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Biomedical subjects

T Minagawa

Publications and source records attributed to T Minagawa.

At least 37 records · Page 2Linked to original sources
PubMed1999

[Clinical practice in nursing, and "re establishment of daily routines"--the nurse's role in inter-professional collaboration].

Clinical practice in adult nursing is given during the 4th year at the School of Health Sciences, Sapporo Medical University. In this paper, we report the achievements in this training on one theme. The theme chosen was the nursing of patients and support of their families particularly their caregivers, for whom re-establishment of daily routines was indispensable. A total of 51 students underwent this nursing practice at a neurological hospital on 26 occasions, over 3 years from 1996. We found that the students learned inter-professional collaboration in their relationships with other students, skilled nurses and other professionals in the hospital and other organizations. We also analyzed the nurses' roles learned through the inter-professional collaboration, which could be summarized as follows: 1. Understanding patients' and their families' living conditions and mental state, as affected by the patient's disease or disability. 2. Supporting the safe care at home of patients helping them to re-establish living routines. 3. Educating caregivers on how to attend to patients and develop better attendance skills. 4. Making sure the patients' and their families' living needs are reflected in the support system. 5. Providing nursing information for the coordination process of the support system, as well as respecting patients' and their families' individuality and lives as a whole.

Aged↗
PubMed1998

Tertiary structure formation in the propeptide of subtilisin BPN' by successive amino acid replacements and its close relation to function.

The propeptide of subtilisin BPN', located between a signal peptide and the mature region of the protease, is known to exhibit inhibitory activity toward subtilisin BPN', in addition to its activity as an intramolecular chaperone that facilitates folding of subtilisin BPN'. Another unique feature is that although the isolated propeptide is in a random-coil state, it forms a defined tertiary structure when it is bound to subtilisin BPN'. In this study, amino acid replacements likely to increase the hydrophobicity of the propeptide have been introduced so that the isolated propeptide forms a defined tertiary structure. By successive replacements of Ala47 by Phe, Gly13 by Ile and Val65 by Ile, the propeptide was found to form a tertiary structure in addition to an increase in its secondary structure content, which were identified by circular dichoism spectra measurements. Concurrently, the propeptide, which is a temporary inhibitor in its wild-type form, became resistant to proteolytic digestion by subtilisin BPN'. These results show not only the close relationship between tertiary structure formation in the propeptide and its function as a protease inhibitor but also the ability of a random-coil protein to form a tertiary structure after a limited number of well-designed amino acid replacements.

Amino Acid Sequence↗
PubMed1998

Neuropeptides in the livers of mice during bacterial infections.

Neuropeptides such as substance P (SP) and vasoactive intestinal peptide (VIP) are known to act as immunomodulators. We investigated the induction of SP and VIP in the livers of mice infected with Listeria monocytogenes or injected with Tsukamurella paurometabolum. VIP was detected in the livers of mice after L. monocytogenes infection by an immunohistochemical technique and preproVIP mRNA, which was detected by reverse transcription-polymerase chain reaction (PCR), was induced post infection. However, no SP was detected. In contrast, SP, but not VIP was detected within granulomas in the livers of T. paurometabolum-injected mice, suggesting VIP and SP might be selectively induced in the liver by different bacterial infections.

Actinomycetales↗
PubMed1998

Clinical effects of the recombinant feline interferon-omega on experimental parvovirus infection in beagle dogs.

The clinical effects of recombinant feline interferon-omega (rFeIFN-omega), produced in silkworm by recombinant baculovirus, were examined in 3-4 month-old beagle dogs given an experimental canine parvovirus type-2 (CPV-2) infection. Clinical symptoms, such as pyrexia, vomiting, anorexia and diarrhea, were observed on day 4 after oral inoculation of 10(7) TCID50 of CPV-2 (cc 238 strain) in almost all the inoculated dogs. From day 4, rFeIFN-omega (1 mega units/kg/day) or physiological saline was administered intravenously to infected dogs for 3 consecutive days. Seven out of 17 dogs treated with physiological saline showed hemorrhagic diarrhea and continuously expressed severe clinical enteritis; one dog died with a large amount of hemorrhagic rice-water stool on day 6 after viral exposure. In contrast, 4 out of 12 dogs treated with rFeIFN-omega showed severe clinical enteritis associated with intermittent diarrhea. Scoring of fecal condition revealed that treatment with rFeIFN-omega significantly shifted the enteritis from a severe to mild form. Furthermore, rFeIFN-omega administered in the morning decreased the number of dogs expressing clinical enteritis in the evening suggesting a rapid effect. Vomiting and anorexia were also improved by treatment with rFeIFN-omega. These results suggest that rFeIFN-omega can reduce severe enteritis caused by CPV-2 infection in dogs.

