A typological study of fundamental philosophies of private universities : The positions of women's universities

The purpose of this paper is to typologically examine fundamental philosophies of private universities, using descriptive materials in 1986 published by the universities. The findings of this examination are the following; 1) Fundamental philosophies tend to emphasize the encouragement of the students and the emphasis are classified into six types; ""industrial development"" (type 1), diligence (type 2), leadership (type 3), cultural enlightment (type 4), Christian mentality (type 5), and Buddhist mentality (type 6). 2) Women's universities give greater importance to philosophies type4-6 than to type1-3. Especially, more women's universities established in 1948-1965 than ones established in other periods encouraged women to be a good wife and wise mother. 3) From 1987 onward, more women's universities with philosophy type4 tend to turn into coeducational universities than others

Rescue with an anti-inflammatory peptide of chickens infected H5N1 avian flu

Chickens suffering from avian flu caused by H5N1 influenza virus are destined to die within 2 days due to a systemic inflammatory response. Since HVJ infection (1,2) and influenza virus infection (3,4) cause infected cells to activate homologous serum complement, the systemic inflammatory response elicited could be attributed to the unlimited generation of C5a anaphylatoxin of the complement system, which is a causative peptide of serious inflammation. In monkeys inoculated with a lethal dose of LPS (4 mg/kg body weight), inhibition of C5a by an inhibitory peptide termed AcPepA (5) rescued these animals from serious septic shock which would have resulted in death within a day (6). Therefore, we tested whether AcPepA could also have a beneficial effect on chickens with bird flu. On another front, enhanced production of endothelin-1 (ET-1) and the activation of mast cells (MCs) have been implicated in granulocyte sequestration (7). An endothelin receptor derived antisense homology box peptide (8) designated ETR-P1/fl was shown to antagonize endothelin A receptor (ET-A receptor) (9) and reduce such inflammatory responses as endotoxin-shock (10) and hemorrhagic shock (11), thereby suppressing histamine release in the circulation (12). Thus, we also administered ETR-P1/fl to bird flu chickens expecting suppression of a systemic inflammatory response

Estrogen receptor alpha and beta differentially mediate C5aR agonist evoked Ca2+-influx in neurons through L-type voltage-gated Ca2+ channels

Complement C5a is associated primarily with inflammation. The widespread expression of its receptors, C5aR and C5L2 in neuronal cells, however, suggests additional regulatory roles for C5a in the CNS. C5aR agonist (PL37-MAP) evokes Ca2+-influx in GT1-7 neuronal cell line and the Ca2+-influx is regulated by estradiol. In the present study, we examined further the mechanism of Ca2+-influx and the contribution of the two estrogen receptor (ER) isotypes, ERα and ERβ, to estrogenic modulation of intracellular Ca2+-content. GT1-7 neurons were treated with isotype selective ER agonists for 24 h then C5aR agonist evoked Ca2+-responses were measured by Ca2+-imaging. Transcriptional changes were followed by real-time PCR. We found that not only estradiol (100 pM), but the ERα selective agonist PPT (100 pM) enhanced the PL37-MAP-evoked Ca2+-influx (E2: 215%, PPT: 175%, compared to the PL37-MAP-evoked Ca2+-influx). In contrast, the ERβ selective agonist DPN (100 pM) significantly reduced the Ca2+-influx (32%). Attenuated Ca2+-response (25%) was observed in Ca-free environment and depletion of the Ca2+-pool by CPA eliminated the remaining elevation in the Ca2+-content, demonstrating that the majority of Ca2+ originated from the extracellular compartment. L-type voltage-gated Ca2+-channel (L-VGCC) blocker nifedipine abolished the Ca2+-influx, while R-type Ca2+-channel blocker SNX-482 had no effect, exemplifying the predominant role of L-VGCC in this process. Acute pre-treatments (8 min) with ER agonists did not affect the evoked Ca2+-influx, revealing that the observed effects of estrogens were genomic. Therefore, we checked estrogenic regulation of C5a receptors and L-VGCC subunits. ER agonists increased C5aR mRNA expression, whereas they differentially regulated C5L2. Estradiol decreased transcription of Cav1.3 L-VGCC subunit. Based on these results we propose that estradiol may differentially modulate C5a-induced Ca2+-influx via L-VGCCs in neurons depending on the expression of the two ER isotypes

Oscillation dynamics underlie functional switching of NF-κB for B-cell activation.

