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Biomedical subjects

K Miyake

Publications and source records attributed to K Miyake.

At least 595 records · Page 33Linked to original sources
PubMed1987

[A case of priapism caused by disseminated intravascular coagulopathy].

A case is presented of priapism resulting from disseminated intravascular coagulopathy (DIC), which was diagnosed by pathological studies of the amputated penis and skin biopsy. To our knowledge, this is the first case reported in Japan. This 72-year-old-man visited a hospital complaining of fever and cough, and was administrated for treatment of bronchitis and liver cirrhosis. A few days after admission, multiple purpura with edema and pain appeared over the skin regions on the bilateral knee joint, foot joint and upper extremities. A week after purpura appeared, priapism began. Regardless of irrigation and aspiration of corpora cavernosa and glans-cavernosa-fistula creation, penile necrosis developed. We had to perform penile amputation. The pathology of the amputated penis and skin, and blood coagulative examination suggested that DIC resulted in priapism. DIC was controllable by the use of FOY and heparin. He was discharged and is an outpatient.

Aged↗
PubMed1987

Catheter-associated urinary tract infections in patients undergoing transurethral surgery.

A study of 75 patients undergoing transurethral surgery with relatively short-term urethral catheterization with a sterile closed gravity drainage system revealed a 72% over-all incidence of negative urine cultures after catheter removal. The combination of prophylactic use of antimicrobials and a standardized catheter care system is valuable for preventing catheter-associated bacteriuria.

Aged↗
PubMed1987

A case of primary carcinoma of the epididymis.

We present a rare case of primary carcinoma of the left epididymis in a 32-year-old man. Pathological diagnosis was anaplastic carcinoma of epididymis. The patient is alive and free of metastases 2 years after orchidectomy. Clinical and pathological aspects of epididymal carcinomas are discussed with reference to previously reported cases.

Adult↗
PubMed1987

Possible mechanism by which coenzyme Q10 improves reoxygenation-induced recovery of cardiac contractile force after hypoxia.

To elucidate possible mechanisms by which coenzyme Q10 enhances reoxygenation-induced recovery of cardiac contractile force after hypoxia, rabbit hearts were subjected to hypoxic perfusion for 20 min, followed by 45 min-reoxygenation with or without pretreatment with coenzyme Q10. Hypoxia induced a decline in cardiac contractile force, a decrease in myocardial high-energy phosphates and a release of ATP metabolites and creatine phosphokinase from the perfused heart. Upon reoxygenation the rate of release of ATP metabolites subsided, but no appreciable recovery of the loss of contractile force and the reduction of myocardial ATP content was seen, and the release of creatine phosphokinase was increased further. Pretreatment of rabbits with coenzyme Q10 resulted in an appreciable recovery of cardiac contractile force and of myocardial ATP content upon reoxygenation. The release of creatine phosphokinase from hearts during hypoxia and reoxygenation was inhibited completely by the pretreatment. Changes in the UV absorbance of the perfusate suggested that coenzyme Q10 reduced the loss of ATP metabolites from hypoxic hearts. Furthermore, high-performance liquid chromatographic analysis indicated that coenzyme Q10 attenuated the release of inosine and hypoxanthine from the hearts and decreased myocardial inosine and adenosine content of the hypoxic heart, suggesting that coenzyme Q10 retards the breakdown of ATP metabolites which are possible substrates for a salvage synthesis of ATP, when oxygen is replenished. This could account for an appreciable restoration of ATP, and eventually provide a significant recovery of cardiac contractile force upon reoxygenation.

Adenosine↗
PubMed1986

Polyclonal B cell activation by a B cell differentiation factor, B151-TRF2. II. Evidence for interaction of B151-TRF2 with glycoprotein on B cell membrane via recognition of terminal N-acetyl-D-glucosamine residue(s).

