DETECTION OF PATHOGENS CAUSING GENITAL ULCER DISEASE BY MULTIPLEX POLYMERASE CHAIN REACTION

Objective To establish a multiplex polymerase chain reaction (M-PCR) assay for simultaneous detection of pathogens causing genital ulcer disease (GUD). Methods Based on the gene-specific region of the following pathogens: Chlamydia trachomatis omp1/ompb, herpes simplex virus (HSV) DNA polymerase, Treponema pallidum tpp47, Haemophilus ducreyi 16s rRNA, four sets of primers were designed and an M-PCR assay was developed to detect four pathogens in one test. The assay was evaluated with diagnostic result of golden standard for each pathogen. Results Of the 51 clinical samples, M-PCR showed slightly higher positive rate (47.1%) of HSV than cell culture (23.6%).Meanwhile, the positive rate of T. pallidum detected by M-PCR and dark-field microscopy was 19.6% (10/51) and 15.7% (8/51), respectively. Only one sample was positive for H. ducreyi and no sample was positive for C. trachomatis detected by both M-PCR assay and culture. Conclusion This primary study indicated that M-PCR assay can simultaneously and rapidly detect the four etiologic pathogens causing GUD.

The Relationship Between Ultraviolet B and DNA Methylation in Skin Cancers

Ultraviolet B is regarded as an important factor in many skin diseases,especially skin cancers.Increasingly more evidence is showing that changes in DNA methylation occur in patients with skin cancers.Changes in DNA methylation have also been observed in ultraviolet B-irradiated cells and mouse models.DNA methylation modifier enzymes are simultaneously affected.We herein review the evidence to date showing that Ultraviolet B affects changes in DNA methylation modifier enzymes in skin cancers.However,the mechanism of how ultraviolet B regulates the changes in DNA methylation modifier enzymes remains to be further elucidated.Understanding the mechanism by which ultraviolet B modulates DNA methylation modifier enzymes can help to identify potential therapeutic markers or targets and develop novel strategies for preventing or treating ultraviolet B-induced skin damage.

Calcineurin/Nuclear Factor of Activated T-Cell Pathway in Cutaneous Squamous Cell Carcinoma

Introduction Cutaneous squamous cell carcinoma (CSCC),a keratinocyte-derived skin neoplasm with malignant potential,1 represents 20%-50% of skin cancers and currently has an increasing incidence in the United States.2 Ultraviolet (UV)solar radiation is the primary risk factor for the development of CSCC,and the cumulative exposure received over a lifetime plays a major role in this development.3 Mutations in the p53 gene are the most common genetic abnormalities,causing nonfunctional p53 protein production and cells with damaged DNA replicate in CSCC.

Aberrant DNA Methylation in Cutaneous Squamous Cell Carcinoma

Introduction Cutaneous squamous cell carcinoma(CSCC)is the secondmost common non-melanoma skin cancer after basal cell carcinoma,accounting for 20%of all cutaneous malignancies.CSCC originates from epidermal keratinocytes or adnexal structures such as eccrine glands or pilosebaceous units.1 According to several studies focused on Caucasian populations in Europe,the USA and Australia,about 15–35 per 100,000 individuals are diagnosed with CSCC each year,and the incidence of CSCC is expected to increase by 2%–4%per year.2 The incidence of primary CSCC has increased by 50%–300%globally,especially amongst Caucasian populations in New Zealand,Australia,and North America over the last 3 decades.