***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: Exercise can have anti-inflammatory effects in obesity , but the optimal type and intensity of exercise are not clear . This study compared short-term high-intensity interval training ( HIIT ) with moderate-intensity continuous training ( MICT ) in terms of improvement in cardiorespiratory fitness , markers of inflammation , and glucose control in previously inactive adults at elevated risk of developing type 2 diabetes . Thirty-nine inactive , overweight/obese adults ( 32 women ) were r and omly assigned to 10 sessions over 2 wk of progressive HIIT ( n = 20 , four to ten 1-min sessions at ∼90 % peak heart rate , 1-min rest periods ) or MICT ( n = 19 , 20 - 50 min at ∼65 % peak heart rate ) . Before and 3 days after training , participants performed a peak O2 uptake test , and fasting blood sample s were obtained . Both HIIT ( 1.8 ± 0.4 vs. 1.9 ± 0.4 l/min , pre vs. post ) and MICT ( 1.8 ± 0.5 vs. 1.9 ± 0.5 l/min , pre vs. post ) improved peak O2 uptake ( P < 0.001 ) and lowered plasma fructosamine ( P < 0.05 ) . Toll-like receptor ( TLR ) 4 ( TLR4 ) expression was reduced on lymphocytes and monocytes after both HIIT and MICT ( P < 0.05 ) and on neutrophils after MICT ( P < 0.01 ) . TLR2 on lymphocytes was reduced after HIIT and MICT ( P < 0.05 ) . Plasma inflammatory cytokines were unchanged after training in both groups , but MICT led to a reduction in fasting plasma glucose ( P < 0.05 , 5.9 ± 1.0 vs. 5.6 ± 1.0 mmol/l , pre vs. post ) . Ten days of either HIIT or MICT can improve cardiorespiratory fitness and glucose control and lead to reductions in TLR2 and TLR4 expression . MICT , which involved a longer duration of exercise , may be superior for reducing fasting glucose Statin treatment and exercise training can reduce markers of inflammation when administered separately . The purpose of this study was to determine the effect of rosuvastatin treatment and the addition of exercise training on circulating markers of inflammation including C-reactive protein ( CRP ) , monocyte toll-like receptor 4 ( TLR4 ) expression , and CD14+CD16 + monocyte population size .  Thirty-three hypercholesterolemic and physically inactive subjects were r and omly assigned to rosuvastatin ( R ) or rosuvastatin/exercise ( RE ) groups . A third group of physically active hypercholesterolemic subjects served as a control ( AC ) . The R and RE groups received rosuvastatin treatment ( 10 mg/d ) for 20 weeks . From week 10 to week 20 , the RE group also participated in an exercise training program ( 3d/wk ) . Measurements were made at baseline ( Pre ) , week 10 ( Mid ) , and week 20 ( Post ) , and included TLR4 expression on CD14 + monocytes and CD14+CD16 + monocyte population size as determined by 3-color flow cytometry . Serum CRP was quantified by enzyme-linked immunosorbent assay . TLR4 expression on CD14 + monocytes was higher in the R group at week 20 . When treatment groups ( R and RE ) were combined , serum CRP was lower across time . Furthermore , serum CRP and inflammatory monocyte population size were lower in the RE group compared with the R group at the Post time point . When all groups ( R , RE , and AC ) were combined , TLR4 expression was greater on inflammatory monocytes ( CD14+CD16 + ) compared with classic monocytes ( CD14+CD16⁻ ) at all time points . In conclusion , rosuvastatin may influence monocyte inflammatory response by increasing TLR4 expression on circulating monocytes . The addition of exercise training to rosuvastatin treatment further lowered CRP and reduced the size of the inflammatory monocyte population , suggesting an additive anti-inflammatory effect of exercise OBJECTIVE : To test the feasibility of creating a valid and reliable checklist with the following features : appropriate for assessing both r and omised and non-r and omised studies ; provision of both an overall score for study quality and a profile of scores not only for the quality of reporting , internal validity ( bias and confounding ) and power , but also for external validity . DESIGN : A pilot version was first developed , based on epidemiological principles , review s , and existing checklists for r and omised studies . Face and content validity were assessed by three experienced review ers and reliability was determined using two raters assessing 10 r and omised and 10 non-r and omised studies . Using different raters , the checklist was revised and tested for internal consistency ( Kuder-Richardson 20 ) , test-retest and inter-rater reliability ( Spearman correlation coefficient and sign rank test ; kappa statistics ) , criterion validity , and respondent burden . MAIN RESULTS : The performance of the checklist improved considerably after revision of a pilot version . The Quality Index had high internal consistency ( KR-20 : 0.89 ) as did the subscales apart from external validity ( KR-20 : 0.54 ) . Test-retest ( r 0.88 ) and inter-rater ( r 0.75 ) reliability of the Quality Index were good . Reliability of the subscales varied from good ( bias ) to poor ( external validity ) . The Quality Index correlated highly with an existing , established instrument for assessing r and omised studies ( r 0.90 ) . There was little difference between its performance with non-r and omised and with r and omised studies . Raters took about 20 minutes to assess each paper ( range 10 to 45 minutes ) . CONCLUSIONS : This study has shown that it is feasible to develop a checklist that can be used