Table 1.
Demographic data of the patients involved in the study.
Figure 1.
Fibre type cross sectional area (FCSA) according to different definitions of cachexia.
(A) Mean (± SEM) fibre size for both MyHC1 and MyHCIIa. A comparison is made between patients with the proposed cachexia definition absent (dark grey) and those with the proposed cachexia definition present (light grey) for the four definitions set out in Methods (I–IV). (*, P<0.05 and **, P<0.01, by Student's t test). (B) Immunohistological sections of muscle for a healthy control, patient with weight loss alone (10.1%) (Group II), and patient with low muscularity and >2% weight loss (Group IV). Laminin is shown in green, MyHC1 shown in red, and MyHCIIa is shown in blue.
Table 2.
Myosin heavy chain fibre data of the patients involved in the study.
Figure 2.
Variations in protein and nucleic acid content according to the different definitions of cancer cachexia.
A comparison is made between patients with the proposed cachexia definition absent (dark grey) and those with the proposed cachexia definition present (light grey) for the four definitions set out in the methods (I–IV). (A) Mean (± SEM) wet weight protein content. (B) Mean (± SEM) RNA content. (C) Mean (± SEM) DNA content. (C) Mean (± SEM) RNA/DNA ratio. (*, P<0.05 by Student's t test).
Table 3.
Protein, DNA, and RNA content of the patients involved in the study.
Figure 3.
Skeletal muscle Beclin and ATG5 protein levels in patients with or without >10% weight loss (Group II).
Western blot analysis with indicated antibodies, α-tubulin was used as a loading control. Graph shows the mean (± SEM) protein level represented in arbitrary units (A.U). (*, P<0.05 and **, P<0.01, by Student's t test).
Figure 4.
Total SMAD3, phospho-SMAD3 and ratio of phospho-SMAD3/SMAD3 in patients with or without >5% WL (Group I) levels.
Western blot analysis with indicated antibodies, α-tubulin was used as a loading control. Graph shows the mean (± SEM) protein level represented in arbitrary units (A.U). (*, P<0.05 by Student's t test).
Figure 5.
Inflammatory pathways in patients with (CRP >10 mg/L) and without (CRP ≤10 mg/L) systemic inflammation.
(A) Western blot analysis in the presence or absence of systemic inflammation with indicated antibodies, α-tubulin was used as a loading control. (B) Graph shows the mean (± SEM) protein level of phospho-NF-κB, represented in arbitrary units (A.U). (C) Representative immunohistochemistry and nuclei count of phospho-STAT3 (area shown is representative of field) of a patient with or without systemic inflammation. (D) Graph shows the staining density of phospho-STAT3 nuclei (A.U.) (± SEM) in the presence or absence of systemic inflammation.
Table 4.
Western blots for protein markers of cellular signalling.