Biomedical subjects

N Miyoshi

Publications and source records attributed to N Miyoshi.

112 records · Page 7Linked to original sources

PubMed1977

Changes in blood catecholamine levels and ultrastructure of dog adrenal medullary cells during hemorrhagic shock.

Blood catcholamine levels and ultrastructural changes in adrenal medullary cells were followed during the course of oligemic and normovolemic shock in dogs. Blood adrenaline concentration rose promptly after hemorrhage, reaching a maximum that was 10-fold greater than normal during the early period of hemorrhagic hypotension. Thereafter, adrenaline levels gradually declined until the end of the critical stage of hemorrhagic shock when the blood concentration rose to a level 8-fold that of normal. Following the critical stage, and throughout the irreversible stages of shock, adrenaline levels remained near normal. Noradrenaline, which was initially undetectable, first appeared in the impending stage of hemorrhagic hypotension and showed little change during the course of severe hemorrhagic hypotension. Ultrastructural studies demonstrated A-cell degranulation as early as 5 min after initiation of hemorrhage. Degranulation continued throughout the impending stage of hemorrhagic hypotension and was associated with an increasing number of autophagic vacuoles containing empty vesicles. At the end of the critical stage, all A cells showed complete degranulation and degenerative hydropic change. Progression to necrosis rather than arrest or reversal of hydropic change was observed after reinfusion of blood. In contrast to the marked alterations in A cells, most N cells were morphologically unchanged.

Adrenal Medulla↗

PubMedDate not supplied

The effect of hyperthermia on murine leukaemia cells in combination with photodynamic therapy.

Mouse leukaemia L1210 cells were subjected to hyperthermia (43.0 +/- 0.05 degrees C, water bath) and photodynamic therapy (50 micrograms/ml haematoporphyrin derivative (HpD), 630 +/- 5 nm at 0.1 mW/cm2) for varying lengths of treatment time in different sequences. Dose-response curves showed that the two modalities interact to make the combination more cytotoxic than the sum of the separate individual treatments, and that a determining factor is the intracellular concentration of HpD of tumour cells during hyperthermia. High cytotoxic (synergistic) effects of photodynamic therapy (PDT) were obtained when PDT was performed after hyperthermia following HpD administration. However, only additive cytotoxic effects were found, when hyperthermia was performed after HpD administration and PDT. These cytotoxic data were supported by DNA damage (the increase in single-stranded DNA) as revealed by flow cytometry in cells stained with acridine orange (AO). These in vitro experiments suggest that clinical applications of PDT after hyperthermia with HpD injection might be useful.

Animals↗

PubMedDate not supplied

Photodynamic therapy based on combined use of 5-aminolevulinic acid with a pheophorbide-a derivative for murine tumors.

BACKGROUND: 5-Aminolevulinic acid (5-ALA)-based photodynamic therapy (PDT) appears to be a promising cancer treatment modality. Here, we investigated whether enhancement of 5-ALA-PDT by combining another photosensitizer, a pheophorbide-a derivative (PH-1126), is an option. MATERIALS AND METHODS: PH-1126 (2.5, 5 or 10 mg/kg.bw) and 5-ALA (168 mg/kg.bw) were injected i.p. into C3H/HeN mice bearing squamous cell carcinoma (SCC) or BALB/c nude mice bearing L5178Y lymphoma. Afterwards, these mice received laser irradiations (630 nm for 5-ALA and 650 nm for PH-1126) with a total dose of 88 J/cm2. The results showed that PDT with 5-ALA plus PH-1126 at a low dose (2.5 mg/kg.bw) were well tolerated by both animal models, with resultant synergistically enhanced inhibition of tumor growth and/or survival advantage for the treated animals. CONCLUSION: This study demonstrated the usefulness of the combination of a low dose PH-1126 with 5-ALA for PDT of experimental tumors in vivo.

Aminolevulinic Acid↗

PubMedDate not supplied

Chronic persistent nodular polioencephalomyelitis presenting with brain atrophy.

A 61-year-old male had a recurrent fever (approx. 38 degrees C) and one month later, disorientation and forgetfullness became gradually apparent. His mental and somatic status deteriorated progressively with the recurrence of fever; 3 years later he was in a persistent vegetative state accompanied by status epilepticus, and died after 5 years. Mononuclear cytosis (8-20/microliters) and increased protein (20-70 mg/100 ml) were observed in the cerebro-spinal fluid (CSF) at each examination. There was no increase of antibody titers against various viruses, chlamydia, mycoplasma and toxoplasma in the serum and CSF. Neuropathologically, the prominent microscopic finding was patchy scarred foci consisting of neuronal loss replaced by glial tissue throughout the gray matter. A few gliomesenchymal nodules were found. In addition, rod-shaped macrophages were found to varying degrees in all areas of the brain and spinal cord. No viral inclusion bodies were identified. Electron microscopic examination revealed no viral particles in the affected areas. Suspensions of the frozen brain and CSF were inoculated into primary neuron cultures derived from fetal mice and into mouse brains, but the results were negative. There had been five reported cases of chronic nodular encephalitis up until 1971; this case seems to differ from the others by the presence of persistent inflammation and by neuropathologic findings.

Atrophy↗