Omega-3 fatty acids can improve radioresponse modifying tumor interstitial pressure, blood rheology and membrane peroxidability.

Several studies provide evidence that hypoxic cells present in animal and human solid tumors, may be critical for the successful treatment of cancer. In particular hypoxic cells are resistant to ionizing radiation, photodynamic treatment and the large majority of chemotherapeutic drugs. Hypoxia is generally due to the inadequacy of vascular beds supporting the tumor and to an abnormal microcirculation. Three parameters, tumor interstitial fluid, hemorheological factors and lipoperoxidation, are considered and tentatively associated as playing a role in hypoxic cell treatment. Omega three fatty acids modify these factors and are discussed for their possible ability to enhance tumor cells susceptibility to radiotherapy.

Pacing thresholds of temporary epicardial electrodes: variation with electrode type, time, and epicardial position.

We compared the variation in pacing thresholds of two widely used temporary pacing electrodes at different epicardial sites in 67 patients after coronary artery operations performed with either cardioplegia or ventricular fibrillation. In 33 patients, a bare, braided pacing wire (DW) was placed on the right ventricle and a Medtronic localized epicardial electrode (MED), on each ventricle. In the other 34 patients, the DW wire was placed on the right atrium and a MED electrode, on each atrium. Pacing thresholds were measured at the time of placement; at 1 hour, 6 hours, and 12 hours postoperatively; and daily for 4 days. The pacing thresholds (mean +/- standard error of the mean) at implantation were as follows: DW wire = 0.93 +/- 0.08 V and MED electrode = 0.63 +/- 0.1 V in the ventricles and DW = 1.28 +/- 0.18 V and MED = 0.65 +/- 0.09 V in the atria. On the fourth postoperative day, the pacing thresholds were DW = 2.08 +/- 0.21 V and MED = 1.19 +/- 0.22 V in the ventricles and DW = 2.33 +/- 0.29 V and MED = 1.04 +/- 0.09 V in the atria. The pacing thresholds of both types of wire increased significantly over time, but this deterioration was more pronounced with the braided wire both on the ventricle and on the atrium. The pacing threshold patterns were not affected by chamber side or mode of myocardial preservation. The braided ventricular wire failed to capture after 24 hours in 9 of 30 patients, whereas the localized epicardial electrode captured in all instances (p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Expression of insulin-like growth factor-1 by human ventricular explants in culture.

There is increasing evidence from animal studies for autocrine and paracrine systems in the heart. As the local role of these peptide systems in the human heart is not clear, we assessed cardiac explants in culture as a model for the study of growth factor expression by the heart in humans. Human right ventricular septal biopsies were maintained as explants for up to 9 days in serum-supplemented medium. Insulin-like growth factor-1 (IGF-1) expression was measured by radioimmunoassay and results corrected for tissue protein content. IGF-1 was synthesised by ventricular explants but not secreted into the culture medium. This culture model has the potential to provide insight into the regulation of and response to growth factor expression by the heart in humans.

Effect of plasma exchange in a patient with prolonged deep coma from thrombotic thrombocytopenic purpura.

The clinical, laboratory and instrumental data of a patient with thrombotic thrombocytopenic purpura (TTP) are reported in detail, with reference to an articulated therapeutic regimen including plasma exchange, high-dose methylprednisolone and dipiridamole. Particular emphasis is placed on the dramatic improvement obtained with this treatment despite a very delayed diagnosis and prolonged, severe neurological involvement. A short discussion and review of the literature concerning the role of plasma-exchange in the treatment of TTP is reported.

Plasma exchange in the treatment of nonadvanced stages of progressive systemic sclerosis.

Ten patients suffering from progressive systemic sclerosis, who responded poorly to conventional therapy, underwent plasma exchange (PE) therapy in conjunction with drug therapy. The frequency of PE was twice weekly for 4-6 weeks, two or three times per year, with a summer interruption, when in our own experience a spontaneous relief of symptoms occurs. To judge the efficacy of our therapeutic device, we assessed several laboratory and clinical parameters before and after therapy. The changes in circulating immune complexes, in IgG and IgA, and in some functional indices were significant (P less than 0.001). Eight of 10 patients improved satisfactorily. The remaining two did not improve sufficiently to continue the apheretic treatment. In conclusion, our study suggests that the PE, together with conventional therapy, can be an effective therapeutic device in the treatment of progressive systemic sclerosis.

Defective platelet aggregation and increased platelet turnover in patients with myelofibrosis and other myeloproliferative diseases.

In 9 patients with myeloproliferative diseases (MPD) (6 with myelofibrosis, MF, 1 with Ph1 positive chronic granulocytic leukaemia, CGL, 1 with primary eosinophilia, PE, 1 with pre-leukaemia syndrome, preL) collagen, epinephrine, and ADP-induced aggregation, N-ethylmaleimide-induced malondialdehyde (MDA) production, beta-thromboglobulin (beta-TG) plasma levels, and platelet turnover were studied. Collagen-induced aggregation was found to be normal in 7 patients, absent in 1, and reduced in 1. In all but 3 patients, aggregation with ADP was markedly reduced. Epinephrine-induced aggregation was decreased in 7 patients. No difference was found between mean MDA production in MPD (3.21 +/- 0.50 nmol/10(9) PLTs) and in control group of 21 normal subjects (3.04 +/- 0.26 nmol/10(9) PLTs). Mean beta-TG levels were significantly higher (P less than 0.01) in MPD patients (165.00 +/- 28.29 ng/ml) than in healthy controls (81.76 +/- 14.63 ng/ml). Mean platelet production half-time was significantly shorter in MPD (2.48 +/- 0.24 d) than in the control group (3.43 +/- 0.17 d), after adjustment for age by covariance analysis (P less than 0.005). Our data do not indicate an abnormal prostaglandin synthesis and are consistent with the hypothesis that a disseminated intravascular platelet aggregation might take place in MPD patients.