231 research outputs found

    Comparison of Combination Posterior Sub-Tenon Triamcinolone and Modified Grid Laser Treatment with Intravitreal Triamcinolone Treatment in Patients with Diffuse Diabetic Macular Edema

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    PURPOSE: To compare the efficacy of posterior sub-Tenon's capsule triamcinolone acetonide injection combined with modified grid macular photocoagulation (PSTI + MP) with intravitreal triamcinolone acetonide (IVTA) injection in the treatment of diffuse diabetic macular edema (DME). MATERIALS AND METHODS: Forty eyes of 33 patients with diffuse DME were randomly allocated into either PSTI + MP (20 eyes) or IVTA (20 eyes). Best corrected visual acuity (VA) and foveal thickness were measured. RESULTS: The ETDRS scores at baseline were 25.2 +/- 13.6 (mean +/- SD) letters in the PSTI + MP group, whereas 21.7 +/- 16.3 letters in the IVTA group. The ETDRS scores improved by 33.2 +/- 15.9, 34.7 +/- 16.6 and 30.9 +/- 19.0 letters in the PSTI + MP group whereas by 30.9 +/- 15.4, 30.1 +/- 17.9 and 31.5 +/- 15.0 letters in the IVTA group at 1, 3, and 6 months after the treatments, respectively. The VA improved significantly at 1 month and 3 months after both treatments (all p 0.05, Student's t-test). The foveal thicknesses at baseline and 1, 3, and 6 months after the treatments were 382.8 +/- 148.3, 309.1 +/- 131.3, 319.3 +/- 93.3, 340.4 +/- 123.5 microm (mean +/- SD) in the PSTI + MP group vs. 369.1 +/- 123.1, 241.4 +/- 52.3, 277.5 +/- 137.4, 290.2 +/- 127.9microm in the IVTA group, respectively. Pairwise comparisons revealed significant decrease in foveal thickness at 1 month (p = 0.01, paired t-test) for the PSTI + MP group, and at both 1 month (p 0.05, Student's t-test). In contrast to the PSTI + MP group, where no complications were noted, the elevation of intra-ocular pressure in 3 of 20 eyes (15%) and a significant increase in average cataract grading were observed in the IVTA group. CONCLUSION: PSTI + MP treatment provides significant improvement of vision in patients with diffuse DME over 3 months, and achieves outcomes comparable to those after IVTA treatment, however, with fewer complications.ope

    The perception of quinine taste intensity is associated with common genetic variants in a bitter receptor cluster on chromosome 12

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    The perceived taste intensities of quinine HCl, caffeine, sucrose octaacetate (SOA) and propylthiouracil (PROP) solutions were examined in 1457 twins and their siblings. Previous heritability modeling of these bitter stimuli indicated a common genetic factor for quinine, caffeine and SOA (22–28%), as well as separate specific genetic factors for PROP (72%) and quinine (15%). To identify the genes involved, we performed a genome-wide association study with the same sample as the modeling analysis, genotyped for approximately 610 000 single-nucleotide polymorphisms (SNPs). For caffeine and SOA, no SNP association reached a genome-wide statistical criterion. For PROP, the peak association was within TAS2R38 (rs713598, A49P, P = 1.6 × 10−104), which accounted for 45.9% of the trait variance. For quinine, the peak association was centered in a region that contains bitter receptor as well as salivary protein genes and explained 5.8% of the trait variance (TAS2R19, rs10772420, R299C, P = 1.8 × 10−15). We confirmed this association in a replication sample of twins of similar ancestry (P = 0.00001). The specific genetic factor for the perceived intensity of PROP was identified as the gene previously implicated in this trait (TAS2R38). For quinine, one or more bitter receptor or salivary proline-rich protein genes on chromosome 12 have alleles which affect its perception but tight linkage among very similar genes precludes the identification of a single causal genetic variant

    Pediatric endurance and limb strengthening for children with cerebral palsy (PEDALS) – a randomized controlled trial protocol for a stationary cycling intervention

