Clemmensenkragh1679

Interventional treatments of aneurysms in the carotid artery are increasingly being supplemented with three-dimensional (3D) x-ray imaging. The 3D imaging provides additional information on device sizing and stent malapposition during the procedure. Standard 3D x-ray image acquisition is a one-size fits all model, exposing patients to additional radiation and results in images that may have cardiac-induced motion blur around the artery. Here, we investigate the potential of a novel dynamic imaging technique Adaptive CaRdiac cOne BEAm computed Tomography (ACROBEAT) to personalize image acquisition by adapting the gantry velocity and projection rate in real-time to changes in the patient's electrocardiogram (ECG) trace.

We compared the total number of projections acquired, estimated carotid artery widths and image quality between ACROBEAT and conventional (single rotation fixed gantry velocity and acquisition rate, no ECG-gating) scans in a simulation study and a proof-of-concept physical phantom experimento intracranial interventional procedures negatively affected by cardiac motion.

Asthmatic children on corticosteroids can develop hypothalamic-pituitary-adrenal axis suppression (HPAS). Single nucleotide polymorphisms (SNPs) rs242941 and rs1876828 of the corticotrophin-releasing hormone receptor 1 (CRHR1) gene were associated with lower stimulated cortisol (F) levels, whereas rs41423247 of the glucocorticoid receptor (NR3C1) gene was associated with higher basal F levels. The objective of the current study was to confirm whether these three SNPs are associated with HPAS in asthmatic children.

DNA was extracted from saliva obtained from 95 asthmatic children, who had previously undergone basal F and metyrapone testing. Thirty-six children were classified as suppressed. Non-suppressed children were subclassified according to their post-metyrapone adrenocorticotropin (PMTP ACTH) level into a middle (106-319pg/mL) and a high (>319pg/mL) ACTH response group. TaqMan

polymerase chain reaction assays were utilized.

Only rs41423247 was inversely associated with HPAS (OR=0.27 [95% CI 0.06-0.90]). Its GC genotype was inversely associated with HPAS (log odds=-1.28, P=.021). Chidamide √PMTP ACTH was associated with CC (effect size=10.85, P=.005) and GC genotypes (effect size=4.06, P=.023). The C allele is inherited as a dominant trait (effect size=-1.31 (95% CI -2.39--0.33; P=.012). In the high ACTH response group, both genotypes affected the PMTP ACTH (effect sizes 1.41 and 15.46; P-values .023 and <2×10

for GC and CC, respectively).

The C allele of rs41423247 was found to be protective against HPAS. CC genotype is associated with the highest PMTP ACTH response.

The C allele of rs41423247 was found to be protective against HPAS. CC genotype is associated with the highest PMTP ACTH response.

Children aged ≥ 6 to < 12 years with severe atopic dermatitis (AD) have limited treatment options. In a 16-week, randomized, placebo-controlled, phase III trial in children, dupilumab, a monoclonal antibody inhibiting interleukin (IL)-4/IL-13 signalling, significantly improved signs and symptoms with acceptable safety; longer-term safety and efficacy data are lacking.

To report the pharmacokinetic profile and long-term safety and efficacy of dupilumab in children (aged ≥ 6 to < 12 years) with severe AD.

Children (aged ≥ 6 to < 12 years) with severe AD were enrolled in a global, multicentre, phase IIa, open-label, ascending-dose, sequential cohort study and subsequent open-label extension (OLE) study. Patients received single-dose dupilumab 2 or 4 mg kg

followed by 8-week pharmacokinetic sampling, then 2 or 4 mg kg

weekly for 4 weeks (phase IIa), followed by the same weekly regimen (OLE). Primary endpoints were dupilumab concentration-time profile and treatment-emergent adverse events (TEAEs support the use of dupilumab as a continuous long-term treatment for children aged ≥ 6 to less then 12 years with severe AD.

To describe an anti-Strongyloides IgA, IgG and IgG immune complex antibody response profile in patients with pulmonary tuberculosis.

Saliva and serum samples were collected from 100 individuals group I, 50 apparently healthy individuals; and group II, 50 pulmonary tuberculosis patients. The IgA, IgG and IgG immune complex detection were carried out via an ELISA immunoenzymatic test. Optical density medians in saliva samples of IgA antibody (median of 7.21) and IgG-IC (median of 4.95) were significantly higher in tuberculosis group compared to control individuals (median IgA of 3.93 and IgG-IC of 2.38).

This study presents antibody data to the field of pulmonary tuberculosis and strongyloidiasis coinfection, including saliva samples, and especially IgG immune complex detection.

This study presents antibody data to the field of pulmonary tuberculosis and strongyloidiasis coinfection, including saliva samples, and especially IgG immune complex detection.Cypermethrin (CYP) is an important type II pyrethroid pesticide widely used to protect crops against pests and insect infestations. However, its toxicity is a risk to both human health and the surrounding environment. The present study was conducted to investigate the nephrotoxic effect and histopathological changes caused by Cypermethrin in the kidney tissues of adult Wistar rats. In this study, 30 Wistar rats were equally divided into three groups. G1, control animals; G2 and G3 treated with various sub lethal doses of CYP for 30 days as follows G2, administered low dose (1/100 of LD50) of CYP; G3, administered high dose (1/50 of LD50) of CYP. The damage to different organelles of renal proximal and distal cells was observed using transmission electron microscopy. Histopathological damage in kidney samples was confirmed using morphological and histological measures. The results showed that CYP caused significant histopathological damage to the renal proximal and distal tubules of treated rats. Compared to control samples, CYP caused marked alterations in the dimensions of nucleus, ovoid and filamentous mitochondria of the treated cells. In conclusion, Cypermethrin is found to be toxic to mammals. It caused marked ultrastructural damage to the renal proximal and distal tubules of Wistar rats and the intensity of nephrotoxicity correlated with the dose of oral administration.