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Biomedical subjects

K Sano

Publications and source records attributed to K Sano.

At least 613 records · Page 34Linked to original sources
PubMed1984

An ultramicro-assay for proteins in biological fluids other than blood using a combination of agarose gel isoelectric focusing and silver staining.

Agarose gel isoelectric focusing and silver staining, is a suitable method for clearly separating 20-30 protein bands in various body fluids other than blood, such as urine, cerebrospinal fluid, tear, sweat, saliva and gingival fluid. A protein concentration of 80 mg/l is sufficient for detection, and a range of 200-600 mg/l is optimum to obtain reliable results. Thus, no preparative concentration or desalting of samples is required, though dilution to the optimum protein level may be needed for some fluid samples. This technique is expected to provide diagnostically useful information.

Body Fluids↗
PubMed1984

Selective vulnerability in the gerbil hippocampus following transient ischemia.

Following brief ischemia, the Mongolian gerbil is reported to develop unusual hippocampal cell injury (Brain Res 239:57--69, 1982). To further clarify this hippocampal vulnerability, gerbils were subjected to ischemia for 3, 5, 10, 20, and 30 min by bilateral occlusion of the common carotid arteries. They were perfusion-fixed after varying intervals of survival time ranging from 3 h up to 7 days. Following brief ischemia (5--10 min), about 90% of the animals developed typical hippocampal damage. The lesion was present throughout the extent of the dorsal hippocampus, whereas damage outside the hippocampus was not observed. Each sector of the hippocampus showed different types of cell reaction to ischemia. Ischemia cell change was seen in scattered CA4 neurons , and reactive change was found in CA2, whereas CA1 pyramidal cells developed a strikingly slow cell death process. Ischemia for 3 min did not produce hippocampal lesion in most cases. Following prolonged ischemia (20--30 min), brain injury had a wide variety in its extent and distribution. These results revealed that the gerbil brief ischemia model can serve as an excellent, reliable model to study the long-known hippocampal selective vulnerability to ischemia. Delayed neuronal death in CA1 pyramidal cells was confirmed after varying degrees of ischemic insult. These findings demonstrated that the pathology of neuronal injury following brief ischemia was by no means uniform nor simple.

Animals↗
PubMed1984

Fine structural nature of delayed neuronal death following ischemia in the gerbil hippocampus.

An unusual, delayed neuronal death (DND) has been noticed in the hippocampus of the Mongolian gerbil following brief ischemia (Kirino 1982). On day 1 following 5--10 min of ischemia, light microscopy showed the CA1 pyramidal cells unchanged. On day 2, the cells showed massive growth of membranous cytoplasmic organelles instead of overt cellular disintegration. These neurons were destroyed extensively by day 4 after ischemic insult. Following longer ischemia (20--30 min), however, the changes in the CA1 pyramidal cells appeared faster and resembled the well-characterized ischemic cell change (ICC). To further clarify the differences between ICC and DND, gerbils were submitted to transient 5--30 min ischemia. They were perfusion-fixed following a given survival period and then processed for electron microscopy. Following transient ischemia, specimens showed slow cell changes with growth of cisterns of the endoplasmic reticulum (ER). In some CA1 neurons, the cytoplasm was shrunken and darkly stained, but they also displayed accumulation of ER cisterns. Occasionally, the CA1 cells demonstrated highly shrunken dark perikarya, no different than in ICC. These results indicate that DND seems to be the typical disease process of the CA1 sector and that a severer insult makes the change faster and more similar to ICC. ICC seems to occur when the CA1 pyramidal cells are damaged so severely that they cannot react with proliferous activity.

Animals↗
PubMed1984

Delayed neuronal death in the rat hippocampus following transient forebrain ischemia.

An unusual, slowly progressing neuronal damage has been reported to occur in the gerbil hippocampus following ischemia (Kirino 1982). Delayed neuronal death following ischemia has also been noticed in the rat four-vessel occlusion model (Pulsinelli et al. 1982). By light microscopy this slow neuronal injury in the rat was not different from the previously known neuronal ischemic cell change. This report lead us to the question as to whether neurons in the rat hippocampus are damaged rapidly following an initial latent period or deteriorate slowly and progressively until they display overt changes. To clarify this point, observation was done on the hippocampal CA1 sector of the rat following ischemia. Rats were subjected to four-vessel occlusion, and those which developed ischemic symptoms were perfusion-fixed. Although the change appeared very slowly and lacked microvacuolation of the cytoplasm, neuronal alteration was practically not different from classical ischemic cell change. By electron microscopy, however, the change was detectable when the neurons still appeared intact by light microscopy. An increase in the membranous organelles and deposition of dark substances were the initial manifestations. It seemed that the CA1 neurons deteriorated very slowly and progressively, and that they retained partial viability in the initial phase of the change. In spite of the difference in light-microscopic findings, the mechanisms underlying delayed neuronal death in the rat and gerbil hippocampus seemed to be identical.

