Splenectomy for idiopathic thrombocytopenic purpura after living-related liver transplantation.
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Biomedical subjects
Publications and source records attributed to S Chiba.
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Chromosome instability, a major property of cancer cells, is believed to promote mutations that establish malignant phenotypes. Centrosome hyperamplification and the consequential increase in the frequency of aberrant mitoses are the major causes of chromosome instability in cancer cells that lack the functional p53 tumor suppressor protein. Here, we examined dynamic changes of chromosome and centrosome behaviors during long-term culturing of primary epithelial cells derived from p53-null mice. The heterogeneity in the number of chromosomes per cell in the early to mid passage cell population diminished in late passage cells, giving rise to distinct subpopulations of cells. Concomitantly, centrosome hyperamplification that was observed at a high frequency in early to mid passage cells was suppressed in late passage cells. These results provide an explanation for the frequent observations that some cancer cell lines and tissues that lack functional p53 show normal centrosome behaviors and altered, yet relatively stable, chromosomes. Moreover, our in vitro findings may provide a model for possible genomic convergence in cultured cells. This may be analogous to the genomic convergence model proposed for in vivo tumor progression in which chromosome instability initially imposed during tumorigenesis becomes suppressed when neoplastic cells have acquired chromosome compositions that promise an optimal growth in a given environment.
Complementary DNA of mouse deafness dystonia peptide 1 (DDP1) was isolated from adipocyte cDNA library and expressed in mammalian cells. The sequence shares homology of 92 and 97% on the nucleic acid and the amino acid levels with human DDP1. In comparison to mouse Bruton's tyrosine kinase (Btk) locus, the coding region spans 2 exons and the splice point is the same as human DDP1. Northern blot analysis suggests that mouse DDP1 expresses ubiquitously. In vitro transcription/translation study showed that the cDNA of mouse DDP1 codes about 11 kDa peptide. DDP1 tagged with FLAG localized in mitochondria and cytoplasm of COS7 cells. P19 embryonal carcinoma cells transfected with anti sense DDP1 cDNA were frequently dead after subculture and all the survivals expressed endogenous DDP1 mRNA. Therefore, mouse DDP1 may play an important role to survive in contrast to Tim8p, a yeast homologue, which was unnecessary in yeast.
The present study is the first to show that superoxide (O(-)(2)) forming NADPH oxidase is activated in Alzheimer's disease (AD) brains by demonstrating the marked translocation of the cytosolic factors p47-phox and p67-phox to the membrane. In conjunction with a recent in vitro study showing that amyloid beta activates O(-)(2) forming NADPH oxidase in microglia, where these phox proteins are localized in this study, the present results suggest that, in AD, NADPH oxidase is activated in microglia, resulting in the formation of reactive oxygen species which can be toxic to neighboring neurons in AD.
Norwalk virus (NV) and Sapporo virus (SV) were approved as type species of the genus Norwalk-like viruses and the genus Sapporo-like viruses, respectively, within the family Caliciviridae. To clarify the importance of NV and SV as causes of gastroenteritis outbreaks in infants, stool samples obtained from 36 outbreaks of nonbacterial gastroenteritis that occurred during 1976-1995 in an infant home in Sapporo, Japan, were examined for diarrhea viruses using electron microscopy, enzyme immunoassays, reverse transcriptase-polymerase chain reaction (PCR), and sequencing of the PCR products. NV and SV were associated with 15 (42%) of the 36 outbreaks and were more prevalent than rotavirus (RV) A, which was associated with 10 (28%) of the 36 outbreaks. Our data indicate that NV and SV were the most common cause of outbreaks of viral gastroenteritis in infants and were indeed more prevalent than RV-A in Sapporo, Japan, during 1976-1995.
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Gelatin-specific T cell response was performed to determine whether a series of vaccinations with gelatin-containing DTP is a primary sensitization process in gelatin allergy. Thirty-seven recipients with gelatin-containing DTP who developed adverse reactions after vaccination and eight recipients of DTP without gelatin who also developed adverse reactions were studied. In addition, 10 subjects receiving gelatin-containing vaccine and 10 subjects inoculated with non-gelatin vaccine who did not show any adverse reactions were also investigated. All subjects inoculated with gelatin-containing DTP vaccine showed positive T cell responses against gelatin, however, occurrence of adverse reactions did not correlate with T cell responses. We conclude that DTP vaccine containing gelatin induces sensitization to gelatin in the recipients, but the mechanism of local reactions remains unknown.
By employing Strutinsky's treatment we demonstrate that the magnetic field gives rise to a phase shift of the shell oscillations in nuclear masses. The proton orbital magnetism is shown to enhance the nuclear shell effect especially when the field influence is comparable to the spin-orbit coupling. The magnetic field of the strength scale B approximately 10(16)-10(17) G is found to shift significantly the nuclear magic numbers of the iron region towards smaller mass numbers.
