Several experimental studies have suggested that specific nutrients might play a role on the risk of liver damage. Nevertheless, few epidemiological studies have evaluated the role of diet on the ...risk of symptomatic liver cirrhosis, giving contradictory results. To evaluate the role of the intake of nutritional factors and dietary patterns on the risk of symptomatic liver cirrhosis and to examine their combined action with alcohol consumption we used data from the Italian Study on Liver Cirrhosis Determinants project. From 1994 to 1998 all the consecutive cirrhotic inpatients admitted to 19 Italian collaborative hospitals for signs of liver decompensation in whom the diagnosis of liver cirrhosis was made for the first time (259 cases) and one or two gender, age and area of residence matched individuals (416 controls) were recruited. Data on lifetime alcohol intake, usual consumption of 191 food items and on markers of hepatitis B and C viral infection were collected. The analysis of principal components identified a nutritional pattern positively correlated with vegetable and fruit intakes and negatively with animal and no-fruit sugar products. With respect to abstainers, relative risks in consumers of use ≤25 and ≥51 g/day of alcohol increased from 0.4 95% confidence interval 0.0, 5.9 to 9.3 1.3, 69.0 and from 2.1 1.1, 4.2 to 18.1 2.8, 118.3 for the lowest and the highest value of this nutritional pattern, respectively. Diet might therefore modulate the damaging effect of alcohol on the liver.
The potential roles of Ca2+ ions in the response of T lymphocytes to stimulation with monoclonal antisera to the T3 antigen were investigated by means of pharmacological agents that predominantly ...inhibit the flux of Ca2+ ions into cells (verapamil, nifedipine) or the activity of Ca2+-dependent kinases (trifluoperazine, polymyxin B). As assessed by uptake of 3Hthymidine, proliferation induced with anti-T3 +/- recombinant IL-2 at 72 h was inhibited by greater than 80% in the presence of nifedipine at 50 microM, and almost completely arrested (greater than 95% inhibition) with the other agents at the same concentration. Further quantitative assays of the effects of polymyxin B and trifluoperazine on C-kinase labelling of exogenous substrate showed a major reduction with both agents, but inhibition was substantially greater with polymyxin B that with trifluoperazine (IC50 = 14 and 70 microM respectively). These results were confirmed by qualitative assessment of Ca2+/phospholipid-dependent phosphorylation of endogenous substrates, which demonstrated major phosphoproteins of MW 56,000, 52,000, 43,000, and 20,000, and dose-dependent reduction in labelling in the presence of polymyxin B. Similar results were obtained under more physiological conditions in intact cells labelled with 32P orthophosphate. These findings indicate several possible roles for Ca2+ in T-cell activation, and several possible levels of activity, including modulation of calmodulin-dependent kinases and effects on Ca2+/phospholipid-dependent kinases and Ca2+ channels.
We have studied the cytotoxicity against rabbit liver cells of lymphocytes from the peripheral blood of 71 patients with various liver diseases. The group with chronic active hepatitis and three ...patients with acute alcoholic hepatitis showed significantly higher mean values of lymphocytotoxicity (P less than 0.001) compared with the other patients with chronic persistent hepatitis, post-necrotic fibrosis and cirrhosis. Wilson's disease, and prolonged viral hepatitis. The mean cytotoxicity of these last groups did not differ significantly from controls. In four out of six patients with chronic active hepatitis a significant decrease of lymphocytotoxicity was found after immunosuppressive therapy with oral prednisolone. A good correlation between the lymphocytotoxicity test and histological signs of activity suggests that a cell-mediated immune aggression is present in this disease.
IntroductionContrast-induced acute kidney injury (CI-AKI) after PCI predicts worse cardiovascular outcomes. Physiologic mechanisms, genetic predisposition and socioeconomic disparities related to ...ethnicity may contribute to the occurrence of CI-AKI.HypothesisWe evaluated the risk of CI-AKI after PCI according to ethnicity and its subsequent impact on 1-year mortality.MethodsPatients undergoing PCI at our Institution from 2009-2018 were grouped by ethnicity into White (n=7,942), Asian (n=2,604), Hispanic (n=1,431) and African American (n=1,748). CI-AKI was defined as a peri-procedural creatinine increase of >0.3 mg/dL or >50% compared to baseline. The association between ethnicity and CI-AKI was assessed using logistic regression. A sensitivity analysis was performed by including only patients with baseline CKD, defined as eGFR <60 mL/min/1.73m. The risk of 1-year mortality after CI-AKI was evaluated with multivariate Cox model.ResultsThe rate of CI-AKI was 5.8% in the overall population. Compared to White patients, the risk of CI-AKI was higher in African Americans (OR 1.45, 95% CI 1.19-1.76; p<0.001), lower in Asians (OR 0.78, 95% CI 0.65-0.98; p=0.03) and similar in Hispanics (OR 0.93, 95% CI 0.73-1.19; p=0.57). However, after adjustment for confounders, the association between ethnicity and CI-AKI was largely attenuated (Figure). Findings of sensitivity analysis in CKD patients were consistent with those in the general population. Overall, 1-year mortality was increased in patients who experienced CI-AKI (adjusted HR 1.92, 95% CI 1.39-2.66; p<0.001), but this risk was not uniform among the different subgroups (Whitep<0.001, African Americanp=0.05, Hispanicp=0.06, Asianp=0.37) (Figure).ConclusionsThe risk of CI-AKI after PCI varies according to ethnicity, however, this might be explained by differences in risk factors observed in each group. The occurrence of CI-AKI is associated with an increased risk of mortality at 1 year.
A glycoprotein termed alpha 1-acid glycoprotein (alpha 1-AGP) is a component of normal human serum; its concentration is often increased in several pathological disorders, including acute ...inflammation and cancer. Inhibitory effects of alpha 1-AGP on some in vitro T and B cell function assays have been reported but our recent data indicated that alpha 1-AGP is indeed a T cell mitogen at physiological concentrations. The present study was designed to investigate: (a) the relationship between this glycoprotein and two other glycoproteins of the T and B cell membrane, i.e. the T3 and Ia antigens; (b) the ability of lymphocytes to take up exogenous alpha 1-AGP; (c) the different expression of alpha 1-AGP on the T cell membrane upon different activation pathways, i.e., autologous non-T-cells (B cells and monocytes) phytohemagglutinin and anti-T3 monoclonal antibody (MAb) stimulations. The data reported herein show no competition at the membrane level between anti-alpha 1-AGP and anti-T3 or anti-Ia MAbs. In addition, (1) the lymphocytes were able to absorb alpha 1-AGP from the culture medium and (2) the expression of this glycoprotein was enhanced upon T cell stimulation (all three stimulants employed induced an increase of alpha 1-AGP positive T cells), thus suggesting a possible role of this glycoprotein in in vitro T cell activation.
Cinoxacin is an oral synthetic antibacterial agent, of the second generation quinolones group, with excellent efficacy in respiratory, intra-abdominal, pelvic, and skin and soft tissue infections. ...Overall, quinolones are well tolerated drugs, although phototoxicity and photoallergenicity is well demonstrated experimentally. In this report we show you a case of a man who presented a anaphylactic reaction associated with myocardial infarction, after taking a capsule of cinoxacin. We suppose that there is a direct participation of the heart in anaphylactic reactions, because acttivated mast-cells mediators can determine cardiovascular effects. Then performed double-blind placebo controlled challenge test with an alternative drug. We did not observe any adverse immediate or late adverse reaction to this drug.
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