Transcription factor nuclear factor kappa B (NF-κB) shows cooperative switch-like activation followed by prolonged oscillatory nuclear translocation in response to extracellular stimuli. These dynamics are important for activation of the NF-κB transcriptional machinery, however, NF-κB activity regulated by coordinated actions of these dynamics has not been elucidated at the system level. Using a variety of B cells with artificially rewired NF-κB signaling networks, we show that oscillations and switch-like activation of NF-κB can be dissected and that, under some conditions, these two behaviors are separated upon antigen receptor activation. Comprehensive quantitative experiments and mathematical analysis showed that the functional role of switch activation in the NF-κB system is to overcome transient IKK (IκB kinase) activity to amplify nuclear translocation of NF-κB, thereby inducing the prolonged NF-κB oscillatory behavior necessary for target gene expression and B-cell activation

Widely Extended [OIII] 88 um Line Emission around the 30 Doradus Region Revealed with AKARI FIS-FTS

We present the distribution map of the far-infrared [OIII] 88um line emission around the 30 Doradus (30 Dor) region in the Large Magellanic Cloud obtained with the Fourier Transform Spectrometer of the Far-Infrared Surveyor onboard AKARI. The map reveals that the [OIII] emission is widely distributed by more than 10' around the super star cluster R136, implying that the 30 Dor region is affluent with interstellar radiation field hard enough to ionize O^{2+}. The observed [OIII] line intensities are as high as (1-2) x 10^{-6} W m^{-2} sr^{-1} on the peripheral regions 4'-5' away from the center of 30 Dor, which requires gas densities of 60-100 cm^{-3}. However the observed size of the distribution of the [OIII] emission is too large to be explained by massive stars in the 30 Dor region enshrouded by clouds with the constant gas density of 10^2 cm^{-3}. Therefore the surrounding structure is likely to be highly clumpy. We also find a global correlation between the [OIII] and the far-infrared continuum emission, suggesting that the gas and dust are well mixed in the highly-ionized region where the dust survives in clumpy dense clouds shielded from the energetic photons.Comment: 17 pages, 9 figures, accepted for publication in Publications of the Astronomical Society of Japan (PASJ

CD59 protects rat kidney from complement mediated injury in collaboration with Crry

CD59 protects rat kidney from complement mediated injury in collaboration with Crry.BackgroundAs previously reported, the membrane-bound complement regulator at the C3 level (Crry/p65) is important in maintaining normal integrity of the kidney in rats. However, the role of a complement regulator at the C8/9 level (CD59) is not clear, especially when activation of complement occurs at the C3 level. The aim of this work was to elucidate the in vivo role of CD59 under C3 activating conditions.MethodsTwo monoclonal antibodies, 5I2 and 6D1, were used to suppress the function of Crry and CD59, respectively. In order to activate alternative the pathway of complement, the left kidney was perfused with 5I2 and/or 6D1 and was recirculated.ResultsIn the kidneys perfused with 5I2 alone, deposition of C3 and membrane attack complex (MAC) was observed in the peritubular capillaries, vasa recta, and tubular basement membranes. Cast formation, tubular dilation and degeneration, and cellular infiltration were observed at days 1 and 4, and they recovered by day 7. Further suppression of CD59 by 6D1 significantly enhanced the deposition of MAC and worsened the already exacerbated tubulointerstitial injury. These effects of 6D1 were dose dependent. Perfusion with 6D1 alone did not induce histologic damage or MAC deposition in the tubulointerstitium.ConclusionsIn rats, CD59 maintains normal integrity of the kidney in collaboration with Crry in rats against complement-mediated damage in vivo

Complement C5a inhibition improves late hemodynamic and inflammatory changes in a rat model of nonocclusive mesenteric ischemia

BACKGROUND: Nonocclusive mesenteric ischemia (NOMI) can evolve in a variety of low-flow states. Although the mechanisms leading to NOMI-related intestinal necrosis are largely unknown, circumstantial evidence suggests that excessive vasoconstriction and complement activation both play important roles in this process. Because targeting of the circulatory malfunction of the splanchnic area could be of therapeutic relevance, we set out to investigate the long-term effects of treatment with a complement C5a antagonist in a rat model of partial aortic occlusion (PAO)-induced transient mesenteric hypoperfusion. METHODS: The mean arterial pressure of the splanchnic area was kept between 30 and 40 mm Hg by 60 minutes of PAO in anesthetized male Sprague-Dawley rats. C5a inhibitor acetyl-peptide-A (AcPepA; 4 mg kg-1 intravenously) or vehicle administration was initiated at the 45th minute of PAO. After 24 hours, the animals were reanesthetized to record the macrohemodynamics and ileal microcirculation, and plasma and tissue samples were taken for determination of high-mobility group box protein-1 (HMGB-1), endothelin-1, tumor necrosis factor (TNF)-alpha levels, and small intestinal leukocyte infiltration. Epithelial structural changes were visualized by in vivo confocal laser scanning endomicroscopy. RESULTS: At 24 hours after PAO, mean arterial pressure, heart rate, and cardiac output were significantly greater, the intestinal intramural microcirculation was significantly impaired, and plasma HMGB-1, endothelin-1, TNF-alpha levels, the degree of epithelial damage and leukocyte infiltration was increased. The AcPepA treatment moderated the hemodynamic and microcirculatory changes, and decreased inflammatory activation and histologic signs of mucosal damage. CONCLUSION: C5a inhibition ameliorated the potentially harmful local mesenteric hypoperfusion and global long-term inflammatory consequences of PAO. This approach is of promise for use in NOMI-associated situations

