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 A role for vitamin D deficiency in Parkinson disease ( PD ) has recently been proposed . OBJECTIVE To compare the prevalence of vitamin D deficiency in a research data base cohort of patients with PD with the prevalence in age-matched healthy controls and patients with Alzheimer disease ( AD ) . DESIGN Survey study and blinded comparison of plasma 25-hydroxyvitamin D ( 25[OH]D ) concentrations of stored sample s in a clinical research data base at Emory University School of Medicine . SETTING Referral center ( PD and AD patients ) , primary care clinics , and community setting ( controls ) . PARTICIPANTS Participants were recruited into the study between May 1992 and March 2007 . Every fifth consecutively enrolled PD patient was selected from the clinical research data base . Unrelated AD ( n = 97 ) and control ( n = 99 ) participants were r and omly selected from the data base after matching for age , sex , race , APOE genotype , and geographic location . MAIN OUTCOME MEASURES Prevalence of suboptimal vitamin D and mean 25(OH)D concentrations . RESULTS Significantly more patients with PD ( 55 % ) had insufficient vitamin D than did controls ( 36 % ) or patients with AD ( 41 % ; P = .02 , chi(2)test ) . The mean ( SD ) 25(OH)D concentration in the PD cohort was significantly lower than in the AD and control cohorts ( 31.9 [ 13.6 ] ng/mL vs 34.8 [ 15.4 ] ng/mL and 37.0 [ 14.5 ] ng/mL , respectively ; P = .03 ) . CONCLUSIONS This report of 25(OH)D concentrations in a predominantly white PD cohort demonstrates a significantly higher prevalence of hypovitaminosis in PD vs both healthy controls and patients with AD . These data support a possible role of vitamin D insufficiency in PD . Further studies are needed to determine the factors contributing to these differences and eluci date the potential role of vitamin D in pathogenesis and clinical course of PD Significant reduction in bone mineral density ( BMD ) occurs in patients with Parkinson 's disease ( PD ) , correlating with immobilization and with vitamin D deficiency , and increasing the risk of hip fracture , especially in elderly women . As a biological indicator of compromised vitamin K status , an increased serum concentration of undercarboxylated osteocalcin ( Oc ) has been associated with reduced BMD in the hip and an increased risk of fracture in otherwise healthy elderly women . We evaluated treatment with vitamin K(2 ) ( menatetrenone ; MK-4 ) in maintaining BMD and reducing the incidence of nonvertebral fractures in elderly female patients with PD . In a r and om and prospect i ve study of PD patients , 60 received 45 mg of MK-4 daily for 12 months , and the remaining 60 ( untreated group ) did not . At baseline , patients of both groups showed vitamin D and K(1 ) deficiencies , high serum levels of ionized calcium , and glutaminic residue ( Glu ) Oc , and low levels of parathyroid hormone ( PTH ) and 1,25-dihydroxyvitamin D [ 1,25-(OH)(2)D ] , indicating that immobilization-induced hypercalcemia inhibits renal synthesis of 1,25-(OH)(2)D and compensatory PTH secretion . BMD in the second metacarpals increased by 0.9 % in the treated group and decreased by 4.3 % in the untreated group ( p < 0.0001 ) .  Vitamin K(2 ) level increased by 259.8 % in the treated group . Correspondingly , significant decreases in Glu Oc and calcium were observed in the treated group , in association with an increase in both PTH and 1,25-(OH)(2)D. Ten patients sustained fractures ( eight at the hip and two at other sites ) in the untreated group , and one hip fracture occurred among treated patients ( p = 0.0082 ; odds ratio = 11.5 ) . The treatment with MK-4 can increase the BMD of vitamin D- and K-deficient bone by increasing vitamin K concentration , and it can also decrease calcium levels through inhibition of bone resorption , result ing in an increase in 1,25-(OH)(2)D concentration 
    Output:
    
agent
