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Biomedical subjects

A Yoshida

Publications and source records attributed to A Yoshida.

At least 235 records · Page 13Linked to original sources

Ondine's curse and Hirschsprung's disease: neurocristopathic syndrome.

We report a female newborn with Ondine's curse and Hirschsprung's disease--neurocristopathic syndrome. The female infant required endotracheal intubation and mechanical ventilation due to apnea which developed soon after birth. She had abdominal distension with bilious vomiting. A barium enema revealed a caliber change at the rectum and rectal biopsies showed no ganglion cells. Colostomy was performed at the age of 17 days. Hypoxemia with hypercapnia was noted during her sleep, and tracheostomy was performed at the age of 55 days. In addition, deafness and pupillary autonomic dysfunction were observed. The definitive surgery for Hirschsprung's disease was performed at the age of 4 months. She is now 2 years old with normal growth but needs ventilator support at home. In this case, we detected no mutation in the RET gene and EDNRB gene.

DNA Mutational Analysis↗

Tissue specific expression and chromosomal mapping of a human UDP-N-acetylglucosamine: alpha1,3-d-mannoside beta1, 4-N-acetylglucosaminyltransferase.

A human cDNA for UDP- N -acetylglucosamine:alpha1,3-d-mannoside beta1,4- N- acetylglucosaminyltransferase (GnT-IV) was isolated from a liver cDNA library using a probe based on a partial cDNA sequence of the bovine GnT-IV. The cDNA encoded a complete sequence of a type II membrane protein of 535 amino acids which is 96% identical to the bovine GnT-IV. Transient expression of the human cDNA in COS7 cells increased total cellular GnT-IV activity 25-fold, demonstrating that this cDNA encodes a functional human GnT-IV. Northern blot analysis of normal tissues indicated that at least five different sizes of mRNA (9.7, 7.6, 5.1, 3.8, and 2.4 kb) forGnT-IV are expressed in vivo. Furthermore, these mRNAs are expressed at different levels between tissues. Large amounts of mRNA were detected in tissues harboring T lineage cells. Also, the promyelocytic leukemia cell line HL-60 and the lymphoblastic leukemia cell line MOLT-4 revealed abundant mRNA. Lastly, the gene was mapped at the locus on human chromosome 2, band q12 by fluorescent in situ hybridization.

Amino Acid Sequence↗

Serum leucine aminopeptidase as an activity indicator in systemic lupus erythematosus: a study of 46 consecutive cases.

OBJECTIVE: To determine whether elevations in serum leucine aminopeptidase (LAP) levels reflected the underlying evolution of active disease in systemic lupus erythematosus (SLE). METHODS: We studied serum LAP levels, other laboratory indicators, and SLE Disease Activity Index (SLEDAI) scores, in 46 consecutive patients with SLE admitted to Tokyo Metropolitan Komagome Hospital. LAP levels in 46 patients with rheumatoid arthritis were also measured. RESULTS: Thirty-three SLE patients had elevated LAP levels. LAP levels correlated positively with levels of lactate dehydrogenase, aspartate aminotransferase, alanine aminotransferase and gamma-glutamyl transpeptidase, and negatively with the total serum haemolytic complement and leucocyte, neutrophil and lymphocyte counts, but showed no correlation with alkaline phosphatase, gamma-globulin, beta2-microglobulin or C-reactive protein levels, or platelet count. The SLEDAI score correlated positively with LAP levels. The LAP level in patients with rheumatoid arthritis was near normal. CONCLUSION: The serum LAP level may be a potential activity indicator for SLE.

Adult↗

Posterior shoulder dislocation associated with fracture of the humeral anatomic neck: treatment guidelines and long-term outcome.

