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: Statin treatment in patients with coronary heart disease is associated with a reduced incidence of short-term adverse events and endpoint cardiac events . However , the effects of statin treatment on atherosclerotic plaques , particularly stable plaques , remain poorly defined . In total , 228 consecutive patients with stable atherosclerotic plaques who had undergone coronary arteriography ( CAG ) and intravascular ultrasound ( IVUS ) were r and omly assigned to receive placebo ( placebo group , n=54 ) or atorvastatin ( ATOR ) at a single daily dose of 10 mg ( ATOR 10 mg group , n=47 ) , 20 mg ( ATOR 20 mg group , n=45 ) , 40 mg ( ATOR 40 mg group , n=43 ) or 80 mg ( ATOR 80 mg group , n=39 ) . Endpoints , including serum lipids , serum inflammation , plaque volume and percentage of plaque necrosis were assessed after 3–6 months . At baseline , mean low-density lipoprotein ( LDL ) , high-density lipoprotein ( HDL ) and high-sensitivity C-reactive protein ( hs-CRP ) levels , as well as plaque volumes and percentages of plaque necrosis , were similar between all groups . At 6 months of follow-up , the LDL levels in the ATOR groups were below those at their respective baselines ( P<0.01 ) . HDL levels in the ATOR 80 mg group following treatment were significantly higher compared with baseline ( P=0.001 ) . Additionally , they were significantly higher compared with those in the placebo , ATOR 10 , 20 and 40 mg groups ( P<0.01 , P=0.001 , P=0.048 , P=0.047 , respectively ) . Hs-CRP levels in the placebo group following treatment were higher compared with baseline levels ( 6.87±2.62 vs. 5.07±1.80 , P<0.01 ) , but hs-CRP levels in the ATOR 80 mg group following treatment were lower compared with baseline ( 3.59±1.07 vs. 6.10±2.12 , P<0.01 ) . According to the virtual histology ( VH ) of IVUS , the percentages of plaque necrosis following treatment in the placebo and ATOR 10 mg groups rose above baseline levels ( 15.51±12.56 vs. 7.69±1.31 % , 13.54±11.76 vs. 7.83±1.43 % , P<0.01 ) and conformed to the diagnostic criteria for unstable plaques ( 15.51±12.56 , 13.54±11.76 % ) . By contrast , in the ATOR 20 , 40 and 80 mg groups , percentages of plaque necrosis remained stable following treatment compared with baseline ( P=0.069 , 0.846 and 0.643 , respectively ) . Plaque volumes following treatment in the placebo , ATOR 10 and 20 mg groups were similar to baseline levels . However , in the ATOR 40 and 80 mg groups , plaque volumes decreased following treatment compared with baseline plaque volumes ( 30.69±8.12 vs. 37.09±12.01 mm3 , 24.99±1.01 vs. 36.47±14.68 mm3 , P=0.019 , P<0.01 , respectively ) . ATOR ( 20 mg/day ) is able to lower LDL to st and ard levels while ATOR 40 mg/day was superior to 20 mg/day and had similar effects to 80 mg/day . Only ATOR 80 mg/day was able to increase HDL levels . Hs-CRP in patients without ATOR was higher and ATOR 80 mg/day decreased levels . ATOR ≥20 mg/day is able to stabilize plaques and ATOR 80 mg/day was superior to 20 and 40 mg/day . Thus , ATOR 40–80 mg/day reduces the volume of plaques The purpose of this 20-week , open-label , r and omized clinical trial was to evaluate the effect of rosuvastatin on fasting serum lipids and lipoproteins , high-sensitivity C-reactive protein ( hs-CRP ) , and the glomerular filtration rate ( GFR ) in 91 patients with chronic kidney disease . Patients were r and omized to rosuvastatin 10 mg/day ( n = 48 ) or to  no lipid-lowering treatment ( n = 43 ) for 20 weeks . In contrast to patients not receiving rosuvastatin , patients receiving rosuvastatin tended to derive more favorable improvements from baseline values in low-density lipoprotein cholesterol ( -43 % , p < 0.001 , vs 7 % , p = NS ; p < 0.001 for change with rosuvastatin treatment vs change with no antilipemic treatment ) , hs-CRP ( -47 % , p < 0.001 , vs 7 % , p = NS ; p < 0.001 for change with rosuvastatin treatment vs change with no antilipemic treatment ) , and GFR ( 11 % , p < 0.05 , vs 4 % , p = NS ; p = NS for change with rosuvastatin treatment vs change with no antilipemic treatment ) AIMS Previously we revealed the effectiveness of a new therapeutic approach