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M Tsujikawa

Publications and source records attributed to M Tsujikawa.

31 records · Page 2Linked to original sources
PubMed1997

Differentiating full thickness macular holes from impending macular holes and macular pseudoholes.

AIMS: The reliability of scanning laser ophthalmoscope (SLO) microperimetry in differentiating full thickness macular holes from macular pseudoholes and impending macular holes was evaluated. METHODS: 106 eyes with the clinical diagnosis of full thickness macular holes, macular pseudoholes, and impending (stage 1) macular holes were examined for the presence of deep or relative scotoma using SLO microperimetry. The relation between these scotomas and the clinical diagnosis was studied. RESULTS: Deep and relative scotomas were detected in all 57 eyes with clinically defined full thickness macular holes. In contrast, among 49 eyes diagnosed with macular pseudoholes or impending macular holes, no deep and only one relative scotoma was observed. The sensitivity of the presence of a deep scotoma as an indicator of the clinical diagnosis of a full thickness macular hole was 100% (57 of 57), and the specificity was 100% (49 of 49). The sensitivity of the presence of a relative scotoma was 100% (57 of 57) and the specificity was 98.0% (48 of 49). CONCLUSION: With SLO microperimetry, full thickness macular holes can be precisely and objectively distinguished from other conditions that mimic macular holes.

Adult↗
PubMed1997

Secondary vitrectomy for the treatment of macular holes occurring after vitrectomy.

Tangential foveal traction by the posterior vitreous cortex is regarded as the main cause of full-thickness macular holes. This report documents two cases of full-thickness macular holes that developed after vitrectomy for other diseases in the apparent absence of the cortical vitreous traction. Autologous serum with pars plana vitrectomy was used to treat these cases. Anatomic closure of the holes was achieved. Macular holes developing after vitrectomy may have an etiology other than tangential vitreous traction, and secondary vitrectomy is useful in treating such holes.

Adult↗
PubMed1996

Secretory production of recombinant urokinase-type plasminogen activator-annexin V chimeras in Pichia pastoris.

To produce a thrombi-targeting plasminogen activator, we expressed a fused gene that contains a modified pre-sequence of Mucor pussilus rennin (MPR) followed by a chimeric gene of single-chain urokinase-type plasminogen activator (scu-PA)::annexin V (AV). The fused gene was ligated into an integrative vector, under the control of the alcohol oxidase 1 (AOX1) promoter (p), and transformed into Pichia pastoris. Transformants were monitored for the secretion of fibrinolytic activity. The highest expressing clone, HB225, secreted as much as 600 international units (IU) of fibrinolytic activity per ml of culture medium under optimal conditions. It contained three tandem copies of the full-size vector disruptively integrated into the AOX1 sequence. Western blot analysis revealed that the secreted chimera was highly susceptible to proteolysis. Addition of excess amino acids (aa) to the culture medium minimized the degree of proteolysis. Two major species of chimera, 85 and 65 kDa, were then isolated from the culture medium. The former was the intact form consisting of a single-chain and showing full enzyme activity after activation by plasmin. The latter was an enzymatically processed form consisting of two chains held by a disulfide bond, having full enzyme activity without activation. Both chimeras exhibited calcium-dependent phospholipid (PL)-binding affinities similar to the parent AV.

Amino Acid Sequence↗
PubMed1996

Secretion of a variant of human single-chain urokinase-type plasminogen activator without an N-glycosylation site in the methylotrophic yeast, Pichia pastoris and characterization of the secreted product.

