The early liver cancer warning can strike at mealtime
Liver cancer is the eight most deadly type of the disease in the UK, with around 5,800 people sadly losing their lives to it each year.
Symptoms of the killer cancer often don't show up until the later stages of the disease making it harder to treat, experts from the American Cancer Society have said. He said: "Generally, people living with liver cancer will find themselves losing their appetite for food or being unable to eat as much as before due to abdominal discomfort or nausea. Additionally, those affected by the disease may find that even eating small amounts causes pain and discomfort in the stomach area."
Top Health Stories Today Liver cancer symptoms According to Ambani, the full list of early symptoms could include:While these symptoms are considered ‘common’ signs of the disease, Cancer Nurse at Perci Health, Lisa Jacques, added that red flags can also be caused by other conditions.
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HDL and LDL have distinct, opposing effects on LPS-induced brain inflammation - Lipids in Health and DiseaseEndotoxemia and sepsis induce neuroinflammation and increase the risk of neurodegenerative disorders although the mechanism by which peripheral infection leads to brain inflammation is not well understood. While circulating serum lipoproteins are known immunometabolites with the potential to modulate the acute phase response and cross the blood brain barrier, their contribution to neuroinflammation during systemic infection is unknown. The objective of this study was to elucidate the mechanisms by which lipoprotein subclasses modulate lipopolysaccharide (LPS)-induced neuroinflammation. Adult C57BL/6 mice were divided into 6 treatment groups, including a sterile saline vehicle control group (n = 9), an LPS group (n = 11), a premixed LPS + HDL group (n = 6), a premixed LPS + LDL group (n = 5), a HDL only group (n = 6) and an LDL only group (n = 3). In all cases injections were administered intraperitoneally. LPS was administered at 0.5 mg/kg, and lipoproteins were administered at 20 mg/kg. Behavioural testing and tissue collection was performed 6 h post-injection. The magnitude of peripheral and central inflammation was determined by qPCR of pro-inflammatory genes in fresh liver and brain. Metabolite profiles of liver, plasma and brain were determined by 1H NMR. Endotoxin concentration in the brain was measured by the Limulus Amoebocyte Lysate (LAL) assay. Co-administration of LPS + HDL exacerbated both peripheral and central inflammation, whilst LPS + LDL attenuated this inflammation. Metabolomic analysis identified several metabolites significantly associated with LPS-induced inflammation, which were partially rescued by LDL, but not HDL. Endotoxin was detected at significantly greater concentrations in the brains of animals that received LPS + HDL compared to LPS + saline, but not those that received LPS + LDL. These results suggest that HDL may promote neuroinflammation through direct shuttling of endotoxin to the brain. In contrast, LDL was shown to have anti-neu
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