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A Ishida

Publications and source records attributed to A Ishida.

At least 73 records · Page 4Linked to original sources
PubMed2000

A new methodology for the measurement of the Wiberg angle in infants under 3 months.

This article describes the measurement of the Wiberg center edge angle in infants under 3 months using sonographic images of their hips. In the literature review, there was no reference of the application of this angle in this particular age group. Thus, a methodology has been developed based upon the fact that, at this age, the acetabular roof constitutes a large portion of hyaline cartilage. In this way, it was concluded that it was not possible to apply the original Wiberg method since the center of the femoral head can be only estimated and not accurately determined in plain radiography. For this present study, 400 hips of 200 infants were analyzed. All these hips were classified as type 1a or 1b, according to Graf. The sonographic images were transferred to a Pentium computer through a video Spigot interface. The images were analyzed by software specially developed for this purpose. Since ultrasonography allows the exact recognition of the anatomical elements of the hip joint in young children, software provided the acetabular cartilaginous roof angle that corresponds to the center edge angle in adults. The authors believe that this method will be helpful in the early detection of morphological alterations in the hip joint.

Cadaver↗
PubMed2000

Racial and geographic differences of Wiberg's angle from 400 ultrasonographic normal hips in Italian and Brazilian infants younger than 3 months old.

The Wiberg center edge angle (CEA) of 400 hip sonographies among 200 infants, 100 Italians and 100 Brazilians, aged from 15 days to 90 days, whose hip joints were considered normal, from the ultrasonographic point of view (1a and 1b) according to Graf's classification were measured. For the CEA measurements in the studied material, the authors used their own methodology developed for this purpose, which is based on basic geometric concepts and applied by one graphic computer program. In the studied material, the statistical analysis of the results obtained in the measurement of the CEA showed a better conformation of the acetabular roof complex in the Brazilian infants compared with the Italian.

Brazil↗
PubMed2000

A clinically oriented video-based system for quantification of eyelid movements.

A field-worthy system was developed to quantify the eyelid movements in clinical sites. The system consists of a home-use charge-coupled device video camera, a processing unit, and a personal computer. A white marker of 4-mm diameter and 30-mg weight is attached to the lower margin of the upper eyelid. The processing unit automatically detects the vertical displacement of the upper edge of the marker. One marker is attached to each eye so that the movements of the both eyelids are measured with one camera simultaneously. The measurement error of the system was evaluated in experiments on eight healthy subjects and eight patients with eyelid paralysis. The mean of the absolute error of peak amplitudes occurring in 2 min was 0.81 mm, with the worst error being +1.7 mm. The reproducibility of the mean peak amplitude measured on five consecutive days was within 1 mm. The mean peak amplitudes of both eyes were measured preoperatively and postoperatively for approximately three months for three patients who were operated on to remove vestibular schwannoma. The results demonstrated basic clinical utility of the system.

Adult↗
PubMed2000

15-Deoxy-Delta(12,14)-prostaglandin J(2) induces G(1) arrest and differentiation marker expression in vascular smooth muscle cells.

In search of substances useful for the treatment of atherosclerotic vascular diseases, we studied the effects of 15-deoxy-Delta(12, 14)-prostaglandin J(2) (15d-PGJ(2)), a natural ligand for peroxisome proliferator-activated receptor gamma, on the proliferation and differentiation of vascular smooth muscle cells (VSMCs). 15d-PGJ(2) but not WY14643, an agonist for peroxisome proliferator-activated receptor alpha, dose-dependently inhibited VSMC proliferation; the effect was maximal at 12 microM. This compound strongly suppressed the activities of cyclin-dependent kinases (Cdk) 4, 6, and 2, thereby preventing the phosphorylation of the retinoblastoma protein. These Cdks seemed to be inhibited through two mechanisms: the down-regulation of cyclin D1 and the up-regulation of Cdk inhibitor p21(Cip1/Waf1/Sdi1). 15d-PGJ(2) was found to inhibit the phosphatidylinositol 3-kinase/protein kinase B signaling pathway, which mediates cyclin D1 expression. Mitogenic stimulation of quiescent cells decreased the level of mRNA for the smooth muscle-specific myosin heavy-chain SM1, whereas this reduction was prevented by 15d-PGJ(2). A long-term treatment of exponentially growing VSMCs with 15d-PGJ(2) markedly elevated the mRNA level of SM1 and, moreover, induced SM2, another isoform expressed exclusively in mature VSMCs. 15d-PGJ(2) also increased the expression levels of calponin-h1 and smooth muscle alpha-actin. These results suggest that 15d-PGJ(2) induces G(1) arrest by two distinct mechanisms and promotes VSMC differentiation.

