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Lichen planus pigmentosus is a variant of lichen planus that is particularly difficult to treat. The aim of this study was to evaluate the efficacy and safety of tranexamic acid in lichen planus pigmentosus.

This prospective study, conducted at the University Hospital of Casablanca from August 2017 to June 2019, included 20 patients with histologically confirmed lichen planus pigmentosus. The exclusion criteria were pregnancy, breastfeeding, known hypersensitivity to tranexamic acid, and thromboembolic disease. Evaluation was carried out by means of clinical examination and measurement of the affected area using the Visioface® RD hardware package at 6 and 12 months (M6 and M12).

Eighteen women and 2 men with an average age of 49 years (range 26-65 years) were included. All patients were phototype 3 or 4. The average disease duration was 2.9 years (range 2 months-15 years). Pigmented, slate-grey, well-delineated macules were observed in all patients on the face (n=19), neck (n=14) or arms (n=2). Pruritus was present in 9 patients. All patients received oral tranexamic acid 250mg/d for 4 to 6 months with external photoprotection that was prolonged beyond 6 months. At M6, partial improvement was noted in 10 patients, 3 patients showed no improvement, and 7 patients were lost to follow-up. Pruritus disappeared in all patients and no relapse was seen at M12.

Our study suggests that tranexamic acid could be an effective treatment for lichen planus pigmentosus with a good safety profile. However, the limitations of the study are the limited population and the high number of patients lost to follow-up at M6. Larger-scale studies are needed to provide more detailed results.

Our study suggests that tranexamic acid could be an effective treatment for lichen planus pigmentosus with a good safety profile. However, the limitations of the study are the limited population and the high number of patients lost to follow-up at M6. Larger-scale studies are needed to provide more detailed results.Surfactant treatment for neonatal respiratory distress syndrome has dramatically improved survival of preterm infants. However, this has resulted in a markedly increased incidence of sequelae such as neonatal chronic inflammatory lung disease. The current surfactant preparations in clinical use lack the natural lung defence proteins surfactant proteins (SP)-A and D. These are known to have anti-inflammatory and anti-infective properties essential for maintaining healthy non-inflamed lungs. Supplementation of currently available animal derived surfactant therapeutics with these anti-inflammatory proteins in the first few days of life could prevent the development of inflammatory lung disease in premature babies. However, current systems for production of recombinant versions of SP-A and SP-D require a complex solubilisation and refolding protocol limiting expression at scale for drug development. Using a novel solubility tag, we describe the expression and purification of recombinant fragments of human (rfh) SP-A and SP-D using Escherichia coli without the need for refolding. We obtained a mean (± SD) of 23.3 (± 5.4) mg and 86 mg (± 3.5) per litre yield of rfhSP-A and rfhSP-D, respectively. rfhSP-D was trimeric and 68% bound to a ManNAc-affinity column, giving a final yield of 57.5 mg/litre of highly pure protein, substantially higher than the 3.3 mg/litre obtained through the standard refolding protocol. Further optimisation of this novel lab based method could potentially make rfhSP-A and rfhSP-D production more commercially feasible to enable development of novel therapeutics for the treatment of lung infection and inflammation.Neural cell adhesion molecule 1 (NCAM1/CD56) is expressed on immune cells, myoblasts, and malignant cells, and there is a growing demand for the genetic detection of CD56 and CD56-targeted therapy. In the present study, we developed a novel peptide ligand (designated Natein) that binds to human CD56 by using T7 phage display technology. Natein recognized the extracellular region of CD56 and could bind to natural killer (NK) cells and CD56-positive (CD56+) cancer cells. CD56+ cells enriched from human peripheral blood mononuclear cells (PBMCs) using biotinylated Natein-conjugated microbeads, similarly to CD56 antibody-isolated cells, demonstrated functional cytotoxicity against K562 cells. In addition, Natein could be used to stain CD56+ lymphoma cells in nasal-type extranodal NK/T-cell lymphoma tissues similarly to a CD56 antibody. These findings suggest that Natein has the potential to be alternative to CD56 antibody that could be used for peptide-based cell isolation and diagnosis.This study aimed to evaluate IL-17A (interleukin 17A) and IL-17RA (IL-17A receptor) in a pediatric population that died with non-pandemic acute viral pneumonia compared to the non-viral pneumonia group. Necropsy lung samples (n = 193) from children that died after severe acute infection pneumonia were selected and processed for viral antigen detection by immunohistochemistry. After this, they were separated into two groups virus-positive (n = 68) and virus-negative lung samples (n = 125). https://www.selleckchem.com/products/ctpi-2.html Immunohistochemistry was performed to assess the presence of IL-17A and IL-17RA in the lung tissue. The virus-positive group showed stronger immunolabeling for IL-17A and IL-17RA (p = 0.020 and p less then 0.001, respectively). The result of this study may suggest that IL-17A and IL-17RA plays an essential role in the maintenance of viral infection and lung injuries. These aspects may increase the severity of the inflammatory response leading to lethal lung injuries in these patients. Children with community-acquired non-pandemic pneumonia that requiring hospitalization could benefit from using IL-17RA/IL-17A monoclonal antibodies to block their injurious effects.Kawasaki disease (KD) has been declared a rare idiopathic condition for a long time. The children age less than five years, as the most susceptible group, are at risk of this disease. Since the cause of the disease is unknown, this study was designed to investigate the cause of KD. We applied metaDE and WGCNA packages in order to perform a meta-analysis and identify network modules of co-expressed genes, respectively, on three expression array datasets and also CEMiTool package to confirm detected modules by WGCNA. Using the Pearson correlation coefficient, the resemblance of KD to other symptomatic-similar diseases, including bacterial infections, viral infections, JIA (juvenile idiopathic arthritis), HSP (Henoch-Schönlein purpura), GAS (group A streptococcal), and HAdV (adenovirus) was accurately estimated. In addition to validation by more three expression array datasets, serum samples of 16 patients and eight control participants have undergone the Real-Time PCR assay so as to evaluate produced bioinformatic results.

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