Chronic kidney disease (CKD) has been associated with an abnormal lipid profile. Our aim was to study the interplay between oxidized low-density lipoprotein (ox-LDL), adiponectin, and blood lipids and lipoproteins in Portuguese patients with CKD under hemodialysis (HD); the influence of the pentanucleotide repeat polymorphism in the apolipoprotein(a)(apo [a]) gene upon lipoprotein(a)(Lp[a]) levels in these patients. We studied 187 HD patients and 25 healthy individuals. ox-LDL and adiponectin were measured using enzyme-linked immunoassays. Apo(a) genotyping was performed by polymerase chain reaction, followed by electrophoresis in polyacrylamide gel. Compared with controls, patients presented with significantly higher levels of adiponectin, Lp(a), and ox-LDL/low-density lipoprotein cholesterol (LDLc) ratio; significantly lower levels of total cholesterol (TC), LDLc, apo A-I, apo B, ox-LDL, and TC/high-density lipoprotein cholesterol (HDLc) ratio were also observed. Similar changes were observed for patients with or without statin therapy, as compared with controls, except for Lp(a). Multiple linear regression analysis showed that body mass index, HDLc, time on HD, and triglycerides (TG) were independent determinants of adiponectin levels, and that apo B, TG and LDLc were independent determinants of ox-LDL concentration. Concerning the apo(a) genotype, the homozygous (TTTTA)8/8 repeats was the most prevalent (50.8%). A raised proportion of LDL particles that are oxidized was observed. Adiponectin almost doubled its values in patients and seems to be an important determinant in HDLc and TG levels, improving the lipid profile in these patients. Apo(a) alleles with a lower number of repetitions are more frequent in patients with higher Lp(a).

Calprotectin is a protein released into stools, used as a marker of inflammation in inflammatory bowel diseases. We tested the hypothesis that cow's milk protein in formula milk may increase the intestinal release of calprotectin, as a consequence of a subclinical inflammatory reaction. At 12 weeks of age, we measured fecal calprotectin by an immunoenzyme assay (Calprest, Eurospital, Trieste, Italy), in 38 exclusively breastfed and in 32 exclusively formula-fed infants. Fecal calprotectin levels were not different in the two groups (p = 0.09), although a trend to higher values in infants with colic, or with family history of allergies was noted. This suggest that, in general, formula milk does not promote activation of an intestinal inflammatory reaction, compared to human milk, although a subclinical activation of the inflammatory response in infants at risk for allergic diseases may be present.

The performance of the QuantiFERON®-cytomegalovirus (CMV) assay was compared to that of a flow-cytometry intracellular cytokine staining method (ICS) for detecting CMV-specific IFN-γ-producing CD8(+) T-cell responses in allogeneic stem cell transplant recipients (allo-SCT) and for estimating their magnitude and functionality. A total of 90 whole blood specimens from 23 allo-SCT recipients was analyzed by both methods. Overall, the percentage of specimens that yielded concordant results by both methods was 68.8%(κ=0.691; 95% CI 0.548-0.835), and the sensitivity of the QuantiFERON®-CMV assay for detecting positive IFN-γ T-cell responses (>0.2 UI/mL), taking the ICS method as the reference, was 76.3%. The magnitude of IFN-γ CD8(+) T-cell responses to CMV-specific peptides measured with the QuantiFERON®-CMV assay correlated significantly (σ=0.695; P=<0.001) with that of the total IFN-γ CD8(+) T cells, functional dual (IFN-γ/TNF-α, σ=0.652; P=<0.001, and IFN-γ/CD107a, σ=0.690; P=<0.001) and trifunctional (IFN-γ/TNF-α/CD107a; σ=0.679; P=>0.001) CMV-specific CD8(+) T-cell responses as quantitated by ICS. In summary, the data indicated that the QuantiFERON®-CMV assay is less sensitive than the ICS method for detecting CMV-specific IFN-γ CD8(+) T-cell responses in the allo-SCT setting; Nevertheless, it allowed the estimation of the total and polyfunctional CMV-specific IFN-γ CD8(+) T-cell responses in specimens testing positive by both methods.

PURPOSE: Despite the recent innovations, complications of prostate biopsy can occur. The aim of this study was a prospective monitoring of major septic complications occurring after transrectal prostate biopsy, to describe their causing agents, to report the clinical course of these patients, and to give guidelines based on our personal experience. METHODS: This prospective study was carried out between January 2009 and September 2010. Complications were evaluated by telephone interviews. RESULTS: Between January 2009 and September 2010, 447 (96.5%) completed the telephone interview. Urosepsis occurred in ten patients (2.2%) and in three cases evolved into septic shock. Of these ten patients, nine had a positive blood culture, of whom eight for Escherichia coli and one for Aeromonas hydrophila, Aeromonas caviae, and Aeromonas sobria. In seven cases, the E. coli isolated were resistant to fluoroquinolone and six produced an extended spectrum beta-lactamase. Six E. coli were classified as multidrug-resistant organisms. Of the 10 patients, one died after the onset of multiorgan failure. For the other nine, the mean time spent in the hospital was 9 days (range, 6-15 days). CONCLUSIONS: Escherichia coli are developing new drug resistances. Early recognition of patients who harbor MDRO E. coli in their rectum or in the urine could be an important strategy for preventing sepsis. If a patient who has recently undergone transrectal prostate biopsy shows clinical signs of sepsis in the 48 h, a multiresistant E. coli infection must be suspected. The patient must be admitted urgently to the hospital, and carbapenem antibiotic therapy should be started.

