ABSTRACT
According to the age of onset, childhood acne can be divided into neonatal acne, infantile acne, preschool acne, and prepubertal acne. Neonatal acne and infantile acne can serve as predictive factors for severe adolescent acne, preschool acne may be related to underlying endocrine diseases, and prepubertal acne is a sign of pubertal maturation. The treatment of childhood acne is similar to that of adolescent acne, and adverse effects of drugs and their impact on the growth and development of children should be considered.
ABSTRACT
Cognitive impairment often occurs in elderly patients with heart failure.In this paper, we reviewed the possible mechanism of cognitive impairment in elderly patients with heart failure.The possible pathological mechanism of cognitive impairment in elderly patients with heart failure was discussed from the aspects of decreased cardiac output, renal damage, atrial fibrillation, inflammatory reaction, neuroregulation, depression and high homocysteine level, and the effect of cognitive impairment on heart failure was also summarized, so as to improve both the clinicians' awareness of cognitive impairment and the level of diagnosis and treatment in elderly patients with heart failure.
ABSTRACT
Objective To determine the expression of caspase-14 in skin lesions of patients with chronic actinic dermatitis (CAD),and to explore the effect of ultraviolet B (UVB) radiation on its mRNA and protein expression in HaCaT cells.Methods In 2016,skin samples were collected from lesions of 10 patients with CAD (test group),10 patients with eczema (positive control group) and from normal skin of 10 healthy controls after cosmetic surgery (negative control group) in the Department of Dermatology,First Affiliated Hospital of Kunming Medical University.Immunohistochemical staining was performed to determine the expression of caspase-14 in the normal skin,CAD and eczema lesions.Cultured HaCaT cells were divided into several groups:UVB groups irradiated with 0,30,60,90 mJ/cm2 UVB separately,and 5-AzaC groups irradiated with 0,30,60,90 mJ/cm2 UVB separately followed by the treatment with the methylase inhibitor 5-AzaC for 24 hours.Then,the cells were collected,and real-time fluorescence-based quantitative PCR (RT-PCR) and Western blot analysis were conducted to determine the mRNA and protein expression of caspase-14 respectively in HaCaT cells in the UVB groups and 5-AzaC groups.Statistical analysis was carried out with SPSS22.0 software by using chi-square test for the comparison of rates,and t test and two-factor analysis of variance for the comparison of means.Results In the CAD and eczema lesions,caspase-14 was mainly expressed in the spinous and granular layers,but not in the stratum comeum.However,caspase-14 was markedly expressed in the stratum corneum of the normal skin tissues.Of the 10 CAD samples,5 were positive for caspase-14,and 9 of 10 normal skin samples were positive for caspase-14.The positive rate of caspase-14 significantly differed between the two above groups (x2 =7.30,P ＜ 0.05).RT-PCR and Western blot analysis showed significant changes in the mRNA and protein expression of caspase-14 in HaCaT cells after irradiation with different doses of UVB (F =87.54,23.46,both P ＜ 0.05),which showed a decreasing trend along with the increase in the dose of UVB.After exposure to 0,30,60 and 90 mJ/cm2 UVB,the mRNA and protein expression of caspase-14 was significantly higher in the 5-AzaC groups than in the UVB groups (all P ＜ 0.05).Conclusions In CAD lesions,the expression of caspase-14 markedly decreased,and was absent in the stratum corneum.UVB radiation can downregulate the mRNA and protein expression of caspase-14 in HaCaT cells.