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    BACKGROUND: In the past, effortful exercises were considered inappropriate for children with spastic cerebral palsy (CP) due to concern that they would escalate abnormalities including spasticity and abnormal movement patterns. Current scientific evidence indicates that these concerns were unfounded and that therapeutic interventions focused on muscle strengthening can lead to improved functional ability. However, few studies have examined the potential benefits of cardiorespiratory fitness exercises in this patient population. METHODS/DESIGN: The rationale and design of a randomized controlled trial examining the effects of a stationary cycling intervention for children with CP are outlined here. Sixty children with spastic diplegic CP between the ages of 7 and 18 years and Gross Motor Function Classification System (GMFCS) levels of I, II, or III will be recruited for this study. Participants will be randomly assigned to either an intervention (cycling) or a control (no cycling) group. The cycling intervention will be divided into strengthening and cardiorespiratory endurance exercise phases. During the strengthening phase, the resistance to lower extremity cycling will be progressively increased using a uniquely designed limb-loaded mechanism. The cardiorespiratory endurance phase will focus on increasing the intensity and duration of cycling. Children will be encouraged to exercise within a target heart rate (HR) range (70 – 80% maximum HR). Thirty sessions will take place over a 10–12 week period. All children will be evaluated before (baseline) and after (follow-up) the intervention period. Primary outcome measures are: knee joint extensor and flexor moments, or torque; the Gross Motor Function Measure (GMFM); the 600 Yard Walk-Run test and the Thirty-Second Walk test (30 sec WT). DISCUSSION: This paper presents the rationale, design and protocol for Pediatric Endurance and Limb Strengthening (PEDALS); a Phase I randomized controlled trial evaluating the efficacy of a stationary cycling intervention for children with spastic diplegic cerebral palsy

    Actos Now for the prevention of diabetes (ACT NOW) study

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    Abstract Background Impaired glucose tolerance (IGT) is a prediabetic state. If IGT can be prevented from progressing to overt diabetes, hyperglycemia-related complications can be avoided. The purpose of the present study was to examine whether pioglitazone (ACTOS®) can prevent progression of IGT to type 2 diabetes mellitus (T2DM) in a prospective randomized, double blind, placebo controlled trial. Methods/Design 602 IGT subjects were identified with OGTT (2-hour plasma glucose = 140–199 mg/dl). In addition, IGT subjects were required to have FPG = 95–125 mg/dl and at least one other high risk characteristic. Prior to randomization all subjects had measurement of ankle-arm blood pressure, systolic/diastolic blood pressure, HbA1C, lipid profile and a subset had frequently sampled intravenous glucose tolerance test (FSIVGTT), DEXA, and ultrasound determination of carotid intima-media thickness (IMT). Following this, subjects were randomized to receive pioglitazone (45 mg/day) or placebo, and returned every 2–3 months for FPG determination and annually for OGTT. Repeat carotid IMT measurement was performed at 18 months and study end. Recruitment took place over 24 months, and subjects were followed for an additional 24 months. At study end (48 months) or at time of diagnosis of diabetes the OGTT, FSIVGTT, DEXA, carotid IMT, and all other measurements were repeated. Primary endpoint is conversion of IGT to T2DM based upon FPG ≥ 126 or 2-hour PG ≥ 200 mg/dl. Secondary endpoints include whether pioglitazone can: (i) improve glycemic control (ii) enhance insulin sensitivity, (iii) augment beta cell function, (iv) improve risk factors for cardiovascular disease, (v) cause regression/slow progression of carotid IMT, (vi) revert newly diagnosed diabetes to normal glucose tolerance. Conclusion ACT NOW is designed to determine if pioglitazone can prevent/delay progression to diabetes in high risk IGT subjects, and to define the mechanisms (improved insulin sensitivity and/or enhanced beta cell function) via which pioglitazone exerts its beneficial effect on glucose metabolism to prevent/delay onset of T2DM. Trial Registration clinical trials.gov identifier: NCT0022096
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