Animals↗
PubMed1998

[The classification and analysis of the blood pathway in left ventricular cavity observed by left ventricular contrast echocardiography].

We can observe and analyse the blood pathway in left ventricular cavity by contrast echocardiography using sonicated albumin, because it can be through the pulmonary capillaries. I. The observational classification of the blood pathway in left ventricular cavity. Group I: The contrast medium comes to the apex directly from the mitral orifice. Group II: The contrast medium comes to the apex along the posterior wall forming the spiral flow and turns back to the outflow tract. Group III: The contrast medium is found like a fireworks only at the apex. II. The factors associated with the blood pathway in left ventricular cavity. 1. Abnormality of left ventricular wall motion, 2. The form of left ventricular cavity, 3. Early diastolic peak velocity of the transmitral flow, 4. A/E, 5. Left ventricular function.

Contrast Media↗
PubMed1997

The propeptide of subtilisin BPN' as a temporary inhibitor and effect of an amino acid replacement on its inhibitory activity.

The propeptide of subtilisin-family proteases is known to exhibit inhibitory activity toward a cognate protease in addition to its function as an intramolecular chaperone. For detailed investigation of its inhibitory properties, the propeptide of subtilisin BPN' was produced in Escherichia coli. Inhibitory activity measurements and electrophoresis showed that the propeptide was a temporary inhibitor, which was initially potent but was gradually degraded by subtilisin BPN' through specific intermediates. The main cleavage site was identified as Glu53-Lys54, with minor sites at Thr17-Met18 and Met21-Ser22, which were located in turn regions of the propeptide in the complex with subtilisin BPN'. Since the isolated propeptide has been shown not to form a tertiary structure, these results indicate that main digestions proceed through proteolytic attack of subtilisin toward the accessible sites of the propeptide in the complex with subtilisin. Therefore, replacement of Glu53 at the main cleavage site by Asp, which is a less favorable amino acid than Glu for subtilisin, makes the propeptide a more resistant temporary inhibitor.

Binding Sites↗
PubMed1997

Macrophage antigen-1 positive cells are essential in the defense against Theiler's virus strain GD VII infection in the spinal cord.

Acute encephalomyelitis caused by Theiler's virus strain GD VII resembles human poliomyelitis, and T cells are essential in eliminating the virus from the brain, though not from the spinal cord. We speculated that macrophage-lineage cells might play a crucial role in eliminating the virus from the spinal cord. To analyse the role of macrophage-lineage cells in the infection, antibodies specific for beta2 integrin, as well as an anti-leukocyte function antigen 1 (LFA-1) monoclonal antibody (MAb) and an anti-complement receptor type 3 (CR3) MAb were used to deplete the corresponding cell populations in Theiler's virus-infected mice. Infiltration of CD8+ T cells into the brain and spinal cord was inhibited by the administration of the anti-LFA-1 MAb, and viral replication was augmented only in the brain. The number of CD4+ T cells and macrophage antigen-1 (Mac-1[+]) cells in the brain and spinal cord were not decreased by anti-LFA-1 MAb treatment. Anti-CR3 MAb treatment led to decrease of Mac-1(+) cells in the brain and spinal cord. The viral replication in the spinal cord of anti-CR3 MAb treated mice was augmented, but not that in the brain. These results indicate that the defense mechanism against Theiler's virus strain GD VII is dependent on Mac-1(+) cells in the spinal cord.

Animals↗
PubMed1997

[Survey of echinococcosis in Hokkaido and measure against it].

