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学者姓名：夏育民
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Abstract ：
Melasma is a common acquired disorder of pigmentation that negatively impacts quality of life. Present treatments show poor therapeutic effect with frequent recurrence. This in large part is due to the currently limited understanding of the disease's etiology. It is urgent to elucidate the pathogenesis of melasma to further the discovery of new therapeutic strategies. Recent studies show that melasma is triggered or aggravated by a variety of factors, including genetic susceptibility, ultraviolet radiation, and sex hormone dysregulation. Ultraviolet B radiation upregulates the expression of several melanocyte-specific genes and stimulates the release of key factors that participate in the synthesis of melanin. There is a significant increase in melanin in both the epidermal and dermal layers of affected skin, possibly due to abnormalities in crosstalk between the melanocytes and other cells. Melanogenesis is regulated through various signaling networks including the Wnt/beta-catenin, PI3K/Akt, cAMP/PKA, and SCF/c-kit-mediated signaling pathways. In addition, inflammatory mediators, oxidative stress, neuroactive molecules, sebocytes, etc, have also been proved to be related to the pathogenesis of melasma. This review provides a comprehensive update on the current understanding of the pathogenesis of melasma.
Keyword ：
genetic predisposition melanocyte melasma sex hormone ultraviolet
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| GB/T 7714 | Liu, Wei , Chen, Qin , Xia, Yumin . New Mechanistic Insights of Melasma [J]. | CLINICAL COSMETIC AND INVESTIGATIONAL DERMATOLOGY , 2023 , 16 : 429-442 . |
| MLA | Liu, Wei 等. "New Mechanistic Insights of Melasma" . | CLINICAL COSMETIC AND INVESTIGATIONAL DERMATOLOGY 16 (2023) : 429-442 . |
| APA | Liu, Wei , Chen, Qin , Xia, Yumin . New Mechanistic Insights of Melasma . | CLINICAL COSMETIC AND INVESTIGATIONAL DERMATOLOGY , 2023 , 16 , 429-442 . |
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Abstract ：
Microsatellite instability (MSI) is detected in approximately 15% of colorectal cancers (CRCs). WD40 and tetratricopeptide repeats 1 (WDTC1) is frequently mutated in MSI CRC, indicating that it may contribute to CRC development. However, the functional evidence of the role of WDTC1 in CRC development remains unknown. Herein, we conducted in vitro assays to examine the function of WDTC1 using knockdown experiments in three CRC cell lines, SW480, CACO2, and LoVo. We provided strong evidence that silencing WDTC1 significantly suppressed cell proliferation, migration, and invasion consistently in all three CRC cell lines. To evaluate the potential role of WDTC1 in regulating CRC-related genes, we conducted RNA sequencing after 24 and 48 h in SW480 cells after treating WDTC1-siRNA and its vehicle control cells. Differential gene expression analysis identified 44 (42 downregulated and 2 upregulated) and 16 (all downregulated) genes, at time points of 24 and 48 h, respectively, whereas 15 downregulated genes were commonly detected at both time points. The ingenuity pathways analysis suggested that the most significant enrichments associated with cancer function and upstream regulator ATM/ATR were observed for these commonly observed genes. We further verified differential gene expression of eight cancer-related genes, ARHGEF12, GSTP1, FNDC3A, TMTC3, RTN4, RRM2, UHMK1, and PTPRF, using RT-PCR in all three cell lines. Our findings provided additional insight into the oncogenic role of WDTC1 in CRC development.
