Prostatic evaluation by transrectal sonography with histopathologic correlation: the echopenic appearance of early carcinoma

Fifty-two patients with clinical stage A and B carcinomas of the prostate were imaged by ultrasound (US) transrectally with a 5-MHz linear array transducer and transabdominally with a 3-MHz sector scanner prior to radical prostatectomy. The fresh specimens of 44 prostate glands were scanned in a water bath with a 5-MHz linear array transducer in multiple planes. In all cases, histopathologic correlation was obtained. Prostatic carcinoma presented as an echopenic lesion in 54% of the specimens, as a slightly hypoechoic area in 22%, and could not be identified in 24% because of its isoechoic characteristics. In contrast to many previous reports, no instance of echogenic cancer was observed.     

Biodegradation potential of some micromycetes for pentachlorophenol

A first screening was performed upon 100 strains of micromycetes cultivated on solid media (malt extract medium and mineral medium) with pentachlorophenol (PCP) (0.5 g/liter). Under these conditions, 50 strains gave a light blurring around the inoculation spot, indicating some PCP degradation. Later, 50 selected strains were cultivated in liquid synthetic medium with PCP (1 g/liter). After 6 days of cultivation, photodegradation occurred for 25%. On the whole, the consumption of PCP was 25% for Zygomycetes, 3% for yeasts, and 10-15% for Deuteromycetes, except 7% for Tuberculariales. It was shown that glucose repressed the PCP consumption. Among degrading fungi, some could grow with PCP when cultures were initiated with spores, others could not. A more detailed study was done with Phoma glomerata cultivated in liquid synthetic medium (PCP 100 mg/liter) in darkness or with light. Photodegradation increased up to 25% but abiotic degradation occurred also in darkness (8%). Consumption of PCP by Ph. glomerata was 27% after 2 days with light and was lower in darkness (19%).     

Detection of Hepatitis B Virus DNA Sequences in Liver in HBsAg Seronegative Patients with Liver Disease with and without Anti-HBc Antibodies

Excluding studies from Brechot and co-workers, little supporthas been found for a role of the hepatitis B virus in the pathogenesisof HBsAg seronegative patients with predominantly chronic liverdiseases, including primary liver cancer. In this study liverDNA from 59 predominantly British patients (four cases withpaired biopsies, 6–12 months apart) with different, mostlychronic, liver diseases was analysed by molecular hybridization.All were seronegative for HBsAg and serum hepatitis B virusDNA (dot blot hybridization) and their liver diseases were believedto be unrelated to hepatitis B virus infection. Hepatitis Bvirus DNA was detected in liver of 11 (18.6 per cent) patients;nine had episomal(3.2 Kb) DNA and eight had higher molecularweight bands suggesting integrated forms. Six patients werealso seronegative for anti-HBc. Patients of UK and non-UK originwere equally represented. Hepatitis B virus DNA was detectedin serum of six of nine patients tested using the polymerasechain reaction. The detection of hepatitis B virus DNA in liverand in serum by this assay in a significant proportion of patientswith chronic liver disease, hitherto unsuspected of being hepatitisB virus-related, suggests a possible role for this virus inlow- as well as high-prevalence countries.     

Neurotoxic mode of action of artemisinin

We recently described a screening system designed to detect neurotoxicity of artemisinin derivatives based on primary neuronal brain stem cell cultures (G. Schmuck and R. K. Haynes, Neurotoxicity Res. 2:37-49, 2000). Here, we probe possible mechanisms of this brain stem-specific neurodegeneration, in which artemisinin-sensitive neuronal brain stem cell cultures are compared with nonsensitive cultures (cortical neurons, astrocytes). Effects on the cytoskeleton of brain stem cell cultures, but not that of cortical cell cultures, were visible after 7 days. However, after a recovery period of 7 days, this effect also became visible in cortical cells and more severe in brain stem cell cultures. Neurodegeneration appears to be induced by effects on intracellular targets such as the cytoskeleton, modulation of the energy status by mitochondrial or metabolic defects, oxidative stress or excitotoxic events. Artemisinin reduces intracellular ATP levels and the potential of the inner mitochondrial membrane below the cytotoxic concentration range in all three cell cultures, with these effects being most dominant in the brain stem cultures. Surprisingly, there were substantial effects on cortical neurons after 7 days and on astrocytes after 1 day. Artemisinin additionally induces oxidative stress, as observed as an increase of reactive oxygen species and of lipid peroxidation in both neuronal cell types. Interestingly, an induction of expression of AOE was only seen in astrocytes. Here, manganese superoxide dismutase (MnSOD) expression was increased more than 3-fold and catalase expression was increased more than 1.5-fold. In brain stem neurons, MnSOD expression was dose dependently decreased. Copper-zinc superoxide dismutase and glutathione peroxidase, two other antioxidant enzymes that were investigated, did not show any changes in their mRNA expression in all three cell types after exposure to artemisinin.