The first patient with echinococcosis who had lived in Rebun island was discovered in 1937 at Otaru and 134 patients had been identified as Rebun cases till 1989. In the meantime, the eradication of echinococcosis succeeded with extermination of dogs and foxes from the island. On the other hand, the first patient of Kon-sen cases was found in 1965 and 208 patients have been treated so far. The patients had been restricted within the Kon-sen region until 1979, but thereafter the patients have been found sporadically all over Hokkaido. This distributional tendency of the patients coincides with the explosion of the infection with Echinococcus multilocularis in foxes in Hokkaido after 1980. Prevention measure against echinococcosis has been carried out by the Committee for the Disorder of Hokkaido, by which we have been successful. We succeed in the early diagnosis and treatment of the patients, but still have no decisive methods to eradicate E. multilocularis in Hokkaido. This is one of the important problems of zoonosis to solve for the next century of Hokkaido.

Animals↗
PubMed1996

Reciprocal action of interferon-gamma and interleukin-4 promotes granulomatous inflammation induced by Rhodococcus aurantiacus in mice.

An intravenous injection of Rhodococcus aurantiacus to mice causes granulomatous inflammation dependent on endogenous interferon-gamma (IFN-gamma). The present study examined the role of endogenous interleukin-4 (IL-4) on granulomatous inflammation. Endogenous IL-4 in the spleen extracts was not detected during the phase of granuloma formation by enzyme-linked immunosorbent assay (ELISA). However, IL-4 protein level was elevated during the phase of granuloma regression. IL-4 mRNA expression in the livers and spleens was also elevated during the phase of granuloma regression. In addition, IL-4 levels during the phase of granuloma formation were increased by treatment with anti-IFN-gamma monoclonal antibody (mAb), suggesting that endogenous IFN-gamma might inhibit IL-4 production during the phase of granuloma formation. Administration of anti-IL-4 mAb on weeks 3 and 4 after the inoculation inhibited the regression of granulomas and augumented IFN-gamma level at 5 weeks. Endogenous IFN-gamma was produced by CD4+ T cells during the phase of granuloma regression and endogenous IL-4 was produced by both CD4+ and CD8+ T cells. These findings suggest that during the phase of granuloma formation endogenous IL-4 might be inhibited by IFN-gamma, while during the phase of granuloma regression endogenous IL-4 might play a crucial role in the reduction of granulomas and IFN-gamma production.

Actinomycetales Infections↗
PubMed1996

Blood-brain-barrier transport of lipid microspheres containing clinprost, a prostaglandin I2 analogue.

Because the permeability of the blood-brain barrier to lipid microspheres (LMs) has not hitherto been demonstrated, blood-brain-barrier permeability to LM containing the prostaglandin I2 analogue clinprost has been evaluated for an in-vitro system of primary cultured monolayers of bovine brain capillary endothelial cells (BCECs), by a capillary depletion study in rats and by an in-situ brain perfusion study in normal and 4-vessel-occluded fore brain ischaemic rats. Although energy-dependency was not observed in [3H]clinprost uptake by BCECs, in accordance with results for simple diffusional transport, uptake of [3H]clinprost contained in lipid microspheres (denoted [3H]clinprost(LM)) was significantly inhibited by the endocytosis inhibitor, dansylcadaverine. The transport of LM into BCECs by endocytosis was also confirmed by fluorescence microscopy and flow-cytometric analysis using LM labelled with a fluorescent probe, 1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate (Dil). The absolute uptake of Dil(LM) by BCECs, measured by HPLC, was, however, almost 1/10 that of [3H]clinprost(LM), results which suggest the superiority of simple diffusion of clinprost over endocytosis of its LM form in the uptake of clinprost(LM) by BCECs. In the capillary-depletion study with rat-brain-perfused [3H]clinprost(LM) from the internal carotid artery, the parenchyma apparent distribution volume was about 45 times larger than that of the capillary, showing that [3H]clinprost(LM) was transported through the blood-brain barrier into the brain. The permeability coefficients of [3H]clinprost and [3H]clinprost(LM) determined by insitu brain perfusion in normal rats were considerably higher than those of the active metabolite [3H]isocarbacyclin and its LM form. In addition, the Blood-brain-barrier permeabilities to [3H]clinprost, [3H]isocarbacyclin and their LM forms in ischaemic rats were almost identical to those in normal rats. It was concluded that clinprost(LM) was transported through the blood-brain barrier by endocytosis of LM, simple diffusion of clinprost released from LM, and transport of isocarbacyclin generated by hydrolysis of clinprost. The blood-brain-barrier permeability of clinprost(LM) is not reduced in ischaemic conditions, because the simple diffusion of clinprost released from LM contributed mainly to clinprost(LM) transport.