Human single-chain urokinase-type plasminogen activator without an N-glycosylation site (scu-PA-Q302) was produced in the methylotrophic yeast, Pichia pastoris using the shortened prepeptide sequence of a fungal aspartic proteinase, Mucor pusillus rennin (MPR). The level of urokinase-type plasminogen activator (u-PA) immunoreactive material in YPM medium was 0.47 mg/l; however, most of the secreted product had been processed to smaller polypeptides. The N-terminal amino acid sequence of major species was identical to that of the low molecular weight two-chain u-PA. Some approaches to minimizing the proteolysis of scu-PA-Q302 were attempted. Addition of Triton X-100, L-arginine and ammonium phosphate to the YPM medium minimized the proteolysis of scu-PA-Q302 and increased the yield of immunoreactive material to approximately 5 mg/l. Use of proteinase A- or proteinase B-deficient strains of yeast did not reduce the degradation. Co-expression of scu-PA-Q302 and urinary trypsin inhibitor resulted in partial reduction of the major species of proteolysis. Scu-PA-Q302 was purified from the culture supernatant of the improved medium by two successive chromatographies on Phenyl-Sepharose and S-Sepharose. The purified protein had a molecular weight of 47 kDa. It did not contain detectable N-linked oligosaccharides, but contained O-linked oligosaccharides attached to the light chain. N-terminal amino acid sequencing of the purified preparation showed that the shortened prepeptide sequence of MPR was correctly processed by the Pichia yeast. Scu-PA-Q302 closely resembles natural scu-PA with respect to its enzymatic activity against the chromogenic substrate S-2444 and its in vitro fibrinolytic properties.

Arginine↗
PubMed1987

Purification and sequencing of a trypsin-sensitive cholecystokinin-releasing peptide from rat pancreatic juice. Its homology with pancreatic secretory trypsin inhibitor.

The trypsin-sensitive cholecystokinin-releasing peptide is a peptide purified from rat pancreatic juice on the basis of its stimulatory activity toward pancreatic enzyme secretion. We postulate that the peptide acts as a mediator of pancreatic enzyme secretion in response to dietary protein intake and that it (designated as "monitor peptide" from its role in the intestine) could be responsible for the feedback regulation of pancreatic enzyme secretion. About 20 nmol of the highly purified peptide were obtained from 800 ml of rat pancreatic juice by reverse-phase high performance liquid chromatography. It was then sequenced. The peptide comprises 61 amino acid residues (Table I). It has a sequence that closely resembles that of a highly conserved region in pancreatic secretory trypsin inhibitors (PSTIs, Kazal type inhibitor): -Ile-Tyr-Asx-Pro-Val-Cys-Gly-Thr-Asx-Gly-. However, the peptide is less related to other mammalian PSTIs than they are to each other. The additional 5 residues at the NH2 terminus make the peptide larger than the common 56-residue PSTIs. The trypsin-sensitive cholecystokinin-releasing peptide is to be classified as a Kazal-type inhibitor and may be one of the rat PSTIs or a related peptide. The present results and increasing evidence from other laboratories and ours suggest that Kazal-type inhibitors play previously unrecognized multiple physiological roles.

Amino Acid Sequence↗
PubMed1986

Stimulation of pancreatic enzyme secretion by a peptide purified from rat bile-pancreatic juice.

We purified a peptide from rat pancreatic juice that enhances pancreatic enzyme secretion in a manner different from that of exogenous trypsin inhibitors, such as soybean trypsin inhibitor, when it is infused into the rat intestine. In this paper, we present evidence for the release of gut hormone(s) into the blood of rats after intestinal administration of the peptide. In the presence of atropine, an anesthetized rat small intestine was washed out with saline containing soybean trypsin inhibitor (Kunitz type) to eliminate proteases. Under these conditions, the rat small intestine was divided into four equal parts by ligation. Administration of the peptide into the first quarter of the small intestine stimulated pancreatic enzyme secretion. However, administration into the more distal parts did not stimulate the enzyme secretion. Moreover, intravenous injection of 1 mL of plasma from rats in which the peptide had been infused into the duodenum caused stimulation of pancreatic enzyme secretion in the recipient rats. It was suggested that the purified peptide acts in the proximal small intestine and that it stimulates the release of gut hormone(s) into the blood to enhance pancreatic enzyme secretion. These findings support the hypothesis that the peptide we purified is responsible in part for the humoral control of pancreatic enzyme secretion in the response to food intake.

Animals↗
PubMed1984

Virological classification of autopsy livers with hepatic disorders.