Antigens, Differentiation↗
PubMed2000

Surgical repair of acute left ventricular free wall rupture: report of a case.

We present a case of acute (blowout) left ventricular free wall rupture (LVFWR) that occurred on the third day after inferior myocardial infarction. Because electromechanical dissociation developed abruptly and pericardiocentesis was no effective, there was no time for establishing a cardiopulmonary bypass (CPB). Emergency thoracotomy and direct closure were successfully performed at the bed-side. We believe that acute type of LVFWR in which initial symptom is electromechanical dissociation without any preceding symptoms can be rescued by emergency thoracotomy and direct closure of the rupture with no aid of CPB provided that the rupture is a small tear located on the anterior, lateral, or even the inferior wall of the left ventricle, if hemodynamical stability is obtained.

Aged↗
PubMed2000

Memory rehabilitation of an amnesic patient following limbic encephalitis and a role of family members: a case report.

We describe problems in daily living that arose in a 46-year-old man with severe amnesia following limbic encephalitis. Amnesic symptoms changed from stage I (difficulty in memory retention) to stage II (loss of continuity of memory) and finally to stage III (paramnesia and confused sequence of events), significantly affecting his ability to function. Questionnaire response assessment, directly observed behavior, neuropsychological testing, and especially interviewing permitted qualitative assessment of clinical changes, promoted patient insight into the memory disturbance, and enhanced motivation to use a memory notebook. Additionally, the family gained a better understanding of the disorder, made appropriate environmental modifications, and provided other necessary assistance. Episodic memory improved, and the memory notebook served as an effective compensatory tool. However, disturbance in prospective memory did not improve, and was not compensated adequately by use of the notebook. Anxiety and significant impairment of everyday functioning resulted. Long-term supportive intervention at home was necessary. The patient's wife in particular needed to make environmental adjustments and aid him in use of the notebook.

Amnesia↗
PubMed1999

Striatal perfusion of indomethacin attenuates dopamine increase in immature rat brain exposed to anoxia: an in vivo microdialysis study.

Using in vivo microdialysis and HPLC, we examined the effects of indomethacin on extracellular dopamine (DA) in the striatum of immature rats submitted to anoxia. Rat pups in two indomethacin groups received intrastriatal perfusion of either 1 mM or 5 mM indomethacin throughout the experiment. The DA level reached 1185+/-400% of the basal level during anoxia; in contrast, the peak levels of DA were only 307+/-63%, 153+/-35% in indomethacin groups (p<0.05). We consider that this suppression would be one of the mechanisms of the protective effect of indomethacin on hypoxic ischemic encephalopathy.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1999

Phosphorylation and activation of Ca2+/calmodulin-dependent protein kinase phosphatase by Ca2+/calmodulin-dependent protein kinase II.

Ca2+/calmodulin-dependent protein kinase phosphatase (CaMKPase) is a protein phosphatase which dephosphorylates autophosphorylated Ca2+/calmodulin-dependent protein kinase II (CaMKII) and deactivates the enzyme (Ishida, A., Kameshita, I. and Fujisawa, H. (1998) J. Biol. Chem. 273, 1904-1910). In this study, a phosphorylation-dephosphorylation relationship between CaMKII and CaMKPase was examined. CaMKPase was not significantly phosphorylated by CaMKII under the standard phosphorylation conditions but was phosphorylated in the presence of poly-L-lysine, which is a potent activator of CaMKPase. The maximal extent of the phosphorylation was about 1 mol of phosphate per mol of the enzyme and the phosphorylation resulted in an about 2-fold increase in the enzyme activity. Thus, the activity of CaMKPase appears to be regulated through phosphorylation by its target enzyme, CaMKII.

Animals↗
PubMed1999

Stable gene expression with VSV-G pseudotyped-retrovirus vector in the rat liver.

