Microalgae recycling improves biomass recovery from wastewater treatment high rate algal ponds.

Microalgal biomass harvesting by inducing spontaneous flocculation (bioflocculation) sets an attractive approach, since neither chemicals nor energy are needed. Indeed, bioflocculation may be promoted by recycling part of the harvested microalgal biomass to the photobioreactor in order to increase the predominance of rapidly settling microalgae species. The aim of the present study was to improve the recovery of microalgal biomass produced in wastewater treatment high rate algal ponds (HRAPs) by recycling part of the harvested microalgal biomass. The recirculation of 2% and 10% (dry weight) of the HRAPs microalgal biomass was tested over one year in an experimental HRAP treating real urban wastewater. Results indicated that biomass recycling had a positive effect on the harvesting efficiency, obtaining higher biomass recovery in the HRAP with recycling (R-HRAP) (92-94%) than in the control HRAP without recycling (C-HRAP) (75-89%). Microalgal biomass production was similar in both systems, ranging between 3.3 and 25.8 g TSS/m2d, depending on the weather conditions. Concerning the microalgae species, Chlorella sp. was dominant overall the experimental period in both HRAPs (abundance >60%). However, when the recycling rate was increased to 10%, Chlorella sp. dominance decreased from 97.6 to 88.1%; while increasing the abundance of rapidly settling species such as Stigeoclonium sp. (16.8%, only present in the HRAP with biomass recycling) and diatoms (from 0.7 to 7.3%). Concerning the secondary treatment of the HRAPs, high removals of COD (80%) and N-NH4+ (97%) were found in both HRAPs. Moreover, by increasing the biomass recovery in the R-HRAP the effluent total suspended solids (TSS) concentration was decreased to less than 35 mg/L, meeting effluent quality requirements for discharge. This study shows that microalgal biomass recycling (10% dry weight) increases biomass recovery up to 94% by selecting the most rapidly settling microalgae species without compromising the biomass production and improving the wastewater treatment in terms of TSS removal.

[Interleukin-4 and cardiac fibrosis in patients with heart failure]. / Interleucina-4 y fibrosis miocárdica en pacientes con insuficiencia cardiaca.

Interleukin-4 (IL-4) stimulates inflammatory responses, activates collagen synthesis, promotes fibrosis progression, and inhibits the production of inflammatory cytokines. We studied the relationship between the urinary IL-4 level and levels of markers of cardiac fibrosis and left ventricular volume in 98 patients with heart failure (HF). The left ventricular end-systolic volume index (LVESVI) and left ventricular end-diastolic volume index (LVEDVI) were calculated, and IL-4, tumor necrosis factor-alpha (TNF-alpha), IL-6, and aminoterminal propeptide of procollagen type III (PIIINP) levels were recorded. Comparison of urinary IL-4 and PIIINP levels in patients and control subjects gave values of 12 (12) pg/mL and 4 (3) pg/mL (P<.0001), respectively, and 5 (2) ng/mL and 4 (1) ng/mL (P<.0001), respectively. The IL-4 level correlated with LVESVI and LVEDVI (r = -0.22, P<.05), and with PIIINP (r = 0.24, P<.05). In patients with hypertensive cardiomyopathy, there was a good correlation between IL-4 and PIIINP levels (r = 0.7, P<.01). Correlations were also observed between IL-4 and TNF-alpha (r = 0.3, P<.01) and IL-6 (r = 0.5, P<.0001). The urinary IL-4 level correlated with cardiac fibrosis and remodeling in patients with HF. The relationship was stronger in those with hypertensive cardiomyopathy.

Interleucina-4 y fibrosis miocárdica en pacientes con insuficiencia cardiaca / Interleukin-4 and cardiac fibrosis in patients with heart failure