with a short-term , very-low dose fluvastatin-valsartan combination on the improvement of arterial function in type 1 diabetes mellitus patients ( T1DM ) . In this study we explored whether this approach influences inflammation and oxidative stress and explored any association of these effects with arterial function improvement . METHODS This was a supplementary analysis of the two previous double blind r and omized studies ( included 44 T1DM patients ) . Treatment group received very-low dose fluvastatin-valsartan , the control group received placebo . Blood sample s were collected and inflammation parameters : high-sensitivity CRP ( hsCRP ) , interleukin 6 ( IL-6 ) , vascular cell adhesion molecule-1 ( VCAM-1 ) and oxidative stress parameter total antioxidant status ( TAS ) were measured . RESULTS Treatment decreased hsCRP values ( by 56.5 % , P<0.05 ) and IL-6 values ( by 33.6 % , P<0.05 ) and increased TAS values ( by 21.1 % ; P<0.05 ) after 30days of treatment . High sensitivity CRP and TAS remained decreased 3months after treatment discontinuation . Importantly , the anti-inflammatory and anti-oxidative action significantly correlated with arterial function improvement . CONCLUSIONS The approach consisting of short-term ( 30days ) treatment with a very low-dose fluvastatin-valsartan combination acts anti-inflammatory and anti-oxidative in T1DM patients . These observations along with the improvement of arterial function support the assumption that this approach could have an important clinical benefit in T1DM patients OBJECTIVE The purpose of this study was to evaluate the efficacy and safety profile of ezetimibe/simvastatin(EZE/SIMVA ) combination tablet , relative to ezetimibe ( EZE ) and simvastatin ( SIMVA ) monotherapy , in patients with primary hypercholesterolemia . METHODS This was a r and omized , multicenter , double-blind , placebo-controlled , factorial design study After a 6- to 8-week washout period and 4-week , single-blind , placebo run in , hypercholesterolemic patients ( low-density lipoprotein cholesterol [ LDL-C ] , 145 - 250 mg/dL ; triglycerides [ TG ] , < or = 350 mg/dL ) were r and omized equally to 1 of 10 daily treatments for 12 weeks : EZE/SIMVA 10/10 , 10/20 , 10/40 , or 10/80 mg ; SIMVA 10 , 20 , 40 , or 80 mg ; EZE 10 mg ; or placebo . The primary efficacy analysis was mean percent change from baseline in LDL-C to study end point Secondary end points included percent changes in other lipid variables and C-reactive protein [ CRP ] . RESULTS There were 1528 patients r and omized to treatment ( 792 women , 736 men ) ; mean ( SD ) age ranged from 54.9 ( 112 ) years to 56.4 ( 10.6 ) years across pooled treatment groups . The treatment groups were well balanced for baseline demographics . Pooled EZE/SIMVA was associated with greater reductions in LDL-C than pooled SIMVA or EZE alone ( P < 0.001 ) . Depending on dose , EZE/SIMVA was associated with reductions in LDL-C of -44.8 % to -602 % , non-high-density lipoprotein cholesterol of -40.5 % to -55.7 % , and TG of -22.5 % to -30.7 % ; high-density lipoprotein cholesterol increased by 5.5 % to 9.8 % . EZE/SIMVA was associated with greater reductions in CRP and remnant-like particle-cholesterol than SIMVA alone ( P < 0.001 ) . More patients receiving EZE/SIMVA versus SIMVA achieved LDL-C concentrations < 100 mg/dL ( 78.6 % vs 45.9 % ; P < 0.001 ) . EZE/SIMVA was generally well tolerated , with a safety profile similar to SIMVA monotherapy There were no significant differences between EZE/SIMVA and SIMVA in the incidence of consecutive liver transaminase levels > or =3 times the upper limit of normal ( ULN ) ( 1 .5 % for EZE/SIMVA and 1.1 % for SIMVA ; P = NS ) or creature kinase levels > or = 10 times ULN ( 0.0 % for EZE/SIMVA and 02 % for SIMVA ; P = NS ) . CONCLUSION The EZE/SIMVA tablet was a highly effective and well-tolerated LDL-C-lowering therapy in this study of patients with primary hypercholesterolemia BACKGROUND Chronic kidney disease ( CKD ) is associated with inflammation . The effects of atorvastatin on biomarkers of inflammation were assessed in CKD patients in the LORD trial . METHODS 117 patients with serum creatinine > 120 μmol/L were r and omized to receive atorvastatin 10 mg/day ( 56 ) or placebo ( 61 ) and followed for a mean of 2.5 years . 