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Objective

The aim of the study was to evaluate the loss of truncal rotation over 54 hours after removing Chêneau brace.

Methods

The studied groups consisted of 39 girls aged 10–18 years old, diagnosed with adolescent idiopathic scoliosis (AIS) and treated with Chêneau brace (CAST) and 20 AIS girls aged 10–18 years old, not treated with bracing. Posterior-anterior radiographs were obtained from the clinical assessment of all subjects and were subsequently used to determine Cobb angles. The measurements of the angle of trunk rotation (ATR) were taken with the Scoliometer® and back-contour device during Adams forward bending test by the two evaluators. The changes in ATRs during 54 hours of observation were performed after the brace had been taken off (0, 2, 24, 30, 48 and 54 hours after debracing). This was described using VATR variable, defined as the change in the absolute Scoliometer® readings in the time intervals against the time interval Δt between the measurements. During back-contour assessment the differential factor (kra) has been used for the digital analysis. The changes in kra over 54 hours of observation were expressed as Vkra factor, defined as the difference in the absolute value of the amplitude differential factor (kra) in the time intervals against the time interval Δt between the measurements.

Results

The highest changes were observed in the thoracic as well as in lumbar spine in patients with Cobb angle ≥30°, axial rotation of the apical vertebrae within 5–15°, Risser sign 0–2. The biggest change in the trunk rotation after Chêneau brace had been taken off was noted within the first two hours of observation.

Conclusion

The patients should be advised to take the brace off for a minimum of two hours before the scheduled x-ray, to allow full relaxation of the trunk in order to obtain reliable radiological images of the deformation.

Level of Evidence

Level III Therapeutic study.  相似文献   
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Increasing evidence suggests that human epidermal melanocytes play an important role in the skin immune system; however, a role of their pigmentation in immune and inflammatory responses is poorly examined. In the study, the expression of Toll‐like receptor 4 (TLR4) and inflammatory cytokines and chemokines by cultured normal melanocytes derived from lightly and darkly pigmented skin was investigated after cell stimulation with lipopolysaccharide (LPS). The basal TLR4 mRNA level in heavily pigmented cells was higher as compared to their lightly pigmented counterparts. Melanocyte exposure to LPS upregulated the expression of TLR4 mRNA and enhanced the DNA‐binding activity of NF‐κB p50 and p65. We found substantial differences in the LPS‐stimulated expression of numerous genes encoding inflammatory cytokines and chemokines between the cells with various melanin contents. In lightly pigmented melanocytes, the most significantly upregulated genes were nicotinamide phosphoribosyltransferase (NAMPT/visfatin), the chemokines CCL2 and CCL20, and IL6, while the genes for CXCL12, IL‐16 and the chemokine receptor CCR4 were the most significantly upregulated in heavily pigmented cells. Moreover, the lightly pigmented melanocytes secreted much more NAMPT, CCL2 and IL‐6. The results of our study suggest modulatory effect of melanogenesis on the immune properties of normal epidermal melanocytes.  相似文献   
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Background

Rosacea is a chronic inflammatory skin condition whose etiology has been linked to mast cells and the antimicrobial peptide cathelicidin LL-37. Individuals with refractory disease have demonstrated clinical benefit with periodic injections of onabotulinum toxin, but the mechanism of action is unknown.

Objectives

To investigate the molecular mechanism by which botulinum toxin improves rosacea lesions.

Methods

Primary human and murine mast cells were pretreated with onabotulinum toxin A or B or control. Mast cell degranulation was evaluated by β-hexosaminidase activity. Expression of botulinum toxin receptor Sv2 was measured by qPCR. The presence of SNAP-25 and VAMP2 was established by immunofluorescence. In vivo rosacea model was established by intradermally injecting LL-37 with or without onabotulinum toxin A pretreatment. Mast cell degranulation was assessed in vivo by histologic counts. Rosacea biomarkers were analyzed by qPCR of mouse skin sections.

Results

Onabotulinum toxin A and B inhibited compound 48/80-induced degranulation of both human and murine mast cells. Expression of Sv2 was established in mouse mast cells. Onabotulinum toxin A and B increased cleaved SNAP-25 and decreased VAMP2 staining in mast cells respectively. In mice, injection of onabotulinum toxin A significantly reduced LL-37-induced skin erythema, mast cell degranulation, and mRNA expression of rosacea biomarkers.

Conclusions

These findings suggest that onabotulinum toxin reduces rosacea-associated skin inflammation by directly inhibiting mast cell degranulation. Periodic applications of onabotulinum toxin may be an effective therapy for refractory rosacea and deserves further study.  相似文献   
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