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This cross-sectional multicenter study aimed to evaluate serum CXCL-10, as an activity marker for vitiligo, and compare it with other putative serum and tissue markers. Serum CXCL-10 was compared to interferon gamma (IFN-γ), interleukin 6 (IL-6), and IL-17 using ELISA in 55 non-segmental vitiligo patients (30 active and 25 stable) and 30 healthy controls. Marginal skin biopsy was taken for immunohistochemical evaluation of CD8+T cells and CXCL-10+ve cells. Serum levels of CXCL-10, IL-17, and IL-6 were elevated in all vitiligo patients compared to controls (p < .05). All investigated serum markers were higher in active versus stable vitiligo. Tissue expression of CXCL-10+ve cells and CD8+ve T cells was stronger in vitiligo patients compared to controls, and tissue CXCL-10+ve cell expression was stronger in active versus stable cases. Positive correlations were noted between the different serum and tissue markers. CXCL-10 was the most specific, whereas IL-6 was the most sensitive serum marker to distinguish active from stable disease.

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Telocytes have been identified as a distinctive type of interstitial cells and have been recognized in most tissues and organs. Telocytes are characterized by having extraordinary long cytoplasmic processes, telopodes, that extend to form three-dimensional networks and commonly constitute specialized forms of cell-to-cell junctions with other neighboring cells. Telocytes have been localized in the stem cell niche of different organs such as the heart, lung, skeletal muscle, and skin. Electron microscopy and electron tomography revealed a specialized link between telocytes and stem cells that postulates a potential role for telocytes during tissue regeneration and repair. In this review, the distribution of telocytes in different stem cell niches will be explored, highlighting the intimate relationship between the two types of cells and their possible functional relationship.

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Melanocyte loss is the main feature of vitiligo, but evidence refers to pathological multiplayers. Transmission electron microscopy was utilized to further explore vitiligo before and after narrow-band ultraviolet B (NB-UVB) therapy. Skin biopsies were retrieved from lesional and perilesional skin and compared to normal control skin. Sections were examined for melanocytes and keratinocytes and the number of melanosomes and thickness of basal lamina were measured. In lesional skin, keratinocytes revealed two types of degeneration with a significant increase in the mean thickness of basal lamina and decrease in the number of melanosomes. After treatment, lesional and perilesional skin showed variable ultrastructural features.

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Spinal cord injury (SCI) results in demyelination of surviving axons, loss of oligodendrocytes, and impairment of motor and sensory functions. We have developed a clinical strategy of cell therapy for SCI through the use of autologous bone marrow cells for transplantation to augment remyelination and enhance neurological repair. In a preclinical large mammalian model of SCI, experimental dogs were subjected to a clipping contusion of the spinal cord. Two weeks after the injury, GFP-labeled autologous minimally manipulated adherent bone marrow cells (ABMCs) were transplanted intrathecally to investigate the safety and efficacy of autologous ABMC therapy. The effects of ABMC transplantation in dogs with SCI were determined using functional neurological scoring, and the integration of ABMCs into the injured cords was determined using histopathological and immunohistochemical investigations and electron microscopic analyses of sections from control and transplanted spinal cords. Our data demonstrate the presence of GFP-labeled cells in the injured spinal cord for up to 16 weeks after transplantation in the subacute SCI stage. GFP-labeled cells homed to the site of injury and were detected around white matter tracts and surviving axons. ABMC therapy in the canine SCI model enhanced remyelination and augmented neural regeneration, resulting in improved neurological functions. Therefore, autologous ABMC therapy appears to be a safe and promising therapy for spinal cord injuries.

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Spinal cord injuries (SCI) cause sensory loss and motor paralysis. They are normally treated with physical therapy, but most patients fail to recover due to limited neural regeneration. Here we describe a strategy in which treatment with autologous adherent bone marrow cells is combined with physical therapy to improve motor and sensory functions in early stage chronic SCI patients. In a phase I/II controlled single-blind clinical trial (clinicaltrials.gov identifier: NCT00816803), 70 chronic cervical and thoracic SCI patients with injury durations of at least 12 months were treated with either intrathecal injection(s) of autologous adherent bone marrow cells combined with physical therapy or with physical therapy alone. Patients were evaluated with clinical and neurological examinations using the American Spinal Injury Association (ASIA) Impairment Scale (AIS), electrophysiological somatosensory-evoked potential, magnetic resonance imaging (MRI), and functional independence measurements. Chronic cervical and thoracic SCI patients (15 AIS A and 35 AIS B) treated with autologous adherent bone marrow cells combined with physical therapy showed functional improvements over patients in the control group (10 AIS A and 10 AIS B) treated with physical therapy alone, and there were no long-term cell therapy-related side effects. At 18 months posttreatment, 23 of the 50 cell therapy-treated cases (46%) showed sustained functional improvement. Compared to those patients with cervical injuries, a higher rate of functional improvement was achieved in thoracic SCI patients with shorter durations of injury and smaller cord lesions. Therefore, when combined with physical therapy, autologous adherent bone marrow cell therapy appears to be a safe and promising therapy for patients with chronic SCI of traumatic origin. Randomized controlled multicenter trials are warranted.

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BACKGROUND: Skin tags (ST) are common benign tumors of the skin but their etiopathogenesis is not well understood. STs arise in sites subjected to trauma. It was proved that mast cells are recruited to sites of skin trauma and increase their tumor necrosis factor-α (TNF-α) content. AIM: STs are linked to obesity and frictional sites, but this has not been studied at the molecular level. We hypothesized that mast cells, TNF-α and its family member, TNF-related apoptosis-inducing ligand (TRAIL) might play a role in the pathogenesis of STs as a response to trauma. MATERIALS AND METHODS: A study was done on 15 patients with STs. Two STs and a snip of normal skin were obtained in each subject. We counted the mast cells after Toluidine blue staining. Enzyme-linked immunosorbant assay was used to measure TNF-α level while reverse transcriptase polymerase chain reaction was used to evaluate the level of TRAIL mRNA expression. RESULTS: Mast cell count in all STs was significantly higher than that in control (P=0.0355). There was a highly significant increase in the level of TNF-α in all STs as compared to its level in controls (P<0.0001). Expression of TRAIL mRNA was significantly higher in STs as compared to its expression in controls (P<0.0001). CONCLUSION: Our study suggests that mast cells, TNF-α and TRAIL may play a role in the pathogenesis of STs.