Imiquimod (IMQ)-induced mouse psoriatic model is one of the useful models displaying most of psoriatic features. To compare the modeling efficacy of different IMQ creams, we induced the psoriatic models by topically applying two different brands of IMQ 5% creams to the shaved Balb/c mice skin and assessed the results. Balb/c female mice (n = 24) 8–12 weeks of age were randomly divided into experimental groups A (Likejie), B (Aldara), and control group C (Vaseline); Likejie, Aldara, or Vaseline was topically applied to the back skin for mice in groups A, B, and C, respectively, for six consecutive days. The total psoriasis area and severity index scores of groups A, B, and C were 3.25 ± 1.56, 9.81 ± 0.84, and 0, respectively; the Baker’s scores were 2.93 ± 1.07, 6.47 ± 1.50, and 0, respectively; and the epidermis thickness was 49.79 ± 14.16, 85.62 ± 17.55, and 20.04 ± 3.68 µm, respectively. The differences between the three groups in dual were statistically significant (P < 0.005 for the groups in dual). Aldara group showed more characteristic alterations of psoriasiform lesions than that of Likejie both macroscopically and histopathologically. The results suggested that different brands of IMQ creams may result in differential efficacy when performing the IMQ-induced psoriasis mouse models.

The pathogenesis of Stevens–Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) is not fully understood. Our previous study reported that chemokine CCL27 was overexpressed in serum of SJS/TEN patients. The objective of this study was to investigate the levels of CCL27 and TNF-α in serum and blister fluid from patients with SJS/TEN during the acute stage or resolution phase. A total of 27 patients with SJS/TEN and 39 healthy donors were recruited to the study. Serum and vesicular levels of CCL27 and TNF-α were determined by enzyme-linked immunosorbent assays. Serum levels of CCL27 and TNF-α were significantly elevated in patients with SJS/TEN during the acute stage as compared to the resolution phase and also compared with levels observed in normal controls (P = 0.001/< 0.001; P = 0.012/< 0.001). Serum TNF-α levels were significantly higher in patients with SJS/TEN during the resolution phase compared with normal controls (P < 0.001). Serum CCL27 levels were positively correlated with TNF-α levels during the acute stage (r s = 0.660; P < 0.001). Blister fluid exhibited much lower CCL27 levels than serum did during the acute stage (P = 0.008). TNF-α levels were much higher in vesicles in contrast to serum from acute stage (P = 0.040) as well as serum from resolution phase (P = 0.029). Our study demonstrated roles of CCL27 and TNF-α in promoting the course of SJS/TEN. CCL27 may act early in the course of disease, via the circulation, whereas TNF-α acts throughout the course of disease, in skin lesions.

Mandibuloacral dysplasia type A (MADA) is a rare autosomal recessive disorder, characterized by growth retardation, skeletal abnormality with progressive osteolysis of the distal phalanges and clavicles, craniofacial anomalies with mandibular hypoplasia, lipodystrophy and mottled cutaneous pigmentation. Some patients may show progeroid features. MADA with partial lipodystrophy, more marked acral, can be caused by homozygous or compound heterozygous mutation in the gene encoding lamin A and lamin C (LMNA). MADA and Hutchinson-Gilford progeria syndrome are caused by the same gene and may represent a single disorder with varying degrees of severity. MAD patients characterized by generalized lipodystrophy (type B) affecting the face as well as extremities and severe progressive glomerulopathy present heterozygous compound mutations in the ZMPSTE24 gene.

We developed the first Ru(ii) complex-based bioorthogonal two-photon photosensitizers. Through bioorthogonal labelling, they realize effective tumour-specific photodynamic therapy against triple-negative breast cancer cells.