Low vitamin D levels are associated with an increased risk of PD
***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 A role for vitamin D deficiency in Parkinson disease ( PD ) has recently been proposed . OBJECTIVE To compare the prevalence of vitamin D deficiency in a research data base cohort of patients with PD with the prevalence in age-matched healthy controls and patients with Alzheimer disease ( AD ) . DESIGN Survey study and blinded comparison of plasma 25-hydroxyvitamin D ( 25[OH]D ) concentrations of stored sample s in a clinical research data base at Emory University School of Medicine . SETTING Referral center ( PD and AD patients ) , primary care clinics , and community setting ( controls ) . PARTICIPANTS Participants were recruited into the study between May 1992 and March 2007 . Every fifth consecutively enrolled PD patient was selected from the clinical research data base . Unrelated AD ( n = 97 ) and control ( n = 99 ) participants were r and omly selected from the data base after matching for age , sex , race , APOE genotype , and geographic location . MAIN OUTCOME MEASURES Prevalence of suboptimal vitamin D and mean 25(OH)D concentrations . RESULTS Significantly more patients with PD ( 55 % ) had insufficient vitamin D than did controls ( 36 % ) or patients with AD ( 41 % ; P = .02 , chi(2)test ) . The mean ( SD ) 25(OH)D concentration in the PD cohort was significantly lower than in the AD and control cohorts ( 31.9 [ 13.6 ] ng/mL vs 34.8 [ 15.4 ] ng/mL and 37.0 [ 14.5 ] ng/mL , respectively ; P = .03 ) . CONCLUSIONS This report of 25(OH)D concentrations in a predominantly white PD cohort demonstrates a significantly higher prevalence of hypovitaminosis in PD vs both healthy controls and patients with AD . These data support a possible role of vitamin D insufficiency in PD . Further studies are needed to determine the factors contributing to these differences and eluci date the potential role of vitamin D in pathogenesis and clinical course of PD Significant reduction in bone mineral density ( BMD ) occurs in patients with Parkinson 's disease ( PD ) , correlating with immobilization and with vitamin D deficiency , and increasing the risk of hip fracture , especially in elderly women . As a biological indicator of compromised vitamin K status , an increased serum concentration of undercarboxylated osteocalcin ( Oc ) has been associated with reduced BMD in the hip and an increased risk of fracture in otherwise healthy elderly women . We evaluated treatment with vitamin K(2 ) ( menatetrenone ; MK-4 ) in maintaining BMD and reducing the incidence of nonvertebral fractures in elderly female patients with PD . In a r and om and prospect i ve study of PD patients , 60 received 45 mg of MK-4 daily for 12 months , and the remaining 60 ( untreated group ) did not . At baseline , patients of both groups showed vitamin D and K(1 ) deficiencies , high serum levels of ionized calcium , and glutaminic residue ( Glu ) Oc , and low levels of parathyroid hormone ( PTH ) and 1,25-dihydroxyvitamin D [ 1,25-(OH)(2)D ] , indicating that immobilization-induced hypercalcemia inhibits renal synthesis of 1,25-(OH)(2)D and compensatory PTH secretion . BMD in the second metacarpals increased by 0.9 % in the treated group and decreased by 4.3 % in the untreated group ( p < 0.0001 ) .  Vitamin K(2 ) level increased by 259.8 % in the treated group . Correspondingly , significant decreases in Glu Oc and calcium were observed in the treated group , in association with an increase in both PTH and 1,25-(OH)(2)D. Ten patients sustained fractures ( eight at the hip and two at other sites ) in the untreated group , and one hip fracture occurred among treated patients ( p = 0.0082 ; odds ratio = 11.5 ) . The treatment with MK-4 can increase the BMD of vitamin D- and K-deficient bone by increasing vitamin K concentration , and it can also decrease calcium levels through inhibition of bone resorption , result ing in an increase in 1,25-(OH)(2)D concentration 
    Output:
    