***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 Endothelial function is known to be abnormal in patients with diabetes and acute hyperglycaemia may play an aetiological role . AIMS The aim of this r and omised controlled study was to determine if acute systemic hyperglycaemia impairs endothelial function in normal subjects . METHODS Endothelial function was assessed by the change in brachial artery diameter in response to forearm ischaemia using B-mode ultrasound in ten healthy subjects ( eight male ) aged 19 - 35 years .  Brachial artery blood flow velocity and diameter were measured before and after five minutes of forearm ischaemia . Measurements were performed in the supine position after an overnight fast , before and after 60 minute infusions of 0.9 % saline or 10 % dextrose . Measurements were made on two separate occasions at least 24 hours apart , and subjects were r and omised to saline first or dextrose first . The largest diameter measured after ischaemia was divided by the resting arterial diameter to calculate percent dilatation of the artery from baseline , and is reported as flow-mediated dilatation ( FMD ) . RESULTS Dextrose infusion result ed in a significant rise in mean ( SD ) serum glucose 5.2 ( 0.1 ) to 9.2 ( 0.3 ) mmol/L and insulin concentration 6.3 ( 1.4 ) to 20.6 ( 3.7 ) mU/L p<0.002 . Brachial artery blood flow velocity and diameter increased significantly from baseline after ischaemia ( p<0.002 ) . Mean FMD ( SEM ) before and after infusion were not , however , significantly different ( p=0.4 ) ( pre-saline 7.3 [1.0]% , post saline 5.2 [1.5]% and predextrose 8.1 [2.0]% , post dextrose 5.9 [1.7]% ) . CONCLUSIONS These data suggest that acute hyperglycaemia does not impair FMD in normal subjects Purpose Energy drinks are beverages containing vasoactive metabolites , usually a combination of caffeine , taurine , glucuronolactone and sugars . There are concerns about the safety of energy drinks with some countries banning their sales . We determined the acute effects of a popular energy drink , Red Bull , on cardiovascular and hemodynamic variables , cerebrovascular parameters and microvascular endothelial function . Methods Twenty-five young non-obese and healthy subjects attended two experimental sessions on separate days according to a r and omized crossover study design . During each session , primary measurements included beat-to-beat blood pressure measurements , impedance cardiography and transcranial Doppler measurements for at least 20 min baseline and for 2 h following the ingestion of either 355 mL of the energy drink or 355 mL of tap water ; the endothelial function test was performed before and two hours after either drink . Results Unlike the water control load , Red Bull consumption led to increases in both systolic and diastolic blood pressure ( p < 0.005 ) , associated with increased heart rate and cardiac output ( p < 0.05 ) , with no significant changes in total peripheral resistance and without diminished endothelial response to acetylcholine ; consequently , double product ( reflecting myocardial load ) was increased ( p < 0.005 ) . Red Bull consumption also led to increases in cerebrovascular resistance and breathing frequency ( p < 0.005 ) , as well as to decreases in cerebral blood flow velocity ( p < 0.005 ) and end-tidal carbon dioxide ( p < 0.005 ) . Conclusion Our results show an overall negative hemodynamic profile in response to ingestion of the energy drink Red Bull , in particular an elevated blood pressure and double product and a lower cerebral blood flow velocity Postpr and ial hyperglycemia induces oxidative stress responses , impairs vascular endothelial function ( VEF ) and increases the risk of cardiovascular disease . We hypothesized that the antioxidant and anti-inflammatory activities of a γ-tocopherol-rich mixture of tocopherols ( γ-TmT ) would protect against vascular dysfunction that is otherwise caused by postpr and ial hyperglycemia by decreasing