La interleucina 4 (IL-4) estimula la respuesta inflamatoria, activa la síntesis de colágeno, promueve la progresión de fibrosis e inhibe la producción de citocinas inflamatorias. Estudiamos las concentraciones urinarias de IL-4, su relación con los marcadores de fibrosis miocárdica y con los volúmenes del ventrículo izquierdo en 98 pacientes con insuficiencia cardiaca. Calculamos el índice de volumen telesistólico (IVTS) y telediastólico (IVTD), los valores de IL-4, factor de necrosis tumoral (TNF) alfa , IL-6 y propéptido aminoterminal del procolágeno tipo III (PIIINP). Comparamos los valores urinarios de IL-4 y PIIINP en pacientes y controles (12 ± 12 frente a 4 ± 3 pg/ml, p < 0,0001 y 5 ± 2 frente a 4 ± 1 ng/ml, p < 0,0001). La IL-4 se correlacionó con IVTS e IVTD (r = ­0,22; p < 0,05) y con PIIINP (r = 0,24; p < 0,05). En la cardiopatía hipertensiva encontramos una correlación entre IL-4 y PIIINP (r = 0,7; p < 0,01). Correlacionamos la IL-4 con TNF-α y la IL-6, obteniendo r = 0,3, p < 0,01 y r = 0,5, p < 0,0001. La IL-4 en orina se relaciona con la fibrosis miocárdica y el remodelado en la insuficiencia cardiaca. La relación es mayor en la cardiopatía hipertensiva (AU)

Interleukin-4 (IL-4) stimulates inflammatory responses, activates collagen synthesis, promotes fibrosis progression, and inhibits the production of inflammatory cytokines. We studied the relationship between the urinary IL-4 level and levels of markers of cardiac fibrosis and left ventricular volume in 98 patients with heart failure (HF). The left ventricular end-systolic volume index (LVESVI) and left ventricular end-diastolic volume index (LVEDVI) were calculated, and IL-4, tumor necrosis factor-alpha (TNF-alpha), IL-6, and aminoterminal propeptide of procollagen type III (PIIINP) levels were recorded. Comparison of urinary IL-4 and PIIINP levels in patients and control subjects gave values of 12 (12) pg/mL and 4 (3) pg/mL (P<.0001), respectively, and 5 (2) ng/mL and 4 (1) ng/mL (P<.0001), respectively. The IL-4 level correlated with LVESVI and LVEDVI (r = ­0.22, P<.05), and with PIIINP (r = 0.24, P<.05). In patients with hypertensive cardiomyopathy, there was a good correlation between IL-4 and PIIINP levels (r = 0.7, P<.01). Correlations were also observed between IL-4 and TNF-alpha (r = 0.3, P<.01) and IL-6 (r = 0.5, P<.0001). The urinary IL-4 level correlated with cardiac fibrosis and remodeling in patients with HF. The relationship was stronger in those with hypertensive cardiomyopathy (AU)

[Myocardial remodeling and immunologic activation in patients with heart failure]. / Remodelado miocárdico y activación inmunitaria en pacientes con insuficiencia cardiaca.

INTRODUCTION AND OBJECTIVES: Immune response-mediated regulation of myocardial collagen remains poorly understood. Our objective was to investigate the relationship between ventricular remodeling and immunologic activation in patients with heart failure (HF) by comparing dilated and ischemic cardiomyopathy. METHODS: We studied 94 patients with HF and dilated cardiomyopathy (n=46) or ischemic cardiomyopathy (n=48). We recorded left ventricular (LV) volumes, E/A ratio, and ejection fraction. Plasma concentrations of tumor necrosis factor alpha (TNFalpha), soluble TNFa receptor I (sTNF-RI), sTNF-RII, interleukin-6 (IL-6) and IL-10 were measured. The serum procollagen type-III amino-terminal propeptide (PIIINP) level was also obtained. RESULTS: Ventricular volumes were greater in the dilated cardiomyopathy than in the ischemic cardiomyopathy group (P< .05). However, sTNF-RI, sTNF-RII and PIIINP levels were higher in the ischemic group (P< .05). In this group, there were significant correlations between ventricular volumes and IL-10 and sTNF-RII levels. There was also a significant correlation between PIIINP and sTNF-RII levels (r=0.30; P< .05). In the dilated cardiomyopathy group, there was a significant correlation between ventricular volumes and IL-10 level, and between PIIINP level and IL-6 (r=0.32; P< .05) and sTNF-RII levels (r=0.32; P< .05). Multiple linear regression analysis, which included cytokine levels, age, sex and ventricular function, showed that the sTNF-RII level was an independent predictor of the PIIINP level (adjusted r(2)=0.16; P< .0001) and of ventricular volumes (LV end-systolic volume index, adjusted r(2)=0.034; P< .05; and LV end-diastolic volume index, adjusted r(2)=.048; P< .05) in both groups. CONCLUSIONS: In HF, there is an interaction between proinflammatory cytokines and the extracellular matrix. Immunologic implications vary according to disease etiology. The elevation in proinflammatory cytokine and PIIINP levels is greater in patients with ischemic cardiomyopathy. Multiple regression analysis showed that the sTNF-RII level was an independent predictor of ventricular remodeling.