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| GB/T 7714 | Wang, Xiaoyu , Cai, Qiuyin , Ping, Jie et al. The putative oncogenic role of WDTC1 in colorectal cancer [J]. | CARCINOGENESIS , 2022 , 43 (6) : 594-600 . |
| MLA | Wang, Xiaoyu et al. "The putative oncogenic role of WDTC1 in colorectal cancer" . | CARCINOGENESIS 43 . 6 (2022) : 594-600 . |
| APA | Wang, Xiaoyu , Cai, Qiuyin , Ping, Jie , Diaz-Zabala, Hector , Xia, Yumin , Guo, Xingyi . The putative oncogenic role of WDTC1 in colorectal cancer . | CARCINOGENESIS , 2022 , 43 (6) , 594-600 . |
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Abstract ：
As a multifunctional cytokine, lipocalin 2 is weakly expressed in skin and serum under normal conditions. However, it is over-expressed by neutrophils and keratinocytes in the skin lesions and sera in several skin diseases. Recent studies demonstrated that lipocalin 2 participates in the pathogenesis of psoriasis by exerting versatile effects on skin resident cells and infiltrating immune cells. Lipocalin 2 inhibits the synthesis of keratin, involucrin, and loricrin in keratinocytes, leading to epidermal parakeratosis via the Tcf7l1lipocalin 2 signaling axis. It also recruits inflammatory cells such as T cells and neutrophils into skin lesions via the IL-23/IL17, p38MAPK, and ERK-1/2 signaling pathways. Additionally, lipocalin 2 and other cytokines such as IL-17 have the synergetic effects on skin cells. The neutralization of lipocalin 2 or relevant cytokines can alleviate psoriasis, verifying that lipocalin 2 is an effective interfering target for psoriasis. In this review, we summarize the roles of lipocalin 2 in the processes of psoriatic inflammation and the promising therapeutic strategies based on lipocalin 2-related molecules.
Keyword ：
differentiation inflammation keratinocyte lipocalin 2 psoriasis
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| GB/T 7714 | Ren, Kaixuan , Xia, Yumin . Lipocalin 2 Participates in the Epidermal Differentiation and Inflammatory Processes of Psoriasis [J]. | JOURNAL OF INFLAMMATION RESEARCH , 2022 , 15 : 2157-2166 . |
| MLA | Ren, Kaixuan et al. "Lipocalin 2 Participates in the Epidermal Differentiation and Inflammatory Processes of Psoriasis" . | JOURNAL OF INFLAMMATION RESEARCH 15 (2022) : 2157-2166 . |
| APA | Ren, Kaixuan , Xia, Yumin . Lipocalin 2 Participates in the Epidermal Differentiation and Inflammatory Processes of Psoriasis . | JOURNAL OF INFLAMMATION RESEARCH , 2022 , 15 , 2157-2166 . |
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Abstract ：
Skin diseases are mainly divided into infectious diseases, non-infectious inflammatory diseases, cancers, and wounds. The pathogenesis might include microbial infections, autoimmune responses, aberrant cellular proliferation or differentiation, and the overproduction of inflammatory factors. The traditional therapies for skin diseases, such as oral or topical drugs, have still been unsatisfactory, partly due to systematic side effects and reappearance. Cold atmospheric plasma (CAP), as an innovative and non-invasive therapeutic approach, has demonstrated its safe and effective functions in dermatology. With its generation of reactive oxygen species and reactive nitrogen species, CAP exhibits significant efficacies in inhibiting bacterial, viral, and fungal infections, facilitating wound healing, restraining the proliferation of cancers, and ameliorating psoriatic or vitiligous lesions. This review summarizes recent advances in CAP therapies for various skin diseases and implicates future strategies for increasing effectiveness or broadening clinical indications.