BACKGROUND: Pseudotyped-retrovirus-mediated gene transfer to the regenerating rat liver was investigated in vivo and the findings were compared with those for retrovirus-mediated gene transfer. MATERIALS AND METHODS: Four weeks prior to gene transfer, the spleen was transpositioned to the left subcutaneous position to develop a port-splenic shunt. Twenty-four hours after a partial hepatectomy (68%) was performed, the liver was perfused in situ and kept in contact with either a pseudotyped-retrovirus vector encoding LacZ (7 x 10(7) cfu/ml, Group 1) or a retrovirus vector encoding LacZ (1 x 10(4) cfu/ml, Group 2) for 30 min. The animals were sacrificed at various points after gene transfer, and X-gal staining, reversed polymerase chain reaction (RT-PCR), and ONPG assay were performed to detect the transferred LacZ cDNA. RESULTS: In X-gal staining, the transferred LacZ cDNA started to show a strong beta-galactosidase activity in 30 to 50% of the hepatocytes at 3 days after gene transfer. Positive staining continued to be recognized until 28 days with a slight decrease in its intensity thereafter. On the other hand, Group 2 animals showed weak staining, which was observed in about 10 to 15% of the hepatocytes from 3 days after gene transfer and then decreased thereafter. In RT-PCR, positive mRNA of LacZ was detected constitutively until 28 days after gene transfer in Group 1, whereas two-thirds of the samples showed a negative band in Groups 2 at 3 days after gene transfer. CONCLUSION: In conclusion, the pseudotyped-retrovirus vector was useful in establishing a stable and strong expression of the in vivo gene transfer, while targeting the regenerating liver.

Animals↗
PubMed1999

Synthesis of caged peptides using caged lysine: application to the synthesis of caged AIP, a highly specific inhibitor of calmodulin-dependent protein kinase II.

N(alpha)-Fmoc-N(epsilon)-(2-nitrobenzyloxycarbonyl)-lysine has been prepared and used in the solid-phase synthesis of caged peptides. The synthesized caged AIP (cagedKcagedKALRRQEAVDAL) showed characteristics required for caged peptides including a significantly reduced inhibitory activity to calmodulin-dependent protein kinase II and instantaneous recovery of the activity with photo-irradiation.

Calcium-Calmodulin-Dependent Protein Kinase Type 2↗
PubMed1999

Accelerated healing of Dacron grafts seeded by preclotting with autologous bone marrow blood.

> Studies have suggested that bone marrow-derived cells in the circulation may have the capacity and potential to endothelialize and heal vascular graft surfaces. We have investigated whether accelerated endothelialization could be achieved for Dacron grafts seeded by preclotting with bone marrow blood (BMB). Five 8 mm x 6 cm Dacron grafts seeded and preclotted with BMB and four controls preclotted with peripheral blood were implanted in the descending thoracic aorta (DTA) of mongrel dogs for 2 and 4 weeks. Two additional BMB DTA grafts were studied for 3 months. Five pairs of BMB and control grafts (4 mm x 6 cm) were bilaterally implanted into the carotids of dogs for 1 week and five pairs for 4 weeks. All grafts remained patent. BMB seeding/preclotting was a simple, effective method to accelerate early graft endothelialization without increasing thrombogenicity. Further studies are needed before clinical application can be recommended.

Animals↗
PubMed1999

Angiotensin II receptor blockade limits kidney injury in two-kidney, one-clip Goldblatt hypertensive rats with special reference to phenotypic changes.

Recent evidence indicates that tubulointerstitial injury plays an important role in hypertensive kidney injury and that phenotypic changes contribute to this pathology. Moreover, angiotensin II is known to be actively involved in the pathogenesis of progressive kidney injury induced by hypertension. The present study was undertaken to see the effect of a newly developed angiotensin II type I receptor (AT1 receptor) antagonist on hypertension-induced kidney injury and to determine the contribution of phenotypic changes to morphologic alterations. Two-kidney, one-clip (2K1C), Goldblatt hypertensive rats (n = 27) were made by clipping the left renal artery. These animals were orally administered 57G709 (a selective non-peptide AT1 receptor antagonist)(10 mg/kg/day), captopril (20 mg/kg/day), or vehicle alone for 23 days beginning 4 weeks after clipping. In the non-clipped kidney of vehicle-treated 2K1 C rats, marked tubulointerstitial injury as well as glomerular sclerosis and/or hyalinosis was found in association with phenotypic changes, as shown by the neoexpression of vimentin in periglomeruli, perivascular walls, distal tubuli, and injured interstitium. Renin expression was markedly suppressed in the non-clipped kidneys of vehicle-treated 2K1C rats as compared with renin expression in normotensive control kidneys of sham-operated rats. Both 57G709 and captopril markedly ameliorated hypertensive kidney injury as reflected by the glomerular sclerosing index and by the tubulointerstitial index as determined by the point-counting method, and this improvement was accompanied by a significant decrease in blood pressure, urinary protein excretion, kidney/body weight ratio, and heart/body weight ratio. In addition, the vimentin neoexpression mentioned above was also suppressed with an inhibition of angiotensin II. These results suggest that in 2K1C Goldblatt hypertensive kidney injury, the AT1 receptor antagonist 57G709 exerts a potent renal protective effect associated with the inhibition of phenotypic changes.

