Decimi Junii Juvenalis et Auli Persii Flacci: satire expurgate. Notis illustratae. Curavit F. P. Leverett.

Mode of access: Internet.

Decii Junii Juvenalis et Auli Persii Satyræ,

Mode of access: Internet.

D. Junii Juvenalis, Auli Persii Flacci, et Sulpiciae Satyrae; ex recensione Henrici Christianii Henninii, et Esaaci Casauboni.

"Nicolai Rigaltii deSatyra Juvenalis Dissertatio": p. [iii]-xliv.

D. Iunii Iuvenalis et Auli Persii Flacci Satyrae /

"Auli Persii Flacci Satyrae sex", p. [151]-189, has special t.-p.

D. Junii Juvenalis et Auli Persii Satyræ omni obscoenitate expurgatæ cum interpretatione ac notis

Mode of access: Internet.

Decii Junii Juvenalis & Auli Persii Satyræ,

Mode of access: Internet.

Decii Junii Juvenalis ex Auli Persii Flacci Satiræ / ex recensione et cum notis Ruperti et Kœnig.

Mode of access: Internet.

Decii J. Juvenalis Satirarum libri quinque. [Auli Persii Satiræ.]

Additional title-page:- Nova scriptorum Latinorum bibliotheca.

Decimi Junii Juvenalis et Auli Persii Flacci Satirae expurgatae /

Mode of access: Internet.

Decimi Junii Juvenalis et Auli Persii Flacci Satirae expurgatæ, notis illustratæ.

Mode of access: Internet.

Decimi Junii Juvenalis et Auli Persii Flacci Satiræ expurgatæ,

Mode of access: Internet.

Decimi Junii Juvenalis et Auli Persii Flacci Satirae expurgatæ, notis illustratæ.

Mode of access: Internet.

The Thrombin Receptor Antagonist for Clinical Event Reduction in Acute Coronary Syndrome (TRA.CER) trial: study design and rationale

Background The protease-activated receptor 1 (PAR-1), the main platelet receptor for thrombin, represents a novel target for treatment of arterial thrombosis, and SCH 530348 is an orally active, selective, competitive PAR-1 antagonist. We designed TRA.CER to evaluate the efficacy and safety of SCH 530348 compared with placebo in addition to standard of care in patients with non-ST-segment elevation (NSTE) acute coronary syndromes (ACS) and high-risk features. Trial design TRA.CER is a prospective, randomized, double-blind, multicenter, phase III trial with an original estimated sample size of 10,000 subjects. Our primary objective is to demonstrate that SCH 530348 in addition to standard of care will reduce the incidence of the composite of cardiovascular death, myocardial infarction (MI), stroke, recurrent ischemia with rehospitalization, and urgent coronary revascularization compared with standard of care alone. Our key secondary objective is to determine whether SCH 530348 will reduce the composite of cardiovascular death, MI, or stroke compared with standard of care alone. Secondary objectives related to safety are the composite of moderate and severe GUSTO bleeding and clinically significant TIMI bleeding. The trial will continue until a predetermined minimum number of centrally adjudicated primary and key secondary end point events have occurred and all subjects have participated in the study for at least I year. The TRA.CER trial is part of the large phase III SCH 530348 development program that includes a concomitant evaluation in secondary prevention. Conclusion TRA.CER will define efficacy and safety of the novel platelet PAR-1 inhibitor SCH 530348 in the treatment of high-risk patients with NSTE ACS in the setting of current treatment strategies. (Am Heart J 2009; 158:327-34.)

Meta-analysis identifies 13 new loci associated with waist-hip ratio and reveals sexual dimorphism in the genetic basis of fat distribution.

Waist-hip ratio (WHR) is a measure of body fat distribution and a predictor of metabolic consequences independent of overall adiposity. WHR is heritable, but few genetic variants influencing this trait have been identified. We conducted a meta-analysis of 32 genome-wide association studies for WHR adjusted for body mass index (comprising up to 77,167 participants), following up 16 loci in an additional 29 studies (comprising up to 113,636 subjects). We identified 13 new loci in or near RSPO3, VEGFA, TBX15-WARS2, NFE2L3, GRB14, DNM3-PIGC, ITPR2-SSPN, LY86, HOXC13, ADAMTS9, ZNRF3-KREMEN1, NISCH-STAB1 and CPEB4 (P = 1.9 × 10⁻⁹ to P = 1.8 × 10⁻⁴⁰) and the known signal at LYPLAL1. Seven of these loci exhibited marked sexual dimorphism, all with a stronger effect on WHR in women than men (P for sex difference = 1.9 × 10⁻³ to P = 1.2 × 10⁻&supl;³). These findings provide evidence for multiple loci that modulate body fat distribution independent of overall adiposity and reveal strong gene-by-sex interactions.