Animals↗
PubMed1996

Endogenous interleukin-4, but not interleukin-10, is involved in suppression of host resistance against Listeria monocytogenes infection in interferon-depleted mice.

The production and roles of endogenous interleukin-4 (IL-4) and IL-10 in a sublethal infection with Listeria monocytogenes were studies in normal mice and anti-gamma interferon (IFN-gamma) monoclonal antibody (MAb)-pretreated mice. In normal mice, the expression of mRNAs for IL-4 and IL-10, which was amplified by reverse transcription-PCR, was induced in the spleens and livers either early or late in infection, although the serum IL-4 and IL-10 were not detectable by enzyme-linked immunosorbent assays. In vivo administration of anti-IL-4 MAb showed no effect on antilisterial resistance, whereas anti-IL-10 MAb partially diminished the defense. In anti-IFN-gamma MAb-pretreated mice, a delay in the bacterial elimination from the spleens and livers was observed and high titers of serum IL-4 and IL-10 were induced late in infection. Production of endogenous IL-4 and IL-10 was suppressed in both CD4+ cell-and CD8+ cell depleted mice. The suppression of antilisterial resistance in anti-IFN-gamma MAb-pretreated mice was canceled when anti-IL-4 MAb was injected late in infection, whereas anti-IL-10 MAb showed no effect. These results suggest that the host immune responses were polarized into the T-helper 2 phenotype in anti-IFN-gamma MAb-pretreated mice and that inhibition of host resistance against L. monocytogenes by depletion of IFN-gamma might be attributable to IL-4 produced by T cells polarized into the T-helper 2 phenotype as well as the inhibition of the IFN-gamma effects.

Animals↗
PubMed1996

Transforming growth factor beta is protective in host resistance against Listeria monocytogenes infection in mice.

The role of transforming growth factor beta (TGF-beta) in host resistance against Listeria monocytogenes infection was studied with mice. The constitutive expression of TGF-beta 1 mRNA was observed in the spleens and livers of mice before and after infection. Injecting the mice with anti-TGF-beta 1 peptide serum resulted in diminished antilisterial resistance, whereas the administration of human platelet-derived TGF-beta 1 enhanced the resistance. Moreover, mice were protected against lethal infection when treated with TGF-beta 1. These results suggest the TGF-beta 1 might be involved in antilisterial resistance. On the other hand, injecting the mice with TGF-beta 1 resulted in a decrease in the titers of endogenous gamma interferon, tumor necrosis factor alpha, and interleukin-6, which are crucial in antilisterial resistance, in sera and in extracts of spleen and liver. Thus, a complicated mechanism might be involved in the role of TGF-beta 1 in host resistance against L. monocytogenes infection.

Animals↗
PubMed1996

[New method for automatic tracking of the endocardial boundary in clinical use].

This study attempted to detect the left ventricular endocardial boundary in six healthy men (volunteers) using a newly developed computerized two-dimensional echocardiography method. Automatic detection of the left ventricular endocardium was achieved by; sampling of pictures, noise reduction of the pictures, filtering, decision of the early loop, detection of the left ventricular endocardial boundary, smoothing the boundary, and correction of the boundary. This process requires only 2-3 sec. Areas of the short-axis cross-sections in systolic and diastolic phases of one cardiac cycle were obtained and the percent change rate of these areas on a cardiac cycle were calculated. These were compared with the results obtained by the manual method. The boundary of the left ventricular endocardium detected by the computerized method almost coincided with that found by the manual method. Areas and the change rates obtained were correlated with those by the manual method (areas: r = 0.86, % change rate of area: r = 0.94). This new method is suitable for clinical use.

Adult↗
PubMed1995

Species differences in hydrolysis of isocarbacyclin methyl ester (TEI-9090) by blood esterases.

