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Biomedical subjects

M Uno

Publications and source records attributed to M Uno.

At least 109 records · Page 6Linked to original sources
PubMed1993

[A case of encephalopathy accompanying Mycoplasma pneumoniae pneumonia in an adult].

We experienced a 39-year-old male who developed neurological complication during a course of Mycoplasma pneumoniae pneumonia. The diagnosis of M. pneumoniae pneumonia was made on the basis of elevation of specific antibody (CF) titer in convalescent serum. Electroencephalogram showed diffuse damage in the brain, but no other abnormalities were not found on brain CT-scan and MRI. In the cerebrospinal fluid, the number of cells did not increase and the M. pneumoniae CF titer was not elevated. From these results, we concluded that encephalopathy in this patient was raised by an allergic reaction of the brain tissue to M. pneumoniae antigen. Until now, encephalitis or meningoencephalitis accompanied with M. pneumoniae infection has been reported by many investigators, but reports on encephalopathy due to M. pneumoniae are few. Therefore, we reported herein a case of encephalopathy following Mycoplasma pneumoniae pneumonia with several references.

Adult↗
PubMed1993

[Renin-secreting renal tumor. A case report].

We reported a case of juxtaglomerular cell tumor, which excessively produced renin, resulting in secondary hypertension. A 25-year-old woman complained of headache and nausea. Hypertension and elevation of plasma renin activity were found by physical and laboratory examination. US and CT showed a space occupying lesion at upper pole of the right kidney. Angiography showed a hypovascular area at the corresponding area of the right kidney. Renin-secreting renal tumor of the right kidney was diagnosed and right nephrectomy was performed. Postoperatively, blood pressure and plasma renin activity became normalized and symptoms ameliorated. The juxtaglomerular cell tumor was pathologically confirmed and localization renin in the tumor cells was shown by immunohistochemical study. Forty one cases of juxtaglomerular cell tumor have been reported, since Robertson reported the first case. We discussed the clinical and pathological characteristics of the disease in this report.

Adult↗
PubMed1993

A case of xanthogranulomatous pyelonephritis in a child.

We report an additional case of histopathologically confirmed xanthogranulomatous pyelonephritis in a 9-year-old boy. He was admitted to hospital with a two-day history of sustained fever. Physical examination revealed tenderness in the right upper quadrant of the abdomen. Results of a complete blood count and serum biochemical investigations showed slight anemia and positive C reactive protein. Culture of urine failed to grow any bacteria. Excretory urography revealed deformity of the right renal calyces. Computed tomography showed a focal area of low density in the right kidney. Nephrectomy was carried out as fever had been sustained despite intensive treatment with antibiotics. Sectioning revealed that the renal parenchyma had been replaced by a butter yellow nodule, which was histopathologically confirmed as xanthogranulomatous pyelonephritis. This is the nineteenth reported case in children in Japan to our knowledge.

Adolescent↗
PubMed1992

The Saccharomyces cerevisiae NPS1 gene, a novel CDC gene which encodes a 160 kDa nuclear protein involved in G2 phase control.

We have cloned the gene NPS1 (nuclear protein of Saccharomyces) which encodes a nuclear protein of mol. wt 156 735 Daltons (1359 amino acids) essential for cell growth. NPS1 contains a 2 kb sequence that is highly homologous to the S. cerevisiae SNF2/GAM1 gene known as a transcriptional regulator for multiple genes. However, the NPS1 gene was found to have a distinct function from SNF2/GAM1. The growth of the cells carrying a nps1 delta :: URA3 deletion allele and galactose-inducible NPS1 on a plasmid was arrested under NPS1-repressed conditions with a cell cycle arrest phenotype, being arrested at the large-bud stage with a single nucleus that had a DNA content of G2/M phase. When the arrested cells were further incubated under NPS1-repressed conditions, re-replication of DNA occurred in some of the arrested cells without passage through mitosis. In the predicted amino acid sequence of NPS1, sequences homologous to the catalytic domain of protein kinases were found. We constructed a mutation which results in the substitution of a highly conserved lysine residue (Lys792) in the presumed ATP-binding site of this kinase-like domain with a glutamic acid codon. The mutant gene failed to rescue the growth defect caused by NPS1 disruption, suggesting that Lys792 is essential for the function of NPS1.

Amino Acid Sequence↗
PubMed1992

Complete prevention of diabetes in transgenic NOD mice expressing I-E molecules.