Keyword ：
cold atmospheric plasma reactive nitrogen species reactive oxygen species skin disease therapy
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| GB/T 7714 | Zhai, Si-yue , Kong, Michael G. , Xia, Yu-min . Cold Atmospheric Plasma Ameliorates Skin Diseases Involving Reactive Oxygen/Nitrogen Species-Mediated Functions [J]. | FRONTIERS IN IMMUNOLOGY , 2022 , 13 . |
| MLA | Zhai, Si-yue et al. "Cold Atmospheric Plasma Ameliorates Skin Diseases Involving Reactive Oxygen/Nitrogen Species-Mediated Functions" . | FRONTIERS IN IMMUNOLOGY 13 (2022) . |
| APA | Zhai, Si-yue , Kong, Michael G. , Xia, Yu-min . Cold Atmospheric Plasma Ameliorates Skin Diseases Involving Reactive Oxygen/Nitrogen Species-Mediated Functions . | FRONTIERS IN IMMUNOLOGY , 2022 , 13 . |
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| GB/T 7714 | Gu, Hanjiang , Xia, Yumin , Tan, Xuanfeng . New repair strategy: Treatment of V-shaped divided nevus on eyelids with fish-mouth flap [J]. | DERMATOLOGIC THERAPY , 2021 , 35 (1) . |
| MLA | Gu, Hanjiang et al. "New repair strategy: Treatment of V-shaped divided nevus on eyelids with fish-mouth flap" . | DERMATOLOGIC THERAPY 35 . 1 (2021) . |
| APA | Gu, Hanjiang , Xia, Yumin , Tan, Xuanfeng . New repair strategy: Treatment of V-shaped divided nevus on eyelids with fish-mouth flap . | DERMATOLOGIC THERAPY , 2021 , 35 (1) . |
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Abstract ：
The skin is a complex organ that faces the external environment and participates in the innate immune system. Skin immune homeostasis is necessary to defend against external microorganisms and to recover from stress to the skin. This homeostasis depends on interactions among a variety of cells, cytokines, and the complement system. Collectins belong to the lectin pathway of the complement system, and have various roles in innate immune responses. Mannose-binding lectin (MBL), collectin kidney 1, and liver (CL-K1, CL-L1) activate the lectin pathway, while all have multiple functions, including recognition of pathogens, opsonization of phagocytosis, and modulation of cytokine-mediated inflammatory responses. Certain collectins are localized in the skin, and their expressions change during skin diseases. In this review, we summarize important advances in our understanding of how MBL, surfactant proteins A and D, CL-L1, and CL-K1 function in skin immune homeostasis. Based on the potential roles of collectins in skin diseases, we suggest therapeutic strategies for skin diseases through the targeting of collectins and relevant regulators.
Keyword ：
collectins immune homeostasis immunity immunotherapy skin
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| GB/T 7714 | Wang, Tian , Li, Ke , Xiao, Shengxiang et al. A Plausible Role for Collectins in Skin Immune Homeostasis [J]. | FRONTIERS IN IMMUNOLOGY , 2021 , 12 . |
| MLA | Wang, Tian et al. "A Plausible Role for Collectins in Skin Immune Homeostasis" . | FRONTIERS IN IMMUNOLOGY 12 (2021) . |
| APA | Wang, Tian , Li, Ke , Xiao, Shengxiang , Xia, Yumin . A Plausible Role for Collectins in Skin Immune Homeostasis . | FRONTIERS IN IMMUNOLOGY , 2021 , 12 . |
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Abstract ：
Background and aim As a proinflammatory cytokine, tumor necrosis factor-like weak inducer of apoptosis (TWEAK) participates in the progression of renal fibrosis by binding to its receptor, fibroblast growth factor-inducible 14 (Fn14). However, the effect of Fn14 inhibition on tubular epithelial cell-mediated tubulointerstitial fibrosis remains unclear. This study aimed to elucidate the role of TWEAK/Fn14 interaction in the development of experimental tubulointerstitial fibrosis as well as the protective effect of Fn14 knockdown on proximal tubular epithelial cells. Methods A murine model of unilateral ureteral obstruction was constructed in both wild-type and Fn14-deficient BALB/c mice, followed by observation of the tubulointerstitial pathologies. Results Fn14 deficiency ameliorated the pathological changes, including inflammatory cell infiltration and cell proliferation, accompanied by reduced production of profibrotic factors and extracellular matrix deposition. In vitro experiments showed that TWEAK dose-dependently enhanced the expression of collagen I, fibronectin, and alpha-smooth muscle actin in proximal tubular epithelial cells. Interestingly, TWEAK also upregulated the expression levels of Notch1/Jagged1. Fn14 knockdown and Notch1/Jagged1 inhibition also mitigated the effect of TWEAK on these cells. Conclusions In conclusion, TWEAK/Fn14 signals contributed to tubulointerstitial fibrosis by acting on proximal tubular epithelial cells. Fn14 inhibition might be a therapeutic strategy for protecting against renal interstitial fibrosis.
