STI declines among sex workers and clients following outreach, one time presumptive treatment, and regular screening of sex workers in the Philippines.

OBJECTIVES: This intervention linked research aimed to reduce prevalence of Neisseria gonorrhoeae (Ng) and Chlamydia trachomatis (Ct) among female sex workers by means of one round of presumptive treatment (PT), and improved prevention and screening services. METHODS: A single round of PT (azithromycin 1 g) was given to all female sex workers reached during a 1 month period of enhanced outreach activity. Routine sexually transmitted infection (STI) screening services were successfully introduced for two groups of unregistered sex workers who work in brothels (BSWs) and on the street (SSWs). No changes were made to existing screening methods for registered sex workers (RSWs) or lower risk guest relations officers (GROs). Cross sectional prevalence of Ng and Ct was measured by PCR on three occasions, and stratified by type of sex work. Ng/Ct prevalence was assessed twice in clients of BSWs. RESULTS: Prevalence of Ng and/or Ct at baseline, 1 month post-PT, and 7 months post-PT was BSWs: 52%, 27%, 23%; SSWs: 41%, 25%, 28%; RSWs: 36%, 26%, 34%; GROs: 20%, 6%, 24%, respectively. Ng/Ct declines 1 month post-PT were significant for all groups. 6 months later prevalence remained low for BSWs (p<0.001), and SSWs (p = 0.05), but had returned to pre-intervention levels for the other groups. Prevalence of Ng/Ct among clients of BSWs declined from 28% early in the intervention to 15% (p = 0.03) 6 months later. CONCLUSIONS: In this commercial sex setting, one round of PT had a short term impact on Ng/Ct prevalence. Longer term maintenance of STI control requires ongoing access to effective preventive and curative services.

4-Aminopyridine inhibits the neuromuscular effects of nitric oxide and 8-Br-cGMP.

The effects induced by nitric oxide (NO) in different tissues depend on direct and/or indirect interactions with K+ channels. The indirect interaction of NO is produced by activation of guanylyl cyclase which increases the intracellular cGMP. Since NO, cGMP and 4-aminopyridine alone induce tetanic fade and increase amplitude of muscular contractions in isolated rat neuromuscular preparations, the present study was undertaken to determine whether or not the neuromuscular effects of NO and 8-Br-cGMP can be modified by 4-aminopyridine. Using the phrenic nerve and diaphragm muscle isolated from male Wistar rats (200-250 g), we observed that L-arginine (4.7 mM) and 8-Br-cGMP (18 M), in contrast to D-arginine, induced an increase in the amplitude of muscle contraction (10.5 0.7%, N = 10 and 8.0 0.7%, N = 10) and tetanic fade (15 2.0%, N = 8 and 11.6 1.7%, N = 8) at 0.2 and 50 Hz, respectively. N G-nitro-L-arginine (4 mM, N = 8 and 8 mM, N = 8) antagonized the effects of L-arginine. 4-Aminopyridine (1 and 10 M) caused a dose-dependent increase in the amplitude of muscle contraction (15 1.8%, N = 9 and 40 3.1%, N = 10) and tetanic fade (17.7 3.3%, N = 8 and 37.4 1.3%, N = 8). 4-Aminopyridine (1 M, N = 8) did not cause any change in muscle contraction amplitude or tetanic fade of preparations previously paralyzed with d-tubocurarine or stimulated directly. The effects induced by 4-aminopyridine alone were similar to those observed when the drug was administered in combination with L-arginine or 8-Br-cGMP. The data suggest that the blockage of K+ channels produced by 4-aminopyridine inhibits the neuromuscular effects induced by NO and 8-Br-cGMP. Therefore, the presynaptic effects induced by NO seem to depend on indirect interactions with K+ channels.

4-Aminopyridine inhibits the neuromuscular effects of nitric oxide and 8-Br-cGMP

The effects induced by nitric oxide (NO) in different tissues depend on direct and/or indirect interactions with K+ channels. The indirect interaction of NO is produced by activation of guanylyl cyclase which increases the intracellular cGMP. Since NO, cGMP and 4-aminopyridine alone induce tetanic fade and increase amplitude of muscular contractions in isolated rat neuromuscular preparations, the present study was undertaken to determine whether or not the neuromuscular effects of NO and 8-Br-cGMP can be modified by 4-aminopyridine. Using the phrenic nerve and diaphragm muscle isolated from male Wistar rats (200-250 g), we observed that L-arginine (4.7 mM) and 8-Br-cGMP (18 æì©, in contrast to D-arginine, induced an increase in the amplitude of muscle contraction (10.5 0.7 percent, N = 10 and 8.0 0.7 percent, N = 10) and tetanic fade (15 2.0 percent, N = 8 and 11.6 1.7 percent, N = 8) at 0.2 and 50 Hz, respectively. N G-nitro-L-arginine (4 mM, N = 8 and 8 mM, N = 8) antagonized the effects of L-arginine. 4-Aminopyridine (1 and 10 æì© caused a dose-dependent increase in the amplitude of muscle contraction (15 1.8 percent, N = 9 and 40 3.1 percent, N = 10) and tetanic fade (17.7 3.3 percent, N = 8 and 37.4 1.3 percent, N = 8). 4-Aminopyridine (1 æì¬ N = 8) did not cause any change in muscle contraction amplitude or tetanic fade of preparations previously paralyzed with d-tubocurarine or stimulated directly. The effects induced by 4-aminopyridine alone were similar to those observed when the drug was administered in combination with L-arginine or 8-Br-cGMP. The data suggest that the blockage of K+ channels produced by 4-aminopyridine inhibits the neuromuscular effects induced by NO and 8-Br-cGMP. Therefore, the presynaptic effects induced by NO seem to depend on indirect interactions with K+ channels