***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: OBJECTIVES Recent reports demonstrated in vitro the efficacy of fluvastatin in inhibiting hepatitis C virus ( HCV ) replication and a synergistic effect in association with interferon-alpha ( IFN-alpha ) . In vivo the inhibition of HCV replication by statins has not been demonstrated . We evaluated in this open-label , r and omized controlled study the efficacy of fluvastatin as adjuvant to pegylated-(PEG)-IFN and ribavirin in HIV/HCV genotype 1 co-infected patients . PATIENTS AND METHODS Forty-four HIV/HCV co-infected patients were r and omized to receive , in addition to PEG-IFN-alpha 2b and ribavirin , 80 mg of fluvastatin once daily or no medication . Primary and secondary endpoints were the achievement of sustained virological response ( SVR ) and rapid virological response ( RVR ) , respectively . RESULTS By intent-to-treat analysis , 25 % of the patients achieved an SVR . An SVR was observed in 8/21 patients in the fluvastatin arm and in 3/23 patients in the st and ard therapy arm ( P = 0.08 ) . A significantly higher RVR rate was obtained in the fluvastatin arm compared with the st and ard therapy [ 7/21 ( 33 % ) and 1/23 ( 4 % ) , respectively ; P = 0.02 ] . Baseline alanine aminotransferase ( ALT ) values and fluvastatin treatment arm were the only predictors of RVR at the univariate analysis ; however , no predictors were independently associated with RVR or SVR at the multivariate analysis . CONCLUSIONS Fluvastatin addition to st and ard therapy did not significantly increase the SVR rate in HIV/HCV genotype 1 co-infected patients ; however , it did significantly improve the RVR . Further studies are needed to confirm these promising results and to investigate the mechanisms of action of statins in HCV infection This pilot aims to better underst and the market for childcare in Saudi Arabia – both the supply and dem and sides – and to design a r and omized controlled experiment to test whether access to affordable day care ( in the form of subsidies , for example ) would incentivize Saudi mothers to search actively for employment and to remain employed once they are hired . In addition , the study seeks to underst and the degree to which employment early on in one ’s life impacts employment in later stages . The pilot will provide information on the groups of women the experiment should target , appropriate levels for the childcare subsidy , and the quality and current geographic locations of daycare sites . Expected Impact Determine the effects of facilitating childcare access on Saudi women ’s employment . PRINCIPAL INVESTIGATORS  Boston University Patricia Cortes  Harvard University Claudia Goldin  Swarthmore College Jennifer Pegylated interferon (PEG-IFN)/ribavirin combination therapy is the st and ard-of-care ( SOC ) treatment for chronic hepatitis C patients infected with hepatitis C virus ( HCV ) genotype 1b and high viral load . The addition of fluvastatin to SOC treatment has been suggested to be effective for better outcome in retrospective pilot analyses . We investigated whether the combination of fluvastatin with PEG-IFN/ribavirin could actually improve sustained viral response ( SVR ) in patients with HCV genotype 1b and high viral load . A r and omized , open-labeled , controlled study was conducted between July 2008 and December 2009 in 101 chronic hepatitis C patients allocated to PEG-IFN/ribavirin combination therapy with or without fluvastatin .  