nils-herrmann/clean_scirepeval huggingface dataset:
Synbiotic supplementation and the effects on clinical and metabolic responses in patients with rheumatoid arthritis: a randomised, double-blind, placebo-controlled trial.

Synbiotic intake may be associated with reduced inflammation in patients with rheumatoid arthritis (RA) due to optimised inflammatory markers, oxidative stress and insulin resistance. This research was conducted to assess the effects of synbiotic supplementation on the clinical and metabolic parameters of patients with RA. A total of fifty-four patients with RA were allocated into two groups to receive either a synbiotic capsule (n 27) or a placebo (n 27) for 8 weeks in this randomised, double-blind, placebo-controlled trial. Fasting blood samples were taken at baseline and week 8 of the study to quantify related markers. After the 8-week intervention, compared with the placebo, synbiotic supplementation resulted in a significant reduction in serum high-sensitivity C-reactive protein (hs-CRP) levels (-1427·8 (sd 3267·2) v. +2833·4 (sd 5639·7) ng/ml, P=0·001). In addition, compared with the placebo, synbiotic supplementation improved disease activity score-28 joints (DAS-28) (-1·6 (sd 0·8) v. -0·3 (sd 0·5), P<0·001) and visual analogue scales (VAS) pain (-30·4 (sd 18·7) v. -11·5 (sd 15·9), P<0·001). In addition, a significant elevation in plasma nitric oxide (NO) (+0·8 (sd 4·4) v. -2·6 (sd 4·5) µmol/l, P=0·008), and significant reductions in insulin values (-13·8 (sd 26·4) v. +4·2 (sd 28·2) pmol/l, P=0·01), homoeostasis model of assessment-estimated insulin resistance (HOMA-IR) (-0·5 (sd 1·0) v.+0·1 (sd 1·1), P=0·03) and homoeostatic model assessment-β-cell function (HOMA-B) (-9·4 (sd 17·9) v. +3·3 (sd 18·9), P=0·01) following supplementation with the synbiotic compared with the placebo. Compared with the placebo, synbiotic supplementation also resulted in a significant increase in plasma GSH (+36·6 (sd 63·5) v. -58·5 (sd 154·4) µmol/l, P=0·005). Overall, our study demonstrated that synbiotic supplementation for 8 weeks among patients with RA had beneficial effects on hs-CRP, DAS-28, VAS, NO, insulin levels, HOMA-IR, HOMA-B and GSH levels.
Clinical features and outcomes of gastric variceal bleeding: retrospective Korean multicenter data

While gastric variceal bleeding (GVB) is not as prevalent as esophageal variceal bleeding, it is reportedly more serious, with high failure rates of the initial hemostasis (>30%), and has a worse prognosis than esophageal variceal bleeding. However, there is limited information regarding hemostasis and the prognosis for GVB. The aim of this study was to determine retrospectively the clinical outcomes of GVB in a multicenter study in Korea.



The data of 1,308 episodes of GVB (males:females=1062:246, age=55.0±11.0 years, mean±SD) were collected from 24 referral hospital centers in South Korea between March 2003 and December 2008. The rates of initial hemostasis failure, rebleeding, and mortality within 5 days and 6 weeks of the index bleed were evaluated.



The initial hemostasis failed in 6.1% of the patients, and this was associated with the Child-Pugh score [odds ratio (OR)=1.619; P<0.001] and the treatment modality: endoscopic variceal ligation, endoscopic variceal obturation, and balloon-occluded retrograde transvenous obliteration vs. endoscopic sclerotherapy, transjugular intrahepatic portosystemic shunt, and balloon tamponade (OR=0.221, P<0.001). Rebleeding developed in 11.5% of the patients, and was significantly associated with Child-Pugh score (OR=1.159, P<0.001) and treatment modality (OR=0.619, P=0.026). The GVB-associated mortality was 10.3%; mortality in these cases was associated with Child-Pugh score (OR=1.795, P<0.001) and the treatment modality for the initial hemostasis (OR=0.467, P=0.001).



