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Biomedical subjects

M Morinaga

Publications and source records attributed to M Morinaga.

12 recordsLinked to original sources
PubMed1991

[Analysis of flow cytometric nuclear DNA content of the thymoma and its relationship to malignant intensity].

Determination was made of the nuclear DNA content of paraffin-embedded specimens of resected thymoma using flow cytometry in 39 patients. Relationships among nuclear DNA content, clinicopathological findings and prognosis were studied. The frequency of DNA aneuploid tumors was 30.8%, 6.7% in stage I (15 patients), 28.6% in stage II (7 patients), 44% in stage III (9 patients) and 62.5% in stage IV (8 patients) according to Masaoka's classification, indicating more in increase with advancing stage and significant (p less than 0.05) more increase invasive thymoma than in noninvasive thymoma. The 5 year and 10 year survival rates of DNA diploid tumors were each 94%, while DNA aneuploid tumors, 75% and 45%. Patients with DNA aneuploid tumors showed less favorable prognosis than those with DNA diploid tumors. Similar results were found in patients with invasive thymoma and in those on whom subtotal or partial resection were performed. The present results indicate DNA aneuploid tumors to have greater malignant intensity than DNA diploid tumors in resected thymoma. Flow cytometric nuclear DNA content analysis provides useful biological data and new indices for evaluating the malignancy of resected thymoma.

Adult↗
PubMed1990

A simple, rapid and simultaneous analysis of complex volatile hydrocarbon mixtures in blood using gas chromatography/mass spectrometry with a wide-bore capillary column.

A screening method for detecting volatile hydrocarbons in blood has been developed using gas chromatography/mass spectrometry with a wide-bore capillary column and a headspace method. Toluene-d8 and indan were used as the internal standards for quantitative analysis. Hydrocarbons with retention indices from 600 to 1200 were simultaneously and quantitatively detected in relatively low concentrations (0.01 microgram/ml) in reconstructed ion chromatography. This method could prove useful in forensic cases in which urgent examination of complex hydrocarbon mixtures, e.g. petroleum components, is required.

Cause of Death↗
PubMed1990

Signet ring cell early gastric cancer presenting as an elevated lesion.

Early gastric cancer composed of signet ring cell carcinoma is usually present as a depressed lesion and rarely manifests as a protruding lesion. To our knowledge, only eight cases have been reported in the literature. We herein report such a rare lesion which developed in an asymptomatic 55-year-old man.

Adenocarcinoma, Mucinous↗
PubMed1990

[Screening of drugs and chemicals by wide-bore capillary gas chromatography. II. Detection of drugs and chemicals in the blood].

This paper describes the detection limit for 23 drugs and chemicals in the blood by means of a screening method that uses a gas chromatographic system equipped with a wide-bore capillary column and a nitrogen phosphorus detector. The detection limit by this method was determined as being 1 mm of peak height at the detector's range of 100 and 8 of attenuation. Using this scale, the absolute detection limit was in the range of 1 pg for malathion and sumithion to 1 ng for meprobamate. The detection limit of drugs and chemicals in the blood was 5 ng/ml for sumithion to 8 micrograms/ml for meprobamate. Therefore, this screening method is able to detect the presence of drugs even a therapeutic-level dosages, with the exception of compounds such as haloperidol, which have extremely low therapeutic dosage levels.

Blood Chemical Analysis↗
PubMed1988

Changes of manganese levels during haemodialysis.

Manganese (Mn) transfer during haemodialysis and plasma Mn concentrations in haemodialysis patients were examined. Also, the correlation with plasma Mn levels and haematocrit levels and total plasma protein levels were studied. Fifteen volunteer outpatients undergoing haemodialysis showed significant increases in plasma Mn from 0.20 +/- 0.02 to 0.22 +/- 0.02 micrograms/dl after a 5-hour dialysis. The increase was mainly the result of haemoconcentration as evidenced by a significant increase in the haematocrit and total plasma protein during dialysis; however, diffusion was not found. There was a significant relationship between plasma Mn levels before dialysis and haematocrit values (r = 0.95, p less than 0.01) and total plasma protein levels (r = 0.92, p less than 0.01).

Female↗
PubMed1988

[Clinical studies on renal function and trace elements].

