ReviewWiener klinische Wochenschrift2007
[Cellular regulation of anabolism and catabolism in skeletal muscle during immobilisation, aging and critical illness].
Review in Wiener klinische Wochenschrift, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- Cardiac Rehabilitation in German Speaking Countries of Europe-Evidence-Based Guidelines from Germany, Austria and Switzerland LLKardReha-DACH-Part 2.Journal of clinical medicine · 2021Review
- Aspects of physical medicine and rehabilitation in the treatment of deconditioned patients in the acute care setting: the role of skeletal muscle.Wiener medizinische Wochenschrift (1946) · 2016Review
- Muscle atrophy in intensive care unit patients.Acta informatica medica : AIM : journal of the Society for Medical Informatics of Bosnia & Herzegovina : casopis Drustva za medicinsku informatiku BiH · 2014Review
- [Frailty from the rehabilitation medicine point of view].Zeitschrift fur Gerontologie und Geriatrie · 2014Review
- Functional performance in community-dwelling and institutionalized elderly women.Wiener klinische Wochenschrift · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Skeletal muscle atrophy is associated with situations of acute and chronical illness, such as sepsis, surgery, trauma and immobility. Additionally, it is a common problem during the physiological process of aging. The myofibrillar proteins myosin and actin, which are essential for muscle contraction, are the major targets during the process of protein degradation. This leads to a general loss of muscle mass, muscle strength and to increased muscle fatigue. In critically ill or immobile patients skeletal muscle atrophy is accompanied by enhanced inflammation, reduced wound healing, weaning complications and difficulties in mobilisation. During aging it results in falls, fractures, physical injuries and loss of mobility. Relating to the primary stimulators - hormones, muscle lengthening, stress, inflammation, neuronal activity - research is now focusing on the investigation of the signal transduction pathways, which influence protein synthesis and protein degradation during skeletal muscle atrophy.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.