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: BACKGROUND Adipose tissue-derived leptin and adiponectin control hunger , energy expenditure , insulin sensitivity , endothelial function , reproduction and immunity and are thought to play a role in autoimmune diseases . However , their role in ankylosing spondylitis ( AS ) is not clearly defined . Tumour necrosis factor ΤNF-α is a potential modulator of adipocytokines . The effect of longterm anti-TNF-α treatment on plasma levels of leptin and adiponectin has not been assessed so far . OBJECTIVES To assess the effect of a 6-month anti-TNF-α treatment on serum leptin and adiponectin levels in AS patients . METHODS Thirty men with AS were included in the study . Thirty age- and weight-matched men served as controls . Clinical and biochemical parameters were assessed and serum levels of leptin and adiponectin were measured with enzyme immunoassay methods prior to and after the 6-month treatment with infliximab . RESULTS Mean age and disease duration of AS patients were 40.6±13.7 and 13.4±8.4 years , respectively . At baseline , AS patients exhibited significantly higher adiponectin ( 15.4±8.3 vs. 8.6±4.2 μg/ml , p<0.05 ) , but no difference in leptin levels ( 7.2±2.9 vs. 8.9±6.4 ng/ml , p = NS ) . Adipocytokines did not correlate with any disease parameter . Body weight of the patients did not change significantly over the 6-month period . Serum levels of leptin and adiponectin did not change significantly after the 6-month treatment . CONCLUSIONS Adiponectin levels were significantly higher in AS patients compared with  controls . Infliximab treatment did not change serum levels of leptin and adiponectin suggesting that the anti-TNF-α treatment may not modulate significantly their levels BACKGROUND Adiponectin is an adipocyte-derived cytokine that has anti-inflammatory properties . A preliminary proteomic evaluation of urine for biomarkers of systemic lupus erythematosus ( SLE ) nephritis demonstrated high levels of adiponectin in SLE urine . This prompted investigation of adiponectin expression in human SLE . METHODS Adiponectin was measured by enzyme-linked immunosorbent assay ( ELISA ) in the urine and plasma of a clinical ly well-characterized SLE cohort , with renal and nonrenal SLE being followed in a prospect i ve longitudinal study to identify risk factors for SLE flare . Renal adiponectin expression was assessed by immunohistochemical analysis of kidney biopsies from SLE nephritis patients . RESULTS Cross-sectional testing showed that plasma adiponectin levels were higher in patients with renal SLE flare than normal controls or patients with nonrenal SLE flare , after accounting for race and body mass index . Urine adiponectin levels increased significantly with renal flare , but not nonrenal SLE flare . Longitudinal testing revealed that the urine adiponectin increase began in the 2 months prior to renal flare . Urine adiponectin correlated with plasma levels and magnitude of proteinuria , and to a lesser extent serum creatinine . Plasma adiponectin levels were independent of renal function and proteinuria . In kidney biopsies , adiponectin was found on endothelial surfaces in normal and SLE kidneys , and on podocytes and in the tubules of SLE kidneys . CONCLUSION Plasma adiponectin levels are increased in patients with renal SLE compared to healthy controls and patients with nonrenal SLE . During renal but not nonrenal SLE flare , urine adiponectin levels increase significantly . Urine adiponectin may be a biomarker of renal SLE flare 
    Output:
    
agent
Subgroup analyses suggested that Asian and African AS patients as well as patients aged < 40 years had higher serum leptin and resistin levels when compared to controls .
Serum adiponectin levels were higher in AS patients compared to controls in subgroup of age ≥ 40 , and serum resistin levels in subgroup of BMI ≥ 25 .
Measurement method was a source of heterogeneity for resistin .
Publication bias was not observed and the robustness of study results was confirmed by sensitivity analysis .
Conclusion : Serum resistin , but not leptin or adiponectin levels may be closely associated with the development of AS .
HighlightsSerum levels of resistin are associated with the pathogenesis of AS.In specific subgroups , leptin and adiponectin may be related to AS.Measuring type is one of sources of heterogeneity for the studies about resistin
***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: BACKGROUND Adipose tissue-derived leptin and adiponectin control hunger , energy expenditure , insulin sensitivity , endothelial function , reproduction and immunity and are thought to play a role in autoimmune diseases . However , their role in ankylosing spondylitis ( AS ) is not clearly defined . Tumour necrosis factor ΤNF-α is a potential modulator of adipocytokines . The effect of longterm anti-TNF-α treatment on plasma levels of leptin and adiponectin has not been assessed so far . OBJECTIVES To assess the effect of a 6-month anti-TNF-α treatment on serum leptin and adiponectin levels in AS patients . METHODS Thirty men with AS were included in the study . Thirty age- and weight-matched men served as controls . Clinical and biochemical parameters were assessed and serum levels of leptin and adiponectin were measured with enzyme immunoassay methods prior to and after the 6-month treatment with infliximab . RESULTS Mean age and disease duration of AS patients were 40.6±13.7 and 13.4±8.4 years , respectively . At baseline , AS patients exhibited significantly higher adiponectin ( 15.4±8.3 vs. 8.6±4.2 μg/ml , p<0.05 ) , but no difference in leptin levels ( 7.2±2.9 vs. 8.9±6.4 ng/ml , p = NS ) . Adipocytokines did not correlate with any disease parameter . Body weight of the patients did not change significantly over the 6-month period . Serum levels of leptin and adiponectin did not change significantly after the 6-month treatment . CONCLUSIONS Adiponectin levels were significantly higher in AS patients compared with  controls . Infliximab treatment did not change serum levels of leptin and adiponectin suggesting that the anti-TNF-α treatment may not modulate significantly their levels BACKGROUND Adiponectin is an adipocyte-derived cytokine that has anti-inflammatory properties . A preliminary proteomic evaluation of urine for biomarkers of systemic lupus erythematosus ( SLE ) nephritis demonstrated high levels of adiponectin in SLE urine . This prompted investigation of adiponectin expression in human SLE . METHODS Adiponectin was measured by enzyme-linked immunosorbent assay ( ELISA ) in the urine and plasma of a clinical ly well-characterized SLE cohort , with renal and nonrenal SLE being followed in a prospect i ve longitudinal study to identify risk factors for SLE flare . Renal adiponectin expression was assessed by immunohistochemical analysis of kidney biopsies from SLE nephritis patients . RESULTS Cross-sectional testing showed that plasma adiponectin levels were higher in patients with renal SLE flare than normal controls or patients with nonrenal SLE flare , after accounting for race and body mass index . Urine adiponectin levels increased significantly with renal flare , but not nonrenal SLE flare . Longitudinal testing revealed that the urine adiponectin increase began in the 2 months prior to renal flare . Urine adiponectin correlated with plasma levels and magnitude of proteinuria , and to a lesser extent serum creatinine . Plasma adiponectin levels were independent of renal function and proteinuria . In kidney biopsies , adiponectin was found on endothelial surfaces in normal and SLE kidneys , and on podocytes and in the tubules of SLE kidneys . CONCLUSION Plasma adiponectin levels are increased in patients with renal SLE compared to healthy controls and patients with nonrenal SLE . During renal but not nonrenal SLE flare , urine adiponectin levels increase significantly . Urine adiponectin may be a biomarker of renal SLE flare 
    Output:
    