Biomedical subjects
Publications and source records attributed to R Giuliani.
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BACKGROUND: Malignant insulinoma is a rare tumor. Metastatic disease confined to the liver can be treated with various locoregional treatments. CASE REPORT: We report a case of a young woman who developed liver metastases twelve years following resection of a pancreatic insulinoma positive to anti-insulin antibodies. With five cycles of intra-arterial locoregional chemotherapy (fluorouracil and epirubicin) to the liver and monthly hormone therapy (octreotide) the patient obtained a clinical complete response. After twelve months she is still disease free. CONCLUSION: Locoregional therapy for insulinoma metastatic to the liver might represent the treatment of choice; hepatic intra-arterial chemotherapy is an interesting therapeutic approach which deserves attention. The role of somatostatin analogs is limited to symptom control.
OBJECTIVES: Mercury (Hg), one of the most diffused and hazardous organ-specific environmental contaminants, exists in a wide variety of physical and chemical states, each of which with unique characteristics of target organ specificity. Exposure to Hg vapour and to organic mercurials specifically affects the CNS, while the kidney is the target organ for inorganic Hg compounds. Despite the increasing number of studies, the molecular bases of the nephrotoxic potential of Hg has not, up to now, been clarified, even if there is evidence suggesting that the ability of the metal to interact with proteins (thiol groups) or to generate oxygen radicals may play a major role. Within this context, the aim of the present study was to investigate, in vitro, the mechanism(s) of the early nephrotoxic potential of mercury chloride (HgCl2), one of the most diffused and biologically active mercury (Hg2+) compounds. For this purpose, two kidney-derived in vitro systems (the MDCK and the LLC-PK1 cell lines) were tested for their sensitivity to the salt, and MDCK was chosen as the most suitable in vitro model for our study. As possible biological markers of the organ-specific toxicity of the metal we analysed: i) critical biochemical parameters related to oxidative stress conditions (effect of Hg2+ on the anti-oxidant status of the cell), and ii) gap-junctional function (GJIC). METHODS: Classical toxicity tests (MTT and NR) were used for assessing the sensitivity (IC50) of LLP-CK1 and MDCK cell lines to the mercuric salt. Complete solubilisation of the salt in the culture media was verified by inductively coupled plasma mass spectrometry (ICP-MS). The influence of the metal on cell growth rate and viability were evaluated by conventional proliferation assays. For the following mechanistic studies, cells were exposed for different time periods (4 to 72 hours) to non-cytotoxic (0.1-50 microM) HgCl2 concentrations. The biochemical analysis of the pro-oxidant properties of the mercuric compound was performed by the measurement of anti-oxidant cellular defences against H2O2 [catalase (Cat), glutathione peroxidase (Gpx), and total glutathione (GSH)]. The influence of the metal on the GJIC capacity of MDCK cells was assessed by the "microinjection/dye-coupling" assay. RESULTS: Among the two kidney-derived in vitro systems, MDCK cell line was the most specifically sensitive to the toxic effect of HgCl2: it was, consequently, chosen as a "tubular cell model" for the following experimental steps. Tested for various time periods at increasing concentrations, the HgCl2 effect on MDCK cell proliferation and viability was found to be time- and dose-related. For concentrations < or = 50 microM, HgCl2 inhibits MDCK cell growth rate, being this effect significant (> 50% in respect to untreated controls) from the 24th from the beginning of the treatment, while, for concentrations > 50 microM, the metal causes cell death. Concerning the influence of HgCl2 on MDCK anti-oxidant defences, the most interesting results were obtained by analysing the influence of the mercury salt on the GSH cell content and Gpx activity. Both were, in fact, significantly affected by the presence of the mercury ion. HgCl2 also induced a rapid, dose- and time-related inhibitory effect on the GJIC capacity of the cells. CONCLUSIONS: Even if further investigations are needed to better clarify the possible causal relationship between our findings, they indicate that: a) MDCK cells represent a suitable in vitro model for the study of Hg nephrotoxicity; b) GJIC function is, among those considered in our study, one of the most sensitive biological endpoints for investigating the mechanism(s) of Hg2+ specific toxicity.
