Magnetospheric plasma pressures in the midnight meridian: Observations from 2.5 to 35 RE

Plasma pressure data from the ISEE 2 fast plasma experiment (FPE) were statistically analyzed to determine the plasma sheet pressure versus distance in the midnight local time sector of the near-earth (12–35 RE) magnetotail plasma sheet. The observed plasma pressure, assumed isotropic, was mapped along model magnetic field flux tubes (obtained from the Tsyganenko and Usmanov [1982] model) to the magnetic equator, sorted according to magnetic activity, and binned according to the mapped equatorial location. In regions (L ≳ 12 RE) where the bulk of the plasma pressure was contributed by particles in the energy range of the FPE (70 eV to 40 keV for ions), the statistically determined peak plasma pressures vary with distance similarly to previously determined lobe magnetic pressures (i.e., in a time-averaged sense, pressure balance normal to the magnetotail magnetic equator in the midnight meridian is maintained between lobe magnetic and plasma sheet plasma pressures). Additional plasma pressure data obtained in the inner magnetosphere (2.5 \u3c L \u3c 7) by the Explorer 45, ATS 5, and AMPTE CCE spacecraft supplement the ISEE 2 data. Estimates of plasma pressures in the “transition” region (7–12 RE), where the magnetic field topology changes rapidly from a dipolar to a tail-like configuration, are compared with the observed pressure profiles. The quiet time “transition” region pressure estimates, obtained previously from inversions of empirical magnetic field models, bridge observations both interior to and exterior to the “transition” region in a reasonable manner. Quiet time observations and estimates are combined to provide profiles of the equatorial plasma pressure along the midnight meridian between 2.5 and 35 RE

Treating arteries instead of risk factors: A paradigm change in management of atherosclerosis

Background and Purpose: Until recently, atherosclerosis was thought to be inexorably progressive. Beginning in 2001 and implemented in our vascular prevention clinics by 2003, we have been treating arteries rather than risk factors. We studied the proportion of patients with plaque progression vs regression before and after this change in paradigm. Methods: Carotid total plaque area was measured by ultrasound at baseline and during follow-up. Before 2003, patients were treated according to consensus guidelines. After 2003, patients with plaque progression were treated more intensively, with the explicit goal of halting plaque progression or achieving regression. RESULTS: Four thousand three-hundred seventy-eight patients had serial plaque measurements in a given year between 1997 and 2007; 47% were female. Mean age at time of referral was 60 (SD, 15); this increased steeply (from age 50 to 62 years over the first 5 years) as we focused on stroke prevention. The annual rate of plaque progression increased steeply as the clinic populations aged but then abruptly decreased after implementation of the new approach to therapy. Before 2003, approximately half the patients had plaque progression and ≈25% had regression; by 2005, this had reversed. Changes in plasma lipids show that the differences were attributable to plaque measurement, not simply more intensive therapy for all patients. By 2007, patients with progression had lower levels of low-density lipoprotein than those with regression. Conclusions: Treating arteries without measuring plaque would be like treating hypertension without measuring blood pressure. A clinical trial to test this approach is being designed. © 2010 American Heart Association, Inc

Decline in the severity of carotid atherosclerosis and associated risk factors from 2002 to 2014

Background and Purpose-Several recent studies suggest declining rates of carotid revascularization for patients with carotid stenosis. We investigated whether carotid atherosclerosis severity has declined in recent years. Methods-We used carotid ultrasound to evaluate stenosis and plaque area in 6039 patients presenting to vascular medicine clinics in 3 eras: 2002 to 2005, 2006 to 2009, and 2010 to 2014. Results-The total plaque area at the time of referral to the clinics declined by 24% between 2002 and 2014; the percentage of patients presenting with carotid stenosis \u3c60% declined by 29.9%, and the number presenting with \u3c80% stenosis declined by 36.4%. There were significant reductions in plasma lipids and blood pressure during the same interval. Conclusions-Atherosclerosis severity seems to be declining over time. Better treatment of risk factors in the community may be responsible

What level of plasma homocyst(e)ine should be treated? Effects of vitamin therapy on progression of carotid atherosclerosis in patients with homocyst(e)ine levels above and below 14 μmol/L

