Distribution of the bloodstream infections over time in the three study periods according to their microbiological and clinical outcomes.

<p>(A) Distribution of the bloodstream infections identified within defined time lapses. (B) Distribution of the bloodstream infections according to the time of complete susceptibility result availability. (C) Distribution of the bloodstream infections benefitting from the optimal antimicrobial treatment within defined time lapses. The “No change” category defines bloodstream infections optimally treated before the detection of positive blood culture. BSI, bloodstream infection.</p

Laboratory workflow of positive blood culture bottles according to time of positivity detection during pre-intervention and intervention periods.

<p>AST, antimicrobial susceptibility testing; BC, blood culture; βLT, βLACTA test; EB, Enterobacteriaceae; ID, identification; MALDI-TOF MS, matrix-assisted laser desorption ionization time-of-flight mass spectrometry; PBP2a, PBP2a Culture Colony Test. *: AST was directly performed from positive blood culture fluid when Gram staining identified a Gram-negative rod. Grey squares highlight the accelerated identification and susceptibility tests applied in the modified workflow.</p

Flowchart of adult monomicrobial blood culture episodes included during pre-intervention and intervention periods.

<p>BC, blood culture; BSI, bloodstream infections.</p

Distribution of microorganisms and main resistances of all bloodstream infections across the three study periods.

<p>3GC, third generation cephalosporin (cefotaxime, ceftriaxone, ceftazidime); AST, antimicrobial susceptibility testing; BSI, bloodstream infection; carbapenem (imipenem, meropenem); ID, identification; P0, pre-intervention period; P1, intervention period 1; P2, intervention period 2. Natural AmpC producers identified during the study periods: <i>Citrobacter freundii</i>, <i>Enterobacter aerogenes</i>, <i>Enterobacter cloacae</i>, <i>Hafnia alvei</i>, <i>Serratia marcescens</i>. Non-natural AmpC producers identified during the study periods: <i>Citrobacter koseri</i>, <i>Escherichia coli</i>, <i>Klebsiella oxytoca</i>, <i>Klebsiella pneumoniae</i>, <i>Proteus mirabilis</i>, <i>Proteus vulgaris</i>, <i>Salmonella spp</i>.</p

Relation between basal metabolism and intakes at the onset of withdrawal.

<p>Relation between basal metabolism and intakes at the onset of withdrawal.</p

Anthropomorphic, calorimetric and meal characteristics of AD and control subjects in Study 2.

<p>Values are means ± SD.</p>*<p>p<0.05,</p>**<p>p<0.01,</p>***<p>p<0.001 (AD vs Controls).</p>#<p>p<0.05,</p>##<p>p<0.01,</p>###<p>p<0.001 (AD-T1 vs AD-T3).</p><p>Theoretical basal metabolism was calculated according to the Schofield equations. Respiratory Quotient was calculated as CO₂ consumed/O₂ output. BMI: body mass index; FM: fat mass; BM: basal metabolism.</p

Characteristics and intakes for AD subjects drinking “low” or “high” quantities of alcohol.

<p>Values are means ± SD.</p>*<p>p<0.05,</p>**<p>p<0.01,</p>***<p>p<0.001 (“low alcohol” vs “high alcohol”).</p><p>The total population of alcoholics was split into two subpopulations depending on whether their consumption was lower or higher than the median value of 12.5 kcal/kg/day of alcohol and described as “low alcohol” or “high alcohol” drinking alcoholics. BMI: body mass index; FM: fat mass.</p

Nutrients intakes in controls and AD subjects at the onset (T1) and end (T3) of withdrawal.

<p>Values are means ± SD.</p>*<p>p<0.05.</p>**<p>p<0.01.</p>***<p>p<0.001 (vs AD-T1).</p>¶<p>p<0.05.</p>¶¶<p>p<0.01 (vs AD-T3).</p

Plasma concentrations of (an)orexigenic peptides, glucose and cortisol, estimation of insulin sensitivity and secretion using the HOMA model in AD subjects during withdrawal and controls.

<p>Values are means ± SD.</p>#<p>p<0.05,</p>##<p>p<0.01, p<0.001 (compared to AD-T1).</p>§<p>p<0.05,</p>§§<p>p<0.01,</p>§§§<p>p<0.001 (compared to AD-T2).</p>¶<p>p<0.05,</p>¶¶<p>p<0.01 (compared to AD-T3).</p

Relation between leptinemia and intakes (A) and between leptinemia and basal metabolism (B).

<p>Relation between leptinemia and intakes (A) and between leptinemia and basal metabolism (B).</p