by multiple, symmetrical brain lesions affecting the bilateral thalami, putamina and cerebral white matter, which often show a concentric structure on CT and MRI. To reveal the pathological substrate of this finding, comparison was made between CT and necropsy findings of three fatal cases of ANE. Cranial CT demonstrated a concentric structure of the thalamocerebral lesions in one patient who died 3.5 days after the onset of encephalopathy, but not in the other two patients who died within 30 h. Neuropathological examination of postmortem brains revealed laminar changes of vascular and parenchymal pathology in all the cases. Excessive permeability of blood vessels and resultant vasogenic edema became more prominent with increasing depth from the cerebral surface. The deep portion of the lesions showed severe perivascular hemorrhage, accounting for the central high density on the CT images of one patient.

Child Welfare↗

Perineal rectosigmoidectomy (Altemeier's procedure): a review of physiology, technique and outcome.

Perineal rectosigmoidectomy (Altemeier's procedure), as used for the surgical treatment of full-thickness rectal prolapse, has a long history. The physiological derangement in patients with rectal prolapse is complex, frequently showing impairment of the rectoanal inhibitory reflex, intermittent high-pressure rectal motor activity, disturbances in anorectal sampling and attendant pudendal neuropathy. There are currently few defined preoperative factors in patients presenting with rectal prolapse and fecal leakage which predict for the restoration of continence after surgery. This review describes our technique of Altemeier's procedure and analyzes the reported results of this operation, presenting those studies which assessed postoperative continence and prolapse recurrence in particular. The lack of prospective randomized data regarding this perineal approach makes clinical interpretation difficult at the present time.

Aged↗

Age related expression of Werner's syndrome protein in selected tissues and coexpression of transcription factors.

AIMS: Werner's syndrome (WS) is an uncommon autosomal recessive disease resulting from mutational inactivation of human WRN helicase, Werner's syndrome protein (WRNp). Patients with WS progressively develop a variety of aging characteristics after puberty. The aim of this study was to determine the distribution of WRNp and the expression of the transcription factors regulating WRN gene expression in a variety of human organs in an attempt to understand the WS phenotype. METHODS: Tissue specimens were obtained from 16 controls aged from 27 gestational weeks to 70 years of age and a 56 year old female patient with WS. The distribution of WRNp and the expression of the transcription factors regulating WRN gene expression-SP1, AP2, and retinoblastoma protein (Rb)- were studied in the various human organs by immunohistochemical and immunoblot analyses. RESULTS: In the healthy controls after puberty, high expression of WRNp was detected in seminiferous epithelial cells and Leydig cells in the testis, glandular acini in the pancreas, and the zona fasciculata and zona reticularis in the adrenal cortex. In addition, the SP1 and AP2 transcription factors, which regulate WRNp gene expression, appeared in an age dependent manner in those regions where WRNp was expressed. In controls after puberty, SP1 was expressed in the testis and adrenal gland, whereas AP2 was expressed in the pancreas. CONCLUSIONS: These findings suggest that the age specific onset of WS may be related to age dependent expression of WRNp in specific organs.

Adolescent↗

Comparison of emptying between gastric and colonic conduits following esophagectomy.

The emptying of gastric and colonic conduits following esophagectomy was evaluated. Ten consecutive patients who underwent esophagectomy for malignant diseases were divided into two groups as follows: Group I which consisted of 5 patients who underwent pyloroplasty and in whom the gastric greater curvature was used for reconstruction; and Group II which consisted of 5 patients in whom the colonic conduit was used because of previous gastrectomy. The conduits were placed in the retrosternal spaces in all the patients. The radiopaque markers swallowing test and digestive tract scintigraphy were performed to evaluate emptying two months after surgery. The radiopaque markers swallowing test demonstrated that marker rings quickly disappeared from the gastric conduits but remained in the colonic conduits for as long as three hours. Digestive tract scintigraphy demonstrated that there was no significant difference in the 60-minute clearance rate of 99mTc-DTPA from the conduits between the two groups. The results suggested that tiny food fragments remained in the haustral pockets of the colonic conduits, which may be a disadvantage of these conduits.