Angiotensin Receptor Antagonists↗
PubMed1999

Immunohistochemical study on transforming growth factor-beta1 expression in liver fibrosis of Down's syndrome with transient abnormal myelopoiesis.

A case of Down's syndrome associated with liver fibrosis is reported. The fibrosis was diffusely distributed along sinusoids, and an excess of megakaryocytes was also found in the liver. To determine the mechanism of liver fibrosis in Down's syndrome, we immunohistochemically stained the liver with markers of myofibroblast-like cells, antialpha smooth muscle actin antibodies and antidesmin antibodies. The myofibroblast-like cells were found along sinusoids, suggesting that liver fibrosis in Down's syndrome is caused by the myofibroblast-like cells derived from Ito cells/lipocytes. The expression of transforming growth factor (TGF)-betal, which is an important mediator of the activation of lipocytes, was immunohistochemically examined. The accumulation of TGF-betal was observed in cells in the sinusoidal spaces, which involve the intracellular expression of megakaryocytes. Together, these findings suggest that megakaryocyte-derived TGF-betal is one of the likely candidates in the lipocyte activation of liver fibrogenesis in Down's syndrome.

Actins↗
PubMed1999

Genetic tracing of arterial graft flow surface endothelialization in allogeneic marrow transplanted dogs.

In order to trace genetically the source of fallout endothelialization on arterial grafts, six beagle dogs with successful autologous bone marrow transplantation received composite tandem aortic grafts with an isolated, totally impervious Dacron graft and a porous Dacron graft for 12 weeks. For impervious segments, five of 12 fresh tissue samples were Factor VIII/von Willebrand factor + (FVIII/vWF) and seven had faint or negative signals; three of the FVIII/vWF + samples had alpha-actin + smooth muscle cells. Polymerase chain reaction (PCR) study showed eight had a pure donor DNA genotype and four had donor/host mixed, with the donor predominant. Of 12 AgNO3-stained samples, 11 showed pure donor type and one had donor/host mixed, with the donor predominant. For porous segments, all 12 fresh samples had positive flow surface FVIII/vWF and alpha-actin cells. PCR showed all these samples and all 12 AgNO3-stained samples had donor/host mixed type, but the host pattern was predominant. Porous graft healing appears to involve both cellular fallout and tissue ingrowth, and bone-marrow-derived cells may be a source for fallout.

Animals↗
PubMed1999

Anoxic and hypoxic immature rat model for measurement of monoamine using in vivo microdialysis.

