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Heme oxygenase-1 (HO-1) is an antioxidant protein implicated in tumor progression, metastasis, and resistance to therapy. Elevated HO-1 expression is associated with stemness in several types of cancer, although this aspect has not yet been studied in colorectal cancer (CRC). Using an in vitro model, we demonstrated that HO-1 overexpression regulates stemness and resistance to 5-FU treatment, regardless of p53. In samples from CRC patients, HO-1 and endothelin converting enzyme-1 (ECE-1) expression correlated significantly, and p53 had no influence on this result. Carbon monoxide (CO) activated the ECE-1/endothelin-1 (ET-1) pathway, which could account for the protumoral effects of HO-1 in p53 wild-type cells, as demonstrated after treatment with bosentan (an antagonist of both ETRA and ETRB endothelin-1 receptors). Surprisingly, in cells with a non-active p53 or a mutated p53 with gain-of-function, ECE-1-produced ET-1 acted as a protective molecule, since treatment with bosentan led to increased efficiency for spheres formation and percentage of cancer stem cells (CSCs) markers. In these cells, HO-1 could activate or inactivate certain unknown routes that could induce these contrary responses after treatment with bosentan in our cell model. However more research is warranted to confirm these results. Patients carrying tumors with a high expression of both HO-1 and ECE-1 and a non-wild-type p53 should be considered for HO-1 based-therapies instead of ET-1 antagonists-based ones.

Ribavirin remains essential to chronic hepatitis C treatment. This paper investigates the influence of ribavirin priming to steady state before combined pegylated-interferon/ribavirin treatment on viral kinetics, ribavirin trough concentrations, genetic variability within HCV-core, -NS5B and -NS5A, and response to antiviral therapy. A prospective cohort study was made of 27 chronic hepatitis C genotype 1 naïve patients who received four weeks of ribavirin followed by pegIFN-α-2a/ribavirin for 48 weeks (Group A). The results obtained were compared with those for a control/historical group (Group B). In addition, direct sequencing and pyrosequencing were applied to determine ribavirin monotherapy-induced sequence changes. The rapid, early, and sustained virological response values obtained were 48%, 89%, and 52%, respectively, in Group A, and 52%, 90%, and 52% in Group B (P > 0.05). In the four-week combined treatment, the Group A patients showed a greater decrease in HCV-RNA (2.3 log10  IU/ml vs. 1.2 log10  IU/ml; P = 0.04), lower alanine aminotransferase levels (23.5 ± 1.33 U/L vs. 60.11 ± 18 U/L; P < 0.001) and higher mean ribavirin trough concentrations (3.28 ± 1.26 mg/L vs. 1.74 ± 0.7 mg/L; P = 0.001). No general increase in rates of nucleotide substitutions in the ribavirin monotherapy-treated patients was observed in NS5B, ISDR, or PKRbd, but there was a decrease in silent mutations in the HCV core (P = 0.04). This result was confirmed by pyrosequencing in the NS5A region. It is concluded that the ribavirin priming combined treatment with pegIFN-α-2a does not improve sustained virological response rates in HCV genotype 1 naïve infected patients. However, the greater reductions in viral load and alanine aminotransferase levels, together with the higher ribavirin trough concentration values obtained, could reflect the greater effectiveness of the treatment. Ribavirin does not have a mutagenic effect on the virus in patients with chronic hepatitis C.

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The objective of this study was to assess the antihypertensive effect and the trough to peak (T:P) ratio of lisinopril and captopril, in patients with essential hypertension.After 2 weeks of placebo, 69 of 115 eligible patients had office diastolic blood pressure (DBP) between 90 and 114 mm Hg and daytime average DBP above 85 mm Hg during a 25-h ambulatory BP monitoring (ABPM) and were randomised to receive lisinopril (20 mg once daily) or captopril (50 mg twice daily) for 4 weeks. Office and ambulatory BP were then repeated. Indices of 24-h BP and T:P ratios were calculated and compared.

<i>Strongyloides stercoralis</i> is an intestinal nematode that colonizes and reproduces in the upper small intestinal mucosa. Infection in immunocompetent hosts is self-limited but in immunocompromised patients it can be complicated and cause hyperinfection. We present a 60-year-old female who was admitted due to an exacerbation of acquired thrombotic thrombocytopenic purpura requiring high doses of corticosteroids. The patient began to experience persistent pyrosis, nausea, vomiting, and oral intolerance. She was di­agnosed with syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Upper endoscopy was performed and showed esophageal, gastric, and duodenal mucosa with edema and erythema. Moreover, there were superficial erosions and thickened folds in duodenum. Gastric and duodenal biopsies were taken. Abdominal computed tomography and magnetic enteroresonance displayed duodenal dilation and inflammatory changes. The histological study of biopsies showed colonization by <i>S. stercolaris</i> in the antrum and duodenum. <i>S. stercolaris</i> is a human parasite that is endemic in tropical, subtropical, and temperate regions. Its lifecycle is complex because it completes its entire cycle within the human host; it penetrates the skin, migrates to the lungs, and reach the gastrointestinal tract. The most affected site is the duodenum and upper jejunum. The lifecycle includes autoinfection through the intestinal mucosa or perianal skin, especially in immunocompromised hosts. Immunossuppression can lead to hyperinfection syndrome and disseminated disease. However, involvement of the stomach has relatively rarely been reported. SIADH has been related to systemic hyperinfection, although the mechanism is not clear. The relatively nonspecific clinical and imaging features and the low sensitivity of routine parasite tests make the diagnosis challenging and delayed.