OBJECTIVE: We describe here 10 cases of posterior shoulder dislocation associated with fracture of the humeral anatomic neck. METHODS: Patients were treated according to our uniform treatment guidelines, in which only the dislocated humeral head (closed, if possible) was reduced, without any concomitant repositioning or internal fixation for fractures. RESULTS: Reduction resulted in an acceptable repositioning of the fractured fragments in all but one case. Anatomic neck fractures were impacted by applying longitudinal pressure for stabilization. Although early physiotherapy was initiated, redisplacement of the bone fragments did not occur. Of nine patients who were followed for more than 2 years, complete recovery of function was achieved in all but two patients. The completely detached humeral head became avascular necrotic accompanied by subchondral collapse in one case, and in the other case the displaced lesser tuberosity caused a decreased range of movement. CONCLUSION: We recommend initially treating such patients by either open or closed reduction of the dislocated humeral head and impaction of the fracture, with neither repositioning nor internal fixation of any of the fractured fragments. A completely detached humeral head or bone fragments displaced more than 10 mm after reduction of the dislocated humeral head contraindicate the use of this method.

Adult↗

Comparison of transcranial Doppler investigation of aneurysmal vasospasm with digital subtraction angiographic and clinical findings.

OBJECTIVE: Transcranial Doppler (TCD) findings for evaluation of the severity of vasospasm (VSP) in patients with ruptured aneurysmal subarachnoid hemorrhage are controversial. To clarify these TCD findings, intra-arterial digital subtraction angiography was used to simultaneously investigate the angiographic features of cerebral vessels and the cerebral circulation time (CCT). METHODS: Fifty patients with ruptured aneurysms, for whom computed tomographic scans indicated Fisher Grade III subarachnoid hemorrhage, were investigated. Aneurysmal neck clipping was performed in the acute stage. The mean flow velocity (MFV) at the M1 segment was measured using TCD ultrasonography. Intra-arterial digital subtraction angiography was used to simultaneously investigate angiographic features and CCTs on Days 7 to 13. The CCT was defined as the time difference between the two peaks in optical density curves recorded at the carotid artery (C3-C4 portion) and the ascending vein, after contrast material injection. Angiographic VSP was categorized using a modification of the Fisher classification. RESULTS: Angiograms for 9, 25, and 16 patients showed no, slight to moderate, and severe VSP, respectively. The MFVs of the patients with no, slight to moderate, and severe VSP were 70, 115, and 116 cm/s, respectively. No significant difference among the three groups could be observed. The mean CCTs of the patients with no, slight to moderate, and severe VSP were 4.1, 4.6, and 6.5 seconds, respectively. The CCTs of the patients with severe VSP differed significantly from those of the patients with no or slight to moderate VSP. The patients with severe VSP were divided into two groups. One group included eight patients with severe VSP at proximal sites (the internal carotid artery to the M1 segment), and the other included eight patients with severe VSP extending to the M2 segment and more peripheral sites. The mean CCT of the former group (5.3 s) was significantly different from that of the latter (7.5 s), and the MFV of the former group (128 cm/s) was significantly higher than that of the latter (81 cm/s). The clinical outcomes for the latter patients were more serious than those for the former patients. CONCLUSION: This study suggests that the MFV at the M1 segment is inadequate for estimation of the severity of VSP extending to vessels more peripheral than the M1 segment. Furthermore, severe VSP extending to more peripheral sites can produce more serious ischemic insults, compared with that localized to basal vessels. Patients with negative TCD results and clinical features suggesting the development of VSP should undergo quantitative investigation of cerebral circulatory parameters, such as the CCT, using intra-arterial digital subtraction angiography.

Aneurysm, Ruptured↗

Posterior vitreous detachment induced by injection of plasmin and sulfur hexafluoride in the rabbit vitreous.

PURPOSE: To investigate whether an injection of plasmin and sulfur hexafluoride (SF6) can induce posterior vitreous detachment (PVD) without vitrectomy. METHODS: One eye each of 15 New Zealand white rabbits was assigned to one of three groups. Eyes in group 1 received a vitreous injection of 1 unit of human plasmin (0.1 mL reconstituted in balanced salt solution) and 0.5 mL of SF6; eyes in group 2 received a vitreous injection of plasmin alone; eyes in group 3 received a vitreous injection of SF6 alone. Seven days after injection, all animals were monitored electroretinographically and killed, and the eyes were enucleated. After fixation, scanning electron microscopy was performed. RESULTS: In group 1 eyes, the retinal surface was smooth except for the vitreous base, which showed complete separation of the vitreous cortex from the retina, indicating PVD. In group 2 and 3 eyes, sparse collagen fibers remained on the retinal surface. CONCLUSION: Vitreous injection of plasmin combined with SF6 can induce PVD without vitrectomy.

