Faulting of the Roman aqueduct of Venafrum (southern Italy): Methods of investigation, results, and seismotectonic implications, in

We present evidence of surface faulting of a poorly known frst-century B.C. aqueduct in central-southern Italy. Data were acquired by means of geological, geophysical, and geodetical surveys along the surfcial trace of a primary active fault (Aquae Iuliae fault). The ~30-km-long Venafrum aqueduct presents a net vertical offset of almost 4 m at the intersection with this normal fault. This fact reveals the occurrence of repeated faulting of the Roman water supply after its construction, i.e., during large historical earthquakes, the last being one of the most violent events to happen in Italy during the Middle Ages (September 1349, Mw = 6.6). We tentatively associate the remaining offset of the aqueduct to other poorly characterized earthquakes in the area, which were not previously associated with any active fault. It is a well-known fact that the recognition of ancient earthquakes on archaeological relics is a matter of debate in archaeoseismology, being diffcult at all times—and often impossible—to ascertain whether the damage observed should be related to seismic shaking or other causes (i.e., wars, floods, fres, decadence, etc.). Conversely, the exceptional case represented by the faulting of an archaeological relic such as this provides certain and reliable data on the causative seismogenic source and the associated earthquakes

CNS invasion by CD14+/CD16+peripheral blood-derived monocytes in HIV dementia: perivascular accumulation and reservoir of HIV infection

Increases in circulating CD14+/CD16+ monocytes have been associated with HIV dementia; trafficking of these cells into the CNS has been proposed to play an important role in the pathogenesis of HIV-induced neurological disorders. This model suggests that events outside the CNS leading to monocyte activation initiate the process leading to HIV dementia. To investigate the role of this activated monocyte subset in the pathogenesis of HIV dementia, we examined brain specimens from patients with HIV encephalopathy (HIVE), HIV without encephalopathy, and seronegative controls. An accumulation of perivascular macrophages was observed in HIVE. The majority of these cells identified in microglial nodules and in the perivascular infiltrate were CD14+/CD16+. P24 antigen colocalized with both CD14 and CD16 suggesting that the CD14+/CD16+ macrophage is a major reservoir of HIV-1 infection in CNS. Using CD45/LCA staining, the perivascular macrophage was distinguished from resident microglia. In addition to perivascular and nodular localizations, CD16 also stained ramified cells throughout the white matter. These cells were more ramified and abundant than cells positive for CD14 in white matter. Double staining for p24 and CD16 suggests that these cells were often infected with HIV-1. The prominent distribution of CD14+ cells in HIVE prompted our analysis of soluble CD14 levels in cerebrospinal fluid. Higher levels of soluble CD14 (sCD14) were observed in patients with moderate-to-severe HIV dementia, suggesting the utility of sCD14 as a surrogate marker. CD14+/CD16+ monocytes may play a role in other neurological disorders and sCD14 may be useful for evaluating these conditions

TNFα kinoid vaccination-induced neutralizing antibodies to TNFα protect mice from autologous TNFα-driven chronic and acute inflammation

The proinflammatory cytokine TNFα is a potent mediator of septic shock and a therapeutic target for chronic inflammatory pathologies including rheumatoid arthritis and Crohn's disease. As an alternative to anti-human TNFα (hTNFα) mAbs and other hTNFα blocker approved drugs, we developed an active anti-hTNFα immunotherapy, based on a vaccine comprised of a keyhole limpet hemocyanin-hTNFα heterocomplex immunogen (hTNFα kinoid) adjuvanted in incomplete Freund's adjuvant. In mice transgenic for hTNFα (TTg mice), hTNFα kinoid vaccination elicited high titers of Abs that neutralized hTNFα bioactivities but did not result in a cellular response to hTNFα. The vaccine was safe and effective in two experimental models. Kinoid-immunized but not control TTg mice resisted hTNFα-driven shock in one model and were prevented from spontaneous arthritis, inflammatory synovitis, and articular destruction in a second model. These data demonstrate an anti-cytokine induction of autoimmune protection against both acute and chronic hTNFα exposure. They show that active vaccination against a human cytokine can be achieved, and that the immune response can be effective and safe

Immunization against an IL-6 peptide induces anti-IL-6 antibodies and modulates the Delayed-Type Hypersensitivity reaction in cynomolgus monkeys

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