Quantitative Characterization of the Thermally Driven Alloying State in Ternary Ir-Pd-Ru Nanoparticles.

Compositional and structural arrangements of constituent elements, especially those at the surface and near-surface layers, are known to greatly influence the catalytic performance of alloyed nanoparticles (NPs). Although much research effort often focuses on the ability to tailor these important aspects in the design stage, their stability under realistic operating conditions remains a major technical challenge. Here, the compositional stability and associated structural evolution of a ternary iridium-palladium-ruthenium (Ir-Pd-Ru) nanoalloy at elevated temperatures have been studied using interrupted in situ scanning transmission electron microscopy and theoretical modeling. The results are based on a combinatory approach of statistical sampling at the sub-nanometer scale for large groups of NPs as well as tracking individual NPs. We find that the solid solution Ir-Pd-Ru NPs (∼5.6 nm) evolved into a Pd-enriched shell supported on an alloyed Ir-Ru-rich core, most notably when the temperature exceeds 500 °C, concurrently with the development of expansive atomic strain in the outer surface and subsurface layers with respect to the core regions. Theoretically, we identify the weak interatomic bonds, low surface energy, and large atomic sizes associated with Pd as the key factors responsible for such observed features.

Antibacterial diterpenes and their fatty acid conjugates from rice leaves.

Six structurally oryzalide-related compounds, oryzadione (1), 2, 3, 4, 5 and 6, were isolated from a neutral fraction of the extract of healthy leaves using a bacterial leaf blight-resistant cultivar of a rice plant, "Norin-27", as a group of antimicrobial substances. Their structures were determined by spectroscopic studies to be kaurane analogues and kaurane analogues conjugated with fatty acids, i.e., 1: ent-15,16-epoxy-kauran-2,3-dione (enol form: ent-15,16-epoxy-2-hydroxy-kauran-1-en-3-one), 2: ent-15,16-epoxy-3beta-hydroxy-kauran-2-one, 3: ent-15,16-epoxy-3-oxa-kauran-2-one, 4: ent-15,16-epoxy-3beta-myristoyloxy-kauran-2-one, 5: ent-15,16-epoxy-3alpha-palmitoyloxy-kauran-2-one, and 6: ent-15,16-epoxy-2beta-palmitoyloxy-kauran-2-one.

[Serial topographic changes at the optic disc in normal-tension glaucoma viewed with scanning laser tomography].

PURPOSE: To evaluate topographic changes in normal-tension glaucoma using serial optic disc images obtained by scanning laser tomography. SUBJECTS AND METHODS: Fifty-six eyes of 30 patients with normal-tension glaucoma were imaged using the Heidelberg Retina Tomography (HRT) four or more times during follow-up periods of more than 3 years. Disc progression was determined by regression analysis of global and segmental changes in optic disc parameters. Visual field progression was determined by Humphrey Field Analyzer (HFA) program 30-2 and was compared with disc progression. RESULTS: The global parameters of the optic disc showed progression in 21 of 56 eyes(37.5%). Progression was found in 30 eyes(53.6%) at the superotemporal segment, in 24 eyes(42.9%) at the temporal segment, in 27 eyes(48.2%) at the inferotemporal segment, in 21 eyes(37.5%) at the superonasal segment, in 23 eyes(41.1%) at the nasal segment, and in 27 eyes(48.2%) at the inferonasal segment. The visual field showed progression in 19 eyes (33.9%). The progression in the optic disc parameters did not necessarily agree with that in the visual field. CONCLUSIONS: Glaucomatous disc changes over time can be determined with HRT using regression analysis.

Characteristics of visual field progression in patients with normal-tension glaucoma with optic disk hemorrhages.

