Relight the Candle: What happens to High Redshift Massive Quenched Galaxies

A puzzling population of extremely massive quiescent galaxies at redshifts beyond z=3 has recently been revealed by JWST and ALMA, some of them with stellar ages that show their quenching times to be as high as z=6, while their stellar masses are already above 5e10Msun. These extremely massive yet quenched galaxies challenge our understanding of galaxy formation at the earliest stages. Using the hydrodynamical cosmological simulation suite Magneticum Pathfinder, we show that such massive quenched galaxies at high redshifts can be successfully reproduced with similar number densities as observed. The stellar masses, sizes, formation redshifts, and star formation histories of the simulated quenched galaxies match those determined with JWST. Following these quenched galaxies at z=3.4 forward in time, we find 20% to be accreted onto a more massive structure by z=2, and from the remaining 80% about 30% rejuvenate up to z=2, another 30% stay quenched, and the remaining 40% rejuvenated on a very low level of star formation. Stars formed through rejuvenation are mostly formed on the outer regions of the galaxies, not in the centres. Furthermore, we demonstrate that the massive quenched galaxies do not reside in the most massive nodes of the cosmic web, but rather live in side-nodes of approximately Milky-Way halo mass. Even at z=0, only about 10% end up in small-mass galaxy clusters, while most of the quenched galaxies at z=3.4 end up in group-mass halos, with about 20% actually not even reaching 1e13Msun in halo mass.Comment: 18 pages, 14 figures. Submitted to ApJ, Comments welcom

Blowing out the Candle: How to Quench Galaxies at High Redshift -- an Ensemble of Rapid Starbursts, AGN Feedback and Environment

Recent observations with JWST and ALMA have revealed extremely massive quiescent galaxies at redshifts of z=3 and higher, indicating both rapid onset and quenching of star formation. Using the cosmological simulation suite Magneticum Pathfinder we reproduce the observed number densities and stellar masses, with 36 quenched galaxies of stellar mass larger than 3e10Msun at z=3.42. We find that these galaxies are quenched through a rapid burst of star-formation and subsequent AGN feedback caused by a particularly isotropic collapse of surrounding gas, occurring on timescales of around 200Myr or shorter. The resulting quenched galaxies host stellar components which are kinematically fast rotating and alpha-enhanced, while exhibiting a steeper metallicity and flatter age gradient compared to galaxies of similar stellar mass. The gas of the galaxies has been metal enriched and ejected. We find that quenched galaxies do not inhabit the densest nodes, but rather sit in local underdensities. We analyze observable metrics to predict future quenching at high redshifts, finding that on shorter timescales <500Myr the ratio M_bh/M_* is the best predictor, followed by the burstiness of the preceding star-formation, t50-t90 (time to go from 50% to 90% stellar mass). On longer timescales, >1Gyr, the environment becomes the strongest predictor, followed by t50-t90, indicating that at high redshifts the consumption of old and lack of new gas are more relevant for long-term prevention of star-formation than the presence of a massive AGN. We predict that relics of such high-z quenched galaxies should best be characterized by a strong alpha enhancement.Comment: 22 pages, 13 figures, Submitted to ApJ, Comments welcom

Preparing for low surface brightness science with the Vera C. Rubin Observatory: a comparison of observable and simulated intracluster light fractions

Intracluster light (ICL) provides an important record of the interactions galaxy clusters have undergone. However, we are limited in our understanding by our measurement methods. To address this, we measure the fraction of cluster light that is held in the Brightest Cluster Galaxy and ICL (BCG+ICL fraction) and the ICL alone (ICL fraction) using observational methods (surface brightness threshold-SB, non-parametric measure-NP, composite models-CM, and multi-galaxy fitting-MGF) and new approaches under development (wavelet decomposition-WD) applied to mock images of 61 galaxy clusters (14 <log10M200c/M⊙ < 14.5) from four cosmological hydrodynamical simulations. We compare the BCG+ICL and ICL fractions from observational measures with those using simulated measures (aperture and kinematic separations). The ICL fractions measured by kinematic separation are significantly larger than observed fractions. We find the measurements are related and provide equations to estimate kinematic ICL fractions from observed fractions. The different observational techniques give consistent BCG+ICL and ICL fractions but are biased to underestimating the BCG+ICL and ICL fractions when compared with aperture simulation measures. Comparing the different methods and algorithms, we find that the MGF algorithm is most consistent with the simulations, and CM and SB methods show the smallest projection effects for the BCG+ICL and ICL fractions, respectively. The Ahad (CM), MGF, and WD algorithms are best set up to process larger samples; however, the WD algorithm in its current form is susceptible to projection effects. We recommend that new algorithms using these methods are explored to analyse the massive samples that Rubin Observatory’s Legacy Survey of Space and Time will provide

