16 research outputs found
Original Article
99 cases were operated while we could not use antibiotics. The author traced X-ray photos on paper and measured areas of the peeled cavities with a planimeter. Results were as follows. 1) 66 cases had increasing stage and the rates were more than 30 %. 2) Cases with good developments showed larger original areas (50〜100cm^2) and smaller increasing rates (less than 30 %). 3) Also their X-ray photos showed coinciding or almost coinciding lines of the apices of lungs and the bases of cavities, but we had to take precautions against suppuration when they showed a horizontal line several days after operation. 4) Most of too high degree of adhesion or thickning of pleura did not show good results. When we found a cord which we must manage with some procedures by pneumolysis we must attend to suppuration too. 5)We ought to resect 4th or 5th rib more than 20 cm and 5th or 4th several cm supplementary. 6) As a method of constriction we commend the INVAGI.NATION method. 7) The author noticed in a considerable number of cases that the areas of cavities increased again after they kept long balanced stages
Atherosclerosis V, Proceeding of the Fifth International Symposium, A.M. Gotto, L.C. Smith, B. Allen, Spring Verlag, 1979(BOOK REVIEW)
Antiviral effect of micafungin on three strains of human rhinoviruses. H1HeLa cells were infected with human rhinovirus type 14 (A), 21 (B), or 71 (C) (100 CCID50) and immediately treated with indicated concentrations of micafungin. Three days after compound treatment antiviral activity was determined by the reduction of cytopathic effect using MTT assay. Cell viability of DMSO-treated cells was set to 0 % and that of uninfected cells was set to 100 %. (TIF 100 kb
A new naphthoquinone analogue and antiviral constituents from the root of <i>Rhinacanthus nasutus</i>
<p><i>Rhinacanthus nasutus</i> (L.) Kurz (Acanthaceae) is known as traditional medicine for the treatment of fungal and herpes virus infections. A new naphthoquinone racemate, rhinacasutone (<b>1</b>) together with seven known compounds, rhinacanthone (<b>2</b>), rhinacanthins C, D, N, Q, and E (<b>3</b>–<b>7</b>), and heliobuphthalmin (<b>8</b>) were isolated from root of <i>R. nasutus.</i> Their structures were determined on the basis of extensive spectroscopic methods, including 1D-, 2D-NMR and MS data. All the isolated compounds were tested for their antiviral activities against PR8, HRV1B, and CVB3-infected vero cells. Compounds <b>3</b>–<b>6</b> exhibited significant antiviral activities with the IC<sub>50</sub> value ranging from 0.03 to 23.7 μM in all three infections.</p
Determination of the effective dose of ivy extract in combination with oseltamivir.
<p>The survival rate (A) and body weight (B) of PR8-infected mice administered oseltamivir (*P<0.05; **P<0.01; ***P<0.001, two-tailed unpaired t-test). C: Survival rate of PR8-infected mice that received ivy extract or vehicle (PBS). D: Survival rate of PR8-infected mice that received oral coadministration of ivy extract and oseltamivir (*P<0.05, log-rank analysis of Mantel-Cox data) E: Body weight of PR8-infected mice that received oral coadministration of ivy extract and oseltamivir (*P<0.05, one-way ANOVA with Tukey’s post hoc test).</p
Cytokine production reduced by the combination of oseltamivir and fraction of ivy extract in mice.
<p>A: Body weight of PR8-infected mice administered with oseltamivir alone or coadministratered with oseltamivir and fraction 4 (*P<0.05, one-way ANOVA with Tukey’s post hoc test). B and C: Proinflammatory cytokines and chemokines measured from lung tissue of PR8-infected mice (n = 5 per group) treated with oseltamivir (5 mg/kg) in combination with fraction 4 of ivy extract (30 mg/kg) for 2 (B) and 5 (C) days. *P<0.05;**P<0.01;***P<0.001; n.s., not significant. one-way ANOVA with Tukey’s post hoc test.</p
TIC chromatograms of chromatography fractions.
<p>The HSF content of each fraction analyzed using a chromatogram. HSF, hederasaponin F; TIC, total ion current.</p
Antiviral activity of combined ivy extract and oseltamivir treatment against PR8 virus in vitro and in vivo.
<p>A: CPE reduction assay using SRB assay in A549 cells infected with PR8 virus were treated with oseltamivir for 48 h at the concentrations indicated. (***P<0.0001) B: Antiviral activity of ivy extract (at the concentrations indicated) combined with 25 μg/mL oseltamivir PR8-infected A549 cells. (***P<0.001) C: HSF, HSB, and hederacoside C were used in the presence of 25 μg/mL oseltamivir to identify its anti-PR8 virus activity in A549 cells. After 48 h of incubation, the antiviral activity was investigated by CPE reduction assay using SRB. (***P<0.001), and the antiviral activity was calculated based on the viability of virus infected cells as a percentage of the corresponding untreated control. Data are expressed as the mean ± SD of the percentage values obtained from 3 independent experiments carried out in triplicate. (***P<0.001). D: Survival of mice (n = 5/group) was monitored as depicted in Materials and Methods after treating PR8-infected mice with PBS, oseltamivir, or HSF (*P<0.05, log-rank analysis of Mantel-Cox data). E: Mice were infected with 5 x 10<sup>3</sup> pfu/mouse of PR8, orally coadministered with HSF and/or oseltamivir from 2 days after PR8 infection for 5 days. Mice were sacrificed at 6h after final administration, and lung sections were prepared as described in Materials and Methods. Representative H&E stained samples of lung section were shown (left). Pathological grade of each mouse was evaluated (right). CPE, cytopathic effect; HSB, hederasaponin B; HSF, hederasaponin F; SRB, sulforhodamane B; H&E, hematoxylin and eosin. (*P<0.05) using one-way ANOVA with Tukey’s post hoc test.</p
Serum cytokine and chemokine levels in mice treated with oroxylin A.
<p>Sera were collected on day 5 post infection and levels of IL-6 (A), CXCL1 (B), CCL2 (C), and TNF-α (D) were determined. <sup>*</sup>P<0.01;<sup>**</sup>P<0.001;<sup>***</sup>P<0.0001 using one-way ANOVA with Tukey’s post hoc test.</p
Oroxylin A inhibits the replication of the CVB3 replicon.
<p>(A) Vero cells were transfected with in vitro-transcribed CVB3-replicon RNAs, immediately treated with the indicated concentrations of oroxylin A for 8h, and then assayed for firefly luciferase activity. The luciferase activity of DMSO-treated cells was considered to be 100%. <sup>**</sup>P<0.001 using one-way ANOVA with Tukey’s post hoc test. (B) In the same conditions, another set of CVB3 replicon-transfected cells was assayed for cell viability using CellTiter-Glo reagent. The activity of DMSO-treated cells was considered to be 100%.</p
The antiviral activity of oroxylin A against CVB3 in vivo.
<p>BALB/c mice were infected with a 1 × 10<sup>6</sup> TCID<sub>50</sub> dose of CVB3 and given oroxylin A or vehicle. Body weights (A) and glucose levels (B) were measured for 5 days. <sup>*</sup>p < 0.05, <sup>**</sup>p < 0.01, <sup>***</sup>p < 0.001 for CVB3 + oroxylin A versus CVB3 + vehicle, using one-way ANOVA. Virus titers of mice were determined 5 days post infection by real-time PCR (C) and western blots (D) in the pancreata. In western blot, densitometric measurement of VP1 expression is normalized to β-actin.</p