Aged↗

The dipole moment of membrane proteins: potassium channel protein and beta-subunit.

The mechanism of ion channel opening is one of the most fascinating problems in membrane biology. Based on phenomenological studies, early researchers suggested that the elementary process of ion channel opening may be the intramembrane charge movement or the orientation of dipolar proteins in the channel. In spite of the far reaching significance of these hypotheses, it has not been possible to formulate a comprehensive molecular theory for the mechanism of channel opening. This is because of the lack of the detailed knowledge on the structure of channel proteins. In recent years, however, the research on the structure of channel proteins made marked advances and, at present, we are beginning to have sufficient information on the structure of some of the channel proteins, e.g. potassium-channel protein and beta-subunits. With these new information, we are now ready to have another look at the old hypothesis, in particular, the dipole moment of channel proteins being the voltage sensor for the opening and closing of ion channels. In this paper, the dipole moments of potassium channel protein and beta-subunit, are calculated using X-ray diffraction data. A large dipole moment was found for beta-subunits while the dipole moment of K-channel protein was found to be considerably smaller than that of beta-subunits. These calculations were conducted as a preliminary study of the comprehensive research on the dipolar structure of channel proteins in excitable membranes, above all, sodium channel proteins.

Animals↗

Cardioprotective effect afforded by transient exposure to phosphodiesterase III inhibitors: the role of protein kinase A and p38 mitogen-activated protein kinase.

BACKGROUND: Phosphodiesterase III inhibitors (PDEIII-Is) improve the hemodynamic status of heart failure via inotropic/vasodilatory effects attributable to the increase in intracellular cAMP level. Direct cardioprotection by PDEIII-Is and its underlying mechanisms, however, have not been identified. We tested the infarct size-limiting effect of PDEIII-Is and the roles of cAMP, protein kinase (PK) A, PKC, and mitogen-activated protein kinase (MAPK) families in open-chest dogs. Methods and Results-- Milrinone, olprinone (PDEIII-Is), or dibutyryl-cAMP (db-cAMP) was injected intravenously 30 minutes before 90-minute ischemia, followed by 6 hours of reperfusion. Olprinone was also examined with an intracoronary cotreatment with a PKA inhibitor (H89), a PKC inhibitor (GF109203X), an extracellular signal-regulated kinase kinase (MEK) inhibitor (PD98059), or a p38 MAPK inhibitor (SB203580) throughout the preischemic period. Either PDEIII-Is or db-cAMP caused substantial hemodynamic changes, which returned to control levels in 30 minutes. Collateral flow and percent risk area were identical for all groups. Both PDEIII-Is and db-cAMP increased myocardial p38 MAPK activity during the preischemic period, which was blocked by H89, but not by GF109203X. Both PDEIII-Is and db-cAMP reduced infarct size (19.1+/-4.1%, 17.5+/-3.3%, and 20.3+/-4.8%, respectively, versus 36.1+/-6.2% control, P<0.05 each). Furthermore, the effect of olprinone was blunted by either H89 (35.5+/-6.4%) or SB203580 (32.6+/-5.9%), but not by GF109203X or PD98059. H89, GF109203X, PD98059, or SB203580 alone did not influence infarct size. CONCLUSIONS: Pretreatment with PDEIII-Is has cardioprotective effects via cAMP-, PKA-, and p38 MAPK-dependent but PKC-independent mechanisms in canine hearts.

3',5'-Cyclic-AMP Phosphodiesterases↗

Respiratory modulation of muscle sympathetic nerve activity in patients with chronic heart failure.