Endogenous itaconate is not required for particulate matter-induced NRF2 expression or inflammatory response

Particulate matter (PM) air pollution causes cardiopulmonary mortality via macrophage-driven lung inflammation; however, the mechanisms are incompletely understood. RNA-sequencing demonstrated Acod1 (Aconitate decarboxylase 1) as one of the top genes induced by PM in macrophages. Acod1 encodes a mitochondrial enzyme that produces itaconate, which has been shown to exert anti-inflammatory effects via NRF2 after LPS. Here, we demonstrate that PM induces Acod1 and itaconate, which reduced mitochondrial respiration via complex II inhibition. Using Acod1-/- mice, we found that Acod1/endogenous itaconate does not affect PM-induced inflammation or NRF2 activation in macrophages in vitro or in vivo. In contrast, exogenous cell permeable itaconate, 4-octyl itaconate (OI) attenuated PM-induced inflammation in macrophages. OI was sufficient to activate NRF2 in macrophages; however, NRF2 was not required for the anti-inflammatory effects of OI. We conclude that the effects of itaconate production on inflammation are stimulus-dependent, and that there are important differences between endogenous and exogenously-applied itaconate

A novel treatment strategy of new onset atrial fibrillation after cardiac surgery: an observational prospective study

Objective: The aim of this prospective observational study was to evaluate the efficiency of a new escalating treatment strategy with vernakalant, flecainide and electrical cardioversion (EC) in patients with new onset atrial fibrillation (AF) after cardiac surgery. Material and methods: 24 patients with new onset AF after aortic valve surgery, coronary artery bypass surgery or combined procedures were evaluated in this study. Additional including criteria were age between 18 and 80, duration of AF less than four days, body weight less than 100 kg and no previous treatment with class I or III antiarrhythmic drugs. Exclusion criteria were poor left ventricular ejection fraction (LVEF < 40%) and history of myocardial infarction within 30 days. The patients were divided into converters and non-converters according to their response to combination treatment with vernakalant and flecainide, and the groups were compared. Results: The mean age of the population was 69.6 +/- 6.3 years and 26.1% of patients were female. There were no statistically significant differences between the two groups in terms of height, weight, gender distribution, comorbidities, preoperative medication, left ventricular function and left atrium diameter. Interventricular septum (IVS) in the non-converted group was significantly thicker compared to the converted group: 14.0 +/- 1.00 vs. 10.40 +/- 2.59 mm (p = 0.036). While 14 patients (60.9%) were successfully converted into stable sinus rhythm by pharmacological treatment with vernakalant and flecainide, 9 patients (39.1%, non-converted group) remained in AF. However, seven of them could be converted after additional EC. Conclusion: The combination of vernakalant and flecainide improves the conversion rate into a stable sinus rhythm in postcardiotomy patients with new onset AF compared to single drug therapy. Furthermore it might be an excellent precondition for successful EC in patients who are not converted after using both antiarrhtythmic drugs. Furthermore, left ventricular hypertrophy might be a potential negative predictor of successful pharmacological cardioversion

HIF-1α induces glycolytic reprograming in tissue-resident alveolar macrophages to promote cell survival during acute lung injury

Cellular metabolism is a critical regulator of macrophage effector function. Tissue-resident alveolar macrophages (TR-AMs) inhabit a unique niche marked by high oxygen and low glucose. We have recently shown that in contrast to bone marrow-derived macrophages (BMDMs), TR-AMs do not utilize glycolysis and instead predominantly rely on mitochondrial function for their effector response. It is not known how changes in local oxygen concentration that occur during conditions such as acute respiratory distress syndrome (ARDS) might affect TR-AM metabolism and function; however, ARDS is associated with progressive loss of TR-AMs, which correlates with the severity of disease and mortality. Here, we demonstrate that hypoxia robustly stabilizes HIF-1α in TR-AMs to promote a glycolytic phenotype. Hypoxia altered TR-AM metabolite signatures, cytokine production, and decreased their sensitivity to the inhibition of mitochondrial function. By contrast, hypoxia had minimal effects on BMDM metabolism. The effects of hypoxia on TR-AMs were mimicked by FG-4592, a HIF-1α stabilizer. Treatment with FG-4592 decreased TR-AM death and attenuated acute lung injury in mice. These findings reveal the importance of microenvironment in determining macrophage metabolic phenotype and highlight the therapeutic potential in targeting cellular metabolism to improve outcomes in diseases characterized by acute inflammation