ABSTRACT
Objective To study the effects of semaphorin 5A (SEMA5A) gene silencing by lentivirus?mediated short hairpin RNA(shRNA)on biological activity of malignant melanoma cell line A375. Methods Two pairs of interference sequences for SEMA5A gene(shRNA1 and A375?shRNA2)and a pair of control interference sequences were designed to build lentiviral vectors, which were then transfected into HEK293T cells to gain lentivirus. A375 cells were divided into three groups:experimental group(A375?shRNA1 and A375?shRNA2 cells)transfected with the lentivirus containing shRNA1 or shRNA2, negative control group (A375?con cells) transfected with that containing the control shRNA, and blank control group(A375 cells)receiving no transfection. The A375 cells with stable knockdown of SEMA5A gene expression were screened by puromycin. Subsequently, reverse transcription?PCR and Western?blot analysis were performed to detect mRNA and protein expressions of Semaphorin 5A in these cells, and methyl thiazolyl tetrazolium(MTT)assay was applied to evaluate the growth of cells. The scratch assay and invasion assay were conducted to estimate migration and invasion ability of cells. Results The lentivirus containing the SEMA5A?targeting shRNAs or control shRNA was successfully transfected into A375 cells, and stably transfected cells were gained after puromycin selection. The expressions of semaphorin 5A mRNA and protein in the A375?shRNA2 cells were significantly reduced compared with those in the A375?con and A375 cells(all P 0.05). The scratch assay showed that there was no obvious cell migration into the scratch in the experiment group, whereas the scratch was almost covered by cells in the negative control group and blank control group. The invasion assay showed that the number of A375?shRNA2 cells passing through the Transwell chamber was significantly smaller than that of A375 and A375?con cells(both P 0.05). Conclusion The silencing of SEMA5A gene by lentivirus?mediated shRNA could effectively down?regulate the expression of semaphorin 5A, and inhibit the growth, invasion and migration of A375 cells.
ABSTRACT
Objective To evaluate the efficacy and safety of hydroxychloroquine combined with butyli flufenamatum ointment and other drugs for the treatment of polymorphous light eruption (PLE).Methods A total of 48 patients with PLE were randomly and equally classified into group 1 and group 2.Both groups took hydroxychloroquine 200 mg twice a day and loratadine 10 mg per day for the initial 4 weeks,then took hydroxychloroquine 100 mg twice a day alone for another 4 weeks.Group 1 also topically applied butyli flufenamatum ointment twice a day during the 8 weeks,while group 2 applied mometasone furoate cream twice a day for the first 2 weeks followed by butyli flufenamatum ointment twice a day for another 6 weeks.Each treatment cycle lasted 2 weeks,and both groups received 4 cycles of treatment.Patients were evaluated for the response rate at the end of each cycle,and for the total symptom score and erythema score before and after the 8-week treatment.Statistical analysis was carried out using t test,chi-square test,Fisher's exact test and repeated-measures analysis of variance with the SPSS17.0 software.Results On day 14,28,42 and 56,the total score improved in 0,3,12 and 19 patients in group 1 respectively,and in 1,4,12 and 20 patients in group 2 respectively;the erythema score improved in 1,5,13 and 18 patients in group 1 respectively,and in 0,5,11 and 17 patients in group 2 respectively.No significant difference was observed between the two groups in response rates at any of the above four time points (P ＞ 0.05).Both the total score and erythema score significantly decreased after the 8-week treatment in both groups compared with the pretreatment scores (both P ＜ 0.05).No serious adverse reaction was observed in either of the two groups.Conclusions Hydroxychloroquine combined with loratadine and butyli flufenamatum ointment shows high efficacy and safety for the treatment of PLE.Topical butyli flufenamatum ointment is highly effective for the treatment of PLE,especially for PLE cases mainly presenting with erythema.