33 individuals with normal kidney function were controls . Outcomes included comparison of changes in pentraxin-3 ( PTX3 ) , TNF-α , CRP , IL-6 , IL-8 , and IL-10 between atorvastatin and placebo-treated patients . RESULTS At baseline , compared with controls , CKD patients had increased PTX3 ( mean , 1.08 vs. 0.58 ng/mL ; p < 0.001 ) , CRP ( 4.9 vs. 1.5 mg/L ; p < 0.001 ) , IL-8 ( 6.00 vs. 4.58 pg/mL ; p = 0.001 ) , IL-10 ( 59.0 vs. 17.6 pg/mL ; p = 0.007 ) , and TNF-α ( 18.0 vs. 5.6 ng/mL ; p < 0.001 ) . In patients with raised baseline plasma IL-6/8/10 and /or PTX3 the eGFR decline during the trial was significantly less in those treated with atorvastatin compared to placebo ( mean change , -3.36 ; vs. + 1.25 mL/min/1.73 m2/year ; difference , 4.61 95 % CI 0.98 - 8.25 ; p = 0.002 ) , whilst those without raised inflammatory biomarkers showed no difference . Placebo treated patients with raised TNF-α levels had no eGFR decline ( p > 0.90 ) , whereas in atorvastatin-treated patients eGFR declined ( p = 0.05 ) . CONCLUSIONS CKD patients with inflammation treated with atorvastatin had significantly less eGFR decline . Larger studies using statin therapy , specifically enrolling CKD patients with inflammation , may be worthwhile exploring Purpose of the study was to investigate whether short-term atorvastatin treatment improves endothelial function and affects inflammatory process in patients with heart failure ( HF ) and normal cholesterol levels . HF is characterized by endothelial dysfunction and increased inflammatory process , while statins restore endothelial function having also anti-inflammatory effects in hypercholesterolemic patients . We investigated the effect of 4-week atorvastatin treatment ( 10 mg/day ) on endothelial function and inflammatory markers in patients with HF and cholesterol levels < 220 mg/dl . Patients were r and omly allocated into groups and received atorvast 
    Output:
    
agent
Our meta‐ analysis showed beneficial effects  of statin use  on reducing inflammatory markers in patients with MetS and related disorders
***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: Statin treatment in patients with coronary heart disease is associated with a reduced incidence of short-term adverse events and endpoint cardiac events . However , the effects of statin treatment on atherosclerotic plaques , particularly stable plaques , remain poorly defined . In total , 228 consecutive patients with stable atherosclerotic plaques who had undergone coronary arteriography ( CAG ) and intravascular ultrasound ( IVUS ) were r and omly assigned to receive placebo ( placebo group , n=54 ) or atorvastatin ( ATOR ) at a single daily dose of 10 mg ( ATOR 10 mg group , n=47 ) , 20 mg ( ATOR 20 mg group , n=45 ) , 40 mg ( ATOR 40 mg group , n=43 ) or 80 mg ( ATOR 80 mg group , n=39 ) . Endpoints , including serum lipids , serum inflammation , plaque volume and percentage of plaque necrosis were assessed after 3–6 months . At baseline , mean low-density lipoprotein ( LDL ) , high-density lipoprotein ( HDL ) and high-sensitivity C-reactive protein ( hs-CRP ) levels , as well as plaque volumes and percentages of plaque necrosis , were similar between all groups . At 6 months of follow-up , the LDL levels in the ATOR groups were below those at their respective baselines ( P<0.01 ) . HDL levels in the ATOR 80 mg group following treatment were significantly higher compared with baseline ( P=0.001 ) . Additionally , they were significantly higher compared with those in the placebo , ATOR 10 , 20 and 40 mg groups ( P<0.01 , P=0.001 , P=0.048 , P=0.047 , respectively ) . Hs-CRP levels in the placebo group following treatment were higher compared with baseline levels ( 6.87±2.62 vs. 5.07±1.80 , P<0.01 ) , but hs-CRP levels in the ATOR 80 mg group following treatment were lower compared with baseline ( 3.59±1.07 vs. 6.10±2.12 , P<0.01 ) . According to the virtual histology ( VH ) of IVUS , the percentages of plaque necrosis following treatment in the placebo and ATOR 10 mg groups rose above baseline levels ( 15.51±12.56 vs. 7.69±1.31 % , 13.54±11.76 