Student or educator? Sign up with your school email and get 6 months of Pro free.
Cited by 282

The DOI matches its Crossref record; 12 of the 12 references it cites were found in a registry or an index.

Mechanisms of Chronic Muscle Wasting and Dysfunction after an Intensive Care Unit Stay. A Pilot Study

Open access
dos Santos, Claudia, Hussain, Sabah N. A., Mathur, Sunita, Picard, Martin, Herridge, Margaret, Correa, Judy, Bain, Alexandra, Guo, Yeting, Advani, Andrew, Advani, Suzanne L., Tomlinson, George, Katzberg, Hans, Streutker, Catherine J., Cameron, Jill I., Schols, Annemie, Gosker, Harry R., Batt, Jane·2016·American Journal of Respiratory and Critical Care Medicine

Abstract

RATIONALE: Critical illness survivors often experience permanent functional disability due to intensive care unit (ICU)-acquired weakness. The mechanisms responsible for long-term weakness persistence versus resolution are unknown. OBJECTIVES: To delineate cellular mechanisms underlying long-term weakness persistence in ICU survivors. METHODS: We conducted a nested, prospective study of critically ill patients mechanically ventilated for 7 days or longer. The patients were recruited from the RECOVER program and serially assessed over 6 months after ICU discharge. Twenty-seven of 82 patients consented to participate; 15 and 11 patients were assessed at 7 days and 6 months after ICU discharge, respectively. MEASUREMENTS AND MAIN RESULTS: We assessed motor functional capacity, quadriceps size, strength, and voluntary contractile capacity and performed electromyography, nerve conduction studies, and vastus lateralis biopsies for histologic, cellular, and molecular analyses. Strength and quadriceps cross-sectional areas were decreased 7 days after ICU discharge. Weakness persisted to 6 months and correlated with decreased function. Quadriceps atrophy resolved in 27% patients at 6 months. Muscle mass reconstitution did not correlate with resolution of weakness, owing to persistent impaired voluntary contractile capacity. Compared with Day 7, increased ubiquitin-proteasome system-mediated muscle proteolysis, inflammation, and decreased mitochondrial content all normalized at 6 months. Autophagy markers were normal at 6 months. Patients with sustained atrophy had decreased muscle progenitor (satellite) cell content. CONCLUSIONS: Long-term weakness in ICU survivors results from heterogeneous muscle pathophysiology with variable combinations of muscle atrophy and impaired contractile capacity. These findings are not explained by ongoing muscle proteolysis, inflammation, or diminished mitochondrial content. Sustained muscle atrophy is associated with decreased satellite cell content and compromised muscle regrowth, suggesting impaired regenerative capacity.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1164/rccm.201512-2344oc

Cites

12 of 12 references verified0 citation errors · 0 not checkable

Statistics

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Show all 12 references

Cited by

See all 282

Metadata

Authors
dos Santos, C., Hussain, S. N. A., Mathur, S., Picard, M., Herridge, M., Correa, J., Bain, A., Guo, Y., Advani, A., Advani, S. L., Tomlinson, G., Katzberg, H., Streutker, C. J., Cameron, J. I., Schols, A., Gosker, H. R., & Batt, J.
Venue
American Journal of Respiratory and Critical Care Medicine
Published
2016-10-01
Volume
194
Issue
7
Pages
821-830
ISSN
  • 1073-449X (ISSN-L)
  • 1535-4970
OpenAlex
W2326471898
Cited by
282
References
12
FWCI
18.67
Type
journal article
Language
en
Open access
green

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review

How to cite

Cite CoChat for the checks on this page, and the paper for its own findings.

This page
CoChat. (2026). Citation check: Mechanisms of Chronic Muscle Wasting and Dysfunction after an Intensive Care Unit Stay. A Pilot Study. https://app.cochat.ai/papers/10.1164/rccm.201512-2344oc
The paper
dos Santos, C., Hussain, S. N. A., Mathur, S., Picard, M., Herridge, M., Correa, J., Bain, A., Guo, Y., Advani, A., Advani, S. L., Tomlinson, G., Katzberg, H., Streutker, C. J., Cameron, J. I., Schols, A., Gosker, H. R., & Batt, J. (2016). Mechanisms of Chronic Muscle Wasting and Dysfunction after an Intensive Care Unit Stay. A Pilot Study. American Journal of Respiratory and Critical Care Medicine. https://doi.org/10.1164/rccm.201512-2344oc

Data sources

Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.