human
***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Recently , novel dietary oils with modified fatty acid profiles have been manufactured to improve fatty acid intakes and reduce CVD risk . Our objective was to evaluate the efficacy of novel high-oleic rapeseed ( canola ) oil ( HOCO ) , alone or blended with flaxseed oil ( FXCO ) , on circulating lipids and inflammatory biomarkers v. a typical Western diet ( WD ) . Using a r and omised , controlled , crossover trial , thirty-six hypercholesterolaemic subjects consumed three isoenergetic diets for 28 d each containing approximately 36 % energy from fat , of which 70 % was provided by HOCO , FXCO or WD . Dietary fat content of SFA , MUFA , PUFA n-6 and n-3 was 6 , 23 , 5 , 1 % energy for HOCO ; 6 , 16 , 5 , 7·5 % energy for FXCO ; 11·5 , 16 , 6 , 0·5 % energy for WD . After 28 d , compared with WD , LDL-cholesterol was reduced 15·1 % ( P < 0·001 ) with FXCO and 7·4 % ( P < 0·001 ) with  HOCO . Total cholesterol ( TC ) was reduced 11 % ( P < 0·001 ) with FXCO and 3·5 % ( P = 0·002 ) with HOCO compared with WD . Endpoint TC differed between FXCO and HOCO ( P < 0·05 ) . FXCO consumption reduced HDL-cholesterol by 8·5 % ( P < 0·001 ) and LDL : HDL ratio by 7·5 % ( P = 0·008 ) v. WD . FXCO significantly decreased E-selectin concentration compared with WD ( P = 0·02 ) . No differences were observed in inflammatory markers after the consumption of HOCO compared with WD . In conclusion , consumption of novel HOCO alone or when blended with flaxseed oil is cardioprotective through lipid-lowering effects . The incorporation of flaxseed oil may also target inflammation by reducing plasma E-selectin BACKGROUND There is conflicting evidence on the benefits of foods rich in vitamin E ( alpha-tocopherol ) , n-3 polyunsaturated fatty acids ( PUFA ) , and their pharmacological substitutes . We investigated the effects of these substances as supplements in patients who had myocardial infa rct ion . METHODS From October , 1993 , to September , 1995 , 11,324 patients surviving recent ( < or = 3 months ) myocardial infa rct ion were r and omly assigned supplements of n-3 PUFA ( 1 g daily , n=2836 ) , vitamin E ( 300 mg daily , n=2830 ) , both ( n=2830 ) , or none ( control , n=2828 ) for 3.5 years . The primary combined efficacy endpoint was death , non-fatal myocardial infa rct ion , and stroke . Intention-to-treat analyses were done according to a factorial design ( two-way ) and by treatment group ( four-way ) . FINDINGS Treatment with n-3 PUFA , but not vitamin E , significantly lowered the risk of the primary endpoint ( relative-risk decrease 10 % [ 95 % CI 1 - 18 ] by two-way analysis , 15 % [ 2 - 26 ] by four-way analysis ) . Benefit was attributable to a decrease in the risk of death ( 14 % [ 3 - 24 ] two-way , 20 % [ 6 - 33 ] four-way ) and cardiovascular death ( 17 % [ 3 - 29 ] two-way , 30 % [ 13 - 44 ] four-way ) . The effect of the combined treatment was similar to that for n-3 PUFA for the primary endpoint ( 14 % [ 1 - 26 ] ) and for fatal events ( 20 % [ 5 - 33 ] ) . INTERPRETATION Dietary supplementation with n-3 PUFA led to a clinical ly important and statistically significant benefit . Vitamin E had no benefit . Its effects on fatal cardiovascular events require further exploration BACKGROUND Since inflammation is believed to have a role in the pathogenesis of cardiovascular events , measurement of markers of inflammation has been proposed as a method to improve the prediction of the risk of these events . METHODS We conducted a prospect i ve , nested case-control study among 28,263 apparently healthy postmenopausal women over a mean follow-up period of three years to assess the risk of cardiovascular events associated with base-line levels of markers of inflammation . The markers included high-sensitivity C-reactive protein ( hs-CRP ) , serum amyloid A , interleukin-6 , and soluble intercellular adhesion molecule type 1 ( sICAM-1 ) . We also studied homocysteine and a variety of lipid and lipoprotein measurements .  