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The level of sFas increased significantly compared to that in normal subjects, consistent with previous reports.
2
This action may protect the hepatocyte from excess of SFAs that are more toxic than MUFAs.
3
Conclusions: Intake of PUFAs and SFAs was independently associated with 1-y all-cause mortality in patients with chronic HF.
4
High levels of sFas and HGF might help to confirm a diagnosis of drug-induced liver injury or acetaminophen-related ALF.
5
Patients with lymphopenia tended to have low levels of sFas, making it possible to hypothesize that sFas protects against apoptosis.
6
Methods: Meta-analysis of genome-wide association studies for circulating SFAs was conducted in two population-based cohorts comprising 3521 participants of Chinese ancestry.
7
We aimed to examine the associations between plasma phospholipid SFAs and the metabolic markers of lipid, hepatic, glycaemic and inflammation pathways.
8
Median of intake as percentage of daily energy was 5.3% for PUFAs and 8.2% for SFAs.
9
Further support is believed to derive from the capacity of SFAs to raise LDL cholesterol, and the evidence that LDL-cholesterol lowering reduces CVD incidence.
10
Conclusions: Long-term feeding of a HC diet to lactating goats induced milk fat depression and FAs profile shift with lower MUFAs but higher SFAs.
11
In fact, although it is possible that dietary intake of SFAs has a causal role in CVD, the evidence to support this contention is inconclusive.
12
Although the change in the level of sFas protects steroid therapy was variable, some relation to the differential activation of T cell subsets was suggested.
13
There was a significant correlation between the level of sFas and that of sCD4, suggesting some relation between sFas and activation of CD4+ T cell.
14
The level of sFas increased significantly compared to that in normal subjects, consistent with previous reports.
15
This action may protect the hepatocyte from excess of SFAs that are more toxic than MUFAs.
16
Conclusions: Intake of PUFAs and SFAs was independently associated with 1-y all-cause mortality in patients with chronic HF.