SVR rates were calculated in groups , stratifying host and viral factors . We also analyzed predictive factors for SVR among patients on fluvastatin  with multivariate regression analysis . Rapid and early virological , and end of treatment response rates in the fluvastatin group were not significantly different from those in the non-fluvastatin group . Notwithst and ing , SVR rate was significantly higher in the fluvastatin group than in the non-fluvastatin group ( 63.0%vs 41.7 % , P = 0.0422 ) . Comparison of the two groups stratifying demographic data and HCV characteristics showed significantly higher SVR rates to more than 80 % in males , more than two mutations in the interferon sensitivity determining region ( ISDR ) , and a history of relapse among the fluvastatin group than the non-fluvastatin group . Being male and major genotype IL28B single nucleotide polymorphisms ( SNPs ) were independent predictive factors for SVR among patients on fluvastatin with multivariate analysis . Fluvastatin-combined with PEG-IFN/ribavirin therapy significantly improves SVR rates in patients with HCV genotype 1b and high viral load . Male and major genotype IL28B SNPs were independent predictors for SVR among patients on fluvastatin combination therapy Cholesterol bio synthesis is an integral part of HCV RNA replication . Not only does HCV RNA replicate on lipid rafts , but it also requires cholesterol intermediates to replicate . In addition , it has been shown in vitro that several HMG‐CoA reductase inhibitors can decrease HCV RNA replication by ≥ 1 log . Therefore , we design ed a clinical trial to evaluate the effect of atorvastatin on HCV RNA levels . In this prospect i ve clinical trial , where patients served as their own control , 10 HCV‐infected patients who required treatment for high cholesterol were given 20 mg atorvastatin per day . Although serum cholesterol and LDL predictably decreased significantly , there was no statistically significant change in week 4 and week 12 HCV RNA levels compared to pretreatment HCV RNA levels by the paired Student t test . It is unclear whether the addition of an HMG‐CoA reductase inhibitor to interferon or a more potent inhibitor of cholesterol bio synthesis may be required to inhibit HCV RNA replication in vivo . In conclusion , atorvastatin , and likely all HMG‐CoA reductase inhibitors , does not inhibit HCV RNA replication in vivo at conventional doses . ( HEPATOLOGY 2007;45:895–898 . Background Nonalcoholic fatty liver disease develops in patients with chronic hepatitis C.  Interferon and ribavirin combination therapy is the st and ard treatment for chronic hepatitis C , but if present , NAFLD can reduce the virological response to anti-HCV therapies . Objectives We determined whether the addition of rosuvastatin to interferon and ribavirin improves the sustained virological response ( SVR ) and reduces steatosis . Patients and Methods This study was a prospect i ve , r and omized , open-label trial . Between January 2004 and December 2007 , 65 patients with chronic hepatitis ( 27 women and 38 men , mean age 48 years ) aged 32 - 63 years ( median 46 years ) were consecutively enrolled . Patients were r and omly assigned to receive leukocyte interferon alpha ( 3 MIU 3 times per week ) plus ribavirin ( 1200 mg per day ) for 12 months or interferon alpha and ribavirin at the same dosages plus rosuvastatin ( 5 mg per day ) . The primary endpoints were measurements in SVR , liver enzyme , cholesterol , triglyceride , CRP , glucose , and insulin levels ; and Homa-IR , fibrosis , and steatosis scores . Results After 12 months of treatment , we observed a significant improvement in SVR in 51 % of patients who received interferon plus ribavirin plus rosuvastatin compared with 18 % of relapsers ( OR 1.52 ; 95 % CI = 0.41 - 5.64 ; RR 1.13 ) . There were 23 responders ( 69 % ) and 10 nonresponders ( 30 % ) ( OR 1.38 ; 95 % CI = 0.49 - 16.5 ; RR 1.11 ) . When comparing interferon plus ribavirin group vs interferon plus ribavirin and rosuvastatin group after 12 months , we observed a significant difference in AST ( 85.70 vs.106.5.00 IU/ml ) ( OR 1.2 ; 95 % CI= 0.29 - 4.94 ; RR 1.04 ; p<0.001 ) , ALT ( 81.80 vs. 126.2 IU/ml ) ( OR 1.2 ; 95 % CI = 0.29 - 4.94 ; RR 