Cardiovascular events were defined as death from coronary heart disease , nonfatal myocardial infa rct ion or stroke , or the need for coronary-revascularization procedures . RESULTS Of the 12 markers measured , hs-CRP was the strongest univariate predictor of the risk of cardiovascular events ; the relative risk of events for women in the highest as compared with the lowest quartile for this marker was 4.4 ( 95 percent confidence interval , 2.2 to 8.9 ) . Other markers significantly associated with the risk of cardiovascular events were serum amyloid A ( relative risk for the highest as compared with the lowest quartile , 3.0 ) , sICAM-1 ( 2.6 ) , interleukin-6 ( 2.2 ) , homocysteine ( 2.0 ) , total cholesterol ( 2.4 ) , LDL cholesterol ( 2.4 ) , apolipoprotein B-100 ( 3.4 ) , HDL cholesterol ( 0.3 ) , and the ratio of total cholesterol to HDL cholesterol ( 3.4 ) . Prediction models that incorporated markers of inflammation in addition to lipids were significantly better at predicting risk than models based on lipid levels alone ( P<0.001 ) . The levels of hs-CRP and serum amyloid A were significant predictors of risk even in the subgroup of women with LDL cholesterol levels below 130 mg per deciliter ( 3.4 mmol per liter ) , the target for primary prevention established by the National Cholesterol Education Program . In multivariate analyses , the only plasma markers that independently predicted risk were hs-CRP ( relative risk for the highest as compared with the lowest quartile , 1.5 ; 95 percent confidence interval , 1.1 to 2.1 ) and the ratio of total cholesterol to HDL cholesterol ( relative risk , 1.4 ; 95 percent confidence interval , 1.1 to 1.9 ) . CONCLUSIONS The addition of the measurement of C-reactive protein to screening based on lipid levels may provide an improved method of identifying persons at risk for cardiovascular events Malnutrition and chronic inflammation in dialysis patients negatively impact their survival prognosis , and nutrients , such as omega-3 oils , are postulated to reduce proinflammatory response . In this r and omized , double-blind , multicenter , placebo-controlled trial , we investigated the effects of flaxseed oil ( FO ) on the inflammatory state of patients with chronic renal failure undergoing renal replacement therapy with hemodialysis ( HD ) . We hypothesized that FO supplementation lowers C-reactive protein ( CRP ) levels .  One hundred sixty patients with chronic renal failure who received HD therapy of 3 dialysis units over a 3-month period in South Brazil were included . The patients received blind doses of FO ( 1 g twice a day ) and placebo ( mineral oil , 1 g twice a day ) for a period of 120 days . Inflammation was observed in 89 patients ( 61 % ) at the beginning of the study . There was a correlation between CRP and the body mass index ( R(s ) = 0.22 ; P = .022 ) and high-density lipoprotein cholesterol ( R(s ) = -0.23 ; P = .032 ) , and the CRP levels decreased significantly over time in the group that received FO compared with the control group ( P < .001 ) . During the study period , 33.3 % of the FO group changed from an inflamed to a not-inflamed category , whereas only 16.9 % changed in the mineral oil group ( P = .04 ) . We conclude that the administration of FO decreases the CRP levels and that inflammation in HD patients appears to be correlated to their body mass index and reduced high-density lipoprotein cholesterol levels . Studies with a larger number of patients and over a longer duration are necessary to corroborate these findings Greatly increasing the amounts of flaxseed oil [ rich in α-linolenic acid ( ALNA ) ] or fish oil ( FO ) ; [ rich in eicosapentaenoic acid ( EPA ) and docosahexaenoic acid ( DHA ) ] in the diet can decrease inflammatory cell functions and so might impair host defense . The objective of this study was to determine the effect of dietary supplementation with moderate levels of ALNA , γ-linolenic acid ( GLA ) , arachidonic acid ( ARA ) , DHA , or FO on inflammatory cell numbers and functions and on circulating levels of soluble adhesion molecules .  