ABSTRACT
Objective To estimate the effect of different doses of ultraviolet (UV) radiation on the proliferation of and apoptosis in kertatinocytes,as well as on the expression of p53,matrix metalloproteinase-2 (MMP2) and-9 (MMP9) in actinic keratosis (AK) lesions and normal human skin.Methods Tissue specimens were obtained from the lesions of 20 patients with AK and sun-exposed normal skin of 20 healthy human subjects,and subjected to an air-exposed culture.Each of the specimens was divided into 4 areas to remain untreated (control area) or be irradiated with UV of 5,10 and 20 J/cm2 (irradiated areas) for 4 consecutive days.After another 24-hour culture,the tissue cultures were collected followed by the evaluation of apoptosis in and proliferation of keratinocytes by using terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) and Ki-67 staining,and determination of mRNA and protein expressions of p53,MMP2 and MMP9 by using real time PCR and immunohistochemistry respectively.Results A statistical increase was observed in the percentage of apoptotic cells in the normal skin irradiated with UV of 10 and 20 J/cm2 (46.8％ ± 2.1％ and 56.7％± 2.4％,both P ＜ 0.05) and in the AK lesions irradiated with UV of 20 J/cm2 (43.5％ ± 1.5％,P ＜ 0.05)compared with the corresponding unirradiated tissues.The normal skin showed a higher percentage of apoptotic cells than the lesional skin after irradiation with UV of 10 and 20 J/cm2 (both P ＜ 0.05).The percentage of Ki67-positive cells was significantly decreased in the normal skin after irradiation with UV of 20 J/cm2 (3.34％ ±0.76％,P ＜ 0.05),but experienced no statistical changes in the lesional skin after different doses of UV irradiation (all P ＞ 0.05).There was a statistical elevation in the expression of p53 mRNA (5 J/cm2:1.106 ± 0.025,10 J/cm2: 1.259 ± 0.045,20 J/cm2:1.425 ± 0.053,all P ＜ 0.05) and protein(10 J/cm2:0.1169 ± 0.0032,20 J/cm2:0.1454 ± 0.0047,both P＜ 0.05) in the normal skin,but a statistical reduction in the expression of p53 mRNA(10 J/cm2.0.611 ± 0.050,20 J/cm2:0.578 ± 0.070,both P ＜ 0.05) and protein (20 J/cm2:0.0404 ± 0.0027,P＜ 0.05) in the lesional skin after irradiation compared with the corresponding unirradiated skin tissues.Further more,a statistical increment was observed in MMP2 mRNA and protein expression in normal skin irradiated with UV of 10 J/cm2 (1.086 ± 0.013,0.0843 ± 0.0024,respectively,both P ＜ 0.05) and 20 J/cm2 (1.417 ± 0.036,0.1236 ±0.0042,respectively,both P ＜ 0.05) and in lesional skin irradiated with UV of 20 J/cm2 (1.296 ± 0.028,0.0744± 0.0032,respectively,both P ＜ 0.05),as well as in MMP9 mRNA and protein expression in normal skin irradiated with UV of 20 J/cm2 (1.395 ± 0.026,0.3065 ± 0.0162,respectively,both P ＜ 0.05) and in lesional skin irradiated with UV of 10 J/cm2 (1.298 ± 0.035,0.0992 ± 0.0053,respectively,both P ＜ 0.05) and 20 J/cm2(1.286 ± 0.032,0.1010 ± 0.0063,respectively,both P ＜ 0.05) compared with the corresponding unirradiated tissues.Conclusion Ultraviolet may accelerate the progression of AK by down-regulating p53 expression but up-regulating MMP2 and MMP9 expression.
ABSTRACT
Objective To study the effect of simvastatin on the mouse model of sclerotic skin. Methods A total of 44 mice were divided into two groups, i.e., early administration group (n=24) and post-induction administration group (n=20), and the former was classified into three subgroups, including negative group, model group and simvastatin-treated group, and the latter into two groups, namely blank control group, simvastatin-treated group. The mouse model of sclerotic skin was established by local injec-tions of bleomycin in the back of BALB/c mice. Simvastatin was administered by gavage at a dose of 5 μg per kilogram body weight per day for 4 weeks to mice at the same time when bleomycin was injected in the early group or after 4-week bleomycin injection in the post-induction group. Skin sections were prepared 24 hours after the last administration of simvastatin for histopathological examination and measurement of derma l thickness with HE staining, determination of hydroxyproline content via colorimetry, and mRNA expression of procollagen α1 (Ⅰ) by RT-PCR. Results In the early administration group, a significant increment was observed in the diameter of dermal collagen, skin thickness, and hydroxyproline content in model group compared with the negative control group (all P <0.01), whereas decreased dermal thickness, hydroxyproline content and mRNA expression of procollagen α1(Ⅰ) were noticed in simvastatin-treated group in comparison with the model group (P<0.05, 0.01 and 0.05, respectively). No obvious improvement was achieved in dermal thickness or hydroxyproline content in simvastatin-treated group compared with blank control group (both P0.05), but the mRNA expression of procollagen α1 (Ⅰ) was inhibited in the former group (P<0.05). Conclusion Skin sclerosis is relieved significantly by administration of simvastatin at the induction of scle- rosis but not by that after the induction of sclerotic skin.