vs. 7.83±1.43 % , P<0.01 ) and conformed to the diagnostic criteria for unstable plaques ( 15.51±12.56 , 13.54±11.76 % ) . By contrast , in the ATOR 20 , 40 and 80 mg groups , percentages of plaque necrosis remained stable following treatment compared with baseline ( P=0.069 , 0.846 and 0.643 , respectively ) . Plaque volumes following treatment in the placebo , ATOR 10 and 20 mg groups were similar to baseline levels . However , in the ATOR 40 and 80 mg groups , plaque volumes decreased following treatment compared with baseline plaque volumes ( 30.69±8.12 vs. 37.09±12.01 mm3 , 24.99±1.01 vs. 36.47±14.68 mm3 , P=0.019 , P<0.01 , respectively ) . ATOR ( 20 mg/day ) is able to lower LDL to st and ard levels while ATOR 40 mg/day was superior to 20 mg/day and had similar effects to 80 mg/day . Only ATOR 80 mg/day was able to increase HDL levels . Hs-CRP in patients without ATOR was higher and ATOR 80 mg/day decreased levels . ATOR ≥20 mg/day is able to stabilize plaques and ATOR 80 mg/day was superior to 20 and 40 mg/day . Thus , ATOR 40–80 mg/day reduces the volume of plaques The purpose of this 20-week , open-label , r and omized clinical trial was to evaluate the effect of rosuvastatin on fasting serum lipids and lipoproteins , high-sensitivity C-reactive protein ( hs-CRP ) , and the glomerular filtration rate ( GFR ) in 91 patients with chronic kidney disease . Patients were r and omized to rosuvastatin 10 mg/day ( n = 48 ) or to  no lipid-lowering treatment ( n = 43 ) for 20 weeks . In contrast to patients not receiving rosuvastatin , patients receiving rosuvastatin tended to derive more favorable improvements from baseline values in low-density lipoprotein cholesterol ( -43 % , p < 0.001 , vs 7 % , p = NS ; p < 0.001 for change with rosuvastatin treatment vs change with no antilipemic treatment ) , hs-CRP ( -47 % , p < 0.001 , vs 7 % , p = NS ; p < 0.001 for change with rosuvastatin treatment vs change with no antilipemic treatment ) , and GFR ( 11 % , p < 0.05 , vs 4 % , p = NS ; p = NS for change with rosuvastatin treatment vs change with no antilipemic treatment ) AIMS Previously we revealed the effectiveness of a new therapeutic approach with a short-term , very-low dose fluvastatin-valsartan combination on the improvement of arterial function in type 1 diabetes mellitus patients ( T1DM ) . In this study we explored whether this approach influences inflammation and oxidative stress and explored any association of these effects with arterial function improvement . METHODS This was a supplementary analysis of the two previous double blind r and omized studies ( included 44 T1DM patients ) . Treatment group received very-low dose fluvastatin-valsartan , the control group received placebo . Blood sample s were collected and inflammation parameters : high-sensitivity CRP ( hsCRP ) , interleukin 6 ( IL-6 ) , vascular cell adhesion molecule-1 ( VCAM-1 ) and oxidative stress parameter total antioxidant status ( TAS ) were measured . RESULTS Treatment decreased hsCRP values ( by 56.5 % , P<0.05 ) and IL-6 values ( by 33.6 % , P<0.05 ) and increased TAS values ( by 21.1 % ; P<0.05 ) after 30days of treatment . High sensitivity CRP and TAS remained decreased 3months after treatment discontinuation . Importantly , the anti-inflammatory and anti-oxidative action significantly correlated with arterial function improvement . CONCLUSIONS The approach consisting of short-term ( 30days ) treatment with a very low-dose fluvastatin-valsartan combination acts anti-inflammatory and anti-oxidative in T1DM patients . These observations along with the improvement of arterial function support the assumption that this approach could have an important clinical benefit in T1DM patients OBJECTIVE The purpose of this study was to evaluate the efficacy and safety profile of ezetimibe/simvastatin(EZE/SIMVA ) combination tablet , relative to ezetimibe ( EZE ) and simvastatin ( SIMVA ) monotherapy , in patients with primary hypercholesterolemia . METHODS This was a r and omized , multicenter , double-blind , placebo-controlled , factorial design study After a 6- to 8-week washout period and 4-week , single-blind , placebo run in , hypercholesterolemic patients ( low-density