Mass and environment as drivers of galaxy evolution in SDSS and zCOSMOS and the origin of the Schechter function

We explore the inter-relationships between mass, star-formation rate and environment in the SDSS, zCOSMOS and other surveys. The differential effects of mass and environment are completely separable to z ~ 1, indicating that two distinct processes are operating, "mass-quenching" and "environment-quenching". Environment-quenching, at fixed over-density, evidently does not change with epoch to z ~ 1, suggesting that it occurs as large-scale structure develops in the Universe. The observed constancy of the mass-function shape for star-forming galaxies, demands that the mass-quenching of galaxies around and above M*, must be proportional to their star-formation rates at all z < 2. We postulate that this simple mass-quenching law also holds over a much broader range of stellar mass and epoch. These two simple quenching processes, plus some additional quenching due to merging, then naturally produce (a) a quasi-static Schechter mass function for star-forming galaxies with a value of M* that is set by the proportionality between the star-formation and mass-quenching rates, (b) a double Schechter function for passive galaxies with two components: the dominant one is produced by mass-quenching and has exactly the same M* as the star-forming galaxies but an alpha shallower by +1, while the other is produced by environment effects and has the same M* and alpha as the star-forming galaxies, and is larger in high density environments. Subsequent merging of quenched galaxies modifies these predictions somewhat in the denser environments, slightly increasing M* and making alpha more negative. All of these detailed quantitative relationships between the Schechter parameters are indeed seen in the SDSS, lending strong support to our simple empirically-based model. The model naturally produces for passive galaxies the "anti-hierarchical" run of mean ages and alpha-element abundances with mass.Comment: 66 pages, 19 figures, 1 movie, accepted for publication in ApJ. The movie is also available at http://www.exp-astro.phys.ethz.ch/zCOSMOS/MF_simulation_d1_d4.mo

Relating Near-Earth Observations of AN Interplanetary Coronal Mass Ejection to the Conditions at its Site of Origin in the Solar Corona

International audienc

Relating Near-Earth Observations of AN Interplanetary Coronal Mass Ejection to the Conditions at its Site of Origin in the Solar Corona

International audienc

Relating Near-Earth Observations of AN Interplanetary Coronal Mass Ejection to the Conditions at its Site of Origin in the Solar Corona

International audienc

An international cohort study of autosomal dominant tubulointerstitial kidney disease due to REN mutations identifies distinct clinical subtypes

There have been few clinical or scientific reports of autosomal dominant tubulointerstitial kidney disease due to REN mutations (ADTKD-REN), limiting characterization. To further study this, we formed an international cohort characterizing 111 individuals from 30 families with both clinical and laboratory findings. Sixty-nine individuals had a REN mutation in the signal peptide region (signal group), 27 in the prosegment (prosegment group), and 15 in the mature renin peptide (mature group). Signal group patients were most severely affected, presenting at a mean age of 19.7 years, with the prosegment group presenting at 22.4 years, and the mature group at 37 years. Anemia was present in childhood in 91% in the signal group, 69% prosegment, and none of the mature group. REN signal peptide mutations reduced hydrophobicity of the signal peptide, which is necessary for recognition and translocation across the endoplasmic reticulum, leading to aberrant delivery of preprorenin into the cytoplasm. REN mutations in the prosegment led to deposition of prorenin and renin in the endoplasmic reticulum-Golgi intermediate compartment and decreased prorenin secretion. Mutations in mature renin led to deposition of the mutant prorenin in the endoplasmic reticulum, similar to patients with ADTKD-UMOD, with a rate of progression to end stage kidney disease (63.6 years) that was significantly slower vs. the signal (53.1 years) and prosegment groups (50.8 years) (significant hazard ratio 0.367). Thus, clinical and laboratory studies revealed subtypes of ADTKD-REN that are pathophysiologically, diagnostically, and clinically distinct