OBJECTIVE Recombinant human erythropoietin (rhEPO) therapy under circumstances of moderate chronic renal failure (CRF), with yet lower kidney and heart lesion, may have a protective cardiac effect beyond the correction of anemia, whose mechanism deserves better elucidation, namely by clarifying the impact on gene expression profile of markers of apoptosis, inflammation, proliferation, angiogenesis, and lesion/stress in the heart. MATERIALS AND METHODS Four groups of rats were studied over a period of 15 weeks (n=7 each): control-without surgery and without drug treatment; rhEPO-treated with 50 IU/kg/week of rhEPO-beta; CRF-submitted to partial nephrectomy (3/4); CRF + rhEPO-CRF with rhEPO treatment after the 3rd week of surgery. The heart was collected in order to evaluate the gene expression, by real-time qPCR, of markers of apoptotic machinery, inflammation/immunology, proliferation/angiogenesis, and lesion/stress. RESULTS The main findings obtained were (a) CRF rats have demonstrated overexpression of EPO-R in the heart without changes on EPO expression, together with overexpression of Bax/Bcl2 ratio, PCNA, and IL-2;(b) rhEPO therapy on the heart of the rats with CRF induced by partial 3/4 nephrectomy promoted nonhematopoietic protection, demonstrated by the apoptosis prevention, viewed by the Bax/Bcl2 balance, by the promotion of proliferation, due to PCNA increment, and by the immunomodulatory action, expressed by a trend to prevent the IL-2 increment. CONCLUSION In this model of moderate CRF, rhEPO treatment showed important cardiac nonhematopoietic effects, expressed mainly by the antiapoptotic and the proproliferative action, suggesting that early rhEPO therapy in moderate stages of CRF might have further therapeutic benefits.

The Gilbert syndrome is a benign form of unconjugated hyperbilirubinemia, mainly associated with alterations in UGT1A1 gene. This work investigated the effect of UGT1A1 variants on total bilirubin levels in Gilbert patients (n=45) and healthy controls (n=161). Total bilirubin levels were determined using a colorimetric method; molecular analysis of exons 1-5 and two UGT1A1 promoter regions were performed by direct sequencing and automatic analysis of fragments. Five in silico methods predicted the effect of new identified variants. A significant different allelic distribution, in Gilbert patients and in controls, was found for two promoter polymorphisms. Among patients, 82.2% were homozygous and 17.8% heterozygous for the c.-41_-40dupTA allele; in control group, 9.9% were homozygous and 43.5% heterozygous for this promoter variant, while 46.6%(n=75) presented the [A(TA)6TAA]. For the T>G transition at c.-3279 promoter region, in patients, 86.7% were homozygous and 13.3% heterozygous; in control group, 33.5% were homozygous for the wild type allele, 44.1% were heterozygous and 22.4% homozygous for the mutated allele. The two polymorphisms were in Hardy-Weinberg equilibrium in both groups. Sequencing of UGT1A1 coding region identified nine novel variants, five in patients and four in controls. In silico analysis of these amino acids replacements predicted four of them as benign and three as damaging. In conclusion, we demonstrated that total bilirubin levels are mainly determined by the TA duplication in the TATA-box promoter and by the c.-3279T>G variant. Alterations in the UGT1A1 coding region seem to be associated with increased bilirubin levels, and, therefore, with Gilbert syndrome.

Immune mechanisms involved in control of cytomegalovirus (CMV) infection in the allogeneic stem cell transplantation setting have not been fully disclosed. CMV pp65 and IE-1-specific CD8(+) T cells expressing IFN-γ, TNF-α, and CD107a, alone or in combination, and NKG2C(+) NK cells were prospectively enumerated during 13 episodes of CMV DNAemia. The expansion of monofunctional and polyfunctional CD8(+) T cells was associated with CMV DNAemia clearance. The size and functional diversity of the expanding CD8(+) T-cell population was greater in self-resolved episodes than in episodes treated with antivirals. These differences were related to the magnitude of expansion of cognate antigen IFN-γ CD4(+) T cells. The resolution of CMV DNAemia was associated frequently with a marked expansion of both CD56(dim)/CD16(+) NK cells and NKG2C(+) CD56(bright)/CD16(-) NK cells. The data lend support to the role of polyfunctional CD8(+) T cells in controlling CMV replication in the allogeneic stem cell transplantation setting, and suggest that NKG2C(+) NK cells may be involved critically in the resolution of CMV DNAemia episodes. J. Med. Virol. 84:259-267, 2012. © 2011 Wiley Periodicals, Inc.

A comparative study of boar taint in cooked and dry-cured pig meat products was performed. Forty-eight cooked loins and 48 dry-cured hams from entire males and castrates were studied. The samples were classified according to the androstenone (AN) and skatole (SK) fat content determined using HPLC. A trained sensory panel evaluated taste, aroma, boar odour, boar flavour, juiciness, tenderness and fatness in cooked and dry-cured samples. Threshold levels of AN and SK to separate (P<0.05) entire and castrate samples according to their boar odour and flavour were determined. The effects of castration and processing on the eating quality were studied. Finally, the relationships among boar taint and other sensory attributes in cooked and dry-cured meat were compared. Results from these studies show that the eating quality of processed meat was affected negatively by boar taint. Threshold values were higher in dry-cured ham (2 μg g(-1) AN and 0.12 SK) than cooked loin (0.5 AN and 0.1 SK). AN and SK had a synergistic effect on boar odour and flavour in both products. AN had a greater influence than SK on the aroma and taste, especially in cooked meat. Boar odour was perceived more intensely than boar flavour in both of the products studied. Castration favoured fatness and improved the aroma and taste of cooked and dry-cured meat. The loss of aroma and taste due to boar taint was more noticeable in cooking than drying and curing. In dry-cured meat boar taint was associated with less aroma, taste, juiciness and tenderness. However, in cooked meat, boar taint affected the aroma and taste more strongly, but was not related with juiciness and tenderness, probably because these attributes are influenced by cooking.