Anti-IL-6 Receptor Antibody Causes Less Promotion of Tuberculosis Infection than Anti-TNF-α Antibody in Mice

Objective. Our aim was to investigate the effects of IL-6 blockade on the progression of Mycobacterium tuberculosis (TB) and compare them with those of TNF-α blockade in mice. Methods. Mice were intravenously infected with TB and injected with antibodies. Survival was monitored and histological and immunological studies were carried out. Results. All anti-IL-6R Ab-treated mice and 8 of 10 control mice survived until sacrificed 224 days after TB challenge, whereas anti-TNF-α Ab-treated mice all died between 120 and 181 days. Anti-IL-6R Ab-treated mice exhibited no significant differences in TB CFU in organs, including the lungs, and no deterioration in histopathology compared to control mice at 4 weeks. In contrast, anti-TNF-α Ab-treated mice exhibited increased TB CFU and greater progression of histopathological findings in organs than control mice. Spleen cells from anti-TNF-α Ab-treated mice had decreased antigen-specific response in IFN-γ release and proliferation assays. The results in anti-IL-6R Ab-treated mice suggest that spleen cell responses were decreased to a lesser degree. Similar results were obtained in IL-6 knockout (KO) mice, compared with TNF receptor 1 (TNFR1) KO and TNFR1/IL-6 double KO (DKO) mice. Conclusion. IL-6R blockade promotes the progression of TB infection in mice far less than TNF-α blockade

Physiological Environment Induces Quick Response – Slow Exhaustion Reactions

In vivo environments are highly crowded and inhomogeneous, which may affect reaction processes in cells. In this study we examined the effects of intracellular crowding and an inhomogeneity on the behavior of in vivo reactions by calculating the spectral dimension (ds), which can be translated into the reaction rate function. We compared estimates of anomaly parameters obtained from fluorescence correlation spectroscopy (FCS) data with fractal dimensions derived from transmission electron microscopy (TEM) image analysis. FCS analysis indicated that the anomalous property was linked to physiological structure. Subsequent TEM analysis provided an in vivo illustration; soluble molecules likely percolate between intracellular clusters, which are constructed in a self-organizing manner. We estimated a cytoplasmic spectral dimension ds to be 1.39 ± 0.084. This result suggests that in vivo reactions initially run faster than the same reactions in a homogeneous space; this conclusion is consistent with the anomalous character indicated by FCS analysis. We further showed that these results were compatible with our Monte-Carlo simulation in which the anomalous behavior of mobile molecules correlates with the intracellular environment, leading to description as a percolation cluster, as demonstrated using TEM analysis. We confirmed by the simulation that the above-mentioned in vivo like properties are different from those of homogeneously concentrated environments. Additionally, simulation results indicated that crowding level of an environment might affect diffusion rate of reactant. Such knowledge of the spatial information enables us to construct realistic models for in vivo diffusion and reaction systems

Crry, a complement regulatory protein, modulates renal interstitial disease induced by proteinuria11See Editorial by Quigg, p. 2315

Crry, a complement regulatory protein, modulates renal interstitial disease induced by proteinuria.BackgroundRecent studies have suggested a role for urinary complement components in mediating tubulointerstitial damage, which is known to have a good correlation with progression of chronic renal diseases. Although accumulating evidence suggests that complement regulatory proteins play an important protective role in glomeruli, their role in renal tubules remains unclear. In order to establish the role of a complement regulatory protein, Crry, in renal tubular injury, we employed a molecular biological approach to block the expression of Crry in tubules of animals with proteinuria induced with puromycin aminonucleoside nephritis (PAN).Methods and ResultsTwo different antisense oligodeoxynucleotides (ODNs) against Crry were designed and applied to cultured rat mesangial cells in vitro in order to establish their efficacy. Antisense ODN treatment resulted in decreased expression of Crry protein associated with increased sensitivity to complement attack in cell lysis assays compared with control ODN treatment or no treatment (44.7, 1.50, and 1.34%, respectively). Antisense ODNs did not affect the expression of Thy1 as a control, confirming the specificity of our ODNs. In vivo, we performed selective right renal artery perfusion to administer antisense ODNs to the kidney and showed prominent uptake of ODNs by proximal tubular cells. Reduced expression of Crry protein was demonstrated in proximal tubular cells in antisense ODNs-treated kidneys. Normal rats treated with the antisense ODNs did not show any pathological changes. However, in PAN, rats with massive proteinuria showed increased deposition of C3 and C5b-9 in tubules in antisense-treated kidneys, and histological assessment revealed more severe tubulointerstitial injury in antisense-treated animals compared with controls.ConclusionThese results establish a pathogenic role for complement in leading to tubulointerstitial injury during proteinuria and, to our knowledge for the first time, show a protective role of a complement regulatory protein, Crry, in renal interstitial disease