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Biomedical subjects

K Obata

Publications and source records attributed to K Obata.

316 records · Page 18Linked to original sources
PubMedDate not supplied

Type IV collagen as an early marker for diabetic nephropathy in non-insulin-dependent diabetes mellitus.

We measured urinary albumin (U-Alb) and type IV collagen (uIV.C) in spot urine collected from 82 patients with non-insulin-dependent diabetes mellitus (NIDDM) and 205 controls. Eighty-two NIDDM patients that had no increased excretion of either U-Alb or uIV.C were observed for 6 months. Prevalence of increased excretion of U-Alb and uIV.C at 6 months in these patients were 32.9%, and 62.2%, respectively. Increased excretion of uIV.C was detected in 27 patients without microalbuminuria. chi(2) analysis suggested that uIV.C was more sensitive than U-Alb, and that hypertension enhanced increased excretion of both U-Alb and uIV.C. uIV.C was significantly correlated (P<0.01) with U-Alb but not glycosylated hemoglobin A1C (HbA1C) in NIDDM patients. Taken together, uIV.C may be a useful marker for early diabetic nephropathy.

Adult↗
PubMedDate not supplied

Human preprovasoactive intestinal polypeptide contains a novel PHI-27-like peptide, PHM-27.

Vasoactive intestinal polypeptide (VIP), a 28-amino acid peptide originally isolated from porcine duodenum, is present not only in gastrointestinal tissues but also in neural tissues, possibly as a neurotransmitter, and exhibits a wide range of biological actions (for example, relaxation of smooth muscle, stimulation of intestinal water and electrolyte secretion and release of insulin, glucagon and several anterior pituitary hormones). As the structure of porcine and bovine VIP shows several similarities to those of mammalian glucagon, secretin and gastric inhibitory peptide (GIP), VIP is considered to be a member of the glucagon-secretin family. Recently, we have found that VIP is synthesized from a precursor, pro-VIP (molecular weight (Mr) 17,500), in human neuroblastoma cells and that the primary translation product of the mRNA encoding VIP is prepro-VIP (Mr 20,000). In an attempt to elucidate the primary structure of the precursor, we have now cloned the DNA sequence complementary to the mRNA coding for human VIP and analysed the nucleotide sequence. The entire amino acid sequence of the precursor, deduced from the nucleotide sequence, indicates that the precursor protein contains not only VIP but also a novel peptide of 27 amino acids. The peptide, designated PHM-27, differs by only 2 amino acids from PHI-27, a peptide recently isolated from porcine intestine, and is also closely related in sequence to VIP.

Amino Acid Sequence↗
PubMedDate not supplied

Low-dose mitomycin C, etoposide, and cisplatin for invasive vulvar Paget's disease.

We report the effect of low-dose mitomycin C, etoposide, and cisplatin (low-dose MEP) therapy for three patients with invasive vulvar Paget's disease (invasive VPD) who declined radical vulvectomy and skin grafting. One patient achieved a complete response, while the other two showed partial responses (PR) without grade 3 or 4 adverse effects. The two patients with PR were undergone partial vulvectomy and inguinal lymph node dissection. All patients have no sign of recurrence for 10 months after chemotherapy. Our present results suggest that low-dose MEP is an effective and safe chemotherapy for invasive VPD and low-dose MEP may significantly improve postoperative quality of life in patients with invasive VPD by avoiding extensive vulvar resection and skin grafting.

Aged↗
PubMedDate not supplied

Successful treatment of essential thrombocythemia evolving into agnogenic myeloid metaplasia with interferon-alpha.

PURPOSE: Essential thrombocythemia and agnogenic myeloid metaplasia as one form of idiopathic myelofibrosis are myeloproliferative disorders and are quite rare in children. A patient with essential thrombocythemia that transformed to "adult-type" agnogenic myeloid metaplasia is described. PATIENTS AND METHODS: A routine examination of an 8-year-old girl with bronchial asthma showed thrombocytosis. Essential thrombocythemia was diagnosed 2 years later. During a 3-year follow-up without treatment, transition of the essential thrombocythemia to agnogenic myeloid metaplasia was noticed. The patient had an excellent response to interferon (IFN)-alpha therapy. CONCLUSION: This case is unique because of the availability of premorbid hematologic data and the natural progression of essential thrombocythemia to agnogenic myeloid metaplasia. Whether IFN-alpha therapy can prevent the progression of idiopathic myelofibrosis to leukemia has not yet been determined.

Child↗
PubMedDate not supplied

Identification of genes expressed in the amygdala during the formation of fear memory.

