***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 Hypotensive therapy leads to a number of trace elements metabolism disturbances . Zinc balance is frequently affected by antihypertensive treatment . AIM To evaluate the effect of a hypotensive treatment , modified diet and zinc supplementation on mineral status and selected biochemical parameters in newly diagnosed hypertensive patients on monotherapy . METHODS In the first stage , arterial hypertension in ninety-eight human subjects was diagnosed . In the second stage , antihypertensive monopharmacotherapy was implemented . In the third stage , patients were r and omized into three groups and continued antihypertensive monotherapy : group D received an optimal-mineral-content diet , group S received zinc supplementation , and group C had no changes in diet or zinc supplementation . Iron , zinc , and copper concentrations in serum , erythrocytes , urine , and hair were determined . Lipids , glucose , ceruloplasmin , ferritin , albumin , C-reactive protein ( CRP ) , tumor necrosis factor α ( TNF-α ) , nitric oxide ( NO ) , superoxide dismutase ( SOD ) and catalase ( CAT ) were assayed in serum . RESULTS Antihypertensive monotherapy decreased zinc concentration in serum and erythrocytes and increased the level of zinc in urine , decreased CAT and SOD activity , TNF-α concentration in serum , and increased the level of NO in the serum . Zinc supply led to an increase in zinc concentration in serum , erythrocytes , and hair ( in group S only ) . In the groups with higher zinc intake , decreased glucose concentration in the serum was observed . Significant correlation was seen between the zinc and glucose serum concentrations . CONCLUSION Hypotensive drugs disturb zinc status in newly diagnosed hypertensive patients .  Antihypertensive monotherapy combined with increased zinc supply in the diet or supplementation favorably modify zinc homeostasis and regulate glucose status without blood pressure affecting in patients with hypertension Flaws in the design , conduct , analysis , and reporting of r and omised trials can cause the effect of an intervention to be underestimated or overestimated . The Cochrane Collaboration ’s tool for assessing risk of bias aims to make the process clearer and more Summary A possible interaction between zinc sulphate and tetracycline or doxycycline was examined in a cross-over study in seven volunteers . A single dose of zinc sulphate ( 45 mg Zn++ ) was given simultaneously with tetracycline hydrochloride ( 500 mg ) or doxycycline chloride ( 200 mg ) . The serum concentration of tetracycline , the area under the serum tetracycline concentration-time curve and the excretion of tetracycline in urine were reduced by about 30 % ( p<0.05 ) from the respective control values . The absorption of doxycycline  was not influenced significantly by zinc sulphate . The clinical significance of the zinc-tetracycline interaction seems to be of limited importance Objective : Zinc is an essential trace element that plays a key role in several cellular processes and has been suggested to be involved in blood pressure regulation . We aim ed to prospect ively investigate the association between baseline concentrations of serum zinc  and incident hypertension . Methods : We analyzed data involving 1652 men aged 42–61 years without a known history of hypertension at baseline in the Kuopio Ischemic Heart Disease population -based cohort study , with the assessment of serum zinc concentrations . Hazard ratios [ 95 % confidence intervals ( CIs ) ] for incident hypertension were assessed . Results : During a median follow-up of 24.7 years , 259 participants developed hypertension . Serum zinc was weakly correlated with several risk markers for hypertension and nonlinearly associated with incident hypertension . In analyses adjusted for age , the hazard ratio ( 95 % CIs ) for hypertension in a comparison of the top quartile vs. bottom quartiles 1–3 of zinc concentration was 1.65 ( 1.27–2.15 ; P < 0.001 ) , which was minimally attenuated on adjustment for several established risk factors 1.48 ( 1.13–1.93 ; P = 0.004 ) . The association remained unchanged on further adjustment for renal function , socioeconomic status , and dietary factors . The findings were generally consistent across several clinical subgroups . There was no evidence of an association of dietary zinc intake with risk of hypertension . Conclusion : This prospect i ve study suggests