Active fluidization of polymer networks through molecular motors

Entangled polymer solutions and melts exhibit elastic, solid-like resistance to quick deformations and a viscous, fluid-like response to slow deformations. This viscoelastic behaviour reflects the dynamics of individual polymer chains driven by brownian motion: since individual chains can only move in a snake-like fashion through the mesh of surrounding polymer molecules, their diffusive transport, described by reptation, is so slow that the relaxation of suddenly imposed stress is delayed. Entangled polymer solutions and melts therefore elastically resist deforming motions that occur faster than the stress relaxation time. Here we show that the protein myosin II permits active control over the viscoelastic behaviour of actin filament solutions. We find that when each actin filament in a polymerized actin solution interacts with at least one myosin minifilament, the stress relaxation time of the polymer solution is significantly shortened. We attribute this effect to myosin's action as a 'molecular motor', which allows it to interact with randomly oriented actin filaments and push them through the solution, thus enhancing longitudinal filament motion. By superseding reptation with sliding motion, the molecular motors thus overcome a fundamental principle of complex fluids: that only depolymerization makes an entangled, isotropic polymer solution fluid for quick deformations.     

Hydrogen Adsorption on Metal-Organic Framework MOF-177

This review summarizes the recent literature on the synthesis, characterization, and adsorption properties of meal-organic framework MOF-177. MOF-177 is a porous crystalline material that consists of Zn4O tetrahedrons connected with benzene tribenzoate (BTB) ligands. It is an ideal adsorbent with an exceptionally high specific surface area (BET4500 m2/g), a uniform micropore size distribution with a median pore diameter of 12.7 ?, a large pore volume (2.65 cm3/g), and very promising adsorption properties for hydrogen storage and other gas separation and purification applications. A hydrogen adsorption amount of 19.6 wt.% on MOF-177 at 77 K and 100 bar was observed, and a CO2 uptake of 35 mmol/g on MOF-177 was measured at 45 bar and an ambient temperature. Other hydrogen properties (kinetics and heat of adsorption) along with adsorption of other gases including CO2, CO, CH4, and N2O on MOF-177 were also be discussed. It was observed in experiments that MOF-177 adsorbent tends to degrade or decompose when it is exposed to moisture. Thermogravimetric analysis showed that the structure of MOF-177 remains intact at temperatures below 330℃ under a flow of oxygen, but decomposes to zinc oxide at 420℃.     

1Alpha,25-dihydroxyvitamin D3 inhibits hepatic chromosomal aberrations, DNA strand breaks and specific DNA adducts during rat hepatocarcinogenesis

The possible promoting effect of streptozotocin (STZ; 65 mg/kg body weight, intraperitoneal)-induced diabetes during 2-acetylaminofluorene (2-AAF; 0.04% in basal diet)-initiated hepatocarcinogenesis and modulatory effect of 1α,25-dihydroxyvitamin D₃ (VD₃; 0.3 μg/0.1 ml in propylene glycol, per os) were investigated by monitoring chromosomal aberrations (CAs), DNA strand breaks and specific DNA adducts in rat liver. VD₃ treatment (twice a week) was started 4 weeks before the 2-AAF regimen and continued throughout the study. Aberrant metaphase chromosomes were counted from the regenerating hepatocytes 15, 30 or 45 weeks after STZ injection, while DNA strand break and adduct assays were performed 45 days post-STZ treatment. Dietary exposure to 2-AAF elicited a substantial increase in CAs and elevated the extent of DNA strand breaks and formation of N-(deoxyguanosin-8-yl)-2-aminofluorene. A promoting effect of STZ was evident from CAs coupled with DNA strand break analysis. VD₃ treatment substantially reducted 2-AAF+STZ-induced CAs as well as DNA strand breaks and adducts. Thus, VD₃ appears to be effective in suppressing liver-specific early chromosomal as well as DNA damage during the process of rat hepatocarcinogenesis initiated with 2-AAF and promoted by STZ contributing to its promise as a cancer chemotherapeutic agent. Received 27 April 2001; accepted 22 May 2001     

Observations on the phloem in three species ofMimosa

Zusammenfassung Anatomische Untersuchungen am Phloem vonMimosa ergaben eine histologische Übereinstimmung der engen Siebröhren des Aussenphloems mit den Siebröhren des Innenphloems. In den engen Siebröhren bleibt der Zellkern erhalten.     

以巯基改性聚酰胺-胺树形分子为稳定剂制备纳米银溶胶

用巯基乙酸甲酯改性3.0~5.0代聚酰胺-胺(PAMAM)树形大分子,用红外、拉曼光谱、核磁共振氢谱和元素分析对其进行了表征。借助巯基端基与银离子的配位作用,以巯基改性PAMAM为稳定剂,硼氢化钠为还原剂,还原AgNO3制备了纳米银溶胶,并用紫外-可见光谱和透射电镜对其分散性和稳定性进行了研究。结果表明:制备的纳米银具有较好的分散性和稳定性。     

Pressor response to oxotremorine in atropinized rats

Zusammenfassung Eine zentrale, nikotinartige Wirkung von Oxotremorin wird am Blutdruck der Ratte beschreiben.     

Critical role of TRAF3 in the Toll-like receptor-dependent and -independent antiviral response

Type I interferon (IFN) production is a critical component of the innate defence against viral infections. Viral products induce strong type I IFN responses through the activation of Toll-like receptors (TLRs) and intracellular cytoplasmic receptors such as protein kinase R (PKR). Here we demonstrate that cells lacking TRAF3, a member of the TNF receptor-associated factor family, are defective in type I IFN responses activated by several different TLRs. Furthermore, we show that TRAF3 associates with the TLR adaptors TRIF and IRAK1, as well as downstream IRF3/7 kinases TBK1 and IKK-epsilon, suggesting that TRAF3 serves as a critical link between TLR adaptors and downstream regulatory kinases important for IRF activation. In addition to TLR stimulation, we also show that TRAF3-deficient fibroblasts are defective in their type I IFN response to direct infection with vesicular stomatitis virus, indicating that TRAF3 is also an important component of TLR-independent viral recognition pathways. Our data demonstrate that TRAF3 is a major regulator of type I IFN production and the innate antiviral response.