A Radio-to-mm Census of Star-forming Galaxies in Protocluster 4C23.56 at Z = 2.5:Gas Mass and Its Fraction Revealed with ALMA

We investigate gas contents of star-forming galaxies associated with protocluster 4C23.56 at z = 2.49 by using the redshifted CO (3-2) and 1.1 mm dust continuum with the Atacama Large Millimeter/submillimeter Array. The observations unveil seven CO detections out of 22 targeted Hα emitters (HAEs) and four out of 19 in 1.1 mm dust continuum. They have high stellar mass ({M}\star > 4× {10}10 M ⊙) and exhibit a specific star-formation rate typical of main-sequence star-forming galaxies at z˜ 2.5. Different gas-mass estimators from CO (3-2) and 1.1 mm yield consistent values for simultaneous detections. The gas mass ({M}{gas}) and gas fraction ({f}{gas}) are comparable to those of field galaxies, with {M}{gas}=[0.3,1.8]× {10}11× ({α }{CO}/(4.36× A(Z))) {M}⊙ , where {α }{CO} is the CO-to-H2 conversion factor and A(Z) is the additional correction factor for the metallicity dependence of {α }{CO}, and < {f}{gas}> =0.53+/- 0.07 from CO (3-2). Our measurements place a constraint on the cosmic gas density of high-z protoclusters, indicating that the protocluster is characterized by a gas density higher than that of the general fields by an order of magnitude. We found ρ ({H}2)˜ 5× {10}9 {M}⊙ {{Mpc}}-3 with the CO(3-2) detections. The five ALMA CO detections occur in the region of highest galaxy surface density, where the density positively correlates with global star-forming efficiency (SFE) and stellar mass. Such correlations possibly indicate a critical role of the environment on early galaxy evolution at high-z protoclusters, though future observations are necessary for confirmation

Remote Effects of Lower Limb Ischemia-Reperfusion: Impaired Lung, Unchanged Liver, and Stimulated Kidney Oxidative Capacities

Remote organ impairments are frequent and increase patient morbidity and mortality after lower limb ischemia-reperfusion (IR). We challenged the hypothesis that lower limb IR might also impair lung, renal, and liver mitochondrial respiration. Two-hour tourniquet-induced ischemia was performed on both hindlimbs, followed by a two-hour reperfusion period in C57BL6 mice. Lungs, liver and kidneys maximal mitochondrial respiration (Vmax⁡), complexes II, III, and IV activity (Vsucc), and complex IV activity (VTMPD) were analyzed on isolated mitochondria. Lower limb IR decreased significantly lung Vmax⁡ (29.4±3.3 versus 24±3.7 μmol O2/min/g dry weight, resp.; P=0.042) and tended to reduce Vsucc and VTMPD. IR did not modify liver but increased kidneys mitochondrial respiration (79.5±19.9 versus 108.6±21.4, P=0.035, and 126±13.4 versus 142.4±10.4 μmol O2/min/g dry weight for Vmax⁡ and Vsucc, resp.). Kidneys mitochondrial coupling was increased after IR (6.5±1.3 versus 8.8±1.1, P=0.008). There were no histological changes in liver and kidneys. Thus, lung mitochondrial dysfunction appears as a new early marker of hindlimb IR injuries in mice. Further studies will be useful to determine whether enhanced kidneys mitochondrial function allows postponing kidney impairment in lower limb IR setting

Remote Effects of Lower Limb Ischemia-Reperfusion: Impaired Lung, Unchanged Liver, and Stimulated Kidney Oxidative Capacities

Remote organ impairments are frequent and increase patient morbidity and mortality after lower limb ischemia-reperfusion (IR). We challenged the hypothesis that lower limb IR might also impair lung, renal, and liver mitochondrial respiration. Two-hour tourniquet-induced ischemia was performed on both hindlimbs, followed by a two-hour reperfusion period in C57BL6 mice. Lungs, liver and kidneys maximal mitochondrial respiration ( max ), complexes II, III, and IV activity ( succ ), and complex IV activity ( TMPD ) were analyzed on isolated mitochondria. Lower limb IR decreased significantly lung max (29.4 ± 3.3 versus 24 ± 3.7 mol O 2 /min/g dry weight, resp.; = 0.042) and tended to reduce succ and TMPD . IR did not modify liver but increased kidneys mitochondrial respiration (79.5 ± 19.9 versus 108.6 ± 21.4, = 0.035, and 126 ± 13.4 versus 142.4 ± 10.4 mol O 2 /min/g dry weight for max and succ , resp.). Kidneys mitochondrial coupling was increased after IR (6.5 ± 1.3 versus 8.8 ± 1.1, = 0.008). There were no histological changes in liver and kidneys. Thus, lung mitochondrial dysfunction appears as a new early marker of hindlimb IR injuries in mice. Further studies will be useful to determine whether enhanced kidneys mitochondrial function allows postponing kidney impairment in lower limb IR setting

Biomed Res Int

Remote organ impairments are frequent and increase patient morbidity and mortality after lower limb ischemia-reperfusion (IR). We challenged the hypothesis that lower limb IR might also impair lung, renal, and liver mitochondrial respiration. Two-hour tourniquet-induced ischemia was performed on both hindlimbs, followed by a two-hour reperfusion period in C57BL6 mice. Lungs, liver and kidneys maximal mitochondrial respiration (V(max)), complexes II, III, and IV activity (V(succ)), and complex IV activity (V(TMPD)) were analyzed on isolated mitochondria. Lower limb IR decreased significantly lung V(max) (29.4 +/- 3.3 versus 24 +/- 3.7 mumol O2/min/g dry weight, resp.; P = 0.042) and tended to reduce V(succ) and V(TMPD). IR did not modify liver but increased kidneys mitochondrial respiration (79.5 +/- 19.9 versus 108.6 +/- 21.4, P = 0.035, and 126 +/- 13.4 versus 142.4 +/- 10.4 mumol O2/min/g dry weight for V(max) and V(succ), resp.). Kidneys mitochondrial coupling was increased after IR (6.5 +/- 1.3 versus 8.8 +/- 1.1, P = 0.008). There were no histological changes in liver and kidneys. Thus, lung mitochondrial dysfunction appears as a new early marker of hindlimb IR injuries in mice. Further studies will be useful to determine whether enhanced kidneys mitochondrial function allows postponing kidney impairment in lower limb IR setting