RESUMEN
Chronic urticaria （CU） is a common skin disease worldwide， and its incidence is increasing year by year in various regions. Clinical manifestations such as severe itching can affect normal work， sleep， and daily life and increase the negative psychological burden caused by stress， anxiety， and depression. Mast cell activation and degranulation induced by immunoglobulin（Ig）E hypersensitivity is one of the core pathogenic mechanisms of CU， and there is no cure. Antihistamines such as cetirizine and loratadine are preferred for the clinical treatment of CU. Although they can effectively improve clinical manifestations such as itchiness， long-term application can increase the risk of adverse reactions and drug resistance. The phosphatidylinositol kinase/serine-threonine protein kinase B（PI3K/Akt） signaling pathway， as a classical signaling pathway regulated by phosphatidylinositol and tyrosine kinase receptor （RTK）， is a key target regulating the production and release of cytokines in macrophages and affecting the migration of leukocytes and the activation of mast cells and inflammation， and it can be involved in a variety of metabolic processes， such as mast cell activation and degranulation induced by IgE hypersensitivity and abnormal activation of the complement system so that the PI3K/Akt molecular pathway could be an important target for the future eradication of CU. However， the mechanism and potential role of the PI3K/Akt signaling pathway in the treatment of CU are less reported in China. Now， this paper reviewed the molecular mechanism of PI3K/Akt signaling pathway regulation in the treatment of CU and provided corroborative evidence and therapeutic strategy choices for the treatment of CU with traditional Chinese medicine （TCM） from the perspectives of molecular regulation and network pharmacology analysis.
RESUMEN
The daily management of medical equipment in the shelter hospital of CAPF was explored, and some measures were put forward including completing administration, determining responsibilities, improving supervising system, creating management tools, strengthening application for military and civilian uses, enhancing professional awareness and etc. The problems were solved in the discrepancies between construction and management, application and maintenance as well as training and daily service, so that the equipment was improved in efficiency, service life, metrology and stability. References may be provided for the shelter hospital or other medical units of CAPF for daily management of medical devices.
RESUMEN
A 69-year-old man presented with a 3-year history of scattered erythematous patches, perifollicular papules, acneiform lesions(such as milia, cysts) on the head, trunk and limbs as well as alopecia and peripheral eosinophilia. Histopathological examination revealed chronic focal dermal and perifollicular inflammatory infiltration with vascular proliferation and presence of a small number of eosinophils. He was initially diagnosed with folliculitis, and treated with antihistamines and antibiotics. Thereafter, lesional inflammation and pruritus were attenuated. However, plaques and alopecia developed in the occipital area 3 months later. The second histopathology of biopsy specimens revealed a dense dermal infiltrate of lymphoid cells and eosinophils, perifollicular infiltrate with numerous lymphoid cells, eosinophils and atypical lymphocytes migrating into hair follicles. Alcian blue stain showed epidermal mucinosis in follicles. Immunohistochemical examination showed positive staining of atypical cells for CD3, CD4, CD5, CD2, CD43 and ubiquitin carboxyl-terminal esterase L1 (UCHL1), but negative staining for CD20, CD79a, Epstein-barr virus, CD56, phosphoglucomutase-1, myeloperoxidase, CD7, or AE1 and AE3 monoclonal anti-keratin antibodies. T-cell receptor gene rearrangement was undetected. He was diagnosed with folliculotropic mycosis fungoides. Novel skin lesions still emerged after treatment with photochemotherapy (PUVA) plus acitretin. Follow up of the patient still continued.
RESUMEN
Objective To explore the mechanism underlying the induction of systemic lupus erythematosus (SLE) by estrogen, hydralazine and ultraviolet irradiation. Methods Peripheral blood mononuclear cells (PBMCs) were harvested from 10 patients with SLE and 9 normal human controls, and cultured with or without the intervention with estrogen, hydralazine or ultraviolet irradiation. The DNA methyltransferase-1 (DNMT1) activity of PBMCs was quantified by using DNMT activity/inhibition assay kit. Results No statistical difference was observed in DNMT1 activity between patients with SLE and normal controls (0.36 ± 0.24 vs 0.46 ± 0.17, P ＞ 0.05). A significant decrease was noted in DNMT1 activity in PBMCs from patients with SLE after intervention with estrogen (0.32 ± 0.18 vs 0.46 ± 0.17, t = 1.725, P ＜ 0.05), hydralazine (0.33 ±0.13 vs 0.46 ± 0.17, t = 1.739, P ＜ 0.05) and ultraviolet irradiation (0.30 ± 0.14 vs 0.46 ± 0.17, t = 1.739,P ＜ 0.05 ) compared with that from normal human controls. The treatment with hydralazine also induced an attenuation of DNMT1 activity in PBMCs from normal human controls (0.38 ± 0.12 vs 0.46 ± 0.17, P＜ 0.05).Conclusion Estrogen, hydralazine and ultraviolet irradiation can inhibit the DNMT1 activity of SLE patients,indicating that they may induce the initiation of SLE by altering the activity of DNMT1.
RESUMEN
Objective To investigate the gene expression of methyl-CpG-binding protein 2 (MeCP2) and methyl-CpG-binding domain 2 (mbd2) in patients with systemic lupus erythematosus(SLE) and their significance in the pathogenesis of SLE. Methods Semiquantitative reverse transcriptase-PCR was applied to detect the mRNA expression of MeCP2 and mbd2 in PBMCs obtained from relieved (n=17), active (n=17) SLE patients and healthy controls (n=17). The correlations were further analyzed among these parameters. Results No significant difference was observed in the expression level of MeCP2 mRNA among active SLE patients, relieved SLE patients and healthy controls (P>0.05). The expression of mbd2 in relieved SLE patients was significantly higher than that in health controls (t=12.8, P<0.01), but lower than that in active SLE patients (t=20.0, P<0.01). The expression of mbd2 positively correlated with SLEDAI (r=0.737, P=0.0001) of patients with SLE, and a positive correlation was also observed between the expression of mbd2 and MeCP2 in healthy controls (r=0.550, P=0.0222). Conclusions The expression of MeCP2 and mbd2 may be mutually constrained in normal human, but this relationship seems to be disturbed in patients with SLE.