Previously, we showed that transgenic expression of the MHC (major histocompatibility complex) class II I-E molecules prevented insulitis in non-obese diabetic (NOD) mice at the age of 19 weeks. To rule out the possibility that the I-E expression merely delays the onset of insulitis, we have further characterized the expression and function of the I-E molecule expressed in transgenic NOD mice and confirmed our previous observations. Northern blot analysis showed that the transgenic E alpha d gene was expressed in a pattern similar to the endogenous E alpha d gene in BALB/c mice. The newly expressed I-E molecules were recognized as an alloantigen by the T lymphocytes of normal NOD mice as shown by mixed lymphocyte reaction (MLR). Transgenic NOD mice were resistant to the treatment by cyclophosphamide, which effectively induces diabetes in normal NOD mice, and did not develop diabetes up to 40 weeks of age. On the basis of these findings, we discuss the role of I-E molecules in the prevention of diabetes in NOD mice.

Animals↗
PubMed1992

Transgenic mouse as a tool for the study of autoimmune disease: insulin-dependent diabetes mellitus.

Transgenic mice have been used for analyses of cis-acting elements which are involved in the tissue-specific and developmental-specific expression, for analyses of physiological function of genes, or for the production of a human disease model. This approach is especially successful in the fields of immunology and oncology. Several years ago it was shown that the major histocompatibility complex (MHC) class II gene is identical to the immune response gene by demonstrating that the immune response can be restored by the new expression of class II molecules on immunocompetent cells. Recent evidence suggests that the class II molecule is involved in the generation of autoimmune disease, such as insulin-dependent diabetes mellitus (IDDM). The NOD (non-obese diabetic) mouse is shown to be a mouse model for human IDDM. Concerning the class II genes, the NOD mouse has two characteristic features, the lack of I-E and the presence of unique I-A. It is discussed how the role of class II molecules in the development of IDDM in the NOD mouse can be analyzed. In addition, the transgenic technique can be applied to the study of differentiation and oncogenesis of lymphoid cells. Factors or molecules that affect these processes will also be discussed.

Animals↗
PubMed1991

Congenital antithrombin III deficiency (AT-III Kyoto): identification of a point mutation altering arginine-406 to methionine behind the reactive site.

A Japanese patient with congenital antithrombin III (AT-III) deficiency, named AT-III Kyoto, is associated with reduced levels (60% of normal) of AT-III antigen, progressive activity and heparin cofactor activity. The antithrombin III gene of this patient was investigated by polymerase chain reaction (PCR) method followed by direct DNA sequencing analysis, which revealed a G to T transitional mutation resulting in the conversion of arginine-406 to methionine in exon 6. Arginine-406 is located at the 12th amino acid residue from the reactive site on the C-terminal side of AT-III in a core region of the molecule which has been highly conserved during evolution of serine protease inhibitor (serpin) family. It is concluded that AT-III Kyoto is a newly described mutation which is similar to AT-III Utah and lends support to the idea that the conserved region near the reactive site is important in maintaining biological function of the AT-III molecule.

Adult↗
PubMed1991

Long-term potentiation of the amygdalo-striatal synaptic transmission in the course of development of amygdaloid kindling in cats.

Limbic projection from the amygdala to the basal forebrain and the neostriatum was studied physiologically during development of amygdaloid kindling in cats. Stimulation of the basolateral amygdaloid nucleus (BL) produced the negative field potential monosynaptically in the nucleus accumbens (Acb), while in the caudate nucleus (Cd) it produced a slight negative deflection with a longer latency. The latter is produced disynaptically as it showed marked facilitation in its amplitude when two stimuli were applied at short intervals. After a single period of tetanic stimulation of the BL with a 2-s train of 50-Hz pulses, there was a long-term potentiation (LTP) of both Acb and Cd responses in amplitude to test pulses to the same electrode. These responses increased up to 140% of the pre-tetanus control for 1 h following tetanic stimulation and declined gradually back to the baseline thereafter. However, a slight or moderate increase in the response was observed even 24 h later. Therefore, trains of stimuli presented once per day had a cumulative effect on the negative field potentials evoked in the Acb and the Cd in the early stage of kindling development. In particular, the disynaptic response in the Cd increased markedly to over 10 times as the prekindled control. These findings suggest that LTP in amygdalo-striatal synaptic transmission following tetanic stimulation represents an example of plastic changes in a neuronal chain within the neostriatum, which would underlie the pathophysiological mechanism for developing motor seizures of amygdaloid kindling.

Amygdala↗
PubMed1991

[Aspects of psychologic disorders in Japanese students].

