OBJECTIVE: This study aimed to investigate the impact of sarcopenia and lumbar paraspinal muscle composition (PMC) on patient-reported outcomes (PROs) after lumbar fusion surgery with 12-month follow-up (12 M-FU).
METHODS: A prospective investigation of patients undergoing elective lumbar fusion was conducted. Preoperative MRI-based evaluation of the cross-sectional area (CSA), the functional CSA (fCSA), and the fat infiltration(FI) of the posterior paraspinal muscles (PPM) and the psoas muscle at level L3 was performed. Sarcopenia was defined by the psoas muscle index (PMI) at L3 (CSAPsoas [cm2]/(patients\' height [m])2). PROs included Oswestry Disability Index (ODI), 12-item Short Form Healthy Survey with Physical (PCS-12) and Mental Component Scores (MCS-12) and Numerical Rating Scale back and leg (NRS-L) pain before surgery and 12 months postoperatively. Univariate and multivariable regression determined associations among sarcopenia, PMC and PROs.
RESULTS: 135 patients (52.6% female, 62.1 years, BMI 29.1 kg/m2) were analyzed. The univariate analysis demonstrated that a higher FI (PPM) was associated with worse ODI outcomes at 12 M-FU in males. Sarcopenia (PMI) and higher FI (PPM) were associated with worse ODI and MCS-12 at 12 M-FU in females. Sarcopenia and higher FI of the PPM are associated with worse PCS-12 and more leg pain in females. In the multivariable analysis, a higher preoperative FI of the PPM (β = 0.442; p = 0.012) and lower FI of the psoas (β = -0.439; p = 0.029) were associated with a worse ODI at 12 M-FU after adjusting for covariates.
CONCLUSIONS: Preoperative FI of the psoas and the PPM are associated with worse ODI outcomes one year after lumbar fusion. Sarcopenia is associated with worse ODI, PCS-12 and NRS-L in females, but not males. Considering sex differences, PMI and FI of the PPM might be used to counsel patients on their expectations for health-related quality of life after lumbar fusion.

OBJECTIVE: The plug-and-play prior ((P3) ) can be flexibly coupled with multiple iterative optimizations, which has been successfully applied to the inverse problems of medical imaging. In this work, for accelerated cardiac cine magnetic resonance imaging (CC-MRI), the Spatiotemporal corrElAtion-based hyBrid plUg-and-play priorS (SEABUS) integrating a local P3and a nonlocal P3are introduced.
METHODS: Specifically, the local P3enforces pixelwise edge-orientation consistency by conducting reference frame guided multiscale orientation projection (MSOP) on a subset containing a few adjacent frames; the nonlocal P3constrains the cubewise anatomic-structure similarity by performing cube matching and 4D filtering (CM4D) on all frames. By using effectively a composite splitting algorithm (CSA), SEABUS is incorporated into a fast iterative shrinkage-thresholding algorithm (FISTA) and a new accelerated CC-MRI approach named SEABUS-FCSA is proposed.
RESULTS: The experiment and algorithm analysis demonstrate the efficiency and potential of the proposed SEABUS-FCSA approach, which has the best performance in terms of reducing aliasing artifacts and capturing dynamic features in comparison with several state-of-the-art accelerated CC-MRI technologies.
CONCLUSIONS: Our approach aims to propose a new hybrid P3based iterative algorithm, which is not only used to improve the quality of accelerated cardiac cine imaging but also extend the FCSA methodology.

Skeletal muscle loss appears to be the most significant clinical event in cancer cachexia and is associated with a poor outcome. With regard to such muscle loss, despite extensive study in a range of models, there is ongoing debate as to whether a reduction in protein synthesis, an increase in degradation or a combination of both is the more relevant. Each model differs in terms of key mediators and the pathways activated in skeletal muscle. Certain models do suggest that decreased synthesis accompanied by enhanced protein degradation via the ubiquitin proteasome pathway (UPP) is important. Murine models tend to involve rapid development of cachexia and may represent more acute muscle atrophy rather than the chronic wasting observed in humans. There is a paucity of human data both at a basic descriptive level and at a molecular/mechanism level. Progress in treating the human form of cancer cachexia can only move forwards through carefully designed large randomised controlled clinical trials of specific therapies with validated biomarkers of relevance to underlying mechanisms. This article is part of a Directed Issue entitled: Molecular basis of muscle wasting.