Objectives: To investigate the microorganisms in expressed prostatic secretions (EPS) of both chronic prostatitis patients and normal young male adults and to determine which microorganisms are associated with the degree of intraprostatic inflammation. Methods: Specific polymerase chain reaction (PCR) technology was performed to confirm Neisseria gonorrhoeae, Mycobacterium tuberculosis, Mycoplasma and Chlamydia trachomatis as well as human papilloma virus (HPV), herpes simplex virus type 2 (HSV-2) and cytomegalovirus (CMV). Universal primer PCR technology was carried out to detect 16S bacteria rDNA, followed by cloning and sequencing of the entire 16S rDNA product. Results: The total number of bacteria and/or viruses detected by PCR assays was significantly associated with disease severity (p < 0.001). The white blood cell count and lecithin level was significantly correlated with the number of detected bacteria and/or viruses (p = 0.001 and p = 0.046, respectively). 17 bacterial isolates were identified from 14 EPS samples by 16S rDNA sequencing. Conclusions: Various microorganisms including Ureaplasma urealyticum, C. trachomatis, CMV, HPV and HSV-2 were identified in the EPS from patients with type III prostatitis. HPV infection may be associated with the degree of intraprostatic inflammation.

Background/Aim: Angiotensin II (Ang II) and hypertension play critical roles in the pathogenesis of the atrial remodeling that contributes to atrial fibrillation (AF). However, the gene expression profiles and signaling pathways in atria during the development of AF induced by Ang II remain unknown. Methods: Wild-type male mice (C57BL/6 background, 10 weeks old) were administered an infusion of Ang II (2000 ng/kg/min) using an osmotic pump for 1, 2, and 3 weeks. Blood pressure (BP) was measured by the tail-cuff method. AF was induced and recorded. Atrial enlargement and remodeling were examined by echocardiography and Masson’s trichrome staining. Time-series microarray analyses were conducted to examine gene expression profiles and pathways. Results: Ang II infusion resulted in marked elevation of systolic BP, increased AF incidence and duration, atrial enlargement, fibrosis, and atrial infiltration of myofibroblasts and F4/80-positive macrophages in a time-dependent manner. Microarray results showed that 1,719 genes were differentially expressed in the atrium at weeks 1, 2, and 3 after Ang II infusion. Gene ontology showed that these genes participate mainly in immune system processes, and regulation of cell migration, cell adhesion, complement activation, and the inflammatory response. Significant pathways included lysosomal and phagosomal pathways, which are involved in antigen processing and presentation, as well as chemokine signaling, and extracellular matrix–receptor interaction, which are known to play important roles in Ang II-induced AF. Moreover, these differentially expressed genes were classified into 50 profiles by hierarchical cluster analysis. Of these, eight profiles were significant and contained a total of 1,157 genes. Gene co-expression network analysis identified that Pik3cg (also known as phosphoinositide-3-kinase regulatory subunit 3) was localized in the core of the gene network, and was the most highly expressed among the Pik3 isoforms at different time points. Conclusion: The present findings revealed that many genes are involved in Ang II-induced AF, and highlighted that Pik3cg may play a central role in this disease.

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