The present study discusses the reasons which moved 88 students during one year from April 1987 till March 1988 to make their first spontaneous visit to the Department of Psychiatry in the Health Service Center of Tokyo University. The number of patients amounted to 0.60% of the total student enrollment during the period mentioned. The sufferings which motivated their visits could be phenomenally divided into two sectors. The first sector was related to the individual problems of the students and could be sub-divided into somatic and psychic spheres. To the other sector belonged the social or intersubjective relationships with either a general or a special point of reference. The majority of cases (ca. 70% of all patients) fell into the individual sector. Some reasons for this distribution are discussed. Among the patients there was a large percentage of freshmen. This seems to be due to the internal and external milieu changes caused by entering the university life. The ICD-9 diagnosis showed that ca. 80% of the patients exhibited Neurotic disorder and Adjustment reactions. This raises the question of applicability of ICD-9 to minor ailments, frequent among the clients of a Student Health Center. The dominant source of troubles motivating students to seek psychiatric help appeared to be problems connected with the academic life, like entrance into the university, examinations, choice of field of study, and graduation.

Adjustment Disorders↗
PubMed1991

(BALB/c x C57BL/6)F1 mice are tolerant to undetectable mixed haplotype A beta dA alpha b and mixed isotype A beta dE alpha d self class II molecules.

The existence of mixed haplotype A beta dA alpha b and mixed isotype A beta dE alpha d molecules was demonstrated in A beta d gene introduced C57BL/6 (B6) transgenic and in A beta dE alpha d double gene introduced B6 transgenic mice, respectively. Using alloreactive and antigen reactive T-cell clones, these mixed class II molecules were shown to function as mixed lymphocyte culture reaction (MLR) stimulating determinants and restriction elements for antigen recognition by T cells. The amounts of expression of these mixed class II molecules were sufficient for the stimulation of alloreactive T cells in primary MLR culture. (BALB/c x B6)F1 (CBF1) mice were shown not to express functional mixed haplotype and mixed isotype class II molecules using alloreactive and antigen reactive T-cell clones. Interestingly, however, CBF1 mice did not respond to such mixed haplotype and mixed isotype class II molecules. These results show that CBF1 mice do not respond to undetectably-expressed class II molecule and suggest that they are tolerant to undetectable self class II molecules. The possible interpretations for this are discussed.

Animals↗
PubMed1991

Effect of cyclic GMP and sulfhydryl on prostacyclin production by human vascular endothelial cells.

The relationship between sulfhydryls and cGMP has been observed in several biological processes. Captopril is a sulfhydryl-containing angiotensin converting enzyme (ACE) inhibitor, that decreases PGI2 production in cultured human vascular endothelial cells. Enalapril does not appear to have this property. The role of cyclic GMP (cGMP) and sulfhydryls in the regulatory mechanisms in captopril-induced PGI2 production and Ca++ kinetics was investigated. Bradykinin and Ca ionophore A23187 enhanced PGI2 production, and increased the cytosolic free Ca++ concentration ([Ca++]i). It was observed that 8-bromo cGMP increased intracellular cGMP concentration ([Ca++]i), and decreased PGI2 production without changing [Ca++]i. Sulfhydryl containing compounds such as captopril, N-acetylcysteine and glutathione decreased PGI2 production via increased [cGMP]i. Enalapril, an ACE inhibitor without sulfhydryls, has no effect on PGI2 production, [Ca++]i and [cGMP]i. These results suggested that the presence of sulfhydryl groups is an important factor in the ability of vasoactive substances to induce PGI2 production.

Acetylcysteine↗
PubMed1991

[Surgical treatment of hypertensive cerebellar hemorrhage; stereotactic aspiration surgery vs suboccipital craniectomy].

Patients with severe types of hypertensive cerebellar hemorrhage have been treated usually by suboccipital craniectomy and hematoma evacuation. However, since 1981, we have treated such patients with stereotactic aspiration surgery. The purpose of this study was to evaluate the prognosis of patients treated by stereotactic aspiration surgery for cerebellar hemorrhage in comparison with those who underwent suboccipital craniectomy. Between May 1976 and December 1989, 246 patients with hypertensive cerebellar hemorrhage were admitted to our university hospital and affiliated hospitals. The patients were classified into four categories according to the grading of hypertensive cerebellar hemorrhage proposed by Matsumoto in 1982; benign, moderate, severe, and fulminant. Then we decided the most appropriate therapy according to this grading. Fifty-nine patients (24.0%) underwent suboccipital craniectomy and 38 (15.4%) underwent stereotactic aspiration surgery. There was no significant difference in the postoperative outcome between suboccipital craniectomy and stereotactic aspiration surgery in the overall study. However prognosis of the fulminant type was significantly better with stereotactic aspiration surgery than with suboccipital craniectomy. Possible reasons for this include: 1) All patients of this type who underwent aspiration surgery had this procedure within 12 hours after the onset of cerebellar hemorrhage. 2) The hematoma volume of most patients of this type who had aspiration surgery was under 30ml. 3) The age of all patients of this type with aspiration surgery was under 70 years old. In conclusion, we suggest that aspiration surgery for hypertensive cerebellar hemorrhage is indicated for all patients with moderate, severe and fulminant types of hemorrhage.

