Two trihydrazine-bridged cobalt(II) chain compounds exhibiting antiferromagnetic ordering and single-chain magnetic behavior.

Two new trihydrazine bridged Co(II) chain compounds have been synthesized and magnetically characterized. The two compounds are both composed of [Co(N2H4)3](2+) chains. One exhibits antiferromagnetic ordering behavior while the other behaves as a single-chain magnet (SCM) at low temperature.

Epigallocatechin gallate inactivates clinical isolates of herpes simplex virus.

In the absence of a fully effective herpes simplex virus (HSV) vaccine, topical microbicides represent an important strategy for preventing HSV transmission. (-)-Epigallocatechin gallate (EGCG) (molecular weight, 458.4) is the primary catechin in green tea. The present study shows that EGCG has greater anti-HSV activity than other green tea catechins and inactivates multiple clinical isolates of HSV type 1 (HSV-1) and HSV-2. EGCG reduced HSV-2 titers by >or=1,000-fold in 10 to 20 min and reduced HSV-1 titers by the same amount in 30 to 40 min. The anti-HSV activity of EGCG is due to a direct effect on the virion, and incubating Vero and CV1 cells with EGCG for 48 h prior to infection with HSV-1 and HSV-2, respectively, does not reduce HSV production. Electron microscopic (EM) studies showed that purified virions exposed to EGCG were damaged, and EM immunogold labeling of the envelope glycoproteins gB and gD was significantly reduced following EGCG treatment while capsid protein labeling was unchanged. When purified HSV-1 envelope glycoproteins gB and gD were incubated with EGCG and then examined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, lower-molecular-weight gB and gD bands decreased and new higher-molecular-weight bands appeared, indicating the EGCG-dependent production of macromolecular complexes. gB and gD are essential for HSV infectivity, and these results suggest that EGCG could inactivate HSV virions by binding to gB, gD, or another envelope glycoprotein. EGCG is stable in the pH range found in the vagina and appears to be a promising candidate for use in a microbicide to reduce HSV transmission.

Inactivation of herpes simplex virus clinical isolates by using a combination microbicide.

A combination microbicide using the lipid-ether 1-0-octyl-sn-glycerol (OG) (3 mM) and peptide LSA5 (9 microM) synergistically inactivated six clinical isolates of herpes simplex virus type 2 (HSV-2) by 30- to 100-fold and five of six HSV-1 isolates by 10-fold more than the sum of OG and LSA5 used individually within 30 min. OG plus LSA5 inactivated all HSV clinical isolates by > or = 1,000-fold in 10 to 40 min.

A lipid-peptide microbicide inactivates herpes simplex virus.

A microbicide combining the lipid-ether 1-0-octyl-sn-glycerol (OG; 3 mM) and peptide D2A21 (9 microM) reduced herpes simplex virus type 1 (HSV-1) and HSV-2 titers by at least 1,000-fold, more than the sum of the inactivations produced by OG and D2A21 alone. OG plus D2A21 reduced HSV-1 and HSV-2 titers by > or =1,000-fold in < or =10 and < or =20 min, respectively, whereas OG and D2A21 used alone produced almost no virus inactivation during these times.

[FTIR investigation of new polymer solid electrolytes].

The conductivity of the porous polymer solid electrolyte blended with PVDF and PMMA, which was made by a micro-wave hot-cross-linking method, reached 2.05 x 10(-3) S x cm(-1) at room temperature. The polymer solid electrolyte was analyzed and investigated by FTIR. The results show that the PVDF, PMMA and LiClO4 in the polymer solid electrolyte were not simply blended, but certain kind of effect existed which was strengthened only when the polymer solid electrolyte came into being.

Pentoxifylline downregulares nitric oxide and tumor necrosis factor-a induced by mycobacterial lipoarabinomannan in a macrophage cell line

Pentoxifylline (PTX), a phosphodiesterase inhibitor, is known to downregulate tumor necrosis factor-alpha (TNF-alpha) secretion induced by lipopolysacchride (LPS) and gamma interferon (IFN-gamma). We have had limited success in treating leprosy reactions, including erythema nodosum leprosum (ENL), in which TNF-alpha has been identified as a major proinflammatory cytokine. PTX inhibited production of NO (IC50 approximately equal to 1.0 mg/ml) and TNF-alpha (IC50 approximately equal to 0.05 mg/ml) in a dose-dependent fashion. As little as 0.5 mg/ml of PTX decreased NO production and 0.01 mg/ml of PTX inhibited TNF-alpha production. Western blot analyses demonstrated that iNOS was suppressed by PTX. Northern blot analyses showed significant reduction of TNF-alpha mRNA. We conclude that PTX is an effective inhibitor of lipoarabinomannan (LAM)-induced TNF-alpha production at both the product and transcriptional levels in our macrophage cell line. PTX also showed moderate inhibition of NO at the product level as well as translation of iNOS.