Healthy subjects aged 55 to 75 yr consumed nine capsules per day for 12 wk . The capsules contained placebo oil ( an 80∶20 mix of palm and sunflowerseed oils ) or blends of placebo oil with oils rich in ALNA , GLA , ARA , or DHA or FO . Subjects in these groups consumed 2 g ALNA ; approximately 700 mg GLA , ARA , or DHA ; or 1 g EPA plus DHA ( 720 mg EPA+280 mg DHA ) daily from the capsules . Total fat intake from the capsules was 4 g per day . None of the treatments affected inflammatory cell numbers in the bloodstream ; neutrophil and monocyte phagocytosis or respiratory burst in response to E. coli ; production of tumor necrosis factor-α , interleukin-1β , and interleukin-6 in response to bacterial lipopolysaccharide ; or plasma concentrations of soluble intercellular adhesion molecule-1 . In contrast , the ALNA and FO treatments decreased the plasma concentrations of soluble vascular cell adhesion molecule-1 ( 16 and 28 % decrease , respectively ) and soluble E-selectin ( 23 and 17 % decrease , respectively ) . It is concluded that , in contrast to previous reports using higher amounts of these fatty acids , a moderate increase in consumption of long-chain n−6 or n−3 polyunsaturated fatty acids does not significantly affect inflammatory cell numbers or neutrophil and monocyte responses in humans and so would not be expected to cause immune impairment . Furthermore , we conclude that moderate levels of ALNA and FO , which could be incorporated into the diet , can decrease some markers of endothelial activation and that this mechanism of action may contribute to the reported health benefits of n−3 fatty acids BACKGROUND Greatly increasing dietary flaxseed oil [ rich in the n-3 polyunsaturated fatty acid ( PUFA ) alpha-linolenic acid ( ALA ) ] or fish oil [ rich in the long-chain n-3 PUFAs eicosapentaenoic ( EPA ) and docosahexaenoic ( DHA ) acids ] can reduce markers of immune cell function . The effects of more modest doses are unclear , and it is not known whether ALA has the same effects as its long-chain derivatives . OBJECTIVE The objective was to determine the effects of enriching the diet with ALA or EPA+DHA on immune outcomes representing key functions of human neutrophils , monocytes , and lymphocytes . DESIGN In a placebo-controlled , double-blind , parallel study , 150 healthy men and women aged 25 - 72 y were r and omly assigned to 1 of 5 interventions : placebo ( no additional n-3 PUFAs ) , 4.5 or 9.5 g ALA/d , and 0.77 or 1.7 g EPA+DHA/d for 6 mo . The n-3 PUFAs were provided in 25 g fat spread plus 3 oil capsules . Blood sample s were taken at 0 , 3 , and 6 mo . RESULTS The fatty acid composition of peripheral blood mononuclear cell phospholipids was significantly different in the groups with higher intakes of ALA or EPA+DHA . The interventions did not alter the percentages of neutrophils or monocytes engaged in phagocytosis of Escherichia coli or in phagocytic activity , the percentages of neutrophils or monocytes undergoing oxidative burst in response to E. coli or phorbol ester , the proliferation of lymphocytes in response to a T cell mitogen , the production of numerous cytokines by monocytes and lymphocytes , or the in vivo delayed-type hypersensitivity response . CONCLUSION An intake of < or= 9.5 g ALA/d or < or= 1.7 g EPA+DHA/d does not alter the functional activity of neutrophils , monocytes , or lymphocytes , but it changes the fatty acid composition of mononuclear cells BACKGROUND Atherosclerosis is a chronic inflammatory disease 
    Output:
    
agent
Subgroup analysis revealed that increasing dietary ALA tends to elevate CRP concentration  in healthy subjects .
However , the null effect of ALA supplementation on other inflammatory markers was not changed in various subgroups , indicating that the results are stable .
Meta-regression results revealed a negative relationship between the effect size on CRP and its baseline concentration .
