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1.
Dermatol Ther ; 34(2): e14720, 2021 03.
Article En | MEDLINE | ID: mdl-33369827

Sporotrichosis is a fungal disease of the human and other mammals, caused by a complex of Sporothrix schenckii. The disease follows the traumatic inoculation to lead to fixed lesions, regional lymphangitic lesions, or even disseminated lesions including internal involvement, which depends on host immunological status and strain virulence. In this work, we observed the role of CD4+ T cells apoptosis and conversion of Th1/Th2-type cytokines in the cellular immunity regulation on mice model sporotrichosis. The experiments showed that there was more CD4+ T cells apoptosis, by endogenous apoptosis signaling pathway (P < .05), and more conversions of Th1/Th2-type cytokines in more severe and longer duration groups (P < .05). Meanwhile, the trends of the conversions of Th1/Th2-type cytokines were almost consistent with the CD4 + T cell's apoptosis in the corresponding groups. These findings suggest that CD4+ T cells apoptosis and conversion of Th1/Th2-type cytokines are contributing to promoting the progress of sporotrichosis.


Apoptosis , Cytokines/immunology , Sporotrichosis/immunology , Th1 Cells/immunology , Animals , Mice , Sporothrix
2.
Chem Biol Interact ; 323: 109061, 2020 May 25.
Article En | MEDLINE | ID: mdl-32194039

Oncogenic alterations in the BRAF gene are identified in an estimate of 50% of melanomas and cause melanoma development. BRAF kinase inhibitors (BRAFi), including vemurafenib and dabrafenib, were discovered and used in the clinical treatment of BRAF-mutant metastatic melanoma. Though, BRAFi's therapeutic advantages are short term and short-lived associated with drug resistance. Although a few pathways of developed BRAFi resistance have also been established, in approximately 40% of melanomas, the cause for inherited resistance remains unclear. Recognizing a new process of developed BRAFi resistance might provide new possibilities to successfully treat BRAF mutant melanoma. In this study, we are exploring the compensatory alternative pathway followed by BRAFi/MEKi treated resistant cell for maintaining the long-term integrity and survival.


Cytoprotection , Drug Resistance, Neoplasm , Melanoma/pathology , Proto-Oncogene Proteins B-raf/antagonists & inhibitors , Signal Transduction , Skin Neoplasms/pathology , Humans , Proto-Oncogene Proteins B-raf/metabolism , Melanoma, Cutaneous Malignant
4.
J Cosmet Dermatol ; 19(6): 1487-1489, 2020 Jun.
Article En | MEDLINE | ID: mdl-31556217

BACKGROUND: Cutaneous squamous cell carcinoma (cSCC) is a malignant tumor of epithelial keratinocytes, with a relatively reduced frequency of lymph node metastasis. Despite the fact that this tumor type is largely preventable, the incidence of cSCC is rising every year. Ultraviolet exposure is a major cause of cSCC and directly contributes to cSCC. Other known environmental risk factors include ionizing radiation, cigarette smoking, and certain chemical exposures. AIMS: In this study, we report a clinical case of cSCC with a novel causative factor. PATIENT/METHODS: The report describes a 72-year-old male who was seen for a dermatosis condition initially. Later, epidermal hyperplasia and granulomatous inflammation of the dermis was diagnosed based on skin biopsy. Fungal culture revealed the presence of Sporothrix schenckii which led to the diagnosis of fixed-type sporotrichosis. RESULTS: Four months of oral terbinafine (250 mg once a day) administration partially resolved the lesions. Patient was subsequently diagnosed with cSCC, and surgical resection with wider margins was performed. CONCLUSION: After a careful and rigorous exclusion of known risk factors, we confirmed that this incidence of cSCC was caused by chronic inflammation which followed fixed-type sporotricosis.


Carcinoma, Squamous Cell/diagnosis , Skin Neoplasms/diagnosis , Sporothrix/isolation & purification , Sporotrichosis/complications , Terbinafine/administration & dosage , Administration, Oral , Aged , Biopsy , Carcinoma, Squamous Cell/microbiology , Carcinoma, Squamous Cell/surgery , Chronic Disease/drug therapy , Face , Humans , Male , Skin/immunology , Skin/microbiology , Skin/pathology , Skin Neoplasms/immunology , Skin Neoplasms/microbiology , Skin Neoplasms/surgery , Sporotrichosis/diagnosis , Sporotrichosis/drug therapy , Sporotrichosis/microbiology
5.
J Cosmet Dermatol ; 19(7): 1699-1701, 2020 Jul.
Article En | MEDLINE | ID: mdl-31660688

BACKGROUND: Discoid lupus erythematosus (DLE) is a most well-known clinical variation of chronic cutaneous lupus erythematosus inside the spectrum of lupus erythematosus (LE). Cutaneous trauma remains a significant and peculiar causative factor for DLE. AIMS: We present a case wherein the patient demonstrated unilateral distribution of DLE on a clinically normal appearing occult facial scald of edible oil, representing Koebner phenomenon (KP) i.e. occurrence of a new skin disease at the site of an unrelated and already healed one. PATIENT/METHODS: The 53 years old female patient was unique because she experienced DLE on the nasal back. RESULTS: The injury was totally settled following a month treatment of oral hydroxychloroquine and topical 0.03% tacrolimus ointment. After three months, she encountered an accidental edible oil scald on the right upper cheek. Several small vesicles appeared on a soybean-sized erythema base with a burning sensation. CONCLUSION: We review the literature and conclude by discussing important histologic highlights to think about while endeavoring to perceive the fundamental character and pathogenicity of such sores.


Burns , Lupus Erythematosus, Discoid , Erythema , Female , Humans , Hydroxychloroquine , Lupus Erythematosus, Discoid/drug therapy , Middle Aged , Tacrolimus
6.
Biosci Rep ; 39(12)2019 12 20.
Article En | MEDLINE | ID: mdl-31710084

Koebner phenomenon refers to the emergence of new psoriatic lesions in the healthy skin regions following an injury/trauma to psoriatic patients. The occurrence of psoriatic lesions at unusual areas of the body regions such as on penis, around eyes and on keloids suggest that the Koebner phenomenon may be responsible for these lesions. A number of agents/triggers have been reported to induce the development of new psoriatic lesions in healthy skin areas and these include, tattooing skin, radiations, skin incision, viral infections and striae etc. The different mechanisms that contribute in inducing the development of new psoriatic lesions as Koebernization include the involvement of mast cell-derived inflammatory mediators such as tryptase, IL-6, IL-8, IL-17, and IL-36γ. Moreover, an increased expression of nerve growth factor (NGF) and vascular endothelial growth factor (VEGF) also contribute in Koebernization. Apart from these, there is a critical role of α 2 ß1 integrins, S100A7 (psoriasin) and S100A15 (koebnerisin), change in the ratio of CD4+/CD8+ T cells, down-regulation of mechanosensitive polycystin 1 protein, decrease in inflammation controlling atypical chemokine receptor 2 (ACKR2), reduced expression of N-methyl-d-aspartate (NMDA) receptors (NMDARs) on the keratinocytes and increase in levels of chemokines (CXCL8 and CCL20) in inducing formation of new psoriatic lesions. The present review discusses the role of Koebner phenomenon in the development of new psoriatic lesions. Moreover, it also describes the mechanisms involved in Koebernization in the form of discussion of different key targets that may be potentially modulated pharmacologically to attenuate/halt the development of new psoriatic lesions.


Psoriasis/metabolism , Animals , CD4-CD8 Ratio , Cytokines/metabolism , Humans , Integrin alpha2beta1/metabolism , Psoriasis/pathology , Receptors, Chemokine/metabolism , Receptors, N-Methyl-D-Aspartate/metabolism , S100 Calcium Binding Protein A7/metabolism , TRPP Cation Channels/metabolism
7.
Neural Regen Res ; 11(12): 1962-1968, 2016 Dec.
Article En | MEDLINE | ID: mdl-28197193

Long-term glucocorticoid use may result in sustained suppression of one or more secreted components from the hypothalamo-pituitary-adrenal axis, and often results in apoptosis. Yougui Pill (YGP), a 10-component traditional Chinese herbal medicine, has been shown to be clinically effective for glucocorticoid-induced suppression of the hypothalamo-pituitary-adrenal axis. However, the pharmacological and molecular mechanisms remain unclear. We hypothesized that YGP would exert an anti-apoptosis effect on dexamethasone-treated anterior pituitary cells. In vivo experiments showed that YGP significantly reduced the number of apoptotic cells, down-regulated mRNA expression of cytochrome c, caspase-3, and caspase-9, and up-regulated mRNA expression of Bcl-2. These findings suggest that YGP reduced glucocorticoid-induced apoptosis in rat anterior pituitary cells by regulating the mitochondria-mediated apoptosis pathway.

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