1.04 ; p < 0.001 ) , LDL-cholesterol ( 0.01 vs. 0.60 mmol/l ) ( OR 14 ; 95 % CI = 3.98 - 49.16 ; p RR 2.96 ; < 0.001 ) , triglycerides ( 0.17 vs. 0.2 mmol/l ) ( OR 20 ; 95 % CI = 4.94 - 80.89 ; RR 5.38 ; p < 0.05 ) , and Viremia ( 1.8 vs. 2.48 UI/ml , p < 0.05 ) . Mean fibrosis score decreased 0.10 vs. 0.50 ( OR 4.5 ; 95 % CI = 0.89 - 22.66 ; RR 1.5 ; p < 0.05 ) , and mean steatosis score declined 0.30 vs. 0.50 ( OR 11.2 ; CI = 2.88 - 43.53 ; RR 2.75 ; p < 0.001 ) . Conclusions In HCV patients with NAFLD , the addition of rosuvastatin to interferon and ribavirin significantly reduces viremia , steatosis , and fibrosis without causing side effects BACKGROUND Hepatitis C viral ( HCV ) infection is the leading cause of death due to liver disease in the United States . Currently , pegylated interferon and ribavirin produce sustained viral remission in only 50 % of patients . Additional agents are needed to increase the cure rate . In vitro experiments show strong antiviral effects of fluvastatin against HCV . OBJECTIVES : To assess the safety and antiviral effects of fluvastatin in chronic HCV carriers . METHODS : 31 veterans with chronic HCV were prospect ively given oral doses of fluvastatin , 20 to 320 mg/day , for 2–12 weeks with weekly monitoring of HCV RNA and liver tests . Reductions of viral load ( P < 0.01 ) versus a control group were considered suppressive . RESULTS : With 80 mg a day or less , 11/22 ( 50 % ) patients responded by lowering HCV RNA . The first lowering occurred within 4 weeks ( 9/11 , 82 % ) . The greatest weekly change in HCV RNA level was a 1.75 log10 reduction . When lowered in responders , the viral load remained relatively constant for 2–5 weeks ( 7/9 , 78 % ) , or on the next test rebounded immediately to a non-significant change from , baseline ( n = 2 ) . Continued lowering of virus was seen in 2/19 ( 22 % ) patients when the study ended . We found no evidence of liver tests worsening . CONCLUSIONS : FLV used as monotherapy in vivo showed suppressive effects of HCV clinical ly that are modest , variable , and often short-lived . These findings support “ proof-of-concept ” for pilot trials combining fluvastatin with st and ard therapy . Statins and fluvastatin , in particular , appear to be safe for use in hepatitis Fluvastatin showed anti-hepatitis C virus ( HCV ) activity in vitro , through the inhibition of geranylgeranylation of cellular proteins , and a synergistic effect with interferon (IFN)-alpha . Nevertheless statins up-regulate low-density lipoprotein ( LDL ) receptor , required for HCV cell entry , and the closely related scavenger receptors SRBI and CD36 ; moreover they reduce class II major histocompatibility complex expression on antigen presenting cell , modulating T-cell activation . In vivo LDL levels have been identified as prognostic indicator of sustained viral response to IFN in patients with HCV infection , suggesting that lipid-lowering agents might conversely favour HCV entry into the hepatocytes and translate into higher viral replication . We evaluated the effect of fluvastatin on HCV-RNA levels , CD36 expression and T-cell homeostasis in HCV-RNA positive patients .  HCV-RNA was measured at baseline and after 4 weeks in 42 HCV/HIV-1 co-infected patients , r and omized to receive either fluvastatin 80 mg qd or no treatment . CD36 expression and markers of T-cell activation were evaluated by means of flow cytometry . Plasma interleukin (IL)-10 , IFN-gamma and IL-7 were measured by ELISA . Serum cholesterol and LDL decreased significantly in the treatment group ( P = 0.0001 and 0.01 , respectively ) . Surprisingly a significant increase of HCV-RNA levels was seen after 4 weeks of fluvastatin ( P = 0.03 ) . The percentages of naive/activated/ 
    Output:
    
There were no significant increases in adverse events and withdrawals with the addition of statins .