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Background: Concerns about the hepatitis C virus (HCV) are due to the high risk of chronic liver disease and poor treatment efficacy. Synthesizing evidence from multiple data sources is becoming widely used to estimate HCVinfection prevalence. This paper aims to estimate the prevalence of HCV infection, and the hepatic and extrahepatic sequelae in at-risk groups, using routinely collected data in the Lazio region, Italy. Methods: HCV laboratory surveillance and dialysis, hospital discharge, and drug-user registers were used as information sources to identify at-risk groups and to estimate HCV prevalence and sequelae. Full name and birth date were used as linkage keys for the various health registries. Prevalence was estimated as the percentage of cases within the general population and the at-risk groups, with 95% confidence intervals (95% CI) from 1997 to 2001. The risk of sequelae was estimated through a follow-up of hospital discharges up to December 31, 2004 and calculated as the prevalence ratio in HCV-positive and HCV-negative people, within each at-risk group, with 95% CI. Results: There were 65,127 HCV-infected people in the study period; the prevalence was 1.24% (95%CI = 1.23%-1.25%) in the whole population, higher in males and older adults. Drug users (35.1%; 95%CI = 34.6-35.7) and dialysis patients (21.1%; 95%CI = 20.2%-22.0%) showed the highest values. Medical procedures with little exposure to blood resulted in higher estimates, ranging between 1.3% and 3.4%, which was not conclusively attributable to the surgical procedures. Cirrhosis, hepatocellular carcinoma and encephalopathy were the most frequent hepatic sequelae; cryoglobulinaemia and non-Hodgkin's lymphoma were the most frequent extrahepatic sequelae. Conclusions: Synthesising data from multiple routine sources improved estimates of HCV prevalence and sequelae in dialysis patients and drug users, although prevalence validity should be assessed in survey and sequelae need a welldefined longitudinal approach. [ABSTRACT FROM AUTHOR]

Protein kinase (PK)C?is a critical regulator of mature T-cell activation and proliferation, being implicated in TCR-triggered nuclear factor (NF)-?B activation and providing important survival signals to leukemic T cells. We previously showed that overexpression of pTa/pre-TCR and constitutive activation of NF-?B characterize the T-cell leukemia/lymphoma developing in Notch3-IC transgenic mice. We report here that PKC?is a downstream target of Notch3 signaling and that its activation and membrane translocation require a functional pre-TCR in order to trigger NF-?B activation in thymocytes and lymphoma cells of transgenic mice. Furthermore, deletion of PKC?in Notch3-IC transgenic mice reduces the incidence of leukemia, correlating with decreased NF-?B activation. This paper therefore suggests that PKC?mediates the activation of NF-?B by pre-TCR in immature thymocytes and contributes to the development of Notch3-dependent T-cell lymphoma.Oncogene (2005) 24, 992-1000. doi:10.1038/sj.onc.1208302 Published online 13 December 2004 [ABSTRACT FROM AUTHOR]

Inflammation plays a key role in coronary artery disease (CAD), but whether it is involved in the pathogenesis of syndrome X (SX) is not known. Thus, we assessed the presence of systemic inflammation in patients with SX and its possible relation to infections from Helicobacter pylori, Chlamydia pneumoniae, cytomegalovirus, and Epstein-Barr virus. We studied 55 patients with SX (57 ± 8 years old; 27 women), 49 with stable angina and obstructive CAD (56 ± 8 years old; 24 women), and 60 healthy controls (57 ± 11 years old; 24 women). Plasma levels of high-sensitivity C-reactive protein and interleukin-1 receptor antagonist were measured in all patients. Infection from Helicobacter pylori, Chlamydia pneumoniae, cytomegalovirus, and Epstein-Barr virus was assessed in 43 patients with SX, 40 patients with CAD, and in 39 controls. Patients with SX had lower serum levels of C-reactive protein than did patients with CAD (4.06 ± 6.8 vs 5.99 ± 7.8 mg/L, p = 0.013) but higher levels of C-reactive protein than did controls (1.75 ± 1.98 mg/L; p = 0.008). Plasma levels of interleukin-1 receptor antagonist were higher in patients with CAD (570 ± 738 pg/ml) and patients with SX (494 ± 677 pg/ml) than in controls (254 ± 174, pg/ml; p = 0.0003 vs CAD and p = 0.013 vs SX) but did not differ significantly between patients with CAD or SX (p = 0.20). There were no differences across groups in the prevalence of infection from Helicobacter pylori, Chlamydia pneumoniae, cytomegalovirus, and Epstein-Barr virus and in the prevalence of 1, 2, 3, and 4 infections (p = 0.99). Among patients with SX, no correlation was found between markers of inflammation and indexes of disease activity (angina episodes, exercise test results). Our data show evidence of increased low-grade systemic inflammation in patients with cardiac SX, which was unrelated to an increased infectious pathogen burden. [Copyright &y& Elsevier]

Deals with a study that assessed the incidence and determinants of bacterial infections in HIV-positive people receiving medications for primary prophylaxis of Pneumocystis carinii pneumonia and toxoplasmic encephalitis within a randomized critical trial. Methodology; Statistical analysis; Results.

Presents a letter to the editor about Helicobacter pylori infections.

Background: The pathogenesis of unstable angina is poorly understood, and predicting the prognosis is problematic. Evidence suggests that there may be active inflammation, possibly in the coronary arteries, in this syndrome. We therefore studied the prognostic value of measurements of the circulating acute-phase reactants C-reactive protein and serum amyloid A protein, which are sensitive indicators of inflammation. Methods: We measured C-reactive protein, serum amyloid A protein, creatine kinase, and cardiac troponin T in 32 patients with chronic stable angina, 31 with severe unstable angina, and 29 with acute myocardial infarction. Results: At the time of hospital admission, creatine kinase and cardiac troponin T levels were normal in all the patients, but the levels of C-reactive protein and serum amyloid A protein were ≥ 0.3 mg per deciliter (exceeding the 90th percentile of the normal distribution) in 4 of the patients with stable angina (13 percent), 20 of the patients with unstable angina (65 percent), and 22 of the patients with acute myocardial infarction (76 percent). The 20 patients with unstable angina who had levels of acute-phase reactants ≥ 0.3 mg per deciliter had more ischemic episodes in the hospital than those with levels <0.3 mg per deciliter (mean [±SD] number of episodes per patient, 4.8 ±2.5 vs. 1.8 ±2.4; P = 0.004); 5 patients subsequently had a myocardial infarction, 2 died, and 12 required immediate coronary revascularization. In contrast, no deaths or myocardial infarction occurred among the 11 patients with levels of acute-phase reactants <0.3 mg per deciliter, and only 2 of them required coronary revascularization. Among the patients admitted with a diagnosis of acute myocardial infarction, unstable angina preceded infarction in 14 of the 22 patients (64 percent) with levels of acute-phase reactants ≥ 0.3 mg per deciliter but in none of the 7 patients with levels <0.3 mg per deciliter. Conclusions: Elevation of C-reactive protein and serum amyloid A protein at the time of hospital admission predicts a poor outcome in patients with unstable angina and may reflect an important inflammatory component in the pathogenesis of this condition. (N Engl J Med 1994;331:417-24). [ABSTRACT FROM AUTHOR]