The serum trace elements aluminum (Al), zinc (Zn), nickel (Ni), and manganese (Mn), and creatinine clearance (Ccr) were measured in twenty normal volunteers and 40 patients; 5 patients had mild renal dysfunction, 10 patients had chronic renal failure 5 patients had uremia and 20 patients had been undergoing chronic hemodialysis. Serum Al, Cu, Zn, Ni and Mn were measured with a flameless atomic absorption spectrophotometer. Serum Al levels increased with decrement of the Ccr value. The serum Al level was abnormally high in chronic hemodialysis patients. The serum Cu level in the patients was similar to that in the healthy subjects. Serum Zn, Ni and Mn levels decreased with the decrement of the creatinine clearance level. These results suggest that measurement of serum Al, Zn, Ni and Mn levels can be used as an indication of renal function clinically. In conclusion, serum Al, Zn, Ni and Mn levels are clinical indicators of renal function.

Aluminum↗
PubMed1987

Enhancing effects of tilorone on collagen arthritis and humoral immune response to type II collagen.

The effect of tilorone, which is known to suppress adjuvant arthritis, on the induction of collagen arthritis in rats was investigated. Combined data of the present experiments show that all of the tilorone-treated rats except one in the lowest dosage group developed arthritis but that the incidence of arthritis in the tilorone-treated groups was not significantly different from that of the control group. The results also show that the two higher dosages (12.5 and 25 mg/kg/day) of tilorone caused a significant increase in the severity of collagen arthritis. Humoral immune response to type II collagen was significantly augmented in these two higher dosage groups; however, delayed-type hypersensitivity response to type II collagen was suppressed while tilorone was administered continuously. In addition, treatment with tilorone caused a significant increase in the concentration of anticollagen IgG extractable from the joint tissue. Anticollagen IgG subclass analysis revealed that the major subclass was IgG2a in both the serum and paw extract, with minor amounts of IgG2b, IgG2c, and IgG1. The response of all these subclasses was almost equally activated by tilorone treatment.

Animals↗
PubMed1986

Effects of cyclosporin on collagen induced arthritis in mice.

We have studied the effect of the immunosuppressive agent cyclosporin on collagen induced arthritis in mice. Cyclosporin, when given prophylactically, was capable of suppressing the development of collagen induced arthritis and the immunological response to native type II collagen in a dose dependent manner. Furthermore, treatment with cyclosporin, started on the same day as the booster injection with type II collagen, also resulted in inhibition of development of arthritis and of immunity to collagen. These findings suggest that the time of a booster injection, three weeks after the initial immunisation, might be still within the induction phase of arthritis since reinoculation is required to produce a high incidence of arthritis in mice. In addition, therapeutic treatment with cyclosporin did not affect the clinical course of the disease or the immune response to collagen.

Animals↗
PubMed1985

Serum transfer of collagen arthritis to cyclosporin-treated, type II collagen-tolerant rats.

Collagen arthritis has been passively transferred with a serum concentrate from immunized donors to immunologically naive recipients as well as cyclosporin-treated, type II collagen-tolerant rats. These findings point to an important role for anticollagen antibody and appear to rule out a role for cellular immunity to type II collagen in the initiation of this disease. The passively transferred arthritis was a transient lesion in the majority of naive recipients and in the cyclosporin-treated, type II collagen-tolerant rats as well when a serum concentrate was transferred after the cessation of cyclosporin treatment. When cyclosporin-treated, type II collagen-tolerant rats received transfer concentrate while cyclosporin was administered continuously, arthritis was significantly enhanced, and lasted as long as cyclosporin was administered and in the majority of rats up to 2 weeks after the cessation of cyclosporin treatment. These results, together with a rapid clearance of anticollagen antibody from the serum, suggest that anticollagen antibody is not the sole regulatory factor and that a cellular suppressor system, sensitive to cyclosporin, might participate in the regulation of this disease process.

Animals↗
PubMed1985

Serum transfer of collagen arthritis in congenitally athymic nude rats.

The role of cellular immunity in collagen arthritis was investigated with congenitally athymic nude rats (rnu/rnu) and their heterozygous littermates (rnu/+). Immunization with type II collagen induced polyarthritis and definite immunity to type II collagen in rnu/+ rats, whereas rnu/rnu rats did not develop arthritis or immunity to collagen. An additional study demonstrated that collagen arthritis could be passively transferred with a serum concentrate from arthritic Sprague-Dawley rats to naive rnu/rnu rats as well as to rnu/+ rats. Histopathologically, the passively transferred arthritis in rnu/rnu rats resembled that in rnu/+ rats. Despite no difference in clearance of anti-type II collagen antibody after transfer between them, the passively transferred arthritis in rnu/rnu rats was significantly enhanced and prolonged in comparison with that in rnu/+ rats. These results indicate that arthritis may be inducible by humoral immunity in the absence of functional T cells and also suggest that anti-type II collagen-antibody is not the sole regulatory factor and that the suppressor cell system might regulate the clinical course of the disease.

Animals↗