While, in general, decamethylzincocene, Zn(C5Me5)2, and other zincocenes, Zn(C5Me4R)2 (R = H, But, SiMe3), react with dialkyl and diaryl derivatives, ZnR'2, to give the half-sandwich compounds (eta5-C5Me4R)ZnR', under certain conditions the reactions of Zn(C5Me5)2 with ZnEt2 or ZnPh2 produce unexpectedly the dizincocene Zn2(eta5-C5Me5)2 (1) in low yields, most likely as a result of the coupling of two (eta5-C5Me5)Zn* radicals. An improved, large scale (ca. 2 g) synthesis of 1 has been achieved by reduction of equimolar mixtures of Zn(C5Me5)2 and ZnCl2 with KH in tetrahydrofuran. The analogous reduction of Zn(C5Me4R)2 (R = H, SiMe3, But) yields only decomposition products, but the isotopically labeled dimetallocene 68Zn2(eta5-C5Me5)2 and the related compound Zn2(eta5-C5Me4Et)2 (2) have been obtained by this procedure. Compound 2 has lower thermal stability than 1, but it has been unequivocally characterized by low-temperature X-ray diffraction studies. As for 1 a combination of structural characterization techniques has provided unambiguous evidence for its formulation as the Zn-Zn bonded dimer Zn2(eta5-C5Me4Et)2, with a short Zn-Zn bond of 2.295(3) A indicative of a strong Zn-Zn bonding interaction. The electronic structure and the bonding properties of 1 and those of related dizincocenes Zn2(eta5-Cp')2 have been studied by DFT methods (B3LYP level), with computed bond distances and angles for dizincocene 1 very similar to the experimental values. The Zn-Zn bond is strong (ca. 62 kcal.mol-1 for 1) and resides in the HOMO-4, that has a contribution of Zn orbitals close to 60%, consisting mostly of the Zn 4s orbitals (more than 96%).

Chemokines are critical for the inflammatory process in autoimmune diseases such as rheumatoid arthritis (RA). The chemokine receptor-5 (CCR5) mediates chemotaxis by CC-chemokines and is expressed by lymphocytes with the Th1 phenotype and monocyte/macrophages. A 32 bp deletion in the CCR5 (CCR5-⌬32 allele) abolishes receptor expression in homozygotes, while CCR5-⌬32 carriers would express less receptor than wild-type homozygotes. This polymorphism is related to the resistance to HIV-1 infection and progression towards AIDS. We hypothesized that the CCR5-⌬32 allele may modulate the severity of disease in RA. A total of 160 RA-patients (71 and 89 with severe and non-severe phenotypes, respectively) and 500 healthy individuals from the same Caucasian population (Asturias, northern Spain) were genotyped. Carriers of the CCR5-⌬32 allele were at a significantly higher frequency (P = 0.012) in non-severe compared to severe patients (17% vs 4%). Our results suggest that the CCR5-⌬32 polymorphism is a genetic marker related to the severity of RA. Genes and Immunity (2000) 1, 288-289.Keywords: chemokines; CCR5-⌬32 allele; rheumatoid arthritis; disease severity Rheumatoid arthritis (RA) is a systemic chronic inflammatory disease of the joints characterized by the infiltration of the synovial membrane with T lymphocytes and macrophages, and pannus formation over the underlying cartilage and bone. The inflammatory process observed in RA is mediated by chemotactic factors released by the inflamed tissues. Chemokines display a potent chemotactic activity for cells of the immune system, playing an important role in both the destructive and the fibrovasculoproliferative phases of RA.1 The chemokine receptor-5 (CCR5) mediates chemotaxis by the CC-chemokines RANTES, MIP-1␣ and MIP-1␤. This receptor is expressed by lymphocytes exhibiting the Th1-phenotype and by monocytes/macrophages. 2In addition to its role in inflammation, CCR5 also acts as an HIV-1 coreceptor to mediate the first step in cell entry:fusion of the viral envelope with the membrane in the the target CD4 + cell. A 32 bp deletion at the coding region of the CCR5 gene, the CCR5-⌬32 mutation, leads to the expression of reduced amounts of the CCR5 protein in heterozygous individuals.3 CCR5-⌬32 homozygotes do not express the receptor and have nearly complete resistence to HIV-1 infection despite repeated exposure, while heterozygotes progress slowly towards AIDS compared to wild-type homozygotes. 4 The CCR5-