BACKGROUND: Sympathoexcitation and respiratory instability are closely related to worsening of chronic heart failure. To elucidate the dynamic nature of respiratory modulation of sympathetic activity in patients with heart failure, we studied within-breath variation of muscle sympathetic nerve activity (MSNA) under various ventilatory volumes. METHODS AND RESULTS: MSNA, blood pressure, and respiratory flow were recorded in 23 patients with left ventricular ejection fraction </=45%. Within-breath suppression of MSNA (neural silence) was found in 11 patients (MSNA bursts: 71+/-10/100 heartbeats) but not in the remaining 12 patients (MSNA bursts: 88+/-8/100 heartbeats). Patients without neural silence had a smaller tidal volume (391+/-70 versus 267+/-75 mL/m(2), P<0.01) and a higher respiratory rate (15+/-2 versus 19+/-4 breaths/min, P<0.01) during spontaneous respiration than those with neural silence. The relationship between tidal volume and minimal amplitude of MSNA bursts in each breath was obtained during random-interval breathing and fitted by an exponential function. The curve of patients without neural silence was shifted to the right and upward, which suggests that a greater tidal volume was required to suppress MSNA (227+/-70 versus 437+/-195 mL/m(2), P<0.01). CONCLUSIONS: Sympathoexcitation in patients with chronic heart failure is closely related to both a decrease in resting tidal volume and an attenuated sympathoinhibitory effect of lung inflation reflex.

Aged↗

Developmental changes of synaptojanin expression in the human cerebrum and cerebellum.

Synaptojanin is a highly abundant polyphosphoinositide phosphatase in nerve terminals, and has been thought to play roles in clathrin-mediated synaptic vesicle endocytosis and signaling. In order to determine the broader role of synaptojanin in the central nervous system, we examined synaptojanin expression in the cerebrum and cerebellum from the fetal to the adult period by means of immunohistochemical and Western blot analyses. Immunohistochemistry consistently revealed the localization of synaptojanin in Cajal--Retzius cells, cortical plate neurons, subplate neurons, intermediate neurons, germinal matrix cells and the ventricular neuroepithelium of the fetal cerebrum. In the fetal cerebellum, synaptojanin immunoreactivity was localized in the external granular cell layer, Purkinje cell layer neuropil, cytoplasm of Purkinje cells and internal granular cells. The immunoreactivity in these structures was decreased around birth. After birth, the synaptojanin immunoreactivity of cortical neurons in the cerebrum, Purkinje cell layer neuropil, and internal granular cells and Purkinje cells in the cerebellum increased and reached a plateau after 11 years of age. These results were consistent with the intensity observed on Western blot analysis. These developmental changes of synaptojanin suggest a broader role in not only synaptic vesicle recycling, but also the regulation of neuronal migration and synaptogenesis in the fetal cerebrum and cerebellum.

Adult↗

Up-regulation of E2F-1 in Down's syndrome brain exhibiting neuropathological features of Alzheimer-type dementia.

We studied the expression of the apoptosis-related protein, E2F-1, in Down's syndrome (DS) brains. The immunoreactivity for E2F-1 was detected in the pyramidal neurons of the cerebral cortex from DS brains exhibiting the neuropathological features of dementia of Alzheimer type (DAT), in accordance with the amyloid beta protein (A beta) deposition in the neuron. Therefore, the implication is that A beta deposition may trigger E2F-1-mediated neuronal apoptosis in DS brains with DAT.

Adolescent↗

The structure and dipole moment of globular proteins in solution and crystalline states: use of NMR and X-ray databases for the numerical calculation of dipole moment.

The large dipole moment of globular proteins has been well known because of the detailed studies using dielectric relaxation and electro-optical methods. The search for the origin of these dipolemoments, however, must be based on the detailed knowledge on protein structure with atomic resolutions. At present, we have two sources of information on the structure of protein molecules: (1) x-ray databases obtained in crystalline state; (2) NMR databases obtained in solution state. While x-ray databases consist of only one model, NMR databases, because of the fluctuation of the protein folding in solution, consist of a number of models, thus enabling the computation of dipole moment repeated for all these models. The aim of this work, using these databases, is the detailed investigation on the interdependence between the structure and dipole moment of protein molecules. The dipole moment of protein molecules has roughly two components: one dipole moment is due to surface charges and the other, core dipole moment, is due to polar groups such as N--H and C==O bonds. The computation of surface charge dipole moment consists of two steps: (A) calculation of the pK shifts of charged groups for electrostatic interactions and (B) calculation of the dipole moment using the pK corrected for electrostatic shifts. The dipole moments of several proteins were computed using both NMR and x-ray databases. The dipole moments of these two sets of calculations are, with a few exceptions, in good agreement with one another and also with measured dipole moments.

Animals↗