Animals↗
PubMed1984

In vitro infection of human B lymphocytes with adult T-cell leukemia virus.

Experimental transmission of adult T-cell leukemia (ATL) virus (ATLV) into human B lymphocytes was attempted. Cocultivation of B-cell rich fraction of peripheral blood from a healthy adult with X-ray irradiated ATLV producer MT-2 cells resulted in the establishment of OKA(B) cell line co-infected with both Epstein-Barr virus (EBV) and ATLV. OKA(B) cells and its subclones contained: (1) B cell markers exclusively; (2) both EBV-specific antigen, EBNA and ATLV-specific antigen, ATLA detected by immunofluorescence test; (3) ATLV-specific polypeptides, p24 and p19; (4) ATLV-specific mRNA in ATLA-positive clones; (5) ATLV and EBV particles detectable by electron microscopy. These data clearly show that human B lymphocytes are susceptible to ATLV infection.

Antigens, Viral↗
PubMed1984

Novel host-vector system for selection and maintenance of plasmid-bearing, streptomycin-dependent Escherichia coli cells in antibiotic-free media.

A novel system for selection and maintenance of cells carrying a recombinant plasmid has been developed, using the streptomycin-dependent (Smd) Escherichia coli 4D host and a plasmid vector carrying an rpsL gene from an Sm-resistant (Smr) mutant of E. coli which masks the Smd phenotype. Strain 4D carrying the Smr pBR322 plasmid can grow without Sm. Using this host-vector system, we can select for cells carrying an Smr recombinant plasmid and maintain them in antibiotic-free media.

Bacterial Proteins↗
PubMed1984

CT findings in patients with gliomas, surviving more than 10 years.

After reviewing the latest CT scans of 23 mostly low grade glioma patients who survived more than 10 years after treatment, it was suggested that loss of the original tumour bulk and frequently the presence of porencephalic cavity replacing the original tumour, with a smooth lining which is not contrast-enhanced is essential to assume a clinical "cure" in the case of intrinsic cerebral gliomas. In the case of gliomas growing within the ventricle or subarachnoid space, tissue with calcium deposit but without contrast-enhancement was noted, although the number of cases was limited.

Adolescent↗
PubMed1984

Nature of the vasoactive substance in CSF from patients with subarachnoid hemorrhage.

The purpose of this experiment was to study the nature of vasoactive substance in cerebrospinal fluid (CSF) from patients with aneurysmal subarachnoid hemorrhage. The authors have examined the effects of disulfide bond-reducing agents, a sulfhydryl group oxidizing agent, and specific antagonists of so-called "classical" neurotransmitters on the in vitro isometric contraction of canine basilar arterial strips induced by bloody human CSF. The disulfide bond-reducing agents dithiothreitol (10(-4) M) and dithioerythritol (10(-4) M) suppressed the contraction induced by bloody CSF by an average of 40.3% and 61.2%, respectively. This suppression was achieved under conditions that did not alter KCl-induced contraction. The sulfhydryl group oxidizing agent, 5,5'-dithiobis-(2-nitrobenzoic acid), 10(-4) M, reversed the inhibitory effect of dithioerythritol on the contractile response to bloody CSF. No significant suppression of any response in any preparation was observed with methysergide (10(-7) M), mepyramine (10(-7) M), phenoxybenzamine (10(-5) M), propranolol (10(-6) M), or atropine (10(-6) M). These results indicate that disulfide bonds in the arterial smooth-muscle cells are involved in the contractile responses of canine basilar artery to bloody CSF. Prostaglandins, hemoglobin, and lipid hydroperoxides may all be spasmogens in bloody CSF, while serotonin, histamine, norepinephrine, and acetylcholine are probably not involved.

Animals↗