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Biomedical subjects

T Yoda

Publications and source records attributed to T Yoda.

8 recordsLinked to original sources
PubMed1992

Urinary glycylprolyl dipeptidyl aminopeptidase (GP-DAP) in insulin-dependent diabetic patients.

Urinary glycylprolyl dipeptidyl aminopeptidase (GP-DAP) concentrations were determined in 36 insulin-dependent diabetic children aged 4-18 years with a duration of diabetes ranging from 1 month to 14 years. Abnormal urinary GP-DAP concentrations were found in 19 of the 36 patients. Twelve of 27 patients without microalbuminuria also had increased urinary concentrations of GP-DAP. There was a significant correlation between urinary GP-DAP and plasma fructosamine (r = 0.52, p < 0.001). Our data suggest that urinary GP-DAP may be used as a marker for diabetic nephropathy. However, there is also a possibility that increased urinary GP-DAP concentrations are functionally related to poor metabolic control. Longitudinal studies are needed to establish the clinical usefulness of urinary GP-DAP.

Adolescent↗
PubMed1991

A case of citrullinemia with abnormal messenger RNA for argininosuccinate synthetase.

A male neonate, thus far healthy and fed with breast milk, developed rapidly increasing apathy on the third day of life. Sucking became poor and hyperhidrosis was present. Hyperammonemia (3,305 micrograms/dl) was noted. He became comatose and died on the fourth day. There was a profound derangement of amino acid concentration in the body fluids, with highly elevated citrulline levels (4.70 mumols/ml in serum and 8.47 mumols/ml in urine). Autopsy showed diffuse pulmonary bleeding, as the only noteworthy pathological finding. The liver contained no detectable argininosuccinate synthetase (ASS) activity. The defect of ASS in the present case was not due to a reduced amount of ASSmRNA, but its structure was found to be abnormal; it was approximately 1.57 kb in length due to a defect of about 0.1 kb near the 3' end of the coding region.

Amino Acid Metabolism, Inborn Errors↗
PubMed1991

[Autogenous dermal grafts for repair of temporomandibular joint disc perforations].

Perforations of the temporomandibular joints (TMJs) disc were made in the rabbits and repaired with autogenous dermal grafts. The healing process was investigated histologically. Twenty-one rabbits (forty-two TMJs) were divided into 3 experimental groups. Group 1. Six TMJs in which the superior aspects of the discs were exposed by the incision of the articular eminence. Group 2. Fifteen TMJs in which the discs were perforated. Group 3. Twenty-one TMJs in which the dermal grafts were sutured on the disc perforations. The results obtained were as follows: In group 2, all perforations were not repaired, except in one case. In group 3, 14/19 grafted disc perforations were repaired. One week after surgery, young, loose, collagenous tissue from the synovial membrane lined the margins of the perforations. Two weeks after surgery, vascularity from the synovial membrane and young collagen fibers were seen in the area of the repaired perforations. Four weeks after surgery, long and thick collagen fibers bridged the perforations.

Animals↗
PubMed1990

Activation of idiotype-specific CD4+ T-cell line: cellular processing of exogenous self-immunoglobulin.

An idiotype (Id)-specific long-term cultured T-cell line has been generated from BALB/c mice immunized with M315 (alpha, lambda 2). The cell line comprises both CD3+ and CD4+ but CD8- cells. The T-cell line is stimulated in a class II major histocompatibility complex (MHC)-restricted manner, and is capable of producing interleukin-2 (IL-2) in response to the Id along with Iad-bearing antigen-presenting cells (APC). Fine Id specificity analysis has shown that changes in amino acid residues, Phe-94, Arg-95 and Asn-96, located on the VL-315, resulting from a somatic mutation mechanism of the mouse V lambda 2 gene, contribute to the T-cell activation. Pretreatment of APC with either glutaraldehyde or paraformaldehyde prevented both Fv-315 and VL-315 from triggering the T cells. This suggested that further processing of VL is required for T-cell activation. To clarify this point, we have generated a synthetic peptide, designated P18, which spans residues 91-108 of VL-315. In sharp contrast to VL, prefixed APC were capable of presenting P18 to stimulate the T-cell line to induce IL-2.

Animals↗