The clinical outcome for GVB was better for the present cohort than in previous reports. Initial hemostasis failure, rebleeding, and mortality due to GVB were universally associated with the severity of liver cirrhosis.
Acute administration of the cannabinoid CB1 antagonist rimonabant impairs positive affective memory in healthy volunteers

Emotional processing measures are sensitive to acute administration of clinically useful antidepressant drugs. We wished to test the hypothesis that these models would also be able to detect agents likely to cause depression as an adverse effect. The anti-obesity drug and cannabinoid type 1 receptor antagonist, rimonabant, is associated with significant rates of depression and anxiety in clinical use. Thirty healthy adult volunteers were randomly assigned to receive a single dose of rimonabant (20 mg) or lactose placebo in a double-blind, between-groups design. Three hours after medication administration, subjects undertook an emotional processing test battery including facial emotion recognition, emotional word attentional dot probe, self-relevant word classification, emotional and declarative memory and the emotion-potentiated acoustic startle response. Subjective state was assessed via self-report measures. A single dose of rimonabant did not alter subjective mood. However, rimonabant selectively reduced incidental recall of positive self-relevant adjectives, an effect contrary to that seen following the administration of antidepressants. There were no effects of rimonabant on the other measures of emotional processing. These results suggest that a single dose of rimonabant decreases positive emotional memory in the absence of changes in subjective state. Further studies are required to examine whether rimonabant might produce a wider range of negative emotional biases with repeated treatment.
Comparison of pharmacokinetics and systemic effects of inhaled fluticasone propionate in patients with asthma and healthy volunteers: a randomised crossover study

Inhaled corticosteroids are currently the cornerstone of asthma treatment. Some studies of high-dose fluticasone propionate in patients with no or mild asthma have, however, suggested substantial systemic absorption. We investigated the pharmacokinetics of fluticasone propionate in patients with asthma receiving appropriate doses for severity.



We did a double-blind, randomised, crossover study in 11 patients with asthma and 13 matched healthy controls (age 20-65 years; asthma patients forced expiratory volume in 1 s <75% and stable on high-dose inhaled corticosteroids). Patients received one 1000 microg intravenous dose or 1000 microg daily for 7 days inhaled (via spacer device) fluticasone propionate. In the 12 h after dosing, we monitored plasma fluticasone propionate and cortisol concentrations by mass spectrometry and competitive immunoassay with use of direct chemiluminescence. Analysis was by intention to treat.



After inhalation, geometric mean values were significantly lower in the asthma group than in controls for fluticasone propionate plasma area under curve (1082 [95% CI 850-1451] vs 2815 pg mL(-1) h(-1) [2262-3949], -62% difference [45-72]; p<0.001), maximum concentrations (117 [91-159] vs 383 pg/mL [302-546], -68% [-50 to -81]; p<0.001), and systemic bioavailability (10.1 [7.9-14.0] vs 21.4% [15.4-32.2], -54% [-27 to -70]; p=0.001). Intravenous-dose clearance, volume of distribution at steady state, plasma half-life, and mean residence time, were similar in the two groups. Less suppression of plasma cortisol concentrations was seen in the asthma group than in controls 4-12 h after inhaled fluticasone propionate.



Systemic availability of fluticasone propionate is substantially less in patients with moderate to severe asthma than in healthy controls. Inhaled corticosteroids that are absorbed through the lungs need to be assessed in patients who are receiving doses appropriate for disease severity, and not in normal volunteers.
Effects of lowering LDL cholesterol on progression of kidney disease.

Lowering LDL cholesterol reduces the risk of developing atherosclerotic events in CKD, but the effects of such treatment on progression of kidney disease remain uncertain. Here, 6245 participants with CKD (not on dialysis) were randomly assigned to simvastatin (20 mg) plus ezetimibe (10 mg) daily or matching placebo. The main prespecified renal outcome was ESRD (defined as the initiation of maintenance dialysis or kidney transplantation). During 4.8 years of follow-up, allocation to simvastatin plus ezetimibe resulted in an average LDL cholesterol difference (SEM) of 0.96 (0.02) mmol/L compared with placebo. There was a nonsignificant 3% reduction in the incidence of ESRD (1057 [33.9%] cases with simvastatin plus ezetimibe versus 1084 [34.6%] cases with placebo; rate ratio, 0.97; 95% confidence interval [95% CI], 0.89 to 1.05; P=0.41). Similarly, allocation to simvastatin plus ezetimibe had no significant effect on the prespecified tertiary outcomes of ESRD or death (1477 [47.4%] events with treatment versus 1513 [48.3%] events with placebo; rate ratio, 0.97; 95% CI, 0.90 to 1.04; P=0.34) or ESRD or doubling of baseline creatinine (1189 [38.2%] events with treatment versus 1257 [40.2%] events with placebo; rate ratio, 0.93; 95% CI, 0.86 to 1.01; P=0.09). Exploratory analyses also showed no significant effect on the rate of change in eGFR. Lowering LDL cholesterol by 1 mmol/L did not slow kidney disease progression within 5 years in a wide range of patients with CKD.
A prospective, randomized clinical trial to compare the effect of hyperbaric to normobaric hyperoxia on cerebral metabolism, intracranial pressure, and oxygen toxicity in severe traumatic brain injury.