higher serum zinc concentration is positively and independently associated with  incident hypertension in men . Further evidence from large-scale population -based studies is needed to support these findings and assess the mechanisms underlying the association OBJECTIVES Oxidative stress can contribute to microvascular complications in diabetes . A decisive event associated with this condition may be the decrease in the synthesis of zinc-containing antioxidant enzymes such as superoxide dismutase and glutathione peroxidase . This consideration led us to investigate the effect of zinc supplementation versus placebo on microalbuminuria in diabetic patients in a r and omized double blind clinical trial . METHODS Fifty diabetic patients with microalbuminuria were enrolled .  Fasting plasma glucose , HbA1c , lipid profiles , plasma zinc levels and r and om urine for albumin and creatinine were measured . Patients r and omly received 30 mg elemental zinc ( group 1 ) or placebo ( group 2 ) for 3 months . After a 4 week wash-out period , the groups were crossed over ( i.e. the zinc group were given placebo , and the placebo group were given zinc ) and the protocol was repeated . RESULTS From an initial number of 50 selected patients ( 25 in each of two groups ) , 39 patients ( 21 in group 1 and 18 in group 2 ) completed the study . In group 1 , after zinc supplementation , urinary albumin excretion decreased significantly from 86.5 + /- 57 to 75 + /- 71 mg/g ( p = 0.01 ) . After placebo , patients in group 1 showed no significant reduction in microalbuminuria ( 85 + /- 72 mg/g to 83 + /- 63 mg/g creatinine ) . In group 2 , no change in albumin excretion was observed after placebo treatment ( 90.5 + /- 63 mg/g to 90 + /- 60 mg/g creatinine ) . After zinc supplementation , a significant reduction was observed in albumin excretion , from 90 + /- 60 mg/g to 85 + /- 57 mg/g creatinine ( p = 0.003 ) . CONCLUSIONS Zinc supplementation reduced albumin excretion in microalbuminuric type 2diabetic patients . This outcome may be due to the antioxidant effect of zinc BACKGROUND This study evaluated the effects of zinc supplementation on glycemic control , other cardiometabolic and anthropometric parameters , and  disease progression in prediabetes . METHODS A r and omized double-blind placebo-controlled Phase 2 clinical trial was conducted over a 12-month period in 200 subjects ( 43 % male ; mean [ ± SD ] age 51.8 ± 7.3 years ) , r and omly assigned ( 1 : 1 ) to the treatment or control group . The treatment group received zinc ( 20 mg daily ) . Subjects were evaluated at baseline and at 1 , 3 , 6 , and 12 months . The primary outcome was the change in glycemic control from baseline . Multiple regression analyses were performed , with change in outcome variables after intervention from baseline used as continuous dependent variables . RESULTS In both groups , mean serum zinc concentrations prior to the trial were below normal ( 15.29 - 21.41 μmol/L ) . During the 12-month follow-up , a significantly higher percentage of participants developed type 2 diabetes in the control compared with zinc-treated group ( 25.0 % vs 11.0 % respectively ; P = 0.016 ) . Fasting plasma glucose ( FPG ) , 2-h glucose levels in the oral glucose tolerance test ( OGTT ) , homeostasis model assessment of insulin resistance ( HOMA-IR ) , total cholesterol ( TC ) , and low-density lipoprotein cholesterol ( LDL-C ) were significantly lower in the treated group , with significant improvement in β-cell function . In all four regression models , the best predictor of the dependent variables ( i.e. change in FPG , 2-h glucose in the OGTT , HOMA-IR , and homeostatic model assessment of β-cell function ) was zinc treatment . CONCLUSIONS Zinc supplementation reduced blood glucose and insulin resistance while improving β-cell function . Furthermore , supplementation reduced disease progression to diabetes and had beneficial effects on TC and 
    Output:
    
Nonlinear analysis failed to indicate a significant influence of supplementation dosage or duration on both SBP and DBP .
In addition , we found no evidence for the presence of small- study effects among studies for both SBP and DBP .
We found a significant reduction in SBP  following zinc supplementation .
However , zinc supplementation had no significant effect on DBP .
In addition , no nonlinear association was found between supplementation dosage and duration with changes in both SBP and DBP .