lipoprotein cholesterol [ LDL-C ] , 145 - 250 mg/dL ; triglycerides [ TG ] , < or = 350 mg/dL ) were r and omized equally to 1 of 10 daily treatments for 12 weeks : EZE/SIMVA 10/10 , 10/20 , 10/40 , or 10/80 mg ; SIMVA 10 , 20 , 40 , or 80 mg ; EZE 10 mg ; or placebo . The primary efficacy analysis was mean percent change from baseline in LDL-C to study end point Secondary end points included percent changes in other lipid variables and C-reactive protein [ CRP ] . RESULTS There were 1528 patients r and omized to treatment ( 792 women , 736 men ) ; mean ( SD ) age ranged from 54.9 ( 112 ) years to 56.4 ( 10.6 ) years across pooled treatment groups . The treatment groups were well balanced for baseline demographics . Pooled EZE/SIMVA was associated with greater reductions in LDL-C than pooled SIMVA or EZE alone ( P < 0.001 ) . Depending on dose , EZE/SIMVA was associated with reductions in LDL-C of -44.8 % to -602 % , non-high-density lipoprotein cholesterol of -40.5 % to -55.7 % , and TG of -22.5 % to -30.7 % ; high-density lipoprotein cholesterol increased by 5.5 % to 9.8 % . EZE/SIMVA was associated with greater reductions in CRP and remnant-like particle-cholesterol than SIMVA alone ( P < 0.001 ) . More patients receiving EZE/SIMVA versus SIMVA achieved LDL-C concentrations < 100 mg/dL ( 78.6 % vs 45.9 % ; P < 0.001 ) . EZE/SIMVA was generally well tolerated , with a safety profile similar to SIMVA monotherapy There were no significant differences between EZE/SIMVA and SIMVA in the incidence of consecutive liver transaminase levels > or =3 times the upper limit of normal ( ULN ) ( 1 .5 % for EZE/SIMVA and 1.1 % for SIMVA ; P = NS ) or creature kinase levels > or = 10 times ULN ( 0.0 % for EZE/SIMVA and 02 % for SIMVA ; P = NS ) . CONCLUSION The EZE/SIMVA tablet was a highly effective and well-tolerated LDL-C-lowering therapy in this study of patients with primary hypercholesterolemia BACKGROUND Chronic kidney disease ( CKD ) is associated with inflammation . The effects of atorvastatin on biomarkers of inflammation were assessed in CKD patients in the LORD trial . METHODS 117 patients with serum creatinine > 120 μmol/L were r and omized to receive atorvastatin 10 mg/day ( 56 ) or placebo ( 61 ) and followed for a mean of 2.5 years . 33 individuals with normal kidney function were controls . Outcomes included comparison of changes in pentraxin-3 ( PTX3 ) , TNF-α , CRP , IL-6 , IL-8 , and IL-10 between atorvastatin and placebo-treated patients . RESULTS At baseline , compared with controls , CKD patients had increased PTX3 ( mean , 1.08 vs. 0.58 ng/mL ; p < 0.001 ) , CRP ( 4.9 vs. 1.5 mg/L ; p < 0.001 ) , IL-8 ( 6.00 vs. 4.58 pg/mL ; p = 0.001 ) , IL-10 ( 59.0 vs. 17.6 pg/mL ; p = 0.007 ) , and TNF-α ( 18.0 vs. 5.6 ng/mL ; p < 0.001 ) . In patients with raised baseline plasma IL-6/8/10 and /or PTX3 the eGFR decline during the trial was significantly less in those treated with atorvastatin compared to placebo ( mean change , -3.36 ; vs. + 1.25 mL/min/1.73 m2/year ; difference , 4.61 95 % CI 0.98 - 8.25 ; p = 0.002 ) , whilst those without raised inflammatory biomarkers showed no difference . Placebo treated patients with raised TNF-α levels had no eGFR decline ( p > 0.90 ) , whereas in atorvastatin-treated patients eGFR declined ( p = 0.05 ) . CONCLUSIONS CKD patients with inflammation treated with atorvastatin had significantly less eGFR decline . Larger studies using statin therapy , specifically enrolling CKD patients with inflammation , may be worthwhile exploring Purpose of the study was to investigate whether short-term atorvastatin treatment improves endothelial function and affects inflammatory process in patients with heart failure ( HF ) and normal cholesterol levels . HF is characterized by endothelial dysfunction and increased inflammatory process , while statins restore endothelial function having also anti-inflammatory effects in hypercholesterolemic patients . We investigated the effect of 4-week atorvastatin treatment ( 10 mg/day ) on endothelial function and inflammatory markers in patients with HF and cholesterol levels < 220 mg/dl . Patients were r and omly allocated into groups and received atorvast 
    Output:
    