OBJECT
Oxygen delivered in supraphysiological amounts is currently under investigation as a therapy for severe traumatic brain injury (TBI). Hyperoxia can be delivered to the brain under normobaric as well as hyperbaric conditions. In this study the authors directly compare hyperbaric oxygen (HBO2) and normobaric hyperoxia (NBH) treatment effects.



Sixty-nine patients who had sustained severe TBIs (mean Glasgow Coma Scale Score 5.8) were prospectively randomized to 1 of 3 groups within 24 hours of injury: 1) HBO2, 60 minutes of HBO(2) at 1.5 ATA; 2) NBH, 3 hours of 100% fraction of inspired oxygen at 1 ATA; and 3) control, standard care. Treatments occurred once every 24 hours for 3 consecutive days. Brain tissue PO(2), microdialysis, and intracranial pressure were continuously monitored. Cerebral blood flow (CBF), arteriovenous differences in oxygen, cerebral metabolic rate of oxygen (CMRO2), CSF lactate and F2-isoprostane concentrations, and bronchial alveolar lavage (BAL) fluid interleukin (IL)-8 and IL-6 assays were obtained pretreatment and 1 and 6 hours posttreatment. Mixed-effects linear modeling was used to statistically test differences among the treatment arms as well as changes from pretreatment to posttreatment.



In comparison with values in the control group, the brain tissue PO2 levels were significantly increased during treatment in both the HBO2 (mean +/- SEM, 223 +/- 29 mm Hg) and NBH (86 +/- 12 mm Hg) groups (p < 0.0001) and following HBO2 until the next treatment session (p = 0.003). Hyperbaric O2 significantly increased CBF and CMRO2 for 6 hours (p < or = 0.01). Cerebrospinal fluid lactate concentrations decreased posttreatment in both the HBO2 and NBH groups (p < 0.05). The dialysate lactate levels in patients who had received HBO2 decreased for 5 hours posttreatment (p = 0.017). Microdialysis lactate/pyruvate (L/P) ratios were significantly decreased posttreatment in both HBO2 and NBH groups (p < 0.05). Cerebral blood flow, CMRO2, microdialysate lactate, and the L/P ratio had significantly greater improvement when a brain tissue PO2 > or = 200 mm Hg was achieved during treatment (p < 0.01). Intracranial pressure was significantly lower after HBO2 until the next treatment session (p < 0.001) in comparison with levels in the control group. The treatment effect persisted over all 3 days. No increase was seen in the CSF F2-isoprostane levels, microdialysate glycerol, and BAL inflammatory markers, which were used to monitor potential O2 toxicity.



Hyperbaric O2 has a more robust posttreatment effect than NBH on oxidative cerebral metabolism related to its ability to produce a brain tissue PO2 > or = 200 mm Hg. However, it appears that O2 treatment for severe TBI is not an all or nothing phenomenon but represents a graduated effect. No signs of pulmonary or cerebral O2 toxicity were present.
Effects of tegaserod and erythromycin in upper gut dysmotility: a comparative study.

Tegaserod may enhance upper gut transit, but, its prokinetic effects on antral/small bowel motility and how this compares with erythromycin is unknown. We prospectively assessed and compared the effects of tegaserod and erythromycin on upper gut motility.