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Diaphragmatic action potentials (DAPs) were mapped on the thorax bilaterally in 16 neurologically normal infants and 8 boys aged 1 to 4 years during artificial ventilation after thoracic surgery. Transcutaneous stimulation was used to activate the phrenic nerve at the supraclavicular fossa at the end of an artificial inspiration. The DAPs were of positive polarity and were recorded on the ipsilateral anterolateral chest wall over the sixth to the eighth intercostal spaces, with a maximal peak at the seventh intercostal space. The DAP latencies gradually decreased from 6 to 8 ms at birth to about 5 ms at the age of 1 year, despite an increase of conduction distance. Statistical analyses revealed that DAP amplitude did not correlate with age. The latencies and amplitudes of the DAPs displayed little interside variation. The results are valuable not only as a reference for the diagnosis of patients with phrenic nerve palsy, but also as an indicator of the normal development of the phrenic nerve.
The role of the sexual transmission of human cytomegalovirus (CMV) as a cause of congenital infection was investigated. Serum samples were collected from 756 pregnant women at 10 to 12 weeks of gestation and at 32 to 36 weeks of gestation. Serum samples were also obtained from the husbands of women who seroconverted and women who were seronegative during pregnancy. Commercially available enzyme immunoassay kits were used to detect serum IgG, IgM, and IgA antibodies against CMV. CMV from neonatal urinary specimens was isolated according to a standard tissue culture technique, using MRC-5 cells. At 10 to 12 weeks of gestation, 634 of the 756 pregnant women (83.9%) had IgG antibody to CMV. At 32 to 36 weeks of gestation, 642 of the 756 women (84.9%) had IgG antibody to CMV. A meaningful rise of serum IgG-antibody titer (seroconversion) occurred in 8 women (1.1%). CMV was isolated from the urine of an infant born to a seroconverted woman within a week after birth. The prevalence of IgG antibody to CMV was significantly higher in the husbands of women who seroconverted during pregnancy than in the husbands of the women who were seronegative during pregnancy (P < 0.01). Understanding the epidemiology of CMV is a key element in the development of strategies for the prevention of infection. The transmission of CMV by sexual contact may be important in the pathogenesis of congenital infection. Entirely new approaches to the prevention and treatment of congenital CMV infection are necessary, including antiviral interventions and the development of a vaccine strategy.
The rostral ventrolateral medulla (RVLM) has cholinergic mechanisms responsible for pressor responses. Stimulation of the hypothalamic paraventricular nucleus (PVN) causes an increase of arterial pressure via activation of neurons in the RVLM. In this study, we examined whether PVN stimulation causes a pressor response via activation of cholinergic mechanisms in the RVLM. Male Wistar rats were used and they were anesthetized, paralyzed and artificially ventilated. Electrical stimulation of the PVN produced a pressor response. Microinjection of the muscarinic receptor antagonist scopolamine and the cholinesterase inhibitor physostigmine into the RVLM inhibited and potentiated, respectively, the pressor response induced by PVN stimulation. PVN stimulation also increased the firing rate of RVLM barosensitive neurons and the increase in the firing rate was inhibited and potentiated by scopolamine and physostigmine, respectively, iontophoretically applied on neurons. Microinjection of L-glutamate into the PVN produced a release of ACh in the RVLM. The inhibitory amino acid gamma-aminobutyric acid injected into the lateral parabrachial nucleus (LPBN) inhibited the pressor response induced by PVN stimulation. These results suggest that PVN stimulation causes an increase in arterial pressure via activation of cholinergic inputs in the RVLM. It appears that the pressor response is mediated, at least in part, via cholinergic inputs from the LPBN.
Children infected with Chlamydia pneumoniae sometimes experience lower respiratory tract infections such as pneumonia and bronchitis. Although numerous anti-microbial compounds have been reported to be active against the organism, most of them have not been in a clinical trial in infants and children with C. pneumoniae infection. Clarithromycin has been shown to express anti-chlamydial effects in vitro. In this study, we evaluated the clinical anti-C. pneumoniae properties of clarithromycin in children with mainly lower respiratory tract infection. We administered clarithromycin orally to 21 infants and children at a dose of 10-15 mg/kg/day divided into two or three doses for 4-21 days. Clinical symptoms, roentgenographic and laboratory abnormal findings improved. The overall clinical efficacy rate was 85.7% (18 of 21 cases). Administration of clarithromycin was considered to be a suitable treatment for improving lower respiratory infections in infants and children caused by C. pneumoniae.