Remodelado miocárdico y activación inmunitaria en pacientes con insuficiencia cardiaca / Myocardial remodeling and immunologic activation in patients with heart failure

Introducción y objetivos. No se comprende bien la regulación del colágeno miocárdico mediada por la respuesta inmunitaria. Nuestro objetivo fue determinar las relaciones entre remodelado ventricular y activación inmunitaria en pacientes con insuficiencia cardiaca comparando miocardiopatía isquémica y dilatada. Métodos. Estudiamos a 94 pacientes con insuficiencia cardiaca: miocardiopatía dilatada (n = 46) e isquémica (n = 48). Determinamos volúmenes ventriculares, E/A y FE. Medimos las concentraciones de TNFα, sTNF-RI, sTNF-RII, IL-6 e IL-10 y calculamos los valores de PIIINP. Resultados. Los volúmenes ventriculares en la miocardiopatía dilatada fueron superiores a los del grupo isquémico (p < 0,05). Sin embargo, los valores de sTNF-RI, sTNF-RII y PIIINP fueron más elevados en el grupo isquémico (p < 0,05). En éste, los volúmenes ventriculares se correlacionaron significativamente con IL-10 y sTNF-RII. El PIIINP se correlacionó significativamente con sTNF-RII (r = 0,30; p < 0,05). En el grupo de miocardiopatía dilatada, los volúmenes ventriculares se correlacionaron significativamente con IL-10 y el PIIINP se correlacionó con IL-6 (r = 0,32; p < 0,05) y sTNF-RII (r = 0,32; p < 0,05). La regresión lineal múltiple, que incluyó citocinas, edad, sexo y función ventricular, demuestra que el sTNF-RII es un factor pronóstico independiente del PIIINP (r² ajustada = 0,16; p < 0,0001) y de los volúmenes ventriculares (IVTSVI, r² ajustada = 0,034; p < 0,05; IVTDVI, r² ajustada = 0,048; p < 0,05) en ambos grupos. Conclusiones. En la insuficiencia cardiaca hay una interacción de citocinas proinflamatorias con la matriz extracelular. La implicación inmunitaria es diferente dependiendo de la etiología. Las citocinas proinflamatorias y los valores de PIIINP son más elevados en los pacientes con miocardiopatía isquémica. La regresión múltiple demostró que el sTNF-RII es un factor pronóstico independiente de remodelado ventricular (AU)

Introduction and objectives. Immune response-mediated regulation of myocardial collagen remains poorly understood. Our objective was to investigate the relationship between ventricular remodeling and immunologic activation in patients with heart failure (HF) by comparing dilated and ischemic cardiomyopathy. Methods. We studied 94 patients with HF and dilated cardiomyopathy (n=46) or ischemic cardiomyopathy (n=48). We recorded left ventricular (LV) volumes, E/A ratio, and ejection fraction. Plasma concentrations of tumor necrosis factor α (TNFα), soluble TNFa receptor I (sTNF-RI), sTNF-RII, interleukin-6 (IL-6) and IL-10 were measured. The serum procollagen type-III amino-terminal propeptide (PIIINP) level was also obtained. Results. Ventricular volumes were greater in the dilated cardiomyopathy than in the ischemic cardiomyopathy group (P<.05). However, sTNF-RI, sTNF-RII and PIIINP levels were higher in the ischemic group (P<.05). In this group, there were significant correlations between ventricular volumes and IL-10 and sTNF-RII levels. There was also a significant correlation between PIIINP and sTNF-RII levels (r=0.30; P<.05). In the dilated cardiomyopathy group, there was a significant correlation between ventricular volumes and IL-10 level, and between PIIINP level and IL-6 (r=0.32; P<.05) and sTNF-RII levels (r=0.32; P<.05). Multiple linear regression analysis, which included cytokine levels, age, sex and ventricular function, showed that the sTNF-RII level was an independent predictor of the PIIINP level (adjusted r²=0.16; P<.0001) and of ventricular volumes (LV end-systolic volume index, adjusted r²=0.034; P<.05; and LV end-diastolic volume index, adjusted r²=.048; P<.05) in both groups. Conclusions. In HF, there is an interaction between proinflammatory cytokines and the extracellular matrix. Immunologic implications vary according to disease etiology. The elevation in proinflammatory cytokine and PIIINP levels is greater in patients with ischemic cardiomyopathy. Multiple regression analysis showed that the sTNF-RII level was an independent predictor of ventricular remodeling (AU)

A study of loculated tuberculous pleural effusions treated with intrapleural urokinase.