Keyword ：
Fibroblast growth factor– Fn14 inducible 14 Proximal tubular epithelial cell Renal fibrosis Tumor necrosis factor-like weak inducer of apoptosis TWEAK Unilateral ureteral obstruction
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| GB/T 7714 | Luo, Mai , Liu, Mengmeng , Liu, Wei et al. Inhibition of fibroblast growth factor-inducible 14 attenuates experimental tubulointerstitial fibrosis and profibrotic factor expression of proximal tubular epithelial cells [J]. | INFLAMMATION RESEARCH , 2021 , 70 (5) : 553-568 . |
| MLA | Luo, Mai et al. "Inhibition of fibroblast growth factor-inducible 14 attenuates experimental tubulointerstitial fibrosis and profibrotic factor expression of proximal tubular epithelial cells" . | INFLAMMATION RESEARCH 70 . 5 (2021) : 553-568 . |
| APA | Luo, Mai , Liu, Mengmeng , Liu, Wei , Cui, Xiao , Zhai, Siyue , Gu, Hanjiang et al. Inhibition of fibroblast growth factor-inducible 14 attenuates experimental tubulointerstitial fibrosis and profibrotic factor expression of proximal tubular epithelial cells . | INFLAMMATION RESEARCH , 2021 , 70 (5) , 553-568 . |
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| GB/T 7714 | Liu Wei , Zhang Dingwei , Luo Mai et al. TNF-Like Weak Inducer of Apoptosis Promotes Angiogenesis, Thereby Exacerbating Cutaneous Psoriatic Disease. [J]. | The Journal of investigative dermatology , 2021 , 141 (5) : 1356-1360 . |
| MLA | Liu Wei et al. "TNF-Like Weak Inducer of Apoptosis Promotes Angiogenesis, Thereby Exacerbating Cutaneous Psoriatic Disease." . | The Journal of investigative dermatology 141 . 5 (2021) : 1356-1360 . |
| APA | Liu Wei , Zhang Dingwei , Luo Mai , Jia Fangyan , Peng Lingling , Li Xiaoli et al. TNF-Like Weak Inducer of Apoptosis Promotes Angiogenesis, Thereby Exacerbating Cutaneous Psoriatic Disease. . | The Journal of investigative dermatology , 2021 , 141 (5) , 1356-1360 . |
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Abstract ：
Psoriasis is a common chronic inflammatory dermatitis in which various cytokines play a detrimental role. The cytokine tumor necrosis factor-related weak inducer of apoptosis (TWEAK) is involved in the pathogenesis of multiple inflammatory disorders. However, the potential role of TWEAK in various subtypes of psoriasis has not been studied in depth. To investigate whether the levels of TWEAK are associated with clinical traits and the levels of some known psoriasis-related cytokines, such as interleukin (IL)-17A, IL-22, interferon (IFN)-γ, and IL-36γ, 20 patients with psoriasis vulgaris (PV), 8 patients with pustular psoriasis (PP), 8 patients with erythrodermic psoriasis (EP), and 20 healthy controls (HCs) were recruited into this study. The levels of serum cytokines were detected by commercial enzyme-linked immunosorbent assay kits. The average levels of TWEAK, IL-17A, IL-22, IFN-γ, and IL-36γ were significantly higher in the psoriasis groups than in the HC group. Furthermore, there was a statistically significant correlation between TWEAK and IL-17A/IFN-γ in PV and IL-36γ in EP, but there was no correlation between TWEAK and IL-22 in any subtype of psoriasis. This study suggests that TWEAK may have a role in the pathogenesis of PV, PP, and EP via synergy with IL-17A, IFN-γ, or IL-36γ, but not with IL-22.