In an open label, non-crossover study, 22 patients (M/; mean age=37 years) with symptoms of upper gut dysmotility underwent 24-hour ambulatory antroduodenojejunal manometry with a six-sensor solid state probe. The effects of 12 mg oral tegaserod were compared with 125 mg intravenous erythromycin by quantifying pressure wave activity and assessing motor patterns.



Motor activity increased (p<0.05) in antrum, duodenum and jejunum with both drugs when compared to baseline period. The motor response with tegaserod was higher (p<0.05) in jejunum and occurred during the second or third hours, whereas with erythromycin, it was higher (p<0.05) in antrum and occurred within 30 minutes. After tegaserod, a 'fed-response' like pattern was seen whereas after erythromycin, large amplitude (>100 mmHg) antral contractions at 3 cycles per minute were seen. Following tegaserod and erythromycin, phase III MMCs occurred in 12 (55%) and 8 (36%) patients respectively (p>0.05).



Both drugs increase upper gut motility and induce MMC's, but exert a differential response. Tegaserod produces a more sustained prokinetic effect in the duodenum/jejunum, whereas erythromycin predominantly increases antral motor activity.
Long-term lipid effects of pioglitazone by baseline anti-hyperglycemia medication therapy and statin use from the PROactive experience (PROactive 14).

Studies have shown that pioglitazone treatment in patients with type 2 diabetes mellitus can improve parameters of diabetic dyslipidemia. The aim of this study was to examine the effect of pioglitazone on triglycerides, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol levels in patients from the Prospective Pioglitazone Clinical Trial in Macrovascular Events (PROactive) to determine whether pioglitazone-induced lipid effects were altered by different baseline antihyperglycemia medication or statin use. PROactive was a long-term, randomized, double-blind, cardiovascular outcomes study in patients with type 2 diabetes at high cardiovascular risk who had pioglitazone or placebo added to existing treatment. The present post hoc study analyzed lipid results from patients who received different baseline antihyperglycemia regimens and the presence or absence of baseline statin use. Independent of antihyperglycemia medication and statin use, triglyceride levels decreased in all subgroups treated with pioglitazone (-9.9% to -12.3%), whereas little change was observed in placebo groups. High-density lipoprotein cholesterol increased nearly twice as much with pioglitazone (18.1% to 20.3%) as with placebo (8.1% to 11.8%) across all subgroups. Low-density lipoprotein cholesterol increased moderately with pioglitazone (5.2% to 9.6%) compared with placebo (3.3% to 7.6%) (placebo-adjusted range 1.11% to 4.37%). In conclusion, long-term pioglitazone therapy led to durable improvements in triglyceride and high-density lipoprotein cholesterol levels, irrespective of baseline antihyperglycemia therapy or statin use.
Influences of spinal anesthesia on exercise tolerance in patients with chronic obstructive pulmonary disease.

Lower limb muscle dysfunction contributes to exercise intolerance in chronic obstructive pulmonary disease (COPD). We hypothesized that signaling from lower limb muscle group III/IV sensory afferents to the central motor command could be involved in premature cycling exercise termination in COPD.



To evaluate the effects of spinal anesthesia, which presumably inhibited central feedback from the lower limb muscle group III/IV sensory afferents on exercise tolerance and cardiorespiratory response during constant work-rate cycling exercise in patients with COPD.



In a crossover and double-blind randomized design, eight patients with COPD (FEV(1), 67 ± 8% predicted) completed a constant work-rate cycling exercise after sham (NaCl, interspinous L(3)-L(4)) or active (fentanyl 25 μg, intrathecal L(3)-L(4)) spinal anesthesia.



When compared with placebo, endurance time was significantly prolonged after spinal anesthesia with fentanyl (639 ± 87 s vs. 423 ± 38 s [mean ± SEM]; P = 0.01). Ventilation and respiratory rate were reduced at isotime points under the fentanyl condition, whereas ventilatory efficiency and dead space ventilation were improved. Patients exhibited less dynamic hyperinflation at isotime points with spinal anesthesia. Consequently, the rise in dyspnea was significantly flatter during the fentanyl condition than with placebo.



Spinal anesthesia enhanced cycling exercise tolerance in patients with COPD, mostly by reducing ventilatory response and dyspnea during exercise; these effects were possibly mediated through the inhibition of group III/IV lower limb sensory muscle afferents.
Efficacy of gait training using a treadmill with and without visual biofeedback in patients after stroke: A randomized study.