In this study we describe changes of gene expression that occur in the basolateral complex of the mouse amygdala (BLA) during the formation of fear memory. Through the combination of a behavioral training scheme with polymerase chain reaction-based expression analysis (subtractive hybridization and virtual Northern analysis) we were able to identify various gene products that are increased in expression after Pavlovian fear conditioning and are of potential significance for neural plasticity and information storage in the amygdala. In particular, a key enzyme of monoamine metabolism, aldehyde reductase, and the protein sorting and ubiquitination factor Praja1, showed pronounced and learning-specific induction six hours after fear conditioning training. Aldehyde reductase and Praja1, including a novel alternatively spliced isoform termed Praja1a, were induced in the BLA depending on the emotional stimulus presented and showed different expression levels in response to associative conditioning, training stress, and experience of conditioned fear. Stress and fear were further found to induce various signal transduction factors (transthyretin, phosphodiesterase1, protein kinase inhibitor-alpha) and structural reorganization factors (e.g., E2-ubiquitin conjugating enzyme, neuroligin1, actin, UDP-galactose transporter) during training. Our results show that the formation of Pavlovian fear memory is associated with changes of gene expression in the BLA, which may contribute to neural plasticity and the processing of information about both conditioned and unconditioned fear stimuli.

Aldehyde Reductase↗
PubMedDate not supplied

Higher seizure susceptibility and enhanced tyrosine phosphorylation of N-methyl-D-aspartate receptor subunit 2B in fyn transgenic mice.

Earlier work has suggested that Fyn tyrosine kinase plays an important role in synaptic plasticity. To understand the downstream targets of Fyn signaling cascade in neurons, we generated transgenic mice expressing either a constitutively activated form of Fyn or native Fyn in neurons of the forebrain. Transgenic mice expressing mutant Fyn exhibited higher seizure activity and were prone to sudden death. Mice overexpressing native Fyn did not show such an obvious epileptic phenotype, but they exhibited accelerated kindling in response to once-daily stimulation of the amygdala. Tyrosine phosphorylation of at least three proteins was enhanced in the forebrains of both native and mutant fyn transgenic mice; tyrosine phosphorylation of these three proteins was reduced in fyn knockout mice, suggesting that they are substrates of Fyn. One of these proteins was identified as the subunit 2B (NR2B) of the N-methyl-D-aspartate (NMDA) receptor. Administration of MK-801, a noncompetitive NMDA receptor antagonist, retarded kindling in mice overexpressing native Fyn, as well as wild-type mice, suggests that the accelerated kindling in mice overexpressing Fyn is also mediated by the NMDA receptor activity. Our results thus suggest that tyrosine phosphorylation by Fyn might be involved in regulation of the susceptibility of kindling, one form of the NMDA receptor-mediated neuronal plasticity.

Amino Acid Sequence↗
PubMedDate not supplied

Increased levels of matrix metalloproteinase-3 in sera from patients with active lupus nephritis.

OBJECTIVE: To determine the matrix metalloproteinase-3 (MMP-3) levels in sera from patients with systemic lupus erythematosus (SLE) and to analyse the relationships between MMP-3 and clinical and laboratory features. METHODS: Serum MMP-3 levels were measured by an enzyme immunoassay in 124 patients with SLE and 237 patients with other systemic rheumatic diseases. RESULTS: The frequencies of patients with high MMP-3 levels were 76% in SLE and 82% in rheumatoid arthritis (RA). The level of MMP-3 in the SLE patients was 193.0 +/- 171.5 ng/ml (mean +/- SD) and was almost equal to the level in the RA patients (259.5 +/- 255.6 ng/ml). The MMP-3 levels were significantly higher in SLE patients who had a history of the following abnormalities: persistent proteinuria, cellular casts, anti-double stranded DNA antibodies, decreased C3, decreased creatinine clearance (p < 0.001), circulating immune complex (p < 0.01), malar rash, hypoalbuminemia, or decreased C4 (p < 0.05). The serum MMP-3 level in patients with SLE at admission showed direct correlations with serum uric acid, total cholesterol (p < 0.001), triglyceride, the white blood cell count, and the neutrophil count (p < 0.05), as well as inverse correlations with the total protein (p < 0.01), and IgG (p < 0.05). In SLE patients with active renal disease, the median MMP-3 level at admission and that at 6 months after admission were significantly higher than that at 6 months before admission. CONCLUSIONS: The increased level of serum MMP-3 in SLE is closely associated with clinical features relevant to lupus nephritis, suggesting that it plays a role in the pathogenesis of this condition.

Adolescent↗