oxidative stress and proinflammatory responses , and improving nitric oxide ( NO• ) homeostasis . In a r and omized , crossover study , healthy men ( n=15 ; 21.8 ± 0.8 years ) completed a fasting oral glucose challenge ( 75 g ) with or without prior supplementation of γ-TmT ( 5 days ) . Brachial artery flow-mediated dilation ( FMD ) , plasma glucose , insulin , antioxidants , malondialdehyde ( MDA ) , inflammatory proteins , arginine and asymmetric dimethylarginine ( ADMA ) were measured at regular intervals during a 3-h postpr and ial period . Supplementation of γ-TmT increased ( P<.05 ) plasma γ-T by threefold and γ-carboxyethyl-hydroxychroman by more than ninefold without affecting α-T , glucose , arginine or ADMA . Baseline FMD , MDA , arginine and ADMA were unaffected by γ-TmT ( P>.05 ) . Postpr and ial FMD decreased 30%-44 % ( P<.05 ) following glucose ingestion , but was maintained with γ-TmT. Supplementation of γ-TmT also attenuated postpr and ial increases in MDA that occurred following glucose ingestion . Plasma arginine decreased ( P<.05 ) in both trials to a similar extent regardless of γ-TmT supplementation . However , the ratio of ADMA/arginine increased time-dependently in both trials ( P<.05 ) , but to a lesser extent following γ-TmT supplementation ( P<.05 ) . Inflammatory proteins were unaffected by glucose ingestion or γ-TmT. Collectively , these findings support that short-term supplementation of γ-TmT maintains VEF during postpr and ial hyperglycemia possibly by attenuating lipid peroxidation and disruptions in NO• homeostasis , independent of inflammation An oral glucose challenge causes transient impairment of endothelial function , probably because of increased oxidative stress . During oxidative stress , endothelial nitric oxide ( NO ) synthase ( eNOS ) becomes uncoupled because of decreased bioavailability of tetrahydrobiopterin ( BH4 ) , an essential cofactor of eNOS . Therefore , we examined whether an acute supplement of BH4 could restore endothelial dysfunction induced by an oral glucose challenge .  Healthy subjects were examined in 53 experiments .  Forearm blood flow was measured by venous occlusion plethysmography . Dose-response studies were obtained during intra-arterial infusion of serotonin to elicit endothelium-dependent , NO-specific vasodilation and during sodium nitroprusside ( SNP ) infusion to elicit endothelium-independent vasodilation . Subjects were examined before ( fasting ) and 1 and 2 h after an oral glucose challenge ( 75 g ) with serotonin ( n = 10 ) and SNP ( n = 8) . On different days (6R)-5,6,7,8-tetrahydro-l-biopterin dihydrochloride ( 6R-BH4 ; n = 10 ) , the active cofactor of eNOS or its stereoisomer (6S)-5,6,7,8-tetrahydro-l-biopterin sulfate ( 6S-BH4 ; n = 10 ) , which is inactive as a cofactor , was added 10 min ( 500 microg/min ) before and during the 1-h postchallenge serotonin dose-response study . In vitro studies showed that 6R-BH4 and 6S-BH4 were equipotent antioxidants . Serotonin response was reduced by 24 + /- 7 % ( at the highest dose ) at 1 h postchallenge compared with fasting ( P = 0.001 ) and was restored 2 h postchallenge . The reduction was reversed by the administration of 6R-BH4 but not by 6S-BH4 . SNP responses were slightly increased 1 and 2 h postchallenge ( increased by 15 + /- 13 % at third dose 2 h postchallenge , P = 0.0001 ) . An oral glucose challenge causes transient , NO-specific , endothelial dysfunction , which may be reversed by BH4 . Transient postpr and ial endothelial dysfunction may be partly explained by reduced bioavailability of BH4 and NO Brachial artery vasoactivity ( BAVA ) is a reliable , noninvasive method of assessing endothelium-dependent vasodilatation ( EDV ) in vivo . Acute hyperglycemia , impaired glucose tolerance ( IGT ) , and diabetes mellitus impair EDV , a precursor to atherosclerosis . Thiamine is a coenzyme important in intracellular glucose metabolism . The purpose of this study was to evaluate the effect of thiamine on BAVA in the presence of hyperglycemia . Ten healthy subjects ( group H , mean age 27 years ) , 10 patients with impaired glucose tolerance by World Health Organization criteria ( group IGT , mean age 65 years ) , and 10 patients with non-insulin-dependent diabetes mellitus ( group NIDDM , mean age 50 years ) were studied .  