AIM: To assess the effect of intrapleural urokinase, vis-à-vis simple pleural drainage, on residual pleural thickening in a series of patients suffering from loculated tuberculous pleural effusion. PATIENTS AND METHOD: Twenty-nine patients (21 males and 8 females) with loculated pleural effusion were studied. These patients were randomly allocated to one of two groups: one group received intrapleural urokinase (n=12) and the other was treated by simple drainage with suction (n=17). The urokinase (125,000 UI) was administered into the pleural cavity via an intrathoracic tube. This procedure was repeated every 12h until the quantity of pleural fluid obtained was less than 50 cm3, at which point the intrathoracic tube was removed. RESULTS: In both groups, the biochemical analysis of the pleural fluid was an exudate and the fluid had a serous appearance. Pleural thickening when the drainage tube was removed was 8.09+/-3.36 mm for the group treated with urokinase, and 14.78+/-17.20mm (P>0.05) for the control group. Residual pleural thickening measured upon completion of medical treatment at 6 months was 1.45+/-0.89 mm for the group treated with urokinase and 7.47+/-10.95 mm for the control group (P<0.05). In the control group, only two patients presented over 10mm of residual pleural thickening. The mean quantity of fluid drained in the two groups was 1.487+/-711 ml for the patients with urokinase, and 795+/-519 ml for the control group (P<0.01). CONCLUSION: Our study shows that patients with loculated tuberculous pleural effusion treated with urokinase suffered less from residual pleural thickening, as measured after six months, than those treated by simple drainage. It is therefore suggested that the administration of intrapleural urokinase is a safe and effective treatment for those patients who drain a larger quantity of pleural fluid.

Soluble TNF-alpha and interleukin-6 receptors in the urine of heart failure patients. Their clinical value and relationship with plasma levels.

BACKGROUND: Proinflammatory cytokines are important mediators in heart failure (HF). Recently, urinary levels of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) have been determined. AIMS: The purpose of this study was to measure the urinary levels of TNF-alpha and IL-6 receptors, sTNF-RI, sTNF-RII, sIL-6R, and the relationship with plasma levels and NYHA classes in HF. METHODS: Plasma and urine were collected from 114 HF patients and sTNF-RI, sTNF-RII and sIL-6R (ng/ml) were analyzed. RESULTS: For the whole population, plasma levels of sTNF-RI were 2.1+/-0.1, of sTNF-RII were 5.0+/-0.3 and of sIL-6R were 49.8+/-2.5. Urinary levels were: sTNF-RI, 2.8+/-0.5, r=0.5, p<0.001; sTNF-RII, 12.6+/-2.1, r=0.4, p<0.001; and sIL-6R, 4.2+/-0.4, NS. In NYHA III subjects, we found sTNF-RI, r=0.6, p<0.01, sTNF-RII, r=0.5, p<0.05, and sILR-6, r=0.5, p<0.05. Both plasma TNF receptors and urinary levels of sTNF-RII were higher in patients in a more severe NYHA class (p<0.05). CONCLUSIONS: Urine is a good environment to study sTNF-RI and sTNF-RII, and this fact has diagnostic and prognostic implications. Plasma and urinary levels of TNF receptors showed a fair correlation, which was increased in higher NYHA classes. Plasma and urinary levels of sIL6R showed a good correlation in NYHA III. The TNF receptor levels in urine increased in patients with more severe HF.

Genetic variability of hepatitis C virus NS3 protein in human leukocyte antigen-A2 liver transplant recipients with recurrent hepatitis C.

The association between the severity of chronic hepatitis C and the variability of the hepatitis C virus (HCV) genome remains controversial, but to our knowledge few data are available to date regarding T-cell epitope coding regions in transplant patients. In the current study, we identified 21 human leukocyte antigen (HLA)-A2-positive Spanish patients with chronic hepatitis C, 14 immunosuppressed liver transplant recipients, and 7 immunocompetent controls. Alanine aminotransferase, aspartate aminotransferase, