The prevalence of causative organisms of community-acquired urethritis in an age group at high risk for sexually transmitted infections in Korean Soldiers.

OBJECTIVES: This study was designed to evaluate the causative organisms in young male soldiers with clinical signs and symptoms after sexual contact that suggests a diagnosis of urethritis. METHODS: Between June 2012 and January 2015, male patients with urethritis symptoms that had resulted from sexual contact within 3 months participated in this study. All patients were evaluated using urinalysis and were screened for Neisseria gonorrhoeae (NG), Chlamydia trachomatis (CT), Ureaplasma urealyticum (UU), Mycoplasma genitalium (MG), Mycoplasma hominis (MH), herpes simplex virus (HSV) type II and Trichomonas vaginalis (TV) using multiplex PCR (mPCR) assay in order to detect sexually transmitted infections (STI) or pathogens. RESULTS: A total of 436 male patients aged 18-28 years were included in the study. The median age was 22.0 years. The prevalence of STI pathogens were as follows: NG in 19.0%, CT in 36.6%, UU in 24.0%, MG in 21.5%, MH in 6.1%, HSV type II in 1.6%, TV in 0.2% and indeterminate STI pathogens in 9.4%. Coinfection of NG with non-NG was detected in 5.7% of the participants, while the coinfection rates for STI pathogens were: with CT in 3.4%, with UU in 2.7%, with MG in 0.2% and with MH in 0.2%. CONCLUSIONS: CT was the most prevalent STI pathogen and coinfections of NG with non-NG appeared less frequently. The young male soldiers with urethritis should be administered suitable antibiotics for STI pathogens that were found by mPCR results, rather than an experimental combination of antibiotics for coinfections.

Lipiodol solution of a lipophilic agent, (188)Re-TDD, for the treatment of liver cancer.

Radiolabeled lipiodol has been used for targeting liver cancer. We developed a lipiodol solution of (188)Re-TDD (2,2,9,9-tetramethyl-4,7-diaza-1,10-decanedithiol) and investigated its feasibility for the treatment of liver cancer. The lipiodol solution of (188)Re-TDD was well-retained in the lipiodol phase in vitro. After injection through the tail veins of mice, high lung-uptake was investigated which is evidence of embolizing activity. We also found high accumulation in hepatoma after injection through the hepatic arteries of hepatoma-bearing rats. In conclusion, the lipiodol solution of (188)Re-TDD is a promising agent for liver cancer therapy.

Effect of DA-6034, a derivative of flavonoid, on experimental animal models of inflammatory bowel disease.

Inflammatory bowel disease (IBD) is a multifactorial disorder with unknown etiology and pathogenesis. DA-6034, 7-carboxymethyloxy-3', 4', 5-trimethoxy flavone, is a synthetic flavonoid known to possess anti-inflammatory activity. This study was performed to evaluate the oral therapeutic effect of DA-6034 in three experimental animal models of IBD: two chemical-induced IBD models of rats and the human leukocyte antigen (HLA)-B27 transgenic rat model known to develop spontaneous colitis without the use of exogenous agents. Acute chemical colitis was induced by intracolonic instillation of 1.2 ml of 4% acetic acid solution. Prednisolone (1 mg/kg), sulfasalazine (100 mg/kg) and DA-6034 (0.3 to approximately 3 mg/kg) were orally administered twice daily for 6 days in these rats. In addition, chronic chemical colitis was induced by intracolonic administration of trinitrobenzene sulfonic acid (TNBS) 30 mg in 50% ethanol and agents were orally administered for 6 or 20 days. In chemical-induced IBD models, all of these agents reduced the severity of colitis and specially, DA-6034 (3 mg/kg) showed more potent effect than other drugs in macroscopic lesion score. In HLA-B27 transgenic rats, DA-6034 (3 mg/kg) and prednisolone (0.5 mg/kg) were treated orally twice daily for 6 weeks. The HLA-B27 transgenic rats showed only mild colitis, compared with the chemical-induced colitis models. DA-6034 ameliorated the loose stool and decreased microscopic damage, which is the important indicator of this model. In conclusion, oral therapy of DA-6034 attenuated the macroscopic and histologic damages of the colon in all three experimental models of IBD, which suggest that DA-6034 could be a promising drug in the treatment of IBD.

Taurine can ameliorate inflammatory bowel disease in rats.

We previously reported that the protective effect of taurine against indomethacin-induced gastric mucosal injury was due to its antioxidant effects which inhibited lipid peroxidation and neutrophil activation. In this study, we examined the effect of taurine on reducing the inflammatory parameters of trinitrobenzene sulfonic acid (TNBS)-induced inflammatory bowel disease (IBD) in rats. To induce IBD, rats were given ethanolic TNBS intracolonically. The rats then received 500 mg/kg/day of taurine per orally. The rats were sacrificed one week after IBD induction. Ulceration and inflammation of the distal colon with formation of granuloma in the vehicle-treated IBD rats after two days of administration of TNBS were observed. Treatment with 0.5 g/kg of taurine by the oral route ameliorated colonic damage and decreased the incidence of diarrhea and adhesions. Colon weight (an index of tissue edema) was markedly increased in the IBD rats after administration of TNBS, but was significantly lower after taurine treatment. Myeloperoxidase (MPO) activity in the vehicle-treated IBD rats was substantially increased compared with that of the control. The taurine-treated animals showed reduced MPO activity (35% lower) when compared with that of the vehicle-treated animals. Taurine treatment decreased basal and formyl-methionyl leucyl phenylalanine (FMLP) stimulated reactive oxygen generation in colonic tissue of the IBD rat compared with vehicle treatment after one week. These results suggest that administration of taurine reduced the inflammatory parameters in this rat model of IBD by increasing the defenses against oxidative insult.

Protective effect of taurine on TNBS-induced inflammatory bowel disease in rats.

We had previously reported that the protective effect of taurine against indomethacin-induced gastric mucosal injury was due to its antioxidant effects, which inhibited lipid peroxidation and neutrophil activation. In this study, we examined the effect of taurine on reducing the inflammatory parameters of trinitrobenzene sulfonic acid (TNBS)-induced inflammatory bowel disease (IBD) in rats. In order to induce IBD, ethanolic TNBS was given to rats intracolonically. Then they received 500 mg/kg/day of taurine orally and were sacrificed one week after IBD induction. While ulceration and inflammation of distal colon with formation of granuloma in the vehicle-treated IBD rats two days after administration of TNBS were observed, treatment with taurine ameliorated colonic damage and decreased the incidence of diarrhea and adhesion. Also, colon weight as an index of tissue edema, which was markedly increased in the IBD rats, became significantly lower after taurine treatment. Myeloperoxidase (MPO) activity in the vehicle-treated IBD rats was substantially increased, compared with that of normal control. The taurine-treated animals significantly reduced MPO activity (35% lower) when compared with that of the vehicle-treated animals. Taurine treatment decreased both basal and formyl-methionyl leucyl phenylalanine-stimulated reactive oxygen generation from colonic tissue in the IBD rats. These results suggest that the administration of taurine reduce the inflammatory parameters in this IBD rat model by increasing defending capacity against oxidative damage.

Protective effect of DA-9601, an extract ofArtemisiae Herba, against naproxen-induced gastric damage in arthritic rats.

Gastrointestinal irritation is the most frequent adverse effect in patients chronically taking nonsteroidal antiinflammatory drugs (NSAIDs) for the treatment of arthritic conditions. Gastroprotective effect of DA-9601, a new antiulcer agent fromArtemisiae Herba extract, against NSAID was evaluated in a rat model of arthritis that is similar in many aspects to human rheumatoid arthritis. Daily oral dosing of naproxen (30 mg/kg), one of the most commonly used NSAID, induced apparent gastric lesions as well as a significant decrease in mucosal prostaglandin E(2) (PGE(2)) and prostaglandin F(1alpha) (PGF(1alpha)) levels. Coadministration of DA-9601 prevents naproxen-induced mucosal injury and depletion, of prostaglandins, in a dose-related manner. DA-9601 did not alter the antiinflammatory or analgesic effect of naproxen. The present results suggest that DA-9601 may be useful as a mucoprotectant against NSAIDs in clinical practice.