Keyword ：
IFN-γ IL-17A IL-22 IL-36γ Psoriasis TWEAK
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| GB/T 7714 | Wang Huixia , Wang Sijia , Li Liang et al. Involvement of the cytokine TWEAK in the pathogenesis of psoriasis vulgaris, pustular psoriasis, and erythrodermic psoriasis. [J]. | Cytokine , 2021 , 138 . |
| MLA | Wang Huixia et al. "Involvement of the cytokine TWEAK in the pathogenesis of psoriasis vulgaris, pustular psoriasis, and erythrodermic psoriasis." . | Cytokine 138 (2021) . |
| APA | Wang Huixia , Wang Sijia , Li Liang , Wang Xiuying , Liu Chengfei , Lu Mei et al. Involvement of the cytokine TWEAK in the pathogenesis of psoriasis vulgaris, pustular psoriasis, and erythrodermic psoriasis. . | Cytokine , 2021 , 138 . |
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Abstract ：
Bullous pemphigoid (BP), the most frequent blistering dermatosis in the elderly, is associated with increased mortality. The severity of BP can be assessed by detecting the anti-BP180 immunoglobulin G (IgG) concentration, but the lab test is not available in many community clinics. BP patients are usually in a hypercoagulable state with increased levels of D-dimer and fibrin degradation products (FDPs). We aimed to evaluate the use of D-dimer and FDPs in assessing BP severity. We compared the levels of plasma D-dimer, plasma FDPs, eosinophil counts, eosinophil cationic protein, and serum anti-BP180 IgG concentration between 48 typical BP patients and 33 Herpes zoster (HZ) patients (control group). Correlational analyses were conducted to determine the relationships between the lab values and common BP severity markers. The plasma D-dimer and FDP levels were higher in BP patients than in HZ controls (D-dimer: 3297 +/- 2517 mu g/L vs. 569.70 +/- 412.40 mu g/L; FDP: 9.74 +/- 5.88 mg/L vs. 2.02 +/- 1.69 mg/L, respectively, P < 0.0001). Significant positive correlations were found between D-dimer/FDP levels and BP severity markers (i.e. anti-BP180 IgG concentration [D-dimer: r = 0.3928, P = 0.0058; FDP: r = 0.4379, P = 0.0019] and eosinophil counts [D-dimer: r = 0.3625, P = 0.0013; FDP: r = 0.2880, P = 0.0472]) in BP patients. We also found an association between FDP and urticaria/erythema lesions (r = 0.3016, P = 0.0372), but no other BPDAI components. In 19 BP patients with complete remission after systemic glucocorticoid treatment, D-dimer and FDP levels decreased post-therapy (D-dimer: 5559 +/- 7492 mu g/L vs. 1738 +/- 1478 mu g/L; P < 0.0001; FDP: 11.20 +/- 5.88 mg/L vs. 5.13 +/- 3.44 mg/L; P = 0.0003), whereas they did not in BP patients with treatment resistant. Plasma D-dimer and FDP are convenient markers to evaluate BP severity assistant on BPDAI and eosinophil counts. FDP is also helpful for inflammatory lesions in BP patients.
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| GB/T 7714 | Wang, Sijia , Lu, Mei , Zhao, Zijun et al. Plasma levels of D-dimer and fibrin degradation products correlate with bullous pemphigoid severity: a cross-sectional study [J]. | SCIENTIFIC REPORTS , 2021 , 11 (1) . |
| MLA | Wang, Sijia et al. "Plasma levels of D-dimer and fibrin degradation products correlate with bullous pemphigoid severity: a cross-sectional study" . | SCIENTIFIC REPORTS 11 . 1 (2021) . |
| APA | Wang, Sijia , Lu, Mei , Zhao, Zijun , Peng, Xueting , Li, Liang , Cheng, Chuantao et al. Plasma levels of D-dimer and fibrin degradation products correlate with bullous pemphigoid severity: a cross-sectional study . | SCIENTIFIC REPORTS , 2021 , 11 (1) . |
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