We investigated the role of carbohydrates in the interaction of a B cell differentiation factor designated as B151-TRF2 derived from B151K12 T cell hybridoma with the corresponding receptor on B cells. Induction of polyclonal differentiation of unprimed B cells into IgM-secreting cells by B151-TRF2 was specifically inhibited by addition of N-acetyl-D-glucosamine (GlcNAc) but not by structurally unrelated monosaccharides such as D-galactose, D-glucose, and N-acetyl-D-galactosamine (GalNAc). Absorption of B151-TRF2 activity with spleen cells was specifically inhibited by the presence of GlcNAc. These results indicate that GlcNAc residues are involved in the interaction of B151-TRF2 with the receptor on B cells. To gain insight into mechanism by which GlcNAc inhibits B151-TRF2-mediated B cell responses, the existence of GlcNAc residues was examined on the B151-TRF2 molecule and the corresponding receptor on the B cell surface. The results revealed that B151-TRF2 molecule was not bound to various lectin-coupled agarose beads so far tested, suggesting absence of carbohydrate moieties on the B151-TRF2 molecule. By contrast, pretreatment of spleen cells with trypsin or glycosidase mixture abolished their ability to absorb B151-TRF2 activity. Moreover, B151-TRF2-absorbing ability of spleen cells disappeared by the pretreatment with beta-N-acetylglucosaminidase, which cleaves terminal GlcNAc. The fact that pnitrophenyl (PNP)-GlcNAc specifically inhibited such enzyme activity on target cells indicates that terminal GlcNAc on the B cell surface plays a crucial role in the interaction with B151-TRF2 molecule. Interestingly, it was also found that B151-TRF2 activity was trapped and eluted from GlcNAc-coupled agarose beads. Taken collectively, these results strongly suggest that B cell membrane receptors for B151-TRF2 comprise glycoproteins with a terminal GlcNAc residue(s), and that binding of B151-TRF2 with terminal GlcNAc on the receptor is important for the subsequent activation of B cells.

Acetylglucosamine↗
PubMed1986

Evidence for existence of two distinct TNP-Ficoll-responsive B cell subpopulations preferentially reactive either to a T cell-replacing factor (B151-TRF) or to a signal from accessory cells.

The ability of B cells to respond to TNP-Ficoll has been shown to correlate with their ability to respond to T cell-replacing factor (TRF). The present study analyzed the relationship of TNP-Ficoll-responsive B cells to a TRF-responsive B cell subpopulation. The B cells from normal, unprimed mice responded to TNP-Ficoll in the presence of accessory cells. Such responses were notably augmented by the addition of TRF derived from a monoclonal T cell hybridoma, B151K12(B151-TRF). Interestingly, B cells of mutant X-linked immunodeficient DBA/2Ha which failed to respond to B151-TRF gave anti-TNP PFC responses to TNP-Ficoll comparable to those of normal mice, depending on the presence of accessory cells. However, under this condition, the addition of B151-TRF did not augment the TNP-Ficoll responses. One explanation of the augmentation of TNP-Ficoll response by TRF for the B cells from nondefective mice was that two distinct B cell subpopulations exist which differ in their respective activation requirement for TRF and accessory cells. To examine this possibility, syngeneic accessory cells were pulsed with TNP-Ficoll and were assayed for their ability to activate normal B cells in the presence or absence of B151-TRF. The results revealed that TNP-Ficoll-pulsed accessory cells were able to induce primary anti-TNP PFC responses in normal B cells to the same magnitude as soluble TNP-Ficoll. However, these B cell responses induced by the TNP-Ficoll-pulsed accessory cells were not augmented by the addition of B151-TRF to the culture. These results support the notion that two distinct TNP-Ficoll-responsive B cell subpopulations exist; one requires accessory cell-B cell interaction to be activated by TNP-Ficoll but fails to respond to TRF, and the other can be activated by TRF in a totally accessory cell-independent manner.

Animals↗
PubMed1986

Evidence for contractility of the human seminiferous tubule confirmed by its response to noradrenaline and acetylcholine.

The experiments reported here demonstrate for the first time that the isolated human seminiferous tubule is capable of undergoing contraction after exposure to noradrenaline and acetylcholine. Isoproterenol produces a relaxation of the seminiferous tubule. It is indicated that there are the adrenergic alpha and beta receptors and muscarinic receptors in the myoid cells of human seminiferous tubules.

Acetylcholine↗