BACKGROUND: Lead (Pb) is an environmental toxin whose acute intoxication causes haematological, gastrointestinal and neurological dysfunctions. Moreover it is well-established that prolonged exposure to low levels of inorganic Pb compounds is closely related to hypertension in experimental animals and occupationally exposed humans. Previous reports have suggested that endothelins (ETs), a family of peptides with potent vasoconstrictive properties, might be involved in the pathogenesis of lead-induced hypertension. In vivo studies demonstrated that rats chronically exposed to Pb low levels exhibited blood pressure elevation coupled with an increase of ET-3 concentration in plasma and urine in comparison with control animals. OBJECTIVE: Since kidney is one of the target organs of lead injury, as well as the site of production/action of ETs, we investigated the effects of an inorganic Pb compound (Pb chloride) on the synthesis and secretion of these peptides, using, as in in vitro model, a renal-derived cell line (MDCK). METHODS: The ETs assays in culture media of sub-confluent cell cultures exposed to different concentration of PbCl2 were performed by Enzyme linked Immunoassay (EIA), using two experimental procedures: a) cultures were exposed to 1100 and 200 microM PbCl2 for 30 min, next cells received Pb-free culture medium up to 24 h (pulse/chase experiment); b) cultures were fed continuously up to 24 h with treatment media containing the same PbCl2 concentrations (pulse experiment). Concomitantly, the Pb influence on cell viability was evaluated by different cytotoxicity assays (LDH release, DAPI staining and cell density assays). The mRNA expression of ET-1 was evaluated in pulse experiments by RT-PCR analysis before and after cell exposure to PbCl2. The Pb2+ cellular content of parallel MDCK cell cultures was assessed by AAS analysis. RESULTS: In our experimental conditions, the administration of PbCl2 to sub-confluent MDCK cell cultures did not significantly affect cell viability. Either in pulse or in pulselchase experiments, the ETs content, evaluated in culture media of cells exposed to 100 microM PbCl2, significantly increased. On the contrary, cell treatment with 1 or 200 microM PbCl2 did not modify the ETs secretion. Because the amounts of ETs released in culture media were similar in both kinds of experiment, our results suggest that the metal induces the ETs secretion already after 30 min of cell exposure to the toxicant. Moreover, the ET-3 EIA specific assay did not reveal any immunoreactivity, excluding the involvement of this isoform in the Pb-induced secretion of ETs. Additionally, our results seem to exclude any Pb-induced up-regulation of ET-1 transcripts. The Pb2+ quantification in cell extracts demonstrated that the uptake of the metal is dose- and time-dependent and, in pulse experiments, it was maximum after six hours from the beginning of treatments, then the intracellular Pb2+ content decreased. This last phenomenon suggests the involvement of an ATP-dependent transporter in the mechanism of Pb cell excretion. Moreover, the ETs cell release in culture media of MDCK cells appears to depend on the intracellular content of Pb ions reached within 30 min of treatment. CONCLUSION: Our results indicate that there is a range of PbCl2 doses (100 microM) at which MDCK cells enhance their ETs secretion. Lower doses (1 microM) of Pb salt seem to be ineffective to stimulate ETs release, while, doses equivalent to 200 microM seem to inhibit this phenomenon.
The Authors go over the different stages that made up the development of the neonatal orthopedic treatment by dwelling upon the most interesting and important aspects of each technique.
The Authors, after dealing with the evolution of this kind of therapy, illustrate the multidisciplinary protocol for the treatment of patients with cleft lip and palate and in particular they explain the technique used for the neonatal orthopedic treatment by analyzing its methods and purposes.
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After a brief examination of the most modern conceptions relating to amyloidosis desease a case of sistemic amyloidosis localized in the oral cavity is presented by the authors. An iconografic series of the lesions affecting the mucous membrane of the lips, checks and tongue is meant to contribute to an easier and immediate finding of analogous cases marked by a primary localization in the oral cavity, thus facilitating an early diagnosis of the sistemic desease.
The Authors have tried Althesin as a medicine for the induction and maintainement of the narcosis in the stomatological, maxillo-facial and extra and intra-oral surgery. They have deduced that CT 1341 does not constitute to the anaesthetics Ethrane and Fluothane because of the anaesthetic-level instability (restlessness of the patient and clonic movements of the limbs during the most painful operations in particular). The Authors, supporters of the balanced anaesthesia, suggest using Althesin in the narcosis induction, the maintaining of which is carried on by the N.L.A. type II medicine and by the Ethrane or Fluothane. The latest ones are to be given in very small, not dangerous quantities. The Authors have so obtained a remarkable oxygenation of the patient, a ready, calm and lucid awakening without any collateral and dangerous consequences.
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