to assess the method ological quality not only of r and omised controlled trials but also non-r and omised studies . It has also shown that it is possible to produce a checklist that provides a profile of the paper , alerting review ers to its particular method ological strengths and weaknesses . Further work is required to improve the checklist and the training of raters in the assessment of external validity Diet-induced weight gain increases disease risk via disruption of the innate immune system . Flow cytometry is commonly used to assess the immune system ; however , in mice such measurements traditionally require terminal procedures and tissue collection to generate sufficient sample . The present study refined an existing flow cytometry method to reduce the number of mice needed to longitudinally measure monocytes . CD-1 male mice were r and omly assigned to one of the three groups : DS ( diet-induced weight gain + sedentary ) , DE ( diet-induced weight gain + forced treadmill running [ total distance 35,755 ± 1832 m ] ) or NS ( normal weight gain + sedentary ) . DS and DE consumed a 60 % fat diet and NS consumed a 10 % fat diet ad libitum . Saphenous vein blood sample s were collected weekly for a period of six weeks and three-colour flow cytometry was used to measure changes in monocyte ( CD11b+/14 + ) concentration and cell-surface toll-like receptor 4 ( TLR4 ) expression . DS ( 18 % ) and DE ( 17 % ) gained more weight than NS ( P < 0.001 ) . On a group basis , DS expressed 17 % more TLR4 than DE and NS ( P = 0.005 ) . The present study demonstrates that a longitudinal survival model can be used to reduce the number of animals needed to complete flow cytometry experiments . Exercise during diet-induced weight prevented some ( decreased monocyte TLR4 expression ) but not all aspects of innate immune system function Obesity causes innate immune dysfunction , contributing to increased disease risk . Weight loss from a combination of caloric restriction and exercise is the most effective treatment of obesity . We compared forced and voluntary exercise as weight-loss treatments in diet-induced obese ( DIO ) mice and assessed the effects of weight loss on monocyte concentration and cell-surface expression of Toll-like receptor ( TLR ) 2 , TLR4 , CD80 , and CD86 .  DIO CD1 male mice were allocated r and omly to 1 of 3 groups ( n = 6 per group ) : voluntary wheel running ( VEX ) ; forced treadmill running ( FEX ) ; and sedentary ( S ) . A fourth ( control ) group ( CN , n = 6 ) of nonDIO mice was included also . During the 8-wk weight-loss treatment , all 4 groups consumed a low-fat ( 10 % fat ) diet . Nonlethal saphenous vein blood sample s collected at baseline , week 4 , and week 8 were analyzed by flow cytometry to assess monocyte concentration and functional receptor expression . The VEX and FEX groups lost significantly more body weight ( 36 % and 27 % , respectively ) over the 8 wk of treatment than did other groups . VEX mice ran 4.4 times more than did FEX animals . VEX mice had higher monocyte concentrations ( 48 % and 58 % , respectively ) than did the CN and FEX groups . Compared with baseline , week 8 cell-surface expression of TLR2 ( 22 % ) , TLR4 ( 33 % ) , and CD86 ( 18 % ) was increased in VEX mice . At week 4 , CD80 expression was 42 % greater for VEX than S mice . The present study confirms that short-term exercise and low-fat diet consumption cause significant weight loss and altered immune profiles Introduction . Physical inactivity and obesity are independent risk factors for atherosclerosis . We analyzed the immunomodulatory capacity of 10-week intensified exercise training ( ET ) in obese and lean athletes . Markers of the innate immune response were investigated in obese ( ONE : ET≤40 km/week ) and lean athletes ( LNE : ET≤40 km/week and LE : ET≥55 km/week ) . Methods . Circulating dendritic cells ( DC ) were analyzed by flow-cytometry for BDCA-1/-2-expression . TLR-2/-4/-7 and MyD88 were analyzed by RT-PCR and Western blot . Circulating oxLDL levels were analyzed by ELISA . Results . BDCA-1 expression at baseline was lower in ONE compared to both other groups ( ONE 0.15 % ; LNE 0.27 % ; LE 0.33 % ; P < .05 ) , but significantly increased in ONE after training ( + 50 % ; P < .05 ) . In contrast , BDCA-2 expression at baseline was higher in ONE ( ONE 0.25 % ; LNE 0.11 % ; LE 0.09 % ; P < .05 ) and decreased in ONE after the 10-week training period ( −27 % ; P < .05 ) . Gene activations of TLR-4 and TLR-7 with corresponding protein increase were found for all three groups ( P < .01/P < .05 ) compared to pre training . A reduction of oxLDL levels was seen in ONE ( −61 % ; P < .05 ) . Conclusions . Intensified exercise induces an increase of BDCA-1 + DCs and TLR-4/-7 in obese athletes . We hereby describe new immune modulatory effects , which — through regular aerobic exercise — modulate innate immunity and pro-inflammatory cytokines in obesity 
    Output:
    
Globally , the animal studies showed a marked tendency towards a down-regulation of TLR2 and 4 expression accompagnied with , a reduced activation of nuclear factorkappaB ( NF-κB ) signaling and cytokine production , and an improvement in insulin sensitivity and body composition .
CONCLUSION While animal studies showed a marked tendency towards TLR2 and 4 down-regulation after chronic endurance exercise , the current evidence in human is not sufficiently robust to conclude any role of TLR in the anti-inflammatory properties of exercise