The participation of Bartonella henselae and Coxiella burnetii in the pathogenesis of fever of unknown origin (FUO) and lymphadenopathy has not been completely clarified. Prevalence of these two agents in Japanese children is also unknown. Serum IgG and IgM antibodies to B. henselae and to C. burnetii were examined by the indirect fluorescence antibody assay. Enzyme immunoassay kits were used to detect serum IgG and IgA antibodies against Chlamydia trachomatis. Out of 200 healthy normal pregnant women, two (1.0%) had serum IgG antibodies to B. henselae, four (2.0%) to C. burnetii and 49 (24.5%) to C. trachomatis. Out of 29 patients with FUO, one (3.4%) had serum IgG antibodies to B. henselae, four (13.8%) to C. burnetii and none to C. trachomatis. Out of 31 patients with cervical lymphadenopathy, three (9.6%) had serum IgG antibodies to B. henselae, two (6.5%) to C. burnetii and none to C. trachomatis. Out of 22 patients with generalized lymphadenopathy, one (4.5%) had serum IgG antibodies to B. henselae, three (13.6%) to C. burnetii and none to C. trachomatis. Prevalences of serum antibodies to C. burnetii in the patients with FUO and generalized lymphadenopathy and to B. henselae in the patients with cervical lymphadenopathy were significantly higher than those of normal pregnant women (Welch's t-test; P<0.01). These two agents may have some roles in the pathogenesis of FUO and lymphadenopathy in Japanese children.
The actions of omega-conotoxin (omega-CTX) and diltiazem on adrenergic and purinergic components of double peaked vasoconstrictor responses to periarterial nerve stimulation have been investigated in the isolated, perfused canine splenic arterial preparation. Double peaked vasoconstrictions (biphases of vasoconstrictors) were consistently observed in the conditions of 30 s trains of pulses at 1 - 10 Hz frequencies. omega-CTX (1 - 30 nM) produced similar inhibitory effects on the first phase and second phase responses in a dose-related manner. Thirty nM omega-CTX almost completely inhibited the biphasic vasoconstrictions at any used frequencies but did not affect the vasoconstrictor responses to exogenous applied ATP (0.01 - 1 micromol) and noradrenaline (0.03 - 3 nmol). Intraluminal application of a large dose of diltiazem (3 - 10 microM) also produced a dose-dependent inhibitory effect on biphasic vasoconstrictions at any used frequencies. Three microM diltiazem exerted rather a larger inhibitory effect on the second phase than the first phase response at low frequencies (1 - 3 Hz), but a similar inhibition on first and second phasic responses at high frequencies (6 - 10 Hz). An extremely high dose of diltiazem (10 microM) almost completely inhibited the biphasic vasoconstrictor responses to nerve stimulation, and slightly inhibited the contractile responses to exogenous applied ATP (0.01 - 1 micromol) and noradrenaline (0.03 - 3 nmol). The present results indicate that omega-CTX selectively acts prejunctionally to inhibit the release of transmitters from sympathetic nerve terminals, and omega-CTX-sensitive calcium channels may produce a parallel controlling of purinergic and adrenergic components of sympathetic cotransmission. A large dose of diltiazem has inhibitory effects on both prejunctional and postjunctional sympathetic co-transmission. British Journal of Pharmacology (2000) 129, 47 - 52
The periarterial electrical nerve stimulation (30 s trains of pulses at a frequency of 1, 4 or 10 Hz) induced a double peaked vasoconstriction consisting of an initial transient constriction (first peak) followed by a prolonged response (second peak) in the isolated, perfused canine splenic artery. At low frequencies (1 and 4 Hz), a neuropeptide Y (NPY) Y(1) receptor antagonist BIBP 3226 (0.1-1 microM) produced a dose-dependent inhibitory effect on the second peak, but did not modify the first peak. At a high frequency (10 Hz), 1 microM BIBP 3226 induced a slight, but significant inhibition on both the first and second peaked responses. At a low frequency (1 Hz), the first peak was not influenced by blockade of alpha(1)-adrenoceptors or NPY Y(1) receptors with prazosin (0.1 microM) or BIBP 3226 (1 microM), respectively, but abolished by P2X receptor desensitization with alpha,beta-methylene ATP (alphabeta-m ATP, 1 microM). At a high frequency (10 Hz), the first peak was mostly inhibited by alphabeta-m ATP and partially by prazosin and BIBP 3226. On the other hand, the second peak at a low frequency was largely decreased by BIBP 3226 and partially by prazosin and alphabeta-m ATP, whereas at a high frequency, it was largely attenuated by prazosin and partially by alphabeta-m ATP and BIBP 3226. The results suggest that at a low frequency, the firstly transient constriction of double peaked responses is mainly induced via an activation of P2X-receptors, whereas at a high frequency, it is mostly mediated by the P2X-receptors, and partially by alpha(1)-receptors and NPY Y(1)-receptors. The secondary prolonged vasoconstriction at frequencies used is predominantly mediated via both alpha(1)-receptor and NPY Y(1) receptor activations, and in part by P2X-receptors. Furthermore, an activation of NPY Y(1) receptors may play an important role in evoking the prolonged vasoconstrictor response to longer pulse trains of stimulation at a low frequency, whereas an alpha(1)-adrenoceptor activation exerts a main vasomotor effect for the prolonged response at a high frequency.
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