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Dear colleagues,
 
The 16th international Conference of the Society on Cachexia, Sarcopenia & Muscle Wasting, will take place on 17-19 June 2023 in Stockholm, Sweden, under the guidance of Chairs of the SCWD, Professor Stefan Anker (Berlin, Germany) and Professor Gianluigi Savarese (Stockholm, Sweden).
 
To make sure the international community around the world keeps abreast with the latest advancements after the challenging COVID 19 pandemic and the recent events in Eastern Europe, the Board of the SCWD is determined to create the best possible
conditions for the cachexia and sarcopenia community to meet in person.
SCWD will also make sure highlights of the conference are accessible with virtual options to attend remotely via our digital interactive platform.
 
We hope to see you in Stockholm and look forward to working with you again to continue the tradition of a mutually rewarding and intellectually stimulating SCWD conference!
 
Best regards,
Prof. Stefan Anker (President, SCWD) and Gianluigi Savarese

From the literature

GDF15 and muscle function in cancer cachexia: a review

In this study, TOV21G cancer cachexia mouse models were used to demonstrate impaired muscle function and performance which is seen in cachexia patients. With growth differentiation factor 15, GDF15, neutralization, the mice were seen to exhibit restored muscle function and performance. GDF15 is a stress-responsive cytokine which is secreted by many cells, including tumour cells and damaged cells. GDF15 functions by activating glial cell line-derived neurotrophic factor, GDNF, receptor GFRAL. This is expressed in the hindbrain and leads to reducing food intake and weight loss. This is relevant to cachexia patients, and patients with chronic diseases such as heart failure, as their GDF15 levels are significantly higher than that of healthy people. In this study, the mice were treated with mAB2, an anti-GDF15 antibody. They demonstrated weight gain in terms of fat mass and lean mass, improved muscle function and physical performance. Hence, it is thought that GDF15-related therapy may be effective for patients with cachexia. However, symptoms of cachexia such as fatigue do not appear to be related to GDF15 levels, so further exploration is necessary.
This review by Kim-Muller JY et al. aimed to explore how GDF15 levels are related to weight loss and highlight how GDF15 neutralization could be an option for treating cachexia.

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Progressive development of cachexia in different organ systems: a review

Cachexia is defined as an unintentional loss of 5% or more of body weight, a complication which often negatively affects survival rates. Cachexia is caused by circulating cytokines in the body which are produced by cancer cells and immune cells, causing behavioural and systemic changes. However, how cachexia impacts different tissues is unknown; there is a large amount of information missing, as it is likely there are more tissues in the body affected by cachexia than we know. There are known differences in tissue wasting: in the heart, atrophy is seen after 2 weeks of tumour implantation, but very little wasting in any other tissues at this point. The heart and skeletal muscles are the tissues affected first and foremost. This study also discovered that tissues such as the brain which do not undergo wasting, experience functional derangement due to transcriptional changes such as the upregulation of angiotensin-converting enzyme (ACE). Using lisinopril, a drug which inhibits ACE, muscle force can be improved, even if wasting is not prevented. However, this study was completed on mice with no T lymphocytes – this is a limitation as T cells have been seen to induce or protect from cachexia, so more studies are needed to understand the involvement of T cells in cachexia.
This review by Graca FA et al. aimed to summarise how cachexia affects different tissue systems in the body.

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Daily walking speed and frailty: a significant association?

Walking speed (WS) is clinically recognized as a crucial vital sign. Associations between daily walking speed (DWS) and health outcomes have been underscored by a number of studies, which have further recognized it as an accurate predictor of dependency and mortality in elderly individuals. Despite this knowledge, very few studies have examined the link between DWS and frailty.

The aim of this study was to investigate a smartphone application’s ability to assess the association between DWS and frailty. This application measured DW parameters such as speed and step length and further conducted an in-app frailty assessment using the Kihon checklist.

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Effects of mitochondrial transplant therapy on the reparation of injured skeletal muscle

It is known that traumatic muscle injury damages mitochondria, which may cause them to leak their contents into the cytoplasm and subsequently trigger calcium accumulation, cell death, endoplasmic reticulum stress, and the release of reactive oxygen species (ROS). The latter reduces mitochondrial quality and increases the number of unhealthy mitochondria present in the cell, which may delay post-injury muscle regeneration. Although this knowledge has informed studies demonstrating the beneficial effects of mitochondrial transplant therapy (MTT) on ischaemia-damaged myocardium, its effects on injured skeletal muscle remain undefined.

The aim of this article was to examine the effects of MTT on skeletal muscle function after neuromuscular injury. The latter was induced using BaCl2, which causes widespread muscle proteolysis via myofibre Ca2+ overload and hyper-contractions.

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