Publications by authors named "Ying-Zhe Cui"

The function and survival of melanocytes is regulated by an elaborate network of paracrine factors synthesized mainly by epidermal keratinocytes (KCs). KCs and melanocytes respond to UV exposure by eliciting a tanning response. However, how KCs and melanocytes interact in the absence of UV exposure is unknown.

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Melanocytes, which originate from the neuroectoderm, are specialized cells responsible for producing pigments and possessing a dendritic morphology. These cells migrate to the epidermis and follicles, contributing to skin and hair pigmentation during embryonic development. The remarkable self-renewal capacity of melanocytes enables them to effectively restore hair and skin pigmentation.

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  • - Atopic dermatitis (AD) is a common inflammatory skin disease linked to issues like skin barrier dysfunction and immune system dysregulation, with STAT3 playing a key role in skin cell function.
  • - Researchers created a mouse model with specific loss of STAT3 in skin cells, which showed worsened AD-like symptoms after exposure to a skin irritant, indicating a negative impact on skin health and microbiome composition.
  • - The study found that mice with STAT3 deficiency exhibited more type-2 inflammatory cells and increased levels of TSLP, a protein that attracts immune cells, suggesting that targeting TSLP could help reduce skin inflammation in AD.
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  • Psoriasis involves excessive skin cell growth and immune cell infiltration, with the exact causes remaining uncertain.
  • Researchers found that glycyl-tRNA synthetase (GARS), typically involved in protein synthesis, is overexpressed in the skin and blood of psoriasis patients, promoting skin inflammation and abnormal growth when present in high levels.
  • The study suggests that targeting GARS could be a potential new treatment strategy for psoriasis, as reducing its expression showed improvements in inflammation and skin condition in laboratory models.
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Background: The Isoleucyl-tRNA synthetase (IARS) catalyzes isoleucine to the corresponding tRNA, maintaining the accuracy of gene translation. Its role in psoriasis has been not investigated so far. In this study, we aimed to investigate the mechanisms underlying the efficacy of IARS inhibitor, mupirocin, treatment for psoriasis.

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  • * Nerve fibers in affected skin are closely associated with immune cells and keratinocytes, and disruptions in sensory nerve-related genes were found in psoriasis.
  • * Treatments that impair skin nerves, like botulinum toxin A, have been found to reduce psoriasiform dermatitis, indicating that targeting the nervous system could offer new therapeutic options for psoriasis.
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Psoriasis is a systemic immune‒mediated inflammatory disease characterized by hyperproliferation and abnormal differentiation of epidermal keratinocytes. Recent studies have identified IL-17 and IL-23 as key drivers of psoriasis pathogenesis, but the underlying molecular mechanisms remain unclear. The 2'-5'-oligoadenylate synthetases (OASs), namely, OAS1, OAS2, OAS3, and OASL, are a family of IFN-induced enzymes with multiple antiviral activities, but their role in psoriasis is unknown.

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Myasthenia gravis (MG) is a prototypical antibody-mediated neurological autoimmune disease with the involvement of humoral immune responses in its pathogenesis. T follicular helper (Tfh) cells have been implicated in many autoimmune diseases. However, whether and how Tfh cells are involved in MG remain unclear.

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Background: Cerebral microbleeds (CMBs) occur frequently in patients suspected of cerebrovascular disease and they are the principle radiographic findings in patients with sub-clinical neurological impairment. The objective of this study was to assess the prevalence, distribution, severity and associated clinical features of CMBs in a prospective hospital patient based cohort undergoing brain MRI for suspected cerebrovascular disease, excluding cases with known intracranial hemorrhage or prior large-area stroke.

Methods: The study population consisted of 447 patients who were evaluated with T2*-gradient echo sequences to detect the CMBs lesion number, location, and their association with white matter hyperintensities and clinical parameters, including blood pressure.

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