No significant publication bias was observed for all inflammatory markers as suggested by funnel plot and Begg ’s test .
Conclusion Our meta- analysis did not find any beneficial effect of ALA supplementation  on reducing inflammatory markers including TNF , IL-6 , CRP , sICAM-1 , and sVCAM-1 .
However , in healthy subjects  , ALA supplementation might increase CRP concentration
***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Recently , novel dietary oils with modified fatty acid profiles have been manufactured to improve fatty acid intakes and reduce CVD risk . Our objective was to evaluate the efficacy of novel high-oleic rapeseed ( canola ) oil ( HOCO ) , alone or blended with flaxseed oil ( FXCO ) , on circulating lipids and inflammatory biomarkers v. a typical Western diet ( WD ) . Using a r and omised , controlled , crossover trial , thirty-six hypercholesterolaemic subjects consumed three isoenergetic diets for 28 d each containing approximately 36 % energy from fat , of which 70 % was provided by HOCO , FXCO or WD . Dietary fat content of SFA , MUFA , PUFA n-6 and n-3 was 6 , 23 , 5 , 1 % energy for HOCO ; 6 , 16 , 5 , 7·5 % energy for FXCO ; 11·5 , 16 , 6 , 0·5 % energy for WD . After 28 d , compared with WD , LDL-cholesterol was reduced 15·1 % ( P < 0·001 ) with FXCO and 7·4 % ( P < 0·001 ) with  HOCO . Total cholesterol ( TC ) was reduced 11 % ( P < 0·001 ) with FXCO and 3·5 % ( P = 0·002 ) with HOCO compared with WD . Endpoint TC differed between FXCO and HOCO ( P < 0·05 ) . FXCO consumption reduced HDL-cholesterol by 8·5 % ( P < 0·001 ) and LDL : HDL ratio by 7·5 % ( P = 0·008 ) v. WD . FXCO significantly decreased E-selectin concentration compared with WD ( P = 0·02 ) . No differences were observed in inflammatory markers after the consumption of HOCO compared with WD . In conclusion , consumption of novel HOCO alone or when blended with flaxseed oil is cardioprotective through lipid-lowering effects . The incorporation of flaxseed oil may also target inflammation by reducing plasma E-selectin BACKGROUND There is conflicting evidence on the benefits of foods rich in vitamin E ( alpha-tocopherol ) , n-3 polyunsaturated fatty acids ( PUFA ) , and their pharmacological substitutes . We investigated the effects of these substances as supplements in patients who had myocardial infa rct ion . METHODS From October , 1993 , to September , 1995 , 11,324 patients surviving recent ( < or = 3 months ) myocardial infa rct ion were r and omly assigned supplements of n-3 PUFA ( 1 g daily , n=2836 ) , vitamin E ( 300 mg daily , n=2830 ) , both ( n=2830 ) , or none ( control , n=2828 ) for 3.5 years . The primary combined efficacy endpoint was death , non-fatal myocardial infa rct ion , and stroke . Intention-to-treat analyses were done according to a factorial design ( two-way ) and by treatment group ( four-way ) . FINDINGS Treatment with n-3 PUFA , but not vitamin E , significantly lowered the risk of the primary endpoint ( relative-risk decrease 10 % [ 95 % CI 1 - 18 ] by two-way analysis , 15 % [ 2 - 26 ] by four-way analysis ) . Benefit was attributable to a decrease in the risk of death ( 14 % [ 3 - 24 ] two-way , 20 % [ 6 - 33 ] four-way ) and cardiovascular death ( 17 % [ 3 - 29 ] two-way , 30 % [ 13 - 44 ] four-way ) . The effect of the combined treatment was similar to that for n-3 PUFA for the primary endpoint ( 14 % [ 1 - 26 ] ) and for fatal events ( 20 % [ 5 - 33 ] ) . INTERPRETATION Dietary supplementation with n-3 PUFA led to a clinical ly important and statistically significant benefit . Vitamin E had no benefit . Its effects on fatal cardiovascular events require further exploration BACKGROUND Since inflammation is believed to have a role in the pathogenesis of cardiovascular events , measurement of markers of inflammation has been proposed as a method to improve the prediction of the risk of these events . METHODS We conducted a prospect i ve , nested case-control study among 28,263 apparently healthy postmenopausal women over a mean follow-up period of three years to assess the risk of cardiovascular events associated with base-line levels of markers of inflammation . The markers included high-sensitivity C-reactive protein ( hs-CRP ) , serum amyloid A , interleukin-6 , and soluble intercellular adhesion molecule type 1 ( sICAM-1 ) . We also studied homocysteine and a variety of lipid and lipoprotein measurements .  