The immature brain is considered relatively resistant to anoxia and ischemia. Although hypoxia without ischemia has not been considered to produce brain damage in immature rats as well as in adult rats (S. Levine, Anoxic-ischemic encephalopathy in rats, Am. J. Pathol., 36 (1960) 1-17 [8]; D.E. Levy, J.B. Brieley, D.G. Silverman, F. Plum, Brief hypoxia-ischemia initially damages cerebral neurons, Arch. Neurol., 32 (1975) 450-456 [9]; J.E. Rice, R.C. Vannucci, J.B., Brieriey, The influence of immaturity on hypoxic-ischemic brain damage in rat, Ann. Neurol., 9 (1981) 131-141 [14]), hypoxia in postnatal period is possible to cause a functional brain damage (T. Hender, P. Lundborg, Regional changes in monoamine synthesis in the developing rat brain during hypoxia, Acta. Physiol. Scand., 106 (1979) 139-143 [3]; W. Ihle, J. Gross, R. Moller, Effect on chronic postnatal hypoxia on dopamine uptake by synaptosomes from striatum of adult rats, Biomed. Biochem. Acta., 44 (1985) 433-437 [7]; A. Lun, J. Gross, M. Beyer, H.D. Fischer, C. Wustmann, J. Schmidt, K. Hecht, The vulnerable period of perinatal hypoxia with regard to dopamine release and behavior in adult rats, Biomed. Biochem. Acta., 45 (1986) 619-627 [10]). Using microdialysis, we studied the anoxic or hypoxic effect on catecholamine metabolism in immature rat brain by measuring extracellular concentrations of norepinephrine (NE), dopamine (DA), and its metabolites and also 5-hydroxyindole-3-acetic acid (5-HIAA), the serotonin metabolite. DA is a well established excitatory neurotransmitter (R.C. Vannucci, Experimental biology of cerebral hypoxia-ischemia: relation to perinatal brain damage, Pediatr. Res., 27 (1990) 317-326 [16]), and in the previous report using hypoxic 7-day-old rat pups increase of DA was not detected without additional stimulations (K. Gordon, D. Johnston, M.V. Robinson, T.E. Statman, J.B. Becker, F. Silverstein, Transient hypoxia alters striatal catecholamine metabolism in immature brain: An in vivo microdialysis study, J. Neurochem., 54 (1990) 605-611 [2]). Whereas recently in newborn piglets, hypoxic hypoxia produced increase of extracellular DA (C.-C. Huang, N.S. Lajevardi, O. Tammela, A. Pastuszko, Relationship of extracellular dopamine in striatum of newborn piglets to cortical oxygen pressure, Neurochem. Res., 19 (1994) 649-655 [6]; Olano, M., Song, D., Murphy, S., Wilson, D. F. and Pastuszko, A., Relationships of dopamine, cortical oxygen pressure, and hydroxyl radicals in brain of newborn piglets during hypoxia and posthypoxic recovery, J. Neurochem., 65 (1995) 1205-1212 [13]). We consider that hypoxic ischemic brain damage of human newborns that we can treat is a damage, which does not show overt neuropathological changes. We therefore tried to show that transient anoxia and hypoxia caused biochemical alteration if the exposure did not produce marked morphological changes. This rodent model is adequate to study perinatal asphyxia and alteration of monoamine level could be useful for evaluation of brain damage, even if it is not detected histologically.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1999

3-Methylglutaconic aciduria type I: clinical heterogeneity as a neurometabolic disease.

3-Methylglutaconic (3-MGC) aciduria with 3-methylglutaconyl-CoA hydratase deficiency (3-MGC aciduria type I) is a rare inherited metabolic disease of L-leucine catabolism. We describe a 9-month-old Japanese boy with this disorder who showed progressive neurological impairments presented as quadriplegia, athetoid movements and severe psychomotor retardation from 4 months of age. This finding indicates the existence of clinical heterogeneity in 3-MGC aciduria type I, suggesting it may present as a neurometabolic disease.

Acidosis, Renal Tubular↗
PubMed1999

Prospective evaluation for upper gastrointestinal tract acute graft-versus-host disease after hematopoietic stem cell transplantation.

The incidence and clinical significance of upper gastrointestinal tract acute graft-versus-host disease (upper GI GVHD) were prospectively evaluated in 44 Japanese patients who underwent allogeneic (n = 26) or autologous (n = 18) stem cell transplantation. Endoscopic examination was routinely performed between days 20 and 50 post-transplant and when symptoms of upper GI and/or acute GVHD of other organs were present. The results were compared with the historical records of 49 allograft and 20 autograft recipients. The diagnosis of upper GI GVHD was confirmed by histologic findings of GVHD and persistent upper GI tract symptoms. The incidence of upper GI GVHD was 46% in the prospective allograft group, higher than in the retrospective group. Upper GI GVHD was not diagnosed in any autograft patients. Twelve of 19 patients with upper GI GVHD had skin GVHD, and two of the 12 had concurrent lower GI GVHD. Upper GI GVHD was successfully treated with steroids and did not progress to symptomatic lower GI GVHD. In addition, upper GI GVHD completely resolved without specific alteration in immunosuppressant therapy in six patients. No risk factors for upper GI GVHD could be identified. The presence of upper GI GVHD did not significantly affect early death rate, incidence of chronic GVHD, and overall survival. In conclusion, by the prospective evaluation of the upper GI tract by endoscopy we could accurately diagnose upper GI GVHD in half our allogeneic recipients. However, upper GI GVHD was successfully controlled with or without additional steroids in all cases and had little impact on transplant outcome.

Adolescent↗