Species differences in the hydrolysis of isocarbacyclin methyl ester (TEI-9090) in whole blood and in its separated components were studied in rats, dogs and human. Esterase activity in rat whole blood was approximately 100 and 400 times higher than that in dog and human whole blood, respectively, and was attributed to high plasma activity. In contrast, TEI-9090 hydrolysis activities in dog and human blood were due to red blood cells (RBC), whose activity in humans was slightly suppressed by albumin. In dogs, activity in RBC membranes was 10 times greater than in the cytosol, while in human membrane and cytosol activity was virtually the same. The effects of the esterase inhibitor diisopropylfluorophosphate, bis-p-nitrophenylphosphate (BNPP), eserine, 5,5'-dithiobis-(2-nitrobenzoic acid) (DTNB) and p-chloromercuribenzoate showed that the rat plasma and RBC cytosol esterases hydrolysing TEI-9090 were carboxylesterase (CarbE) and arylesterase (ArE), respectively. The esterases in dog plasma and RBC membrane were CarbE, and RBC cytosol esterase was ArE. In humans, the esterase activities in plasma, RBC membrane and cytosol were butyrylcholinesterase, CarbE and ArE, respectively.

Animals↗
PubMed1995

Paralysis caused by acute myelitis in Theiler's murine encephalomyelitis virus strain GD VII infection is induced by CD4+ lymphocytes infiltrating the spinal cord.

Intravenous infection by Theiler's murine encephalomyelitis virus strain GD VII causes acute encephalomyelitis and paralysis in infected mice. However, nude mice and cyclophosphamide-treated ddY mice did not show paralysis when they were able to survive until day 20 post-infection (p.i.). Of ddY mice infected with 5 x 10(7) p.f.u./mouse, 70-80% showed symptoms of paralysis on day 20 p.i. The viral titres in the brain and spinal cord in infected mice were not significantly different between paralytic and non-paralytic mice. In all of the mice infected with the virus, CD4+ lymphocytes and CD8+ lymphocytes had infiltrated the brain on days 10, 12, 14 and 20 p.i. as demonstrated by flow cytometric analysis. In contrast, few T lymphocytes infiltrated the spinal cord in the non-paralytic mice. Administration of an anti-CD4 monoclonal antibody (MAb) or anti-T cell receptor-alpha beta MAb on day 6 p.i. inhibited paralysis until day 20 p.i., though 20% of the MAb-treated mice and 80% of the control mice showed paralysis. Administration of anti-CD8 MAb was not effective in the suppression of paralysis. The MAb treatment did not significantly augment viral replication in the spinal cord, although the viral titres in the brain of the MAb-treated mice increased significantly. After the transfer of spleen cells from infected C3H mice, the recipient mice infected with a small amount of the virus showed paralysis, though uninfected mice did not. This transfer could be blocked by CD4+ lymphocyte depletion of the donor mice. These results indicate that paralysis caused by acute myelitis in Theiler's virus strain GD VII infection is induced by CD4+ lymphocytes infiltrating the spinal cord.

Acute Disease↗
PubMed1995

CD3+/TCR-alpha beta- cells are important in protecting spinal cord tissues against Theiler's virus strain GD VII infection.

Intravenous infection with Theiler's virus strain GD VII causes acute encephalomyelitis in mice. Endogenous IFN-gamma produced in the spinal cord is important to protect the tissue in mice infected with this virus. Neither CD4+ cells nor CD8+ cells infiltrated the spinal cords of infected mice until Day 9 postinfection. However, the number of CD3+/TCR-gamma delta+ cells increased in the spinal cords of mice infected with the virus. These cells resided in the spinal cords of normal mice, and produced IFN-gamma as a result of stimulation by immobilized anti-CD3 mAb. Elimination of CD3+ cells by the administration of a specific mAb augmented viral replication and suppressed production of endogenous IFN-gamma. Depletion of TCR-alpha beta+ cells and ASGM1+ cells did not affect the viral replication, and did not alter the production of IFN-gamma. Therefore, CD3+/TCR-alpha beta- cells producing IFN-gamma play an important role in the protection of the spinal cord against Theiler's virus infection. These results suggest that CD3+/TCR-alpha beta- cells might be identical to TCR-gamma delta+ cells.

Animals↗