Plasma and platelet taurine concentrations were assayed in 39 patients with insulin-dependent diabetes mellitus (IDDM) and in 34 control subjects matched for age, sex, and both total and protein-derived daily energy intake. Platelet aggregation induced by arachidonic acid in vitro at baseline and after oral taurine supplementation (1.5 g/d) for 90 d was also studied. Plasma and platelet taurine concentrations (mean +/- SEM) were lower in diabetic patients (65.6 +/- 3.1 mumol/L, or 0.66 +/- 0.07 mol/g protein) than in control subjects (93.3 +/- 6.3 mumol/L, or 0.99 +/- 0.16 mol/g protein, P < 0.01). After oral supplementation, both plasma and platelet taurine concentrations increased significantly in the diabetic patients, reaching the mean values of healthy control subjects. The effective dose (mean +/- SEM) of arachidonic acid required for platelets to aggregate was significantly lower in diabetic patients than in control subjects (0.44 +/- 0.07 mmol compared with 0.77 +/- 0.02 mmol, P < 0.001, whereas after taurine supplementation it equaled the mean value for healthy control subjects (0.72 +/- 0.04 mmol). In in vitro experiments, taurine reduced platelet aggregation in diabetic patients in a dose-dependent manner, whereas 10 mmol taurine/L did not modify aggregation in healthy subjects.

No abstract

This work was undertaken to determine whether Acanthamoeba could play a role in the survival and transmission of coxsackieviruses and focused on in vitro interactions between Acanthamoeba castellanii and coxsackie B3 viruses (CVB-3). Residual virus titer evaluations and immunofluorescence experiments revealed a remarkable CVB-3 adsorption on amoeba surfaces and accumulation inside cells. The survival of viruses was independent of the dynamics of amoeba replication and encystment. In addition, our results indicated that virus-infected amoebas can release infectious viruses during interaction with human macrophages. On the basis of these data, Acanthamoeba appears to be a potential promoter of the survival of coxsackieviruses and their transmission to human hosts.Free-living amoebas of the genus Acanthamoeba are ubiquitous in nature (34); they have been isolated from air (19, 32, 33), soil (2, 3, 6, 29), and water environments, including chlorinated swimming pools (10), drinking water (17, 28), cooling towers (5), natural thermal water (31), hospital water networks (35), and marine water (4). Acanthamoeba is characterized by a feeding and replicating trophozoitic stage which under adverse conditions can develop to a dormant cyst stage (34). Cysts are highly resistant forms capable of withstanding disinfection, desiccation, and extremes of temperature. When favorable conditions occur, the cysts hatch and the trophozoites emerge to feed and replicate. Acanthamoeba species are not parasites, as they do not require the infection of a host organism to complete their life cycles (11, 37). However, these amoebae can infect a variety of mammals, including humans, thereby producing severe and often fatal diseases. They act as opportunistic as well as nonopportunistic pathogens, are the causative agents of granulomatous amoebic encephalitis and amoebic keratitis, and have been associated with cutaneous lesions and sinusitis (18,20,(37)(38)(39). Both trophozoites and cysts have been shown to be resistant to chlorination used for disinfecting water systems (30,35,36).In addition, Acanthamoeba amoebas play a role as reservoirs for Legionella pneumophila and other amoeba-resistant microorganisms that include bacteria, fungi, and viruses (15).Enteroviruses (polioviruses, coxsackieviruses, echoviruses, and newer enteroviruses) are naked small RNA viruses of the Picornaviridae family. They are important human pathogens often causing mild febrile illness, but clinical manifestations of enterovirus infections also include meningitis, encephalitis, paralysis, and myocarditis (16,27). Gastrointestinal involvement may also result. Transmission from person to person proceeds through the fecal-oral route. These viruses are widespread in marine water and also may be acquired by eating contaminated aquatic organisms (14). Although labile, they may persist in free-flowing estuarine or marine waters for several months and in some cases during the winter months (21). Although their life span in water may be prolonged by the influence of estu...

No abstract

The present study demonstrates the in vitro effectiveness of the macrolide rokitamycin and the phenothiazine compound chlorpromazine against Acanthamoeba castellanii. Growth curve evaluations revealed that both drugs inhibit trophozoite growth in dose-and time-dependent ways. The effects of both drugs when they were used at the MICs at which 100% of isolates are inhibited were amoebistatic, but at higher doses they were amoebicidal as well as cysticidal. Experiments showed that when rokitamycin was associated with chlorpromazine or amphotericin B, rokitamycin enhanced their activities. Furthermore, low doses of rokitamycin and chlorpromazine, alone or in combination, blocked the cytopathic effect of A. castellanii against WKD cells derived from the human cornea. These results may have important significance in the development of new anti-Acanthamoeba compounds.Acanthamoebas are small, ubiquitous, free-living amoebas which can exist in two forms: the motile trophozoite form and the double-walled cyst form (26,32). In the encysted state they are protected from unfavorable environmental conditions and are resistant to extremes of temperature, desiccation, and microbial agents (3,18,19,42). Human infections are generally site specific: corneal and neural tissues are the primary targets, although other tissues can be affected. These amoebas have been associated with amoebic keratitis, especially in contact lens wearers, and with chronic but fatal granulomatous amoebic meningoencephalitis (GAE) (27). They have also been identified as agents of cutaneous nodules and abscesses, arthritis, and rhinosinusitis (16,24,40,41). Most recently, Acanthamoeba has been recognized as an opportunistic pathogen of humans and other animals and is known to cause a spectrum of infections in immunocompromised individuals, including those with AIDS (4,6,8,20,37). Eradication of these protozoa from infection sites is difficult because under adverse conditions the amoeba encyst and medical therapy is often less effective against cysts than against trophozoites. There are numerous reports of drugs that have the potential for the treatment of Acanthamoeba keratitis. Infections with this organism are usually treated with a combination of cationic antiseptics (polyhexamethylene biguanide), which inhibit the membrane, and aromatic diamidines (propamidine isethionate), which inhibit DNA synthesis (23,25,28,31). More recently, chlorhexidine, alone or in combination with propamidine isethionate, has also been successfully applied (35). The therapeutic treatment for GAE or disseminated acanthamoebiasis is more problematic. Although two GAE cases were successfully treated by chemotherapy with ketoconazole or fluconazole and sulfadiazine after surgical excision of the lesions (29, 36), at present, no clinical trial of these treatments for Acanthamoeba systemic infections has yet been attempted. This is due to the low sensitivity of Acanthamoeba to many antiamoebic agents and, in the case of GAE, to the weak abilities of these agents to cross the blood...