Fluxiod jumps coupled high critical current density of nano-Co3O4 doped MgB2

Polycrystalline MgB2 samples with 0, 2, 4 and 6 percent added nano-Co3O4 being synthesized by vacuum (10-5 Torr) annealing at 750 0C for three hours each are found to be nearly single phase with presence of only a small quantity of Mg/MgO in pristine sample and in addition the Co2O3 in doped compounds. All the samples exhibited clear and sharp diamagnetic transitions at around 38 K, in Zero-field-cooled (ZFC) magnetic susceptibility measurements with sizeable signal. The Field cooled (FC) measurements though having sharp transitions, but showed a very small signal, indicating high level of pinning centers in these samples. Further some of the doped samples exhibited Paramagnetic-Meissner-Effect (PME) in applied field of 5 Oe. The critical current density (Jc), being estimated by invoking Bean model for the pristine compound increase by nearly an order of magnitude for 2 and 4 percent nano-Co3O4 doping and later the same decreases sharply for 6 percent sample at nearly all studied temperatures and applied fields. Further the increased Jc (~ 10^8 A/cm2) is coupled with fluxiod jumps (T = 20 K and H = 1 T). Fluxiod Jumps are not seen in relatively low Jc pristine or 6 percent sample. This means the fluxiod-jumps are intrinsic only to the high Jc samples.Comment: 14 pages including TEXT + Figs. Comments Welcome ([email protected]) OR [email protected]

Mucus trap in coral reefs: formation and temporal evolution of particle aggregates caused by coral mucus

Corals exude large volumes of nutrient-containing mucus when exposed to air during low spring tides, as a protective mechanism against desiccation and UV radiation. Currents and waves of the incoming flood detach the mucus from the corals, thereby increasing organic carbon and nutrient concentrations in the reef water. During transport into the reef lagoon, a large fraction of the mucus dissolves. Roller-table experiments demonstrated that this dissolved mucus leads to the formation of marine snow. The non-dissolving gel-like fraction of the mucus rapidly accumulates suspended particles from the flood water and forms in temporal sequence mucus strings, flocs, surface films, surface layers and thick mucus floats. In a platform reef in the Great Barrier Reef, Australia, we characterized each of these mucus phases and observed the exponential increase of algal and bacterial cells in the ageing mucus aggregates. Within 3 hours, the dry weight of the aggregates increased 35-fold, chlorophyll a 192-fold, bacteria cell density 546-fold, C 26-fold, and N 79-fold. After waves destroy the buoyant mucus floats, the mucus aggregates release enclosed gas bubbles and quickly sink to the lagoon sediments, where they are consumed by the benthic community. This releases aggregate-bound nutrients, which fuel benthic and planktonic production in the lagoon. During ebb tide, corals filter the lagoon water and close the recycling loop. We conclude that coral mucus enhances the filtration capacity of coral reefs and fuels reef benthos, thereby increasing the import of oceanic particles and enhancing recycling in the reef ecosystem

Pegylated TRAIL retains anti-leukemic cytotoxicity and exhibits improved signal transduction activity with respect to TRAIL

To improve the pharmacokinetic profile of tumor necrosis factor-related apoptosis inducing ligand (TRAIL) an N-terminal specific pegylation was performed to generate pegylated TRAIL (PEG-TRAIL). In in vitro experiments, we found that although PEGTRAIL was slightly less efficient than recombinant TRAIL in promoting leukemic cell apoptosis, it showed an improved ability to promote migration of bonemarrow mesenchymal stem cells and to elicit the ERK1/2 intracellular signal transduction pathway. Overall, these data suggest that TRAIL pegylation retains, or even enhances, the biological activities of TRAIL relevant for its therapeutic applications

A preliminary report of the association between human herpes virus 7 (HHV-7) and chronic gatritis

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U94 of human herpesvirus 6 is expressed in latently infected peripheral blood mononuclear cells and blocks viral gene expression in transformed lymphocytes in culture

Human herpesvirus 6 (HHV-6) like other herpesviruses, expresses sequentially immediate early (IE), early, and late genes during lytic infection. Evidence of ability to establish latent infection has not been available, but by analogy with other herpesviruses it could be expected that IE genes that regulate and transactivate late genes would not be expressed. We report that peripheral blood mononuclear cells of healthy individuals infected with HHV-6 express the U94 gene, transcribed under IE conditions. Transcription of other IE genes (U16/17, U39, U42, U81, U89/90, U91) was not detected. To verify that U94 may play a role in the maintenance of the latent state, we derived lymphoid cell lines that stably expressed U94. HHV-6 was able to infect these cells, but viral replication was restricted. No cytopathic effect developed. Furthermore, viral transcripts were present in the first days postinfection and declined thereafter. A similar decline in the level of intracellular viral DNA also was observed. These findings are consistent with the hypothesis that the U94 gene product of HHV-6 regulates viral gene expression and enables the establishment and/or maintenance of latent infection in lymphoid cells

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and tumor necrosis factor-a (TNF- a) promote the NF- kB-dependent maturation of both normal and leukemic myeloid cells.

Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) and TNF-alpha induced monocytic maturation of primary normal CD34-derived myeloid precursors and of the M2/M3-type acute myeloid leukemia HL-60 cell line, associated to increased nuclear factor (NF)-B activity and nuclear translocation of p75, p65, and p50 NF-B family members. Consistently, both cytokines also induced the degradation of the NF-B inhibitors, IB and IB, and up-regulated the surface expression of TRAIL-R3, a known NF-B target. However, NF-B activation and IB degradation occurred with different time-courses, since TNF-alpha was more potent, rapid, and transient than TRAIL. Of the two TRAIL receptors constitutively expressed by HL-60 (TRAIL-R1 and TRAIL-R2), only the former was involved in IB degradation, as demonstrated by using agonistic anti-TRAIL receptor antibodies. Moreover, NF-B nuclear translocation induced by TRAIL but not by TNF-alpha was abrogated by z-IETD-fmk, a caspase-8-specific inhibitor. The key role of NF-B in mediating the biological effects of TNF-alpha and TRAIL was demonstrated by the ability of unrelated pharmacological inhibitors of the NF-B pathway (parthenolide and MG-132) to abrogate TNF-alpha and TRAIL-induced monocytic maturation. These findings demonstrate that NF-B is essential for monocytic maturation and is activated via distinct pathways, involving or not involving caspases, by the related cytokines TRAIL and TNF-alpha

Evidence for a proangiogenic activity of TNF-related apoptosis-inducing ligand

Starting from the observation that tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)/Apo-2L protein is expressed in both malignant and inflammatory cells in some highly vascularized soft tissue sarcomas, the angiogenic potential of TRAIL was investigated in a series of in vitro assays. Recombinant soluble TRAIL induced endothelial cell migration and vessel tube formation to a degree comparable to vascular endothelial growth factor (VEGF), one of the best-characterized angiogenic factors. However, the proangiogenic activity of TRAIL was not mediated by endogenous expression of VEGF. Although TRAIL potentiated VEGF-induced extracellular signal-regulated kinase (ERK) phosphorylation and endothelial cell proliferation, the combination of TRAIL + VEGF did not show additive effects with respect to VEGF alone in inducing vessel tube formation. Thus, although TRAIL has gained attention as a potential anticancer therapeutic for its ability to induce apoptosis in a variety of cancer cells, our present data suggest that TRAIL might also play an unexpected role in promoting angiogenesis, which might have therapeutic implications