Animals↗

Sudden death with malignant hemangioendothelioma originating in the pericardium--a case report.

The authors report a rare case of a malignant hemangioendothelioma (MH) originating in the pericardium. In this case, a metastatic skin lesion was found first, and subsequently the existence of a primary cardiac lesion was confirmed. Generally, primary cardiac tumors grow slowly, and the prognosis of MH is relatively good. In this case, however, the patient died suddenly during the creation of a pericardial window for drainage. An autopsy showed that the MH originated from a pericardial lesion in the right atrium.

Death, Sudden↗

A vanadyl sulfate-bovine serum albumin complex stimulates the release of lipoprotein lipase activity from isolated rat fat pads through an increase in the cellular content of cAMP and myo-inositol 1,4,5-trisphosphate.

A vanadyl sulfate-bovine serum albumin complex (vanadyl-BSA) prolonged the stability of the V4+ oxidation state, although vanadyl alone can readily change the oxidation state from V4+ to V5+ under physiological conditions. Vanadyl-BSA stimulated the release of lipoprotein lipase (LPL) activity from isolated rat fat pads and increased the cellular LPL activity in a time-dependent manner. These effects were independent of protein synthesis. Propranolol, quin 2-AM, ruthenium red, and neomycin all inhibited LPL release more potently than the increase in activity. In contrast, potent inhibition of the increase effect was observed with genistein and wortmannin. Short-term incubation of the fat pads with vanadyl-BSA showed a transient increase in the cellular content of cAMP and myo-inositol 1,4,5-trisphosphate (IP3), which was inhibited by propranolol and neomycin, respectively. These results suggest that vanadyl-BSA stimulates the release of LPL activity through an increase in the cellular content of cAMP and IP3, leading to an increased intracellular Ca2+ concentration, and that it also increases cellular LPL activity via process(es) sensitive to genistein and wortmannin.

Adipose Tissue↗

Role of ornithine in the N-acetylglutamate turnover in the liver of rats.

We determined whether the synthesis and degradation of N-acetylglutamate would regulate urea synthesis when the ornithine status was manipulated. Experiments were done on two groups of rats, each being treated with ornithine or saline (control). The plasma concentration of urea and the liver concentration of N-acetylglutamate in rats given ornithine were each significantly higher than in the control rats. Compared with the control rats, the liver N-acetylglutamate degradation was significantly lower in those rats treated with ornithine. Treatment of the rats with ornithine did not affect N-acetylglutamate synthesis in the liver. An inverse correlation between the liver N-acetylglutamate degradation and liver concentration of N-acetylglutamate was found. These results suggest that the lower degradation of N-acetylglutamate in the ornithine treatment group would be likely to increase the hepatic concentration of this compound and stimulate urea synthesis.

Animals↗

Intraocular neovascularization.

An important character of the eye is transparency, so intraocular neovascularization, which is fragile and likely to result in hemorrhage, would cause a functional disorder of the eye and contribute to loss of vision associated with such diseases as retinopathy of prematurity, diabetic retinopathy, retinal vein occlusion, and age-related macular degeneration. Recently interest in the mechanisms of intraocular neovascularization has increased, and the mechanisms have been gradually elucidated using several in vitro and in vivo angiogenesis models. Blood vessels in the eye are composed of, and surrounded by, various types of cells that produce multiple factors. Neovascularization is regulated by complex interactions among these angiogenic factors, angiostatic factors, and adhesion molecules, and some of these angiogenesis-related molecules have also been suggested as new targets for novel therapeutic agents of intraocular neo-vascularization. This review focuses on in vivo representative angiogenesis models of the corneal pocket model and the model of oxygen-induced retinopathy, and discusses the role of some angiogenesis-related factors and adhesion molecules in intraocular neovascularization.

