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S Nakao

Publications and source records attributed to S Nakao.

At least 109 records · Page 6Linked to original sources

Generalized peritonitis with pneumoperitoneum caused by the spontaneous perforation of pyometra without malignancy: report of a case.

Spontaneous perforation is a very rare complication of pyometra. We report herein the case of an 88-year-old woman who presented with muscular rigidity and free air on abdominal X-ray films. Perforation of the gastrointestinal tract was diagnosed preoperatively, and an emergency laparotomy was performed. A total hysterectomy with bilateral salpingo-oophorectomy was carried out under the diagnosis of generalized peritonitis caused by the spontaneous perforation of pyometra. The culture of purulent fluid from the abdominal cavity showed only Escherichia coli, with no anaerobic bacteria. Histological examination revealed pyometra with necrosis of the endometrium and no evidence of malignancy. The patient was discharged on postoperative day 68 without any major complications. Pyometra is an unusual cause of peritonitis, but it must be considered as a possible diagnosis in elderly women presenting with an acute abdomen. Following this case report, we discuss the problems associated with establishing a correct preoperative diagnosis of generalized peritonitis caused by the spontaneous perforation of pyometra.

Aged↗

Impaired response of granulocyte-committed progenitor cells to stem cell factor and granulocyte colony-stimulating factor in human cyclic neutropenia.

Although cyclic neutropenia (CN) has been the subject of extensive studies due to its striking clinical picture, the abnormality of hematopoietic progenitor cells in patients with CN has been poorly defined. We studied the sensitivity of progenitor cells of a CN patient to colony-stimulating factors (CSF) including G-CSF, interleukin-3 (IL-3), and stem cell factor (SCF). Peripheral blood progenitor cells of the patient required a significantly higher dose of G-CSF to give rise to colonies than those of normal controls. While the presence of SCF enhanced the number of G-CSF-induced colonies regardless of the concentration of G-CSF in normal controls, this synergistic effect of SCF was limited to the high concentration of G-CSF in the patient, indicating that the abnormality in hematopoiesis in CN involved more immature progenitor cells responsive to SCF.

Adult↗

Involvement of prostaglandins in histamine H1 receptor-operated Ca2+ entry in human gingival fibroblasts.

In the absence of external Ca2+, 100 microM histamine evoked a transient increase in intracellular Ca2+ ([Ca2+]i), and subsequent addition of Ca2+ to the medium resulted in a sustained increase in [Ca2+]i in fura-2-loaded human gingival fibroblasts. These Ca2+ mobilizations are attributed to Ca2+ release from intracellular stores and Ca2+ entry, respectively. When the histamine H1 antagonist chlorpheniramine was added after the histamine-induced transient increase in [Ca2+]i, the Ca2+ entry induced by the addition of Ca2+ was inhibited. In the fibroblasts pretreated with cyclooxygenase inhibitors, indomethacin (1 microM) or aspirin (100 microM), histamine-induced Ca2+ entry was significantly inhibited, but not the transient [Ca2+]i increase. These results suggest that the histamine-induced Ca2+ entry requires the continuous binding of histamine to the H1 receptors and is regulated by prostaglandins, which are probably produced due to the H1 receptor activation.

Aspirin↗

Administration of G-CSF to normal individuals diminishes L-selectin+ T cells in the peripheral blood that respond better to alloantigen stimulation than L-selectin- T cells.

To determine whether administration of G-CSF induces phenotypic or functional changes in T cells, we examined peripheral blood T cells from normal individuals receiving G-CSF for activation antigen and adhesion molecule expression before and after G-CSF administration. G-CSF (10 microg/kg/day) was administered subcutaneously to 14 normal individuals for 3-5 days and their PBMC were serially analyzed with monoclonal Ab (mAb) directed to HLA-DR, CD45RO, CD45RA, CD25, CD122, CD95, CD11a, CD49d, CD44 and CD62L (L-selectin) coupled with anti-CD3 mAb. Among T cells positive for these antigens, only the proportion of T cells expressing L-selectin significantly decreased from 68% to 37% after 3-day G-CSF administration. When peripheral blood CD3+ T cells obtained before and after G-CSF administration were sorted into two populations depending on the expression of L-selectin and tested for their proliferative response to allogeneic B cells, the reactivity of L-selectin- cells to alloantigen stimulation was consistently lower than that of L-selectin+ cells regardless of the exposure to G-CSF. The decrease in the relative number of L-selectin+ cells induced by G-CSF administration may contribute to the unexpectedly low incidence of severe acute GVHD after allogeneic PBSC transplantation.