PURPOSE: To study the characteristics of visual field progression in patients with normal-tension glaucoma (NTG) with optic disk hemorrhages. DESIGN: Observational study. METHODS: Fifty-eight eyes of 58 untreated patients with NTG who had at least five reliable visual fields of the Humphrey Field Analyzer (central 30-2) within the follow-up period of more than 24 months were enrolled. Of these, 27 eyes had optic disk hemorrhages in their clinical courses. Pointwise linear regression analysis was done using total deviation values of the fields at each of 74 test locations in each patient. Progression was defined as the points of negative slopes with P <.01. A whole visual field was concentrically divided into three clusters: the areas within 10 degrees, 10 to 20 degrees, and 20 to 30 degrees. Percentages of the progressed points of the three clusters and a whole field were compared between the groups with and without optic disk hemorrhages. RESULTS: No significant differences were found in patients' backgrounds, including initial mean deviation values, follow-up periods, and the number of visual field examinations between the 27 patients with optic disk hemorrhages and the 31 without. The group with optic disk hemorrhages showed significantly higher percentages of progressed points within the 10-degree area compared with the group without optic disk hemorrhages (mean +/- SD: 13.1 +/- 13.7%; 5.1 +/- 8.5%, respectively; P =.0086, Student t test), whereas no significant differences were found in the other two clusters or in a whole field. CONCLUSIONS: Patients with NTG with optic disk hemorrhages tend to show visual field progression in areas within 10 degrees.

Mepanipyrim, a novel inhibitor of pharmacologically induced Golgi dispersion.

Mepanipyrim inhibited retrograde Golgi-to-ER trafficking induced by brefeldin A (BFA), nordihydroguaiaretic acid, clofibrate, and arachidonyltrifluoromethyl ketone in NRK and other types of cells, but did not inhibit anterograde trafficking of Golgi-resident proteins translocated to ER by BFA and newly synthesized VSV-G. However, mepanipyrim did not block the TGN38 dispersion induced by any of these compounds. Mepanipyrim acted on the Golgi, and swollen vesicular Golgi structures were formed and similar structures accumulated during rebuilding of the Golgi after BFA removal. These actions of mepanipyrim were readily reversed after its removal. Mepanipyrim did not stabilize microtubules, but prevented nocodazole-induced fragmentation and dispersion of the Golgi. These results suggest that the mepanipyrim-sensitive molecules participated in stabilizing the Golgi and its anchoring in the perinuclear region, and equally importantly, that the novel action of mepanipyrim may be used as a pharmacological tool for investigating membrane transport, Golgi membrane dynamics, and differentiation of the Golgi from TGN.

Nordihydroguaiaretic acid, of a new family of microtubule-stabilizing agents, shows effects differentiated from paclitaxel.

Nordihydroguaiaretic acid (NDGA) protected microtubules in NRK cells from depolymerization caused by structurally and functionally diverse drugs such as nocodazole, colchicine, vinblastine, and ilimaquinone. Hitherto reported drugs, although structurally unrelated to paclitaxel, stabilize microtubules in a way similar to that of paclitaxel and compete for paclitaxel binding to tubulin. However, NDGA had activity toward microtubules different from the effects of paclitaxel. In NRK cells, paclitaxel caused microtubule bundle formation in the presence and absence of microtubule-depolymerizing drugs. However, microtubule bundle did not form, and microtubules radiated from the microtubule-organizing center, in cells treated with NDGA. Acceleration of tubulin polymerization in vitro by paclitaxel was strong but that by NDGA was weak. Microtubules polymerized in vitro in the presence of paclitaxel, but not those polymerized in the presence of NDGA, resisted the effects of cold. NDGA seemed to bind to tubulin, but did not compete for [3H]paclitaxel binding to tubulin. These observations indicate that NDGA belongs to a novel family of microtubule-stabilizing drugs.

Possible implication of Golgi-nucleating function for the centrosome.

The Golgi apparatus breaks down at mitosis, resulting in the dispersal of Golgi-resident proteins. In NRK cells, however, subsets of both TGN38 and golgin-97, but not ManII and GM130, remained associated with the centrosome throughout the cell cycle. This centrosome association of TGN38 and golgin-97 was not disrupted by treatment with brefeldin A, additional inducers of retrograde trafficking and inhibitors of either kinases or protein phosphatases. Anchoring of the Golgi apparatus within the juxtanuclear region depends on microtubules; the association of TGN38 and golgin-97 subsets with the centrosome, however, was insensitive to nocodazole treatment. Drugs such as PDMP, which block Golgi dispersal both by nocodazole, despite microtubule depolymerization, and by inducers of retrograde trafficking, strengthened the microtubule-nucleating activity of the centrosome. These observations cumulatively suggest the centrosome is implicated in nucleation of the Golgi apparatus through interactions with Golgi-resident proteins, such as TGN38 and golgin-97.