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We consider the Cauchy problem for the damped wave equations with variable coefficients a(x) having power type nonlinearity |u|^p. We discuss the global existence of solutions for small initial data and investigate the relation between the range of a(x) and the order p., Comment: Describes the wrong facts in the text

We examined whether an additive treatment with an angiotensin receptor blocker, olmesartan, reduces the mortality and morbidity in hypertensive patients with chronic heart failure (CHF) treated with angiotensin-converting enzyme (ACE) inhibitors, β-blockers, or both. In this prospective, randomized, open-label, blinded endpoint study, a total of 1147 hypertensive patients with symptomatic CHF (mean age 66 years, 75% male) were randomized to the addition of olmesartan (n = 578) to baseline therapy vs. control (n = 569). The primary endpoint was a composite of all-cause death, non-fatal acute myocardial infarction, non-fatal stroke, and hospitalization for worsening heart failure. During a median follow-up of 4.4 years, the primary endpoint occurred in 192 patients (33.2%) in the olmesartan group and in 166 patients (29.2%) in the control group [hazard ratio (HR) 1.18; 95% confidence interval (CI), 0.96–1.46, P = 0.112], while renal dysfunction developed more frequently in the olmesartan group (16.8 vs. 10.7%, HR 1.64; 95% CI 1.19–2.26, P = 0.003). Subgroup analysis revealed that addition of olmesartan to combination of ACE inhibitors and β-blockers was associated with increased incidence of the primary endpoint (38.1 vs. 28.2%, HR 1.47; 95% CI 1.11–1.95, P = 0.006), all-cause death (19.4 vs. 13.5%, HR 1.50; 95% CI 1.01–2.23, P = 0.046), and renal dysfunction (21.1 vs. 12.5%, HR 1.85; 95% CI 1.24–2.76, P = 0.003). Additive use of olmesartan did not improve clinical outcomes but worsened renal function in hypertensive CHF patients treated with evidence-based medications. Particularly, the triple combination therapy with olmesartan, ACE inhibitors and β-blockers was associated with increased adverse cardiac events. This study is registered at clinicaltrials.gov-NCT00417222.

Vernalization, the promotion of flowering in response to low temperatures, is one of the best characterized examples of epigenetic regulation in plants. The promotion of flowering is proportional to the duration of the cold period, but the mechanism by which plants measure time at low temperatures has been a long-standing mystery. We show that the quantitative induction of the first gene in the Arabidopsis vernalization pathway, VERNALIZATION INSENSITIVE 3 (VIN3), is regulated by the components of Polycomb Response Complex 2, which trimethylates histone H3 lysine 27 (H3K27me3). In differentiated animal cells, H3K27me3 is mostly associated with long-term gene repression, whereas, in pluripotent embyonic stem cells, many cell lineage-specific genes are inactive but exist in bivalent chromatin that carries both active (H3K4me3) and repressive (H3K27me3) marks on the same molecule. During differentiation, bivalent domains are generally resolved to an active or silent state. We found that H3K27me3 maintains VIN3 in a repressed state prior to cold exposure; this mark is not removed during VIN3 induction. Instead, active VIN3 is associated with bivalently marked chromatin. The continued presence of H3K27me3 ensures that induction of VIN3 is proportional to the duration of the cold, and that plants require prolonged cold to promote the transition to flowering. The observation that Polycomb proteins control VIN3 activity defines a new role for Polycomb proteins in regulating the rate of gene induction. © 2010 Blackwell Publishing Ltd.

The purpose of this study is to evaluate the significance of serum antithrombin ILE (AT III) in acute cerebrovascular stroke. AT III levies were determined by means of single radial immunodiffusion method in 73 serum specimens of 19 patients with cerebral hemorrhage (CH.), 129 of 24 patients with cerebral infarction (C.I.) and 82 of 82 healthy controls. AT III levels of patients with C.H. and with C.I. on the 1st day of the attacks were significantly higher than the value of controls. The high levels maintained from the 1st to the 25th day exculding 7th and 8th days in hemorrhagic patients. In patients with C.I., the levels from the 6th to the 25 day were significantly higher than that from the 1st to the 5th day. No difference was found in the types of the diseases. In 150 serum specimens obtained from the 1st to the 7th day, AT III levels were significantly lower in the patients with high fever, disturbance of consciousness and abnormal ECG findings than those in patients without these clinical findings. In serum specimens obtained from the 5th to the 7th day, AT III level of survivals were significantly higher than that of the dead.AT III levels in patients with high FDP levels were higher than those in patients with normal FDP levels. In C.I., AT III levels were directly proportional to prothormbin and plasminogen levels, and were inversely proportional to α1-antitrypsin levels. It is supposed that high AT III levels in acute stroke patients are caused by the protective effects on excess thrombus formation occurring parimarily in C.I. and secondarily in C.H. The high levels in both types of strokes and the close relation to outcome of patients indicate usefulness in the clinical evaluation of patient’s prognosis.