Duplex ultrasound  was used to measure brachial artery flow changes in response to reactive hyperemia following brachial artery tourniquet occlusion for 5 min . This test was performed after a 10 hr fast and at 30 , 60 , and 120 min after a 75 g oral glucose challenge along with measurements of blood glucose level ( BGL ) . A week later , BAVA evaluation was repeated after administration of 100 mg of intravenous thiamine . BAVA ( % increased blood flow ) at peak and trough BGL was compared with and without thiamine . BAVA at peak glucose improved from 69.0 ± 6.4 % to 152.8 ± 22.9 % in group H ( p < 0.005 ) , from 57.6 ± 12.6 % to 139.7 ± 12.4 % in group IGT ( p < 0.005 ) , and from 57.8 ± 8.3 % to 167.8 ± 11.6 % in group NIDDM ( p < 0.005 ) following administration of thiamine . On the other h and , at trough glucose levels , BAVA remained essentially unchanged in group H ( prethiamine 83.8 ± 6.5 % vs. post-thiamine 83.8 ± 17.0 % , p > 0.05 ) as well as group IGT ( prethiamine 96.7 ± 8.5 % vs. post-thiamine 104.0 ± 17.4 % , p > 0.05 ) . BAVA at trough glucose was not measured in group NIDDM secondary to trough BGL > 140 mg/dL. EDV was improved by thiamine in the presence of hyperglycemia in healthy subjects and in patients with IGT and NIDDM . The mechanism by which thiamine  improves EDV is not due to a glucose-lowering effect as thiamine had no effect on EDV under normoglycemic conditions . Routine administration of thiamine might improve endothelial function and therefore slow the development and progression of atherosclerosis , especially in patients with IGT and NIDDM who are prone to develop accelerated atherosclerosis In perinatal psychiatry , r and omized controlled trials are often not feasible on ethical grounds . Many studies are observational in nature , while others employ large data bases not design ed primarily for research purpose s. Quality assessment of the result ing research is complicated by a lack of st and ardized tools specifically for this purpose . The aim of this paper is to describe the  Systematic Assessment of Quality in Observational Research ( SAQOR )  , a quality assessment tool our team devised for a series of systematic review s and meta‐analyses of evidence ‐based literature regarding risks and benefits of antidepressant medication during pregnancy . Copyright © 2011 John Wiley & Sons , Background Postpr and ial hyperglycemia is believed to affect vascular endothelial function . The aim of our study was to compare the effects of acarbose and nateglinide on postpr and ial endothelial dysfunction . Methods We recruited a total of 30 patients with newly diagnosed type 2 diabetes ( 19 men and 11 women , age 67.8 ± 7.3 years ) . Patients were r and omly assigned to 3 groups receiving either 300 mg/day acarbose , 270 mg/day nateglinide , or no medication . A cookie test ( consisting of 75 g carbohydrate , 25 g butter fat , and 7 g protein for a total of 553 kcal ) was performed as dietary tolerance testing . During the cookie test  , glucose and insulin levels were determined at 0 , 30 , 60 , and 120 min after load . In addition , endothelial function was assessed by % flow-mediated dilation ( FMD ) of the brachial artery at 0 and 120 min after cookie load . Results Postpr and ial gluc 
    Output:
    
Macrovascular endothelial function was inversely associated with age , blood pressure , and low-density lipoprotein cholesterol and was positively associated with the postocclusion interval of vascular assessment .
In healthy and diseased subjects , we found evidence for macrovascular but not microvascular endothelial dysfunction during acute hyperglycemia