Granulocyte Colony-Stimulating Factor↗

Effects of nitrous oxide on haemodynamic and electroencephalographic responses induced by tetanic electrical stimulation during propofol anaesthesia.

We studied the effect of nitrous oxide on haemodynamic and electroencephalographic responses caused by noxious stimulation during propofol anaesthesia. Thirty-four patients (ASA I-II) were anaesthetised with propofol 3 mg x kg(-1) and were randomly allocated to receive either 60% nitrous oxide in oxygen or 40% oxygen in air. Anaesthesia was maintained using propofol infusion of 10 mg x kg(-1) x h(-1) for the first 10 min, 8 mg x kg(-1) x h(-1) for the next 10 min and 6 mg x kg(-1) x h(-1) thereafter. Thirty minutes after the induction of anaesthesia, tetanic electrical stimulation (80 mA, 100 Hz) was applied to the ulnar nerve. Tetanic stimulation significantly increased blood pressure and heart rate in both groups (p < 0.005 or less), but did not induce any arousal pattern on the electroencephalograph. Nitrous oxide significantly attenuated the tetanic stimulation-induced increase in blood pressure (p < 0.05 or less), but not the heart rate.

Adult↗

Electroencephalographic arousal response during tracheal intubation and laryngeal mask airway insertion after induction of anaesthesia with propofol.

Laryngoscopy and tracheal intubation, or insertion of a laryngeal mask airway may lead to an arousal response on the electroencephalogram. We studied whether more intense stimulation (laryngoscopy and tracheal intubation) causes a greater arousal response than less intense stimulation (laryngeal mask airway insertion). Thirty-four patients (ASA I-II) were anaesthetised with propofol 3 mg.kg-1, followed by vecuronium 0.15 mg.kg-1 and a propofol infusion of 10 mg.kg-1.h-1. Three minutes after induction of anaesthesia, either laryngoscopy and tracheal intubation (n = 18), or laryngeal mask airway insertion (n = 16) was performed. Laryngoscopy and tracheal intubation caused a significantly greater increase in blood pressure (but not heart rate) than laryngeal mask airway insertion (p < 0.05). Electroencephalogram responses were not different. More intense stimulation does not cause a greater arousal response during propofol anaesthesia.

Adult↗

CD59-deficient blood cells and PIG-A gene abnormalities in Japanese patients with aplastic anaemia.

Patients with aplastic anaemia (AA) frequently develop paroxysmal nocturnal haemoglobinuria (PNH) as a late complication. We investigated the frequency of the development of PNH features including a glycosyl phosphatidylinositol (GPI) anchoring defect in 73 Japanese patients with AA. A deficient expression of CD59 was found on erythrocytes and/or granulocytes in 21/73 (28.8%) of the patients. A Ham/sugar water test was positive in 13/21 patients. We also examined mutations of the PIG-A gene in 11 patients with CD59 deficiency. A heteroduplex analysis detected PIG-A gene abnormality in 10/11 patients tested. Nucleotide sequencing was performed in six patients and identified eight mutations including three mutations in one patient. The mutations of the PIG-A gene were all different and included two single-base insertions, one single-base deletion, two two-base deletions, and one each of eight-base insertion and nine- and ten-base deletions. All mutations but one caused frameshifts. Our findings indicate that a high proportion of Japanese patients with severe AA have a GPI-anchoring defect and that the PIG-A gene is mutated in the AA patients who had a GPI deficiency. We found no significant difference in the pattern of the PIG-A gene mutation between the AA patients with a GPI deficiency and those with de novo PNH.

Adolescent↗

High inducibility of heat shock protein 72 (hsp72) in peripheral blood mononuclear cells of aplastic anaemia patients: a reliable marker of immune-mediated aplastic anaemia responsive to cyclosporine therapy.

