Characterizations of Student's t-distribution via regressions of order statistics

Utilizing regression properties of order statistics, we characterize a family of distributions introduced by Akhundov, Balakrishnan, and Nevzorov (2004), that includes the t-distribution with two degrees of freedom as one of its members. Then we extend this characterization result to t-distribution with more than two degrees of freedom.Comment: To appear in "Statistics

BIOSYNTHESIS OF LYCORINE BY IN VITRO CULTURES OF PANCRATIUM MARITIMUM L. (AMARYLLIDACEAE)

ABSTRACT Seeds of Pancratium maritimum collected from the natural populations along Bulgaria

Theragnostics of TRK-targeting agents (trackins): a challenge that promises reward

Therminologically, theragnostics combines therapeutics and diagnostics. Life at cellular and molecular level is a binary event (e.g., phosphorylation-dephosphorylation of proteins, methylation-demethylations of DNA and acetylation-deacetylation of histones) aimed at the maintenance of a sanogenic phenotype of the homeostasis. Herein, we focus on the neurotrophins with metabotrophic or pathogenic potentials, particularly nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) and their receptors Trk (tyrosine/tropomyosin receptor kinase; pronounced “track”). Accordingly, the term trackins was introduced which stands for Trk-targeting agents influencing agonistically or antagonistically the activity of TrkANGF, TrkBBDNF, and TrkCNT-3 receptor. We argue that multiple diseases may be trackins curable, for instance: (i) agonistic trackins may have therapeutic potentials for cardiometabolic diseases (e.g., atherosclerosis, obesity, T2DM, and metabolic syndrome) and for neurometabolic diseases (e.g., Alzheimer’s disease/T3DM), whereas (ii) antagonistic trackins may be drugs for prostate, breast, gastric, pancreatic and colon cancers, also for pain, and eye, skin and male genitourinary track diseases. Moreover, TrkANGF, TrkBBDNF and TrkCNT-3 receptor may be promising biomarkers for diagnosis and prognosis of these diseases. Altogether, the presented data may be a challenge that promises reward requiring a further pursuit

Space Charge at Nanoscale: Probing Injection and Dynamic Phenomena Under Dark/Light Configurations by Using KPFM and C-AFM

International audienc

Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease

Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.