High levels of plasma homocyst(e)ine (H[e]) are associated with increased vascular risk. Treatment is being contemplated, but the level at which patients should be treated is not known. We compared the response of carotid plaque to vitamin therapy in patients with H(e) above and below 14 μmol/L, a level commonly regarded as high enough to warrant treatment. Two-dimensional B-mode ultrasound measurement of carotid plaque was used to assess the response to vitamin therapy with folic acid 2.5 mg, pyridoxine 25 mg, and cyanocobalamin 250 μg daily, in 101 patients with vascular disease (51 with initial plasma levels above, and 50 below 14 μmol/L). Among patients with plasma H(e) \u3e14 μmol/L, the rate of progression of plaque area was 0.21 ± 0.41 cm2/year before vitamin therapy, and -0.049 ± 0.24 cm2/year after vitamin therapy (P2 = .0001; paired t test). Among patients with levels \u3c14 μmol/L, the rate of progression of plaque was 0.13 ± 0.24 cm2/ year before vitamin therapy and -0.024 ± 0.29 cm2/year after vitamin therapy (P2 = .022, paired t test). The change in rate of progression was -0.15 ± .44 cm2/year below 14 μmol/L, and -0.265 ± 0.46 cm2/year above 14 μmol/L (P = 0.20). Vitamin therapy regresses carotid plaque in patients with H(e) levels both above and below 14 μmol/L. These observations support a causal relationship between homocyst(e)ine and atherosclerosis and, taken with epidemiologic evidence, suggest that in patients with vascular disease, the level to treat may be \u3c9 μmol/L. © 2000 American Journal of Hypertension, Ltd

Expression profiling and QTL analysis: a powerful complementary strategy in drug abuse research

Alcoholism is a complex disease exhibiting a multifactorial mode of transmission. To simplify the genetic and phenotypic complexity of the alcoholic phenotype, alcohol-preferring (P) and -non-preferring (NP) rats were developed on the basis of alcohol preference and consumption as an animal model of alcoholism. Total gene expression analysis (TOGA) and quantitative trait loci (QTL) analysis were applied to selectively bred, inbred P and NP rats as complementary studies to identify genetic factors that contribute to alcohol preference and consumption. TOGA analysis was utilized to screen for differential expression in several brain regions involved in the mesocorticolimbic dopamine (DA) system. Genes exhibiting differences in expression were then screened for an association to the alcohol preference phenotype, the quantitative trait of a previously identified QTL. By evaluating differences in gene expression for linkage to a quantitative trait, this combined approach was implemented to identify alpha-synuclein, a candidate gene for alcohol preference

Convergence of parallel overlapping domain decomposition methods for the Helmholtz equation

We analyse parallel overlapping Schwarz domain decomposition methods for the Helmholtz equation, where the subdomain problems satisfy first-order absorbing (impedance) transmission conditions, and exchange of information between subdomains is achieved using a partition of unity. We provide a novel analysis of this method at the PDE level (without discretization). First, we formulate the method as a fixed point iteration, and show (in dimensions 1,2,3) that it is well-defined in a tensor product of appropriate local function spaces, each with $L^2$ impedance boundary data. Given this, we then obtain a bound on the norm of the fixed point operator in terms of the local norms of certain impedance-to-impedance maps arising from local interactions between subdomains. These bounds provide conditions under which (some power of) the fixed point operator is a contraction. In 2-d, for rectangular domains and strip-wise domain decompositions (with each subdomain only overlapping its immediate neighbours), we present two techniques for verifying the assumptions on the impedance-to-impedance maps which ensure power contractivity of the fixed point operator. The first is through semiclassical analysis, which gives rigorous estimates valid as the frequency tends to infinity. These results verify the required assumptions for sufficiently large overlap. For more realistic domain decompositions, we directly compute the norms of the impedance-to-impedance maps by solving certain canonical (local) eigenvalue problems. We give numerical experiments that illustrate the theory. These also show that the iterative method remains convergent and/or provides a good preconditioner in cases not covered by the theory, including for general domain decompositions, such as those obtained via automatic graph-partitioning software