Vis-NIR disk-integrated photometry of asteroid 25143 Itokawa around opposition by AMICA/Hayabusa

We present photometry of the S-type near-Earth asteroid 25143 Itokawa based on both ground-based observations in the UBVRI bands and measurements from the AMICA/Hayabusa spacecraft observations with ul-, b-, v-, w-, x-, and p-filters. Hayabusa observed Itokawa around opposition during the rendezvous, thus providing a unique set of observations of this asteroid. We fit the phase curve measurements with both the Classic Hapke Model (Hapke, 1981, 1984, 1986) and Modern Hapke Model (Hapke, 2002, 2008, 2012a) and thereby extract the physical properties of Itokawa's surface regolith. The single-scattering albedo (0.57 ± 0.05) is larger than that derived for Eros (0.43 ± 0.02), another S-type near-Earth asteroid visited by a spacecraft. Both models indicate a regolith that is forward-scattering in nature. From the hockey stick relationship derived for the single-particle phase function (Hapke, 2012b), both modeling results suggest a regolith comprised of rough surfaced particles with a low density of internal scatterers. Application of the Modern Hapke model derives porosity parameter values from 1 to 1.1, for BVR bands, which corresponds to porosity values between 77–79%. This suggests the surface of Itokawa is very fluffy and the large boulders may be bonded with smaller size particles, typical of the particle sizes observed in Muses Sea. Both models also provide similar geometric albedo values (0.27 ± 0.02) at the V-band wavelength, which are equivalent to Eros’ geometric albedo

Introduction: P.A.V.B. Swamy's contribution to Econometrics

This paper introduces this special issue of Economic Modelling which marks the significant contribution made by P.A.V.B Swamy to econometrics. His work spans almost 50 years and has been both innovative and challenging. The many distinguished authors who have contributed to this volume attests to the high regard in which he is held in the profession.Econometrics Swamy

Combination propranolol and bepridil therapy in stable angina pectoris

The safety and efficacy of bepridil plus propranolol therapy were investigated in a placebo-controlled, parallel-design, double-blind trial in 56 patients who were not responding to propranolol alone. Patients entering the study were receiving an average propranolol dosage of 131 mg/day (range 20 to 240). For the first 2 weeks of the study they were given placebo in addition to their propranolol dose, and then were randomized to receive continued placebo plus propranolol or bepridil plus propranolol therapy. The bepridil dosage was adjusted over the 8 weeks of active treatment to an average of 273 mg/day (range 200 to 400). The double-blind treatment period was followed by a 3-week washout period during which all patients received propranolol and placebo. The effects of treatment on the frequency of angina attacks, nitroglycerin consumption, exercise performance (treadmill-modified Bruce protocol) and Holter electrocardiogram (ECG) were assessed. Propranolol and bepridil plasma levels also were obtained. Improved antianginal efficacy and reduced nitroglycerin consumption were noted when bepridil was added to propranolol (p \u3c 0.01). During 8 weeks of combination treatment, exercise tolerance increased 1.0 ± 1.2 minutes from a baseline of 7.3 ± 2.2 with bepridil plus propranolol compared with an increase of 0.02 ± 1.3 minutes from a baseline of 7.6 ± 2.9 with placebo plus propranolol (p \u3c 0.01). With bepridil plus propranolol, there were also increases in exercise time to onset of angina (p \u3c 0.04), exercise time to 1-mm electrocardiographic ST-segment depression (p \u3c 0.06) and total work (p \u3c 0.03) compared with placebo plus propranolol therapy. Resting heart rate was reduced a maximum of 2 beats/min with combination treatment compared with propranolol alone, and no differences in blood pressure between treatment groups were observed. There were no clinically significant rhythm changes on Holter ECG with combination treatment, and bepridil treatment had no effect on plasma propranolol levels. Bepridil did prolong the QTc interval on resting ECG by a mean of 37 ± 39 millisecond. Adverse effects were mild with bepridil plus propranolol and greater in frequency than those with placebo plus propranolol. With cessation of bepridil, patients returned toward the angina frequency and exercise tolerance levels seen at baseline with propranolol alone. The addition of bepridil to propranolol provided safe and effective antianginal therapy in patients whose angina was not controlled by propranolol alone. © 1985

Identification of Four Gene Variants Associated with Myocardial Infarction

Family history is a major risk factor for myocardial infarction (MI). However, known gene variants associated with MI cannot fully explain the genetic component of MI risk. We hypothesized that a gene-centric association study that was not limited to candidate genes could identify novel genetic associations with MI. We studied 11,053 single-nucleotide polymorphisms (SNPs) in 6,891 genes, focusing on SNPs that could influence gene function to increase the likelihood of identifying disease-causing gene variants. To minimize false-positive associations generated by multiple testing, two studies were used to identify a limited number of nominally associated SNPs; a third study tested the hypotheses that these SNPs are associated with MI. In the initial study (of 340 cases and 346 controls), 637 SNPs were associated with MI (P<.05); these were evaluated in a second study (of 445 cases and 606 controls), and 31 of the 637 SNPs were associated with MI (P<.05) and had the same risk allele as in the first study. For each of these 31 SNPs, we tested the hypothesis that it is associated with MI, using a third study (of 560 cases and 891 controls). We found that four of these gene variants were associated with MI (P<.05; false-discovery rate <10%) and had the same risk allele as in the first two studies. These gene variants encode the cytoskeletal protein palladin (KIAA0992 [odds ratio (OR) 1.40]), a tyrosine kinase (ROS1 [OR 1.75]), and two G protein–coupled receptors (TAS2R50 [OR 1.58] and OR13G1 [OR 1.40]); all ORs are for carriers of two versus zero risk alleles. These findings could lead to a better understanding of MI pathophysiology and improved patient risk assessment