Cardiovascular events were defined as death from coronary heart disease , nonfatal myocardial infa rct ion or stroke , or the need for coronary-revascularization procedures . RESULTS Of the 12 markers measured , hs-CRP was the strongest univariate predictor of the risk of cardiovascular events ; the relative risk of events for women in the highest as compared with the lowest quartile for this marker was 4.4 ( 95 percent confidence interval , 2.2 to 8.9 ) . Other markers significantly associated with the risk of cardiovascular events were serum amyloid A ( relative risk for the highest as compared with the lowest quartile , 3.0 ) , sICAM-1 ( 2.6 ) , interleukin-6 ( 2.2 ) , homocysteine ( 2.0 ) , total cholesterol ( 2.4 ) , LDL cholesterol ( 2.4 ) , apolipoprotein B-100 ( 3.4 ) , HDL cholesterol ( 0.3 ) , and the ratio of total cholesterol to HDL cholesterol ( 3.4 ) . Prediction models that incorporated markers of inflammation in addition to lipids were significantly better at predicting risk than models based on lipid levels alone ( P<0.001 ) . The levels of hs-CRP and serum amyloid A were significant predictors of risk even in the subgroup of women with LDL cholesterol levels below 130 mg per deciliter ( 3.4 mmol per liter ) , the target for primary prevention established by the National Cholesterol Education Program . In multivariate analyses , the only plasma markers that independently predicted risk were hs-CRP ( relative risk for the highest as compared with the lowest quartile , 1.5 ; 95 percent confidence interval , 1.1 to 2.1 ) and the ratio of total cholesterol to HDL cholesterol ( relative risk , 1.4 ; 95 percent confidence interval , 1.1 to 1.9 ) . CONCLUSIONS The addition of the measurement of C-reactive protein to screening based on lipid levels may provide an improved method of identifying persons at risk for cardiovascular events Malnutrition and chronic inflammation in dialysis patients negatively impact their survival prognosis , and nutrients , such as omega-3 oils , are postulated to reduce proinflammatory response . In this r and omized , double-blind , multicenter , placebo-controlled trial , we investigated the effects of flaxseed oil ( FO ) on the inflammatory state of patients with chronic renal failure undergoing renal replacement therapy with hemodialysis ( HD ) . We hypothesized that FO supplementation lowers C-reactive protein ( CRP ) levels .  One hundred sixty patients with chronic renal failure who received HD therapy of 3 dialysis units over a 3-month period in South Brazil were included . The patients received blind doses of FO ( 1 g twice a day ) and placebo ( mineral oil , 1 g twice a day ) for a period of 120 days . Inflammation was observed in 89 patients ( 61 % ) at the beginning of the study . There was a correlation between CRP and the body mass index ( R(s ) = 0.22 ; P = .022 ) and high-density lipoprotein cholesterol ( R(s ) = -0.23 ; P = .032 ) , and the CRP levels decreased significantly over time in the group that received FO compared with the control group ( P < .001 ) . During the study period , 33.3 % of the FO group changed from an inflamed to a not-inflamed category , whereas only 16.9 % changed in the mineral oil group ( P = .04 ) . We conclude that the administration of FO decreases the CRP levels and that inflammation in HD patients appears to be correlated to their body mass index and reduced high-density lipoprotein cholesterol levels . Studies with a larger number of patients and over a longer duration are necessary to corroborate these findings Greatly increasing the amounts of flaxseed oil [ rich in α-linolenic acid ( ALNA ) ] or fish oil ( FO ) ; [ rich in eicosapentaenoic acid ( EPA ) and docosahexaenoic acid ( DHA ) ] in the diet can decrease inflammatory cell functions and so might impair host defense . The objective of this study was to determine the effect of dietary supplementation with moderate levels of ALNA , γ-linolenic acid ( GLA ) , arachidonic acid ( ARA ) , DHA , or FO on inflammatory cell numbers and functions and on circulating levels of soluble adhesion molecules .  