This OCT study suggests that neointima within the BMS often transforms into lipid-laden tissue during an extended period of time and that expansion of neovascularization from peristent to intraintima contributes to atherosclerotic progression of neointima.

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Since the catastrophic releases of CO2 in the 1980s, Lakes Nyos and Monoun in Cameroon experienced CO 2 recharge at alarming rates of up to 80 mol͞m 2 per yr. Total gas pressures reached 8.3 and 15.6 bar in Monoun (2003) and Nyos (2001), respectively, resulting in gas saturation levels up to 97%. These natural hazards are distinguished by the potential for mitigation to prevent future disasters. Controlled degassing was initiated at Nyos (2001) and Monoun (2003) amid speculation it could inadvertently destabilize the lakes and trigger another gas burst. Our measurements indicate that water column structure has not been compromised by the degassing and local stability is increasing in the zones of degassing. Furthermore, gas content has been reduced in the lakes Ϸ12-14%. However, as gas is removed, the pressure at pipe inlets is reduced, and the removal rate will decrease over time. Based on 12 years of limnological measurements we developed a model of future removal rates and gas inventory, which predicts that in Monoun the current pipe will remove Ϸ30% of the gas remaining before the natural gas recharge balances the removal rate. In Nyos the single pipe will remove Ϸ25% of the gas remaining by 2015; this slow removal extends the present risk to local populations. More pipes and continued vigilance are required to reduce the risk of repeat disasters. Our model indicates that 75-99% of the gas remaining would be removed by 2010 with two pipes in Monoun and five pipes in Nyos, substantially reducing the risks.gas disaster ͉ limnology ͉ natural hazard V olcanoes can release massive amounts of CO 2 at the Earth's surface (1), and in the last 20 years natural lakes with CO 2 -rich waters have also proven to be highly dangerous (2-4). Before the nature of these gas-charged lakes was understood, sudden releases of large clouds of CO 2 gas from Lakes Nyos and Monoun in Cameroon, in 1986 and 1984, respectively, claimed the lives of Ϸ1,800 people by asphyxiation (2, 3). The gas originates from magma at great depth, but dissolves into groundwater near the Earth's surface. The CO 2 -charged water enters the lake bottoms through springs (2, 4) and accumulates in the deep, stratified lakes. Although the timing of sudden releases may be modulated by climate (5), it is now clear that continuous gas recharge into the lakes ensures a natural cycle of repeating disasters (6-8).Unlike most natural hazards, the certainty of future disasters at these lakes can be averted by directed mitigation. The solution is to degas the lakes through controlled piping of gas-rich bottom water to the lake surface where the gas is released harmlessly to the atmosphere in low concentrations. Once flow in a pipe is mechanically initiated, lift is provided by the buoyant rise of bubbly water and the process becomes spontaneous and selfsustaining. Theoretical models (9-11) indicated that this mitigation was feasible, and pumping began at Lake Nyos in 2001 and Lake Monoun in 2003 (12). However, questions still arose about the safety of this hazard miti...

Abstract. We made field explosion experiments as an analogue of volcanic explosion to understand the relationship between the explosion condition and the resultant surface phenomena. The main parameters we employed were explosion depth and explosion energy. Through the experiments we confirmed that scaled depth, which is the depth divided by cube root of energy, is the main parameter determining the properties of explosive volcanism. The energy assigned to blast wave decreased exponentially against the scaled depth. The scaled crater diameter became maximum when the scaled depth was about 4x 10 -3 m/J •/3 Scaled crater diameters by nuclear, chemical subsurface and some volcanic explosions were almost the same. From the scaling law, the overpressure at crater rim was estimated to be several MPa, which corresponded to typical rock strength. Probably the ground-forming materials were broken inside the area where overpressure exceeded their strength.

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Cross ResistanceCidofovir-resistant isolates selected in vitro following exposure to increasing concentrations of cidofovir were assessed for susceptibility to ganciclovir and foscarnet 4 . All were cross resistant to ganciclovir, but remained susceptible to foscarnet. Ganciclovir-or ganciclovir/foscarnet-resistant isolates that are cross resistant to cidofovir have been obtained from drug naive patients and from patients following ganciclovir or ganciclovir/ foscarnet therapy. To date, the majority of ganciclovir-resistant isolates are UL97 gene product (phosphokinase) mutants and remain susceptible to cidofovir 5 . Reduced susceptibility to cidofovir, however, has been reported for DNA polymerase mutants of CMV which are resistant to ganciclovir [6][7][8][9] . To date, all clinical isolates which exhibit high level resistance to ganciclovir, due to mutations in both the DNA polymerase and UL97 genes, have been shown to be cross resistant to cidofovir. Cidofovir is active against some, but not all, CMV isolates which are resistant to foscarnet [10][11][12] . The incidence of foscarnet-resistant isolates that are resistant to cidofovir is not known.A few triple-drug resistant isolates have been described. Genotypic analysis of two of these triple-resistant isolates revealed several point mutations in the CMV DNA polymerase gene. The clinical significance of the development of these cross-resistant isolates is not known. CLINICAL PHARMACOLOGY PHARMACOKINETICSVISTIDE must be administered with probenecid. The pharmacokinetics of cidofovir, administered both without and with probenecid, are described below.The pharmacokinetics of cidofovir without probenecid were evaluated in 27 HIV-infected patients with or without asymptomatic CMV infection. Dose-independent pharmacokinetics were demonstrated after one hr infusions of 1.0 (n = 5), 3.0 (n = 10), 5.0 (n = 2) and 10.0 (n = 8) mg/kg (See Table 2 for pharmacokinetic parameters). There was no evidence of cidofovir accumulation after 4 weeks of repeated administration of 3 mg/kg/ week (n = 5) without probenecid. In patients with normal renal function, approximately 80 to 100% of the VISTIDE dose was recovered unchanged in urine within 24 hr (n = 27). The renal clearance of cidofovir was greater than creatinine clearance, indicating renal tubular secretion contributes to the elimination of cidofovir.The pharmacokinetics of cidofovir administered with probenecid were evaluated in 12 HIV-infected patients with or without asymptomatic CMV infection and 10 patients with relapsing CMV retinitis. Dose-independent pharmacokinetics were observed for cidofovir, administered with probenecid, after one hr infusions of 3.0 (n = 12), 5.0 (n = 6), and 7.5 (n = 4) mg/kg (See Table 2). Approximately 70 to 85% of the VISTIDE dose administered with concomitant probenecid was excreted as unchanged drug within 24 hr. When VISTIDE was administered with probenecid, the renal clearance of cidofovir was reduced to a level consistent with creatinine clearance, suggesting that probenecid blocks ac...