Animals↗

A three-month repeated oral administration study of a low viscosity grade of hydroxypropyl methylcellulose in rats.

The toxicity of the lowest viscosity grade of hydroxypropyl methylcellulose (HPMC) that is currently commercially available was investigated by means of a three-month repeated oral administration study in male and female Crj:CD (SD) IGS rats at doses of 505, 1,020 and 2,100 mg/kg/day. Body weights of males and females in the 2,100 mg/kg group were lower than those of the control group on and after day 28 of administration, but the differences were not statistically significant. The degree of suppression of body weight gain in males was higher than that in females. This tendency was similar to the results in other toxicity studies of HPMC that have been reported. Males in the 2,100 mg/kg group showed a tendency (not significant) for decreased food consumption and urine volume. Examinations of general signs, hematology, blood chemistry, ophthalmology, absolute and relative organ weights, autopsy and histopathology revealed only a few, apparently coincidental, statistically significant differences from the control, and no evidence of any dose-dependent changes was found. It was concluded that the lowest viscosity grade of HPMC showed extremely low toxicity under the conditions of this study, as has been found for higher viscosity grades.

Administration, Oral↗

[Levofloxacin-induced neurological adverse effects such as convulsion, involuntary movement (tremor, myoclonus and chorea like), visual hallucination in two elderly patients].

Levofloxacin-induced-neurological adverse events such as convulsion, involuntary movement (tremor, myoclonus and chorea-like) and visual hallucination in two elderly patients are reported. A 67-year-old man with minor alcoholism and a past-history of gastrectomy and cholecystectomy was given 300 mg/day of oral levofloxacin and fulfenamic acid for an upper respiratory infection. On the 4th day, he reported gradual exacerbation of hand tremor which resembled chorea-like involuntary movement and gait disturbance. He also experienced visual hallucinations. On the 7th day, he suffered generalized convulsions and was admitted. Serum concentration of levofloxacin at this time (3 hours after last administration of a 100 mg tablet of levofloxacin) was 3.6 micrograms/ml. Cessation of the agents promoted complete recovery of these neurological adverse effects within a week. Another 85-year-old man with chronic bronchitis and slight renal impairment received long term administration of 200 mg/day of levofloxacin. On the 68th day of administration, gradual exacerbation of gait disturbance, dysarthria and chorea-like involuntary movement occurred. On the day of admission, 76 days after the start of administration, the serum level of levofloxacin was 2.55 micrograms/ml and that of spinal fluid was 1.12 micrograms/ml (3 hours after the last administration of a 100 mg tablet of levofloxacin). Cessation of the agents promoted complete recovery of these neurological adverse effects within the next two weeks. Both patients had no apparent neurological disorders except age-related brain atrophy. Age-related renal and brain impairment might have contributed to the neurological adverse effects of levofloxacin.

Aged↗

Effect of dietary protein quality on the brain protein synthesis rate in aged rats.

The purpose of this study was to determine whether the quality of dietary protein affects the rate of brain protein synthesis in aged rats. Experiments were conducted on three groups of aged rats (30 wk) given diets containing 20 g casein, 20 g gluten or 20 g gelatin/100 g for 10 d. The fractional rates of protein synthesis in the brain, liver and kidney declined with the decrease in quality of dietary protein. In the brain, liver and kidney, the RNA activity [g protein synthesized/(g RNA.d)] correlated significantly with the fractional rate of protein synthesis. The RNA concentration (mg RNA/g protein) was not related to the fractional rate of protein synthesis in any organ. The results suggest that the rate of protein synthesis in the brain declines with the decrease in quality of dietary protein consumed by aged rats, and that RNA activity is at least partly related to the fractional rate of brain protein synthesis.

Aging↗

Lipid alterations in the liver and serum of rats in histidine-excess and copper deficiency.