Healthy subjects aged 55 to 75 yr consumed nine capsules per day for 12 wk . The capsules contained placebo oil ( an 80∶20 mix of palm and sunflowerseed oils ) or blends of placebo oil with oils rich in ALNA , GLA , ARA , or DHA or FO . Subjects in these groups consumed 2 g ALNA ; approximately 700 mg GLA , ARA , or DHA ; or 1 g EPA plus DHA ( 720 mg EPA+280 mg DHA ) daily from the capsules . Total fat intake from the capsules was 4 g per day . None of the treatments affected inflammatory cell numbers in the bloodstream ; neutrophil and monocyte phagocytosis or respiratory burst in response to E. coli ; production of tumor necrosis factor-α , interleukin-1β , and interleukin-6 in response to bacterial lipopolysaccharide ; or plasma concentrations of soluble intercellular adhesion molecule-1 . In contrast , the ALNA and FO treatments decreased the plasma concentrations of soluble vascular cell adhesion molecule-1 ( 16 and 28 % decrease , respectively ) and soluble E-selectin ( 23 and 17 % decrease , respectively ) . It is concluded that , in contrast to previous reports using higher amounts of these fatty acids , a moderate increase in consumption of long-chain n−6 or n−3 polyunsaturated fatty acids does not significantly affect inflammatory cell numbers or neutrophil and monocyte responses in humans and so would not be expected to cause immune impairment . Furthermore , we conclude that moderate levels of ALNA and FO , which could be incorporated into the diet , can decrease some markers of endothelial activation and that this mechanism of action may contribute to the reported health benefits of n−3 fatty acids BACKGROUND Greatly increasing dietary flaxseed oil [ rich in the n-3 polyunsaturated fatty acid ( PUFA ) alpha-linolenic acid ( ALA ) ] or fish oil [ rich in the long-chain n-3 PUFAs eicosapentaenoic ( EPA ) and docosahexaenoic ( DHA ) acids ] can reduce markers of immune cell function . The effects of more modest doses are unclear , and it is not known whether ALA has the same effects as its long-chain derivatives . OBJECTIVE The objective was to determine the effects of enriching the diet with ALA or EPA+DHA on immune outcomes representing key functions of human neutrophils , monocytes , and lymphocytes . DESIGN In a placebo-controlled , double-blind , parallel study , 150 healthy men and women aged 25 - 72 y were r and omly assigned to 1 of 5 interventions : placebo ( no additional n-3 PUFAs ) , 4.5 or 9.5 g ALA/d , and 0.77 or 1.7 g EPA+DHA/d for 6 mo . The n-3 PUFAs were provided in 25 g fat spread plus 3 oil capsules . Blood sample s were taken at 0 , 3 , and 6 mo . RESULTS The fatty acid composition of peripheral blood mononuclear cell phospholipids was significantly different in the groups with higher intakes of ALA or EPA+DHA . The interventions did not alter the percentages of neutrophils or monocytes engaged in phagocytosis of Escherichia coli or in phagocytic activity , the percentages of neutrophils or monocytes undergoing oxidative burst in response to E. coli or phorbol ester , the proliferation of lymphocytes in response to a T cell mitogen , the production of numerous cytokines by monocytes and lymphocytes , or the in vivo delayed-type hypersensitivity response . CONCLUSION An intake of < or= 9.5 g ALA/d or < or= 1.7 g EPA+DHA/d does not alter the functional activity of neutrophils , monocytes , or lymphocytes , but it changes the fatty acid composition of mononuclear cells BACKGROUND Atherosclerosis is a chronic inflammatory disease 
    Output:
    