We report on 17 Australian cases of human infection or colonization with Scedosporium inflatum. The spectrum of clinical manifestations was similar to that in infection caused by Scedosporium apiospermum. The patients were classified into three groups. Four immunocompetent patients who presented with localized infections of a joint, nail bed, eye, or sphenoidal sinus made up the first group. Our first case, in a boy with posttraumatic septic arthritis, responded to surgical drainage with amphotericin B followed by treatment with itraconazole. The other three cases were cured by surgery alone. The second group consisted of five immunocompromised patients who presented with disseminated infections in a variety of sites. Four of these patients did not respond to antifungal therapy and died. The fifth apparently responded to antifungal drugs after correction of his neutropenia. The third group included eight patients with asymptomatic colonization in the external ear (five cases) or respiratory secretions (three cases). The nine isolates of S. inflatum tested by both disk and agar dilution methods were resistant to antifungal drugs. In our first case, which responded clinically to itraconazole, the MIC of this drug for the fungal isolate was 25 micrograms/mL. Thus S. inflatum can cause a broad spectrum of human infections whose severity and prognosis depend largely on the host's immune status.

Prostatectomy is effective in reducing symptoms in most men. Men who experience a substantial reduction in symptoms were more likely to report a favourable outcome. The study confirmed that approximately one-third of men reported an unfavourable result 3 months after their operation.

The clinical management of prostatectomy has been defined in a large and representative UK sample. In some circumstances consistent variations have been identified. It is not yet clear whether these variations influence outcome. These data can be used by surgeons wishing to compare their own patient management with that described here.

Cobalamins are stored in high concentrations in the human liver and thus are available to participate in the regulation of hepatotropic virus functions. We show that cyanocobalamin (vitamin B12) inhibited the HCV internal ribosome entry site (IRES)-dependent translation of a reporter gene in vitro in a dose-dependent manner without significantly affecting the cap-dependent mechanism. Vitamin B12 failed to inhibit translation by IRES elements from encephalomyocarditis virus (EMCV) or classical swine fever virus (CSFV). We also demonstrate a relationship between the total cobalamin concentration in human sera and HCV viral load (a measure of viral replication in the host). The mean viral load was two orders of magnitude greater when the serum cobalamin concentration was above 200 pM (P < 0.003), suggesting that the total cobalamin concentration in an HCV-infected liver is biologically significant in HCV replication.T he hepatitis C virus (HCV) is an important human pathogen, infecting about 1% of the global population. Approximately 30% of chronically infected carriers develop serious liver disease, making it the single leading indicator for liver transplantation (1). HCV is believed to be noncytopathic, and hepatocellular injury likely results from an abortive immune response to virus-infected cells. During HCV infection, HCV RNA replicates by using a virally encoded RNA-dependent RNA polymerase without a DNA intermediate (2). Because the virion presumably contains only the positive-strand genomic RNA and the virally encoded structural proteins, translation of the HCV genome to produce the viral proteins required for replication is an early obligatory step in the replication cycle. Translation initiates in the 5Ј untranslated region (UTR) and proceeds 5Ј to 3Ј along the positive strand genomic RNA, whereas transcription to synthesize the negative-strand RNA is thought to initiate in the 3Ј UTR of the positive strand and proceeds from 3Ј to 5Ј. It is unlikely that the transcription complex (replicase) of a positive-strand RNA virus can compete with actively translating ribosomal subunits for the same RNA template (3-5). Therefore, HCV should down-regulate its own translation to achieve initiation of transcription. Such regulatory mechanisms probably affect initiation, rather than elongation, thus allowing the translation machinery to clear the template (4). The virus can use a virally encoded protein or cellular factor as a regulatory agent, targeting the HCV internal ribosome entry site (IRES) (6). It is reasonable to suggest that a highly tissue-specific virus like HCV may evolve to use a compound in which that tissue is rich for such a regulatory purpose.HCV initiates translation by a mechanism that is distinct from the usual eukaryotic cap-dependent mechanism (7). Antiviral drug design targeting this mechanism has been proposed (8, 9), because it may yield a therapy with high viral specificity and low host cellular toxicity. The putative regulatory mechanism outlined above suggests that partial inhibition of H...