The hot gas that constitutes the intracluster medium (ICM) has been studied at X-ray and millimeter/sub-millimeter wavelengths (Sunyaev-Zeldovich effect) for decades. Fast radio bursts (FRBs) offer ...an additional method of directly measuring the ICM and gas surrounding clusters, via observables such as dispersion measure (DM) and Faraday rotation measure (RM). We report the discovery of two FRB sources detected with the Deep Synoptic Array (DSA-110) whose host galaxies belong to massive galaxy clusters. In both cases, the FRBs exhibit excess extragalactic DM, some of which likely originates in the ICM of their respective clusters. FRB 20220914A resides in the galaxy cluster Abell 2310 at z=0.1125 with a projected offset from the cluster center of 520 kpc. The host of a second source, FRB 20220509G, is an elliptical galaxy at z=0.0894 that belongs to the galaxy cluster Abell 2311 at projected offset of 870 kpc. These sources represent the first time an FRB has been localized to a galaxy cluster. We combine our FRB data with archival X-ray, SZ, and optical observations of these clusters in order to infer properties of the ICM, including a measurement of gas temperature from DM and ySZ of 0.8-3.9 keV. We then compare our results to massive cluster halos from the IllustrisTNG simulation. Finally, we describe how large samples of localized FRBs from future surveys will constrain the ICM, particularly beyond the virial radius of clusters.
We present the Deep Synoptic Array (DSA-110) discovery and interferometric localization of the so far non-repeating FRB 20220319D. The FRB originates in a young, rapidly star-forming barred spiral ...galaxy, IRAS 02044\(+\)7048, at just 50 Mpc. Although the NE2001 and YMW16 models for the Galactic interstellar-medium (ISM) contribution to the DM of FRB 20220319D exceed its total observed DM, we show that uncertainties in these models accommodate an extragalactic origin for the burst. We derive a conservative upper limit on the DM contributed by the circumgalactic medium (CGM) of the Milky Way: the limit is either 28.7 pc cm\(^{-3}\) and 47.3 pc cm\(^{-3}\), depending on which of two pulsars nearby on the sky to FRB 20220319D is used to estimate the ISM DM. These limits both imply that the total Galactic CGM mass is \(<10^{11}M_{\odot}\), and that the baryonic mass of the Milky Way is \(\lesssim60\%\) of the cosmological average given the total halo mass. More stringent albeit less conservative constraints are possible when the DMs of pulsars in the distant globular cluster M53 are additionally considered. Although our constraints are sensitive to possible anisotropy in the CGM and to the assumed form of the radial-density profile, they are not subject to uncertainties in the chemical and thermal properties of the CGM. Our results strongly support scenarios commonly predicted by galaxy-formation simulations wherein feedback processes expel baryonic matter from the halos of galaxies like the Milky Way.
We report the detection and interferometric localization of the repeating fast radio burst (FRB) source FRB 20220912A during commissioning observations with the Deep Synoptic Array (DSA-110). Two ...bursts were detected from FRB 20220912A, one each on 2022 October 18 and 2022 October 25. The best-fit position is (R.A. J2000, decl. J2000) = (23:09:04.9, +48:42:25.4), with a 90% confidence error ellipse of \(\pm2\) arcsec and \(\pm1\) arcsec in right ascension and declination respectively. The two bursts have disparate polarization properties and temporal profiles. We find a Faraday rotation measure that is consistent with the low value of \(+0.6\) rad m\(^{-2}\) reported by CHIME/FRB. The DSA-110 localization overlaps with the galaxy PSO J347.2702+48.7066 at a redshift \(z=0.0771\), which we identify as the likely host. PSO J347.2702\(+\)48.7066 has a stellar mass of approximately \(10^{10}M_{\odot}\), modest internal dust extinction, and a star-formation rate likely in excess of \(0.1\,M_{\odot}\) yr\(^{-1}\). The host-galaxy contribution to the dispersion measure is likely \(\lesssim50\) pc cm\(^{-3}\). The FRB 20220912A source is therefore likely viewed along a tenuous plasma column through the host galaxy.
Summary Background Glutamate excitotoxicity might contribute to the pathophysiology of amyotrophic lateral sclerosis. In animal models, decreased excitatory aminoacid transporter 2 (EAAT2) ...overexpression delays disease onset and prolongs survival, and ceftriaxone increases EAAT2 activity. We aimed to assess the safety and efficacy of ceftriaxone for amyotrophic lateral sclerosis in a combined phase 1, 2, and 3 clinical trial. Methods This three-stage randomised, double-blind, placebo-controlled study was done at 59 clinical sites in the USA and Canada between Sept 4, 2006, and July 30, 2012. Eligible adult patients had amyotrophic lateral sclerosis, a vital capacity of more than 60% of that predicted for age and height, and symptom duration of less than 3 years. In stages 1 (pharmacokinetics) and 2 (safety), participants were randomly allocated (2:1) to ceftriaxone (2 g or 4 g per day) or placebo. In stage 3 (efficacy), participants assigned to ceftriaxone in stage 2 received 4 g ceftriaxone, participants assigned to placebo in stage 2 received placebo, and new participants were randomly assigned (2:1) to 4 g ceftriaxone or placebo. Participants, family members, and site staff were masked to treatment assignment. Randomisation was done by a computerised randomisation sequence with permuted blocks of 3. Participants received 2 g ceftriaxone or placebo twice daily through a central venous catheter administered at home by a trained caregiver. To minimise biliary side-effects, participants assigned to ceftriaxone also received 300 mg ursodeoxycholic acid twice daily and those assigned to placebo received matched placebo capsules. The coprimary efficacy outcomes were survival and functional decline, measured as the slope of Amyotrophic Lateral Sclerosis Functional Rating Scale-Revised (ALSFRS-R) scores. Analyses were by intention to treat. This study is registered with ClinicalTrials.gov , number NCT00349622. Findings Stage 3 included 66 participants from stages 1 and 2 and 448 new participants. In total, 340 participants were randomly allocated to ceftriaxone and 173 to placebo. During stages 1 and 2, mean ALSFRS-R declined more slowly in participants who received 4 g ceftriaxone than in those on placebo (difference 0·51 units per month, 95% CI 0·02 to 1·00; p=0·0416), but in stage 3 functional decline between the treatment groups did not differ (0·09, −0·06 to 0·24; p=0·2370). No significant differences in survival between the groups were recorded in stage 3 (HR 0·90, 95% CI 0·71 to 1·15; p=0·4146). Gastrointestinal adverse events and hepatobiliary adverse events were more common in the ceftriaxone group than in the placebo group (gastrointestinal, 245 of 340 72% ceftriaxone vs 97 of 173 56% placebo, p=0·0004; hepatobiliary, 211 62% vs 19 11%, p<0·0001). Significantly more participants who received ceftriaxone had serious hepatobiliary serious adverse events (41 participants 12%) than did those who received placebo (0 participants). Interpretation Despite promising stage 2 data, stage 3 of this trial of ceftriaxone in amyotrophic lateral sclerosis did not show clinical efficacy. The adaptive design allowed for seamless transition from one phase to another, and central venous catheter use in the home setting was shown to be feasible. Funding National Institute of Neurological Disorders and Stroke.
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