To obtain further information on lipid metabolism in the histidine-excess and copper-deficiency, rats were fed basal, histidine-excess (the addition of 50 g L-histidine/kg diet) or copper-deficient diets for 0, 7, 21 and 42 d ad libitum. Liver triacylglycerol accumulated and the serum triacylglycerol level decreased after feeding of the histidine-excess diet for 21 or 42 d, but not after feeding of the copper-deficient diet. Serum cholesterol level increased in rats fed the histidine-excess diet for 7, 21 and 42 d, but not in rats fed the copper-deficient diet. Copper content in the liver and serum significantly decreased in rats fed the histidine-excess diet. Copper content in the liver and serum was markedly decreased in rats fed the copper-deficient diet. Liver zinc content was constant, but the serum zinc level decreased in rats fed the histidine-excess diet. Feeding of the copper-deficient diet hardly affected zinc content in the liver and serum. Urinary copper and zinc increased in rats fed the histidine-excess diet, and decreased or showed a decreasing tendency in rats fed the copper-deficient diet. Overall results indicated that feeding the histidine-excess diet caused copper deficiency, whereas hypercholesterolemia was not shown in rats fed the copper-deficient diet although the livers of rats fed the copper-deficient diet contained less copper than those of rats fed the histidine-excess diet. Thus, the responses on liver triacylglycerol and serum cholesterol to copper deficiency induced by the feeding of a histidine-excess diet are different from those to copper deficiency induced by feeding of a copper-deficient diet.

Animals↗

[Iris vessel involvement in iris-nevus syndrome].

PURPOSE: To report a case of iris-nevus syndrome accompanied by disruption of the blood-aqueous barrier in the iris which was confirmed angiographically and histopathologically. CASE: The patient was a 39-year-old woman. She noticed blurred vision in the left eye which was diagnosed as left glaucoma. Specular microscopy revealed low endothelial cell density in the left cornea. The left iris showed atrophy with clusters of nodular iris nevus and distorted pupil. The left iridocorneal angle was closed with peripheral anterior synechia. FINDINGS: Indocyanine green iris angiography revealed more vessels on the surface of the left iris than on the right. In fluorescein iris angiography, the dye leaked from the iris vessels in areas where the iris showed advanced atrophy. The trabecular tissue obtained by trabeculectomy from the patient's left eye showed histopathologically a lining of corneal endothelial cells on the surface of the iris. The density of the vessels was high in the iris stroma. Some cells covering the vessel wall showed degeneration with opening of the zonula occludens. Schlemm's canal had narrowed lumina, and the intertrabecular spaces were closed. CONCLUSION: Disruption of the blood-aqueous barrier may occur in iris-nevus syndrome.

Adult↗

Successful salvage treatment with irinotecan (CPT-11) of recurrent malignant lymphoma in an aged patient; and CPT-11 pharmacokinetics.

A 72-year-old patient with relapsed non-Hodgkin's lymphoma (diffuse large B-cell type) in the tongue was treated with irinotecan (CPT-11) as the 4th salvage therapy. A two-thirds reduced dose of 40 mg/m2 of CPT-11 was administered, as were granulocyte-colony stimulating factor and antidiarrheal agents. Complete remission was achieved. Although grade 3 leukopenia and grade 1 diarrhea were observed, these adverse reactions did not interrupt the treatment schedule and CPT-11 was administered without interruption for a total of 12 weeks. Despite the dose reduction, the area under the concentration-time curve of SN-38, the active metabolite of CPT-11, was nearly equal to the values reported in phase I and II studies of CPT-11. The patient's ratio of SN-38 to the SN-38 glucuronide (SN-38G) was low, suggesting a low risk of diarrhea. The optimal dose modification provided a sufficient amount of the active metabolite. Supportive therapy managed therapy-related toxicities and resulted in a stable treatment schedule. This is a rare case of a patient successfully treated with CPT-11 after a 4th relapse, in which the agent was administered at the total dose of 960 mg/m2, despite the patient's advanced age.

Aged↗