Cerebellar Diseases↗
PubMed1991

[A case report of adjacent tumor of sphenoid ridge meningioma and GH producing pituitary adenoma].

A case of sphenoid ridge meningioma and pituitary adenoma adjacent in the brain is reported. A 70-year-old female was admitted to our hospital with headache. She had no neurological deficit but did have acromegalic change. Hormonal examination showed elevation of plasma levels of HGH (19.0 ng/ml), with normal levels of the other hormones. CT examination revealed a tumor with calcification in the inner third of the sphenoid ridge and another in the pituitary fossa with suprasellar expansion. MRI showed flow void of ICA between these tumors. Intensity of the T1-weighted image of the tumor in the sphenoid ridge was homogeneously iso intensity, and low intensity in the pituitary fossa. The diagnosis of adjacent tumors in the sphenoid ridge meningioma and pituitary adenoma had been made preoperatively. Left front-temporal craniotomy and removal of these tumors were performed. These tumors were close to each other, but were separated by the internal carotid artery and anterior cerebral artery. Pathological examination demonstrated meningotheliomatous meningioma in the sphenoid ridge and sparsely granulated somatotroph adenoma in the pituitary fossa. Fourteen cases showing association of meningioma and pituitary adenoma, which had no history of radiation and trauma, have been reported previously. Although GH producing pituitary adenoma may stimulate adjacent dura and arachnoid cells resulting in the formation of meningioma, the possibility of coincidental occurrence of the two tumors cannot be ignored.

Adenoma↗
PubMed1991

[Simultaneous supra- and infratentorial hypertensive intracerebral hemorrhage].

Multiple intracerebral hemorrhage may occur as rebleeding at the site of the previous lesion or in other places. However, multiple intracerebral hemorrhage occurring simultaneously in the supra-and infratentorial regions is rare. We experienced 9 such cases between May 1976 and December 1989. The clinical symptoms, CT findings and outcome of our cases and of 4 cases which were previously reported in the literature are reviewed in this paper. Out of 13 cases, 11 patients had cerebellar hemorrhage, and the others had pontine hemorrhage in the infratentorium. Among the supratentorial lesions, 11 involved hemorrhage in the putamen or the thalamus, and the others were in the subcortical region. There were no characteristic initial symptoms or neurological signs which suggested that hemorrhage had occurred in both the supra-and infratentorial regions. The only methods by which we could recognize this exceptional situation were the CT scan and MRI scan. The outcome in those patients whose initial neurological grading (NG) was 1 to 3 was good with conservative therapy or surgical treatment. On the other hand, the outcome in patients whose initial NG was 4 or 5 was very poor no matter what treatment was used. As far as surgical treatment is concerned, we believe that hematoma evacuation is necessary when the cerebellar hematoma is bigger than the supratentorial hematoma.

Aged↗
PubMed1990

Direct evidence for the contribution of the unique I-ANOD to the development of insulitis in non-obese diabetic mice.

Insulin-dependent diabetes mellitus is characterized by the infiltration of lymphocytes into the islets of Langerhans of the pancreas (insulitis) followed by destruction of insulin-secreting beta-cells leading to overt diabetes. The best model for the disease is the non-obese diabetic (NOD) mouse. Two unusual features of the class II major histocompatibility complex (MHC) of the NOD mouse are the absence of I-E and the presence of unique I-A molecules (I-ANOD), in which aspartic acid at position 57 of the beta-chain is replaced by serine. This feature is also found in the HLA-DQ chain of many Caucasians with insulin-dependent diabetes mellitus. We have previously reported that the expression of I-E prevents the development of insulitis in NOD mouse. Here we report that the expression of I-Ak (A alpha kA beta k) in transgenic NOD mice can also prevent insulitis, and that this protection is seen not only when the I-A beta-chain has aspartic acid as residue 57, but also when this residue is serine. These results show that the single amino-acid substitution at position 57 of the I-A beta-chain from aspartic acid to serine is not sufficient for the development of the disease.

Animals↗