To evaluate the effects of gait training using a treadmill with and without visual biofeedback in patients in the late period after stroke, and to compare both training methods.



A randomized, controlled study.



Fifty people at least 6 months after stroke, randomly enrolled into groups with a rehabilitation programme of treadmill training with or without visual biofeedback.



Spatio-temporal gait parameters, walking speed, walking distance, self-reliant mobility and functional capacity were evaluated during a programme of 10 sessions over 2 weeks.



Patients in both groups achieved statistically significant improvement. Participants in the intervention group revealed a significantly greater improvement in the shortening of the stance phase (p = 0.0045) and lengthening of the swing phase of the unaffected limb (p = 0.0042) and an increase in the unaffected limb cycle length (p = 0.0021). There were no significant differences between groups in other spatio-temporal parameters of gait or additionally assessed parameters.



Gait training using a treadmill resulted in improvements in the gait and functional capacity of patients. The use of biofeedback gives better results in improving gait cycle length, duration of gait phases and swing phase speed compared with exercise on a treadmill alone.
Interferon treatment of chronic hepatitis C in patients with hemophilia or von Willebrand's disease in Japan

Seven patients with chronic hepatitis C, six hemophiliacs and a patient with von Willebrand's disease, were treated with interferon-alpha (IFN-alpha). Either 9 MU of recombinant IFN-alpha 2a or 3 MU of lymphoblastoid alpha-IFN was administered daily for 2 weeks and then three times a week for 22 weeks. Liver histology, hepatitis C virus (HCV) genotypes, and HCV-RNA levels in sera were investigated in all of the patients before IFN therapy was instituted. Liver histology was classified by the European classification. HCV genotyping conformed to the so-called Okamoto's classification. HCV-RNA levels in sera were quantitated by competitive polymerase chain reaction, using mutant RNA. Liver histology, HCV genotype, and serum HCV-RNA level (copies/ml) in each patient were: patient 1, chronic persistent hepatitis, type II, 3×103 respectively; patient 2, chronic active hepatitis (CAH) 2a, type III, 6×104; patient 3, CAH2a, type IV, 2×105; patient 4, CAH2b, type I, 2×107; patient 5, CAH2b, type II, 8×104; patient 6, CAH2b, type III, 7×106; and patient 7, CAH2b, type IV, 1×107. Sustained elimination of HCV was achieved in patient 3 and temporary elimination was achieved in patients 1 and 2. The other patients showed persistent HCV-RNA positivity in sera both during and after IFN treatment. Poor responsiveness to IFN was observed in patients with relatively progressive liver histology and high levels of HCV viremia.
Ketogenic diet treatment in adults with refractory epilepsy: A prospective pilot study

To assess the efficacy of ketogenic diet (KD) in adults with refractory epilepsy.



Eligible subjects were 18-45 years old with at least two monthly focal seizures (with or without secondary generalization) documented by 8 weeks' follow-up. Classic form of KD treatment (90% fat) was planned for 12 weeks: daily seizure diaries were kept and measurements of the urinary ketones were recorded. Blood studies were done monthly and resting energy expenditure (REE), substrate utilization; body composition and quality of life (QOL) were measured before and after intervention.



Nine patients were enrolled (average age 28+/-6 years; seven women). Only two subjects concluded the study per protocol due to an early drop-out. The average length of KD treatment was 8+/-4 weeks (two patients completed 12 weeks of KD; feelings of hunger and lack of efficacy resulted in withdrawal of the rest). The two patients who concluded the study had a more than 50% reduction in the frequency of the seizures. The others experienced no improvement. Adherence to the KD protocol (100%) was documented by constant ketonuria and increased fat utilization as indicated by the change in respiratory quotient (p<0.031). The KD increased the cholesterol levels (mainly LDL; p=0.0001).



In our experience with relatively small adult population, adherence to KD is difficult. In patients who had compliance over 3 weeks (6/8), KD does not seem to have a significant effect. Yet, the significant reduction in the two patients who concluded the study per protocol may indicate that some patients may benefit from this diet. Significant increase in LDL levels and the unlikable dietary changes are additional impediments to its implementation among adults with refractory epilepsy.