Forty six selected autopsy livers with hepatic disorders were classified histologically into three groups, i.e., hepatitis 8, liver cirrhosis 16 and hepatocellular carcinoma 22, chiefly by histological findings. These groups were subdivided into two categories after determining the presence or absence of three HBV associated markers, i.e., the hepatitis B surface antigen (HBsAg), the antibody to hepatitis B surface antigen (anti-HBs) and the antibody to hepatitis B core antigen (anti-HBc) in the sera and liver homogenates. At least one of these markers was found to be present in the sera and homogenates of 38% of the livers with hepatitis, 69% of the livers with liver cirrhosis and 77% of the livers with hepatocellular carcinoma. When the liver tissues were examined for the presence of HBV DNA using Southern blot technique, the majority of them (10 out of 11) which proved to be positive for at least one HBV associated marker were also positive for HBV DNA. However, HBV DNA could not be detected in the other 10 livers which contained no HBV associated markers. These results showed that a HBV associated serological marker was always expressed, when liver tissue HBV DNA was demonstrable. The results of the two detection methods we used in this study were found to be almost equivalent. These results showed no evidence of nucleic acid homology between DNA from the liver of patients with non-B type liver disorders and HBV DNA.

Autopsy↗
PubMed1981

Effect of exposure to cold on pantothenic acid metabolism in rat liver.

Exposure to a cold environment increased the incorporation of labeled pantothenic acid (PaA) into the liver and total PaA content. These increases were mainly due to an increase of free coenzyme A (CoA). The specific activity of the free CoA fraction was particularly high. These results suggest that exposure to a cold environment accelerates the rate of synthesis of CoA from PaA in the liver.

Animals↗
PubMed1981

Effect of litter size on glucose metabolism in rat pup adipose tissue during the suckling period.

The effect of milk intake on the glucose tolerance capacity, lipogenesis, ATP citrate lyase and acetyl CoA carboxylase activities in rat adipose tissues during the suckling period was studied. The glucose tolerance capacity in the suckling rats was far lower than that in rats at the age of 5 weeks. However, glucose tolerance capacity in the suckling animals of 4-membered litters at the age of 2 weeks was higher than that in control animals of 8-12 membered litters at the same age. Lipid synthesis, fatty acid synthesis and ATP citrate lyase activity in subcutaneous adipose tissues of animals of 4-membered litters in the suckling period were higher than those of control animals. It was observed that ATP citrate lyase activity in subcutaneous adipose tissues of animals of 4-membered litters in the suckling period were higher than those of control animals. It was observed that ATP citrate lyase activity in adipose tissues during the suckling period was increased by glucose injection alone. These results suggest that the development of the glucose tolerance capacity and the lipogenesis in adipose tissues during the suckling period were influenced by nutritional status as well as chronological age.

ATP Citrate (pro-S)-Lyase↗
PubMed1980

Changes in lipid synthesis in rat adipose tissue during development.

Lipogenesis in rat adipose tissue during postnatal development has been studied by measuring the incorporation of labeled glucose into lipid in fat cells and the activities of certain enzymes which participate in lipogenesis. It was found that: (1) Fatty acid synthesis from glucose is negligible in the suckling period. After weaning, it increases rapidly and reaches a plateau at the age of 10 weeks. (2) Insulin sensitivity is negligible in the suckling period. After weaning it rises and then declines. (3) Activities of ATP citrate lyase and acetyl CoA carboxylase are maintained at a low level in the suckling period. After weaning, these activities rise rapidly and then decline. (4) Weaning rats onto a high-fat diet showed decreases in glucose incorporation into fatty acids, insulin sensitivity, ATP citrate lyase activity and acetyl CoA carboxylase activity.

Adipose Tissue↗
PubMed1980

Effect of early feeding on cellularity of rat adipose tissue.

Effect of food intake at various ages (fetal, suckling and weaning periods) on adipose tissue cellularity was studied. 1) Rats were given a restricted diet on weaning and later allowed free access to diet. Fat pads of these animals recovered normal weight on refeeding and no differences in cell number or cell size were observed. 2) Food intake was varied by changing the litter size during the suckling period and, after weaning, animals were given free access to diet. Fat pads of rats raised in small litters were heavier than those of rats raised in large litters. The differences in adipose tissue weight were accounted for by differences in cell size and cell number 3) Maternal rats were given a restricted diet during pregnancy. The pups were irregular in their weight. Pups of the restricted group which were smaller than pups of the control group at birth were chosen and raised normally. Fat pads of these animals were lighter than those of control animals and could be explained in terms of differences in cell size. From these findings, it was suggested that cellular effects of early feeding depended on the phase of growth in the rat.

Adipose Tissue↗