Because hepatitis C virus (HCV) and human immunodeficiency virus (HIV) share common transmission pathways, HIV-HCV co-infection is frequent, involving about 40% of seropositive subjects particularly ...injection drug users and patients with hemophilia. We performed a retrospective analysis on clinical, epidemiological and therapeutical aspects in a population of HIV-HCV coinfected patients, observed in our Department during the period 2001-2003. Forty per cent of 404 observed patients had a co-infection; 90% of those were drug addicts and most (90.2%) were on HAART treatment. Seventy-three per cent of co-infected patients showed transaminases alterations, and 85% had detectable viremia. Prevalent genotypes were 1 (44.6%) and 3 (36.4%). The association PEG-IFN and ribavirine obtained sustained responses in 55% of 9 treated patients.
Acute kidney injury (AKI) is considered largely reversible based on the capacity of surviving tubular cells to dedifferentiate and replace lost cells via cell division. Here we show by tracking ...individual tubular cells in conditional Pax8/Confetti mice that kidney function is recovered after AKI despite substantial tubular cell loss. Cell cycle and ploidy analysis upon AKI in conditional Pax8/FUCCI2aR mice and human biopsies identify endocycle-mediated hypertrophy of tubular cells. By contrast, a small subset of Pax2+ tubular progenitors enriches via higher stress resistance and clonal expansion and regenerates necrotic tubule segments, a process that can be enhanced by suitable drugs. Thus, renal functional recovery upon AKI involves remnant tubular cell hypertrophy via endocycle and limited progenitor-driven regeneration that can be pharmacologically enhanced.
Thromboembolic complications are common in patients with cancer and represent the second cause of death in patients with overt malignant disease. The aim of this study was to investigate the ...activated protein C pathway in cancer.
We studied the coagulation cascade, natural clotting inhibitors, fibrinolytic proteins and resistance to activated protein C in 20 patients with advanced gastrointestinal cancer and 84 volunteers by measuring PT, APTT, fibrinogen, AT III, PC, PS, APC resistance, fibrinolytic system (PLG, ANPL, PAI-1, and t-PA) and activation peptides (D-Dimers, prothrombin 0 fragment 1 + 2/F1 + 2).
Laboratory tests confirmed coagulation abnormalities in cancer patients. Fibrinogen, D-Dimers and F1 + 2 were increased, while t-PA activity was significantly lower than that of controls. APC resistance was higher in cancer patients compared to the control group (55% vs 2%; P < 0.0001). Excess thrombin generation was manifested by increased F1 + 2 plasma levels in APC-resistant cancer patients. Genetic analyses showed that only one patient with a poor response to APC carried a factor V R506Q mutation in exon 10.
Our findings show a high prevalence of APC resistance in cancer, compatible with an acquired defect in the APC pathway.
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