To better characterize immunologic aberrations in aplastic anaemia (AA), we examined peripheral blood mononuclear cells (PBMC) of 67 patients with AA and other patients with various haematological diseases for the expression of heat shock protein 72 (hsp72), which is inducible in lymphocytes by various stressors including antigenic stimulation. When freshly obtained PBMC were examined using flow cytometry, the proportion of cells expressing hsp72 in cytoplasm was significantly higher in allogeneic marrow transplant recipients (22 +/- 15%, mean +/-standard deviation (SD)) and AA patients (17 +/- 21%) than in normal individuals (6 +/- 3%). When PBMC were tested after heat treatment, only the proportion of hsp72+ cells of AA patients (37 +/- 30%) was significantly higher than that of the normal control (17 +/- 11%). Dual fluorescence analysis of the PBMC revealed that the majority of hsp72+ cells was CD3+. For 28 untreated AA patients, the proportion of hsp72+ cells in those who later responded to cyclosporine (CyA) (62 +/- 24%) was higher than that in non-responders (19 +/- 13%). Immunoblotting analysis revealed predominant expression of hsp72 in T cells. These findings indicate that high inducibility of hsp72 in PBMC by heat treatment is an immunologic aberration characteristic of CyA-responsive AA and that this simple test may be useful for identifying a subset of AA patients responsive to immunosuppressive therapy.

Adolescent↗

Cytotoxicity against lymphoblastoid cells mediated by a T-cell clone from an aplastic anaemia patient: role of CD59 on target cells.

In an attempt to elucidate the pathogenic role of a CD4+ cytotoxic T-cell clone NT4.2 isolated from the bone marrow of a patient with cyclosporine-dependent aplastic anaemia, we characterized the T-cell clone as well as its cytotoxicity against an autologous Epstein-Barr (EB) virus-transformed B-lymphoblastoid cell line (LCL). NT4.2 expressed BV21+ BJ2.7+ with a complementarity-determining region (CDR) 3 motif of SQGQGEVEQY which was homologous to that of a T-cell clone isolated from a patient with connective tissue disease. NT4.2 started to lyse LCL cells within 2 h and exerted maximal cytotoxicity within 3 h of incubation. The cytotoxicity required the presence of divalent cations and was not associated with DNA fragmentation of the target cells. Anti-CD59 monoclonal antibodies (MoAb) blocked the cytotoxicity to the same degree as anti-CD3, HLA-DR or CD2 mAb. Flow cytometric analysis of the peripheral blood of this patient during remission after cyclosporine therapy revealed 1.7% of granulocytes to be deficient in CD59. These findings indicate that NT4.2 exerts its cytotoxicity through a perforin-mediated pathway, not a Fas/Fas ligand-dependent pathway, and that haemopoietic stem cells lacking CD59 may evade cytotoxic T lymphocytes, leading to the in vivo expansion of a paroxysmal nocturnal haemoglobinuria clone.

Aged↗

Semi-automatic laser beam microdissection of the Y chromosome and analysis of Y chromosome DNA in a dioecious plant, Silene latifolia.

Silene latifolia has heteromorphic sex chromosomes, the X and Y chromosomes. The Y chromosome, which is thought to carry the male determining gene, was isolated by UV laser microdissection and amplified by degenerate oligonucleotide-primed PCR. In situ chromosome suppression of the amplified Y chromosome DNA in the presence of female genomic DNA as a competitor showed that the microdissected Y chromosome DNA did not specifically hybridize to the Y chromosome, but hybridized to all chromosomes. This result suggests that the Y chromosome does not contain Y chromosome-enriched repetitive sequences. A repetitive sequence in the microdissected Y chromosome, RMY1, was isolated while screening repetitive sequences in the amplified Y chromosome. Part of the nucleotide sequence shared a similarity to that of X-43.1, which was isolated from microdissected X chromosomes. Since fluorescence in situ hybridization analysis with RMY1 demonstrated that RMY1 was localized at the ends of the chromosome, RMY1 may be a subtelomeric repetitive sequence. Regarding the sex chromosomes, RMY1 was detected at both ends of the X chromosome and at one end near the pseudoautosomal region of the Y chromosome. The different localization of RMY1 on the sex chromosomes provides a clue to the problem of how the sex chromosomes arose from autosomes.

Base Sequence↗

Clonidine inhibits and phorbol acetate activates glutamate release from rat spinal synaptoneurosomes.

UNLABELLED: Glutamate is a major neural transmitter of noxious stimulation in the spinal cord. We measured glutamate release from rat spinal synaptoneurosomes by using an enzyme-linked fluorimetric assay. Glutamate was released from spinal cord synaptoneurosomes in response to the addition of 30 mM potassium chloride, 1 mM 4-aminopyridine, or 1 microM ionomycin in the presence of external calcium. There was less release of glutamate in the absence, versus the presence, of external calcium. Clonidine significantly reduced the level of glutamate released from the spinal cord synaptoneurosomes. Tetradecanoyl phorbol acetate, an activator of protein kinase C, enhanced glutamate release. Forskolin, a protein kinase A activator, had no effect on the glutamate efflux. Our data indicate that glutamate released in the spinal cord is dependent on protein kinase C but is independent of the protein kinase A pathway. They also suggest that the inhibition of glutamate release may be the underlying mechanism of antinociception by clonidine at the spinal cord level. IMPLICATIONS: We demonstrated that synaptoneurosomes from rat spinal cord could release glutamate in response to depolarization. We showed that an activator of protein kinase C increased glutamate released from spinal cord synaptoneurosomes but that clonidine decreased it. Glutamate release may be one of the mechanisms of antinociception at the spinal cord level.

4-Aminopyridine↗

Early establishment of hematopoietic chimerism following allogeneic peripheral blood stem cell transplantation in comparison with allogeneic bone marrow transplantation.

To characterize the process of the establishment of complete chimerism after allogeneic peripheral blood stem cell transplantation (allo-PBSCT), we determined the origin of leukocytes in peripheral blood (PB) obtained from 23 patients in the very early period after allo-PBSCT using amplification of mini- or microsatellite regions of genomic DNA. Donor-specific alleles were amplified from the PB obtained at day 8 post-transplant for 19 allo-PBSCT patients. Among the 19 patients, 12 showed only donor-specific alleles (complete chimerism) while 7 did both donor and host-specific alleles (mixed chimerism). Although donor specific alleles were amplified in 10 of 12 patients who received allogeneic bone marrow transplantation (allo-BMT) similarly to allo-PBSCT, all of these ten showed mixed chimerism. When the chimeric state was examined in PB samples obtained serially at 2-3-day intervals post-transplant, host-specific alleles in allo-PBSCT patients were not detectable in the PB much earlier than those in allo-BMT patients. These findings indicate that the appearance of donor-derived cells associated with the disappearance of host-derived cells in the circulation occurs earlier after allo-PBSCT as compared with allo-BMT, leading to the rapid establishment of complete chimerism.

Adolescent↗

Morphological effects on in-stent restenosis assessed by intravascular ultrasound imaging.

The purpose of this study was to evaluate the rupture and dissection of the vessel wall immediately after balloon dilatation by intravascular ultrasound (IVUS) imaging and to predict restenosis in patients who underwent subsequent coronary stent implantation. Stent implantation improves the long-term results of coronary angioplasty by reducing lesion elastic recoil and arterial remodeling. However, several studies have suggested that neointimal hyperplasia is the cause of instant restenosis. We recruited 60 patients in whom IVUS studies were performed immediately after successful balloon dilatation and just before stent implantation. We compared IVUS parameters with 6-month follow-up quantitative coronary angiography. This was performed in 51 lesions of 51 patients (85%). Qualitative analysis included assessment of plaque composition, plaque eccentricity, plaque fracture and the presence of dissection. In addition, minimal luminal diameter, percent diameter stenosis, percent area stenosis and plaque burden were quantitatively analyzed. Two morphological patterns after balloon dilatation were classified by IVUS. Type I was defined as absence or partial tear of the plaque without disclosure of the media to lumen (22 lesions). Type II was defined as a split in the plaque or dissection of the vessel wall with disclosure of the media to the lumen (29 lesions). At 6 months follow-up, angiographic restenosis occurred in 17 of the 51 lesions (33%). Restenosis was significantly (p < 0.05) more likely to occur in type II (13/29: 45% incidence) than in type I (4/22: 18% incidence). The assessment of plaque morphology immediately after balloon dilatation and before stent implantation provides important therapeutic and prognostic implications.

Aged↗

Monitoring of human herpesviruses after allogeneic peripheral blood stem cell transplantation and bone marrow transplantation.

Herpesviruses frequently cause serious complications after allogeneic bone marrow transplantation (allo-BMT). Recent studies have shown more rapid immune reconstitution after allogeneic peripheral blood stem cell transplantation (allo-PBSCT) compared with allo-BMT. However, it has not been clarified whether the improved immune reconstitution after allo-PBSCT is associated with a lower incidence of herpesvirus infections. We monitored the emergence of Epstein-Barr virus (EBV), cytomegalovirus (CMV), human herpesvirus 6 (HHV-6) and HHV-7 DNA by a nested-double polymerase chain reaction in peripheral blood leucocytes from 22 allo-BMT and 16 allo-PBSCT patients. Each virus had an unique temporal profile of detection. HHV-6 DNA was detected most frequently at 3 weeks after transplantation, whereas CMV and EBV DNA were detected later (2-3 months). Detection rates of HHV-6 DNA at 3 and 4 weeks after allo-BMT were significantly higher than those after allo-PBSCT (9/16 v 2/13 at 3 weeks, P < 0.01; 10/21 v 1/15 at 4 weeks, P < 0.01). Detection rates of the other three herpesviruses after the two types of allogeneic transplantation were not significantly different throughout observation period. Furthermore, detection of HHV-6 DNA within the first 4 weeks was associated with delayed platelet engraftment after both allo-BMT and allo-PBSCT (P < 0.01). These results suggest an advantage for allo-PBSCT over allo-BMT in terms of suppression of HHV-6 reactivation and prevention of subsequent complications.

Adolescent↗

[Nationwide survey of allogeneic peripheral blood stem cell transplantation from related donors in Japan: current trends and issues].

In December 1997, we conducted a nationwide survey of cases of primary allogeneic peripheral blood stem cell transplantation (allo-PBSCT) performed in Japan between December 1994 and November 1997 Data was collected on 103 patients with hematologic malignancies, aplastic anemia, or solid tumors. Eighty-seven patients received transplants from HLA-identical siblings, and 16 from HLA-mismatched related donors. Granulocyte-colony stimulating factor (G-CSF) mobilized peripheral blood stem cells (PBSC) were collected from donors by 1 to 3 aphereses. Apheresis products contained a median 5.4 (1.0-30.4) x 10(6) CD34 + cells/kg. Most patients were given cyclosporine and methotrexate for graft-versus-host disease (GVHD) prophylaxis. Median days to ANC > 500/microliter and platelets > 50,000/microliter were 13 (7-49) and 16 (10-94), respectively. Grade II-IV acute GVHD developed in 37/99 (37.4%) and chronic GVHD in 59/86 (68.6%) patients. The incidence of treatment-related mortality within 100 days after transplant was 16.1%. Fifty-five patients (59.6%) were alive after a median follow-up of 794 days. More patients and longer follow-up periods will be required to assess the efficacy of allo-PBSCT and evaluate graft-versus-leukemia effect along with the incidence of acute and chronic GVHD.

Adolescent↗

Successful therapy of myelodysplastic syndrome with menatetrenone, a vitamin K2 analog.

Although vitamin K2 is an inducer of the in vitro differentiation of myeloid leukemic cell lines, its clinical efficacy in the treatment of myelodysplastic syndrome (MDS) is unclear. We administered a vitamin K2 analog, menatetrenone, at 45 mg daily to an 80-year-old woman with MDS (refractory anemia) heavily dependent on red-cell transfusions. The patient's pancytopenia gradually improved, and she became transfusion-independent after 14 months. Pancytopenia recurred when menatetrenone was discontinued but recovered again with readministration. Administration of menatetrenone at a dose effective in improving osteoporosis may also be useful in restoring hematopoiesis in MDS patients, possibly by way of inducing differentiation.

Aged↗