Biomedical subjects
Publications and source records attributed to A Russo.
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A study on the prevalence of seropositivity to T.gondii, Rubella virus, Cytomegalovirus and Herpes simplex virus (type 1 and type 2) was carried out in pregnant women aged 15-45 years. An overall prevalence of 40.7% to T.gondii, of 90.1% to Rubella virus, of 80.8% to Cytomegalovirus, of 82.3% and of 69% to Herpes simplex virus, respectively type 1 and type 2 was found. Cytomegalovirus infection was prevalent in women from low socioeconomic background. Herpes simplex 1 infection was higher in women living in quarters of high density population, whereas antibody prevalence to Rubella virus was higher in women from high socioeconomic setting. The expected fetal risk for T.gondii, Rubella and Cytomegalovirus infections has been assessed on the basis of the yearly seroconversion rate for each pathogen in the study population and of the known transplacental transmission rates after primary and recurrent infection in pregnancy. Thus, the expected incidence of congenital T.gondii infection in this geographic area is 0.2-0.3%, of congenital Rubella infection of 0.02% and of congenital Cytomegalovirus infection of 0.3-1.15%.
The cellular response to radiation and various chemotherapy drugs, whose mechanism in part includes production of free radicals or DNA damage, may be altered by modification of cellular thiols. The recent introduction of agents which either inhibit glutathione (GSH) biosynthesis (buthionine sulfoximine, BSO) or stimulate GSH synthesis (oxothiazolidine-4-carboxylate, OTZ) has enabled detailed studies assessing the role of GSH in the radiation and chemotherapy response. GSH depletion by BSO has resulted in radiosensitization of both aerobic and hypoxic cells, with some discrepancy among laboratories as to the extent of sensitization of hypoxic cells. GSH elevation (by approximately 200% of control) has resulted in modest protection of aerobic and hypoxic cells. GSH has been shown to play an important role in the radiosensitization of hypoxic cells using nitroimidazoles. The extent of nitroimidazole hypoxic radiosensitization has recently been shown to depend on intracellular GSH levels. Recent findings that some human tumour cell lines, as opposed to rodent cell lines, are high in cellular GSH have prompted a need to evaluate in vivo, GSH levels in human tumours. Possible roles of GSH in the chemotherapy response include: (1) detoxification of H2O2 and/or organoperoxides through GSH peroxidase, (2) non-catalyzed nucleophilic reaction of GSH and drug, (3) binding of the drug with GSH catalyzed by GSH transferase, and (4) activation of certain drugs to toxic species by GSH. The role of GSH as it relates to the various topics mentioned above is discussed with emphasis on direction for future studies.
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One case of lumbar extradural abscess of brucellar etiology without spondylodiscitis is described. The recovery was obtained only with antibiotic therapy.
Some clinical studies that were performed for the purpose of assessing the potential cardiotoxicity of mitoxantrone (DHAD) have shown that repeated administrations of the drugs in some patients cause a mild impairment of cardiac functions and morphological changes in the myocardial cells qualitatively similar to those elicited by anthracyclines. Since doxorubicin has been reported to cause acute cardiac effects, probably related to its chronic cardiotoxicity, experiments were carried out on the rabbit heart to investigate whether DHAD is also able to induce acute cardiac effects. Our results show that this drug caused a reversible dose-related impairment of cardiac contractility on the isolated and perfused rabbit heart while it was not able to induce ECG alterations in normal rabbits. These findings demonstrate that in the rabbit DHAD induces an acute cardiac activity qualitatively similar to that of doxorubicin and suggest that this animal model could be a useful tool to study the cardiac actions and related pathogenetic mechanism(s) of this antitumor drug.
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Although the susceptibility of resting B lymphocytes to radiation-induced interphase death is well known, the mechanism by which this occurs is not understood. In this report, we use three measures of plasma membrane integrity (increase in cell volume, uptake of trypan blue, and release of 51Cr) to assess the effect of radiation on the resting B cell plasma membrane. The delivery of 500 to 1000 rad caused the majority of resting B cells to enlarge slightly, whereas 3000 rad caused virtually all of the cells to approximately double in size within 3 to 4 hr. Measurement of the release of 51Cr from resting B cells revealed a similar relationship between the dose of radiation and the loss of radioactive label. Trypan blue exclusion was also found to diminish as a function of radiation dose. An analysis of a variety of lymphoid cells suggested that sensitivity to the membrane damaging effects of gamma radiation was in the order of resting B cells greater than resting T cells greater than a long-term L3T4+ T cell clone greater than a B cell lymphoma. LPS-induced B cell blasts treated with 3000 rad were equivalent to 1000 rad-treated resting B cells. The effects of the gamma radiation could be ameliorated by excluding oxygen (a diradical molecule that can potentially enhance the generation and propagation of highly reactive free radicals) at the time of irradiation, or by adding the free radical scavenging agent cysteamine. These data are compatible with the hypothesis that gamma radiation results in damage to the plasma membrane of resting lymphocytes via the generation of highly reactive free radical species. This damage is reflected in a rapid increase in plasma membrane permeability and swelling of the cells, and may play a major role in causing interphase death.
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Ovariectomy caused a significant increase of immunoreactive dynorphin-like material (IR-DYAN) in the anterior pituitary lobe of intact as well as of medial basal hypothalamus-lesioned rats. No change of IR-DYAN was observed in the neurointermediate lobe of the gland or in the hypothalamus. Estradiol benzoate reversed the increase of anterior pituitary IR-DYAN induced by ovariectomy and caused a reduction in sham-ovariectomized rats.
Lymphocyte subpopulations were studied by means of sheep red blood cell (SRC)-rosetting technique and OKT11, OKT3, OKT4, and OKT8 monoclonal antibodies in ten Sicilian glucose-6-phosphate dehydrogenase-deficient children during the hemolytic crisis due to fava bean ingestion. The number of SRC-rosetting lymphocytes was significantly reduced, while the number of OKT3-positive cells was normal. An inversion of the OKT4/OKT8 ratio was observed, due to a decrease of OKT4-positive cells and an increase of OKT8-positive cells. All these abnormalities reverted to normal in the four children studied after recovery.
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