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Green nail syndrome (GNS) is a paronychial infection mainly due to Pseudomonas aeruginosa, characterized by green discoloration of the nail plate. Although the diagnosis of GNS may be straightforward with its distinctive color change, the clinical management of the disease can be sometimes confusing, especially when the bacterial culture result is inconsistent. There is, however, a paucity of comprehensive reviews regarding the treatment of GNS in the actual clinical setting. In this retrospective review of 34 patients, we found that GNS mostly occurs on a single digit (79.4%) on the big toe or thumb (85.3%) with frequent concurrent fungal infection (67.6%). The prevalence of inconsistent bacterial culture result with no evidence of P. aeruginosa was unexpectedly high (n = 22, 64.7%), in which case coagulase-negative staphylococci were most frequently detected. The P. aeruginosa-negative group did not demonstrate any statistically significant differences compared with the P. aeruginosa-positive group, and it still responded well to the typical topical and/or oral fluoroquinolone treatment. GNS without the evidence of P. aeruginosa may be a more common occurrence than reported in the literature, and it can be managed successfully with the same strategy employed to treat P. aeruginosa-positive cases. It may result from the low detection rate of P. aeruginosa due to the limited sensitivity of the test, or inadequate amount and/or contamination of the sample, warranting close scrutiny by clinicians.Retinoblastoma is known as childhood rare malignancy of the retina. Ciliary neurotrophic factor (CNTF) was previously found to reduce degeneration and promote retina survival. This work investigated the effects of CNTF supplementation on in-vitro model cells including retinoblastoma (Y79) and adipose-derived mesenchymal stem cells (AMSCs) viability, proliferation, gene expression and cell cycle. A drop of viability was detected in Y79 treated with CNTF in a dose-dependent manner (P less then .05). However, the proliferation of AMSCs was increased at lower concentrations of CNTF (5 ng/mL), but declined in higher doses (50 and 100 ng/mL). The BrdU assay confirmed the MTT assay results. Cell cycle was arrested in both Y79 and AMSCs in the G0/G1 phase by CNTF treatment. A considerable down-regulation of Bcl2, CycD1 and N-Myc genes expression (P less then .05) inversely, P15 and P21 genes up-regulation in treated Y79 cells was observed. Besides, stemness genes' transcription was reduced in AMSCs (P less then .05), and levels of neuronal-specific markers such as neuron-specific enolase (NSE) and neuronal nuclei (NeuN) were increased (P less then .05). The findings of this study suggest a promising potential of CNTF in terms of arresting Y79 retinoblastoma cells, and differentiation-inducing to AMSCs, which could be valuable for managing future innovative treatments targeting retinoblastoma. SIGNIFICANCE OF THE STUDY We demonstrate that CNTF has the potential to reduce proliferation of Y79 cells and induce the cell cycle arrest of them. Also, down-regulation of oncogenes (such as N-Myc) while up-regulation of tumour suppressor genes (such as P21) was detected by exposure of Y79 cells to CNTF. Furthermore, we observed the cell cycle arrest, reduction of stemness gene and up-regulation of neural differentiation markers in AMSCs treated with CNTF. These results support the probable promising effects of CNTF for controlling retinoblastoma.Hidradenitis suppurativa (HS) is a chronic inflammatory skin condition that is clinically defined by lesions ranging from painful, deep seated nodules to abscesses, draining sinus tracts, and ultimately, irreversible fibrotic scars. While the etiology remains unclear, a number of mechanisms ranging from genetics to aberrations of the immune system have been proposed. In addition, HS has a number of associations and may occur in conjunction with several diseases that span a host of medical specialties. The estimated prevalence ranges are from 1% to 4%; however, a large degree of under-reporting and misdiagnosis of this condition likely underestimates its true clinical significance. The debilitating consequences of missed diagnoses or improper management leads to severe pain and irreversible cutaneous manifestations (i.e., fistulae, sinus tracts, disfiguring scarring). HS has been found to significantly impair patients' quality of life to a greater degree when compared with other skin conditions. Early recognition and treatment are critical for a favorable prognosis, and diagnostic delays may be related to variable presentations within numerous comorbidities. Here we provide an in-depth, clinical-based review of HS, highlighting the clinical presentation, pathophysiology, grading systems, epidemiology, and comorbidities, in hopes of shedding light on an often misunderstood disease and ultimately moving closer to a more conclusive understanding of its various presentations and association.Periodontal Ehlers-Danlos syndrome (pEDS) is a rare condition caused by pathogenic variants in the C1R and C1S genes, encoding subunits C1r and C1s of the first component of the classical complement pathway. It is characterized by early-onset periodontitis with premature tooth loss, pretibial hyperpigmentation and skin fragility. Rare arterial complications have been reported, but venous insufficiency is rarely described. PD173212 mouse Here we report 13 novel patients carrying heterozygous pathogenic variants in C1R and C1S including three novel C1S variants (c.962G > C, c.961 T > G and c.961 T > A). In addition to the pEDS phenotype, three patients and one relative displayed widespread venous insufficiency leading to persistent varicose leg ulcers. One patient suffered an intracranial aneurysm with familial vascular complications including thoracic and abdominal aortic aneurysm and dissection and intracranial aneurysm rupture. This work confirms that vascular complications can occur, although they are not frequent, which leads us to propose to carry out a first complete non-invasive vascular evaluation at the time of the diagnosis in pEDS patients. However, larger case series are needed to improve our understanding of the link between complement pathway activation and connective tissue alterations observed in these patients, and to better assess the frequency, type and consequences of the vascular complications.