Publications by authors named "N Cacciani"
Article Synopsis
- Critical illness myopathy (CIM) leads to severe muscle function decline in ICU patients, characterized by muscle mass loss where the reduction in specific force outpaces the muscle mass decrease.
- The hallmark of CIM is marked by a significant reduction in the molecular motor protein myosin, which severely impacts the muscle's ability to generate force.
- An innovative study using cadmium telluride quantum dots revealed that muscle efficiency declines before myosin loss occurs, highlighting early changes in myosin function as potential targets for future CIM treatments.
Due to an unexpected activation of different zinc (Zn) transporters in a recent prospective clinical study, we have revisited the role of Zn homeostasis and the activation of matrix metalloproteinases (MMPs) in skeletal muscle exposed to the intensive care unit (ICU) condition (immobilization and mechanical ventilation). ICU patients exposed to 12 days ICU condition were followed longitudinally with six repeated muscle biopsies while they showed a progressive preferential myosin loss, i.e.
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- - The CAS3D image processing method combines Fourier and real space algorithms to analyze 3D volumetric images of skeletal muscle fibers, allowing for automated quantification of myofibrillar orientation and mean sarcomere length (SL).
- - The method demonstrated strong reliability, reproducing expected results from ideal data sets, while showing that slight random noise (up to 20%) had a linear effect on CAS3D values without significantly affecting SL and orientation detection.
- - When applied to a rat ICU model studying ventilator-induced diaphragm dysfunction, CAS3D improved the standard deviation of cosine angle sum detection from 0.03 to 0.008 by processing entire 3D images rather than slice-by-slice, enhancing
Aim: Mechanical ventilation (MV) results in diminished diaphragm size and strength, termed ventilator-induced diaphragm dysfunction (VIDD). VID increases dependence, prolongs weaning, and increases discharge mortality rates. The Janus kinase (JAK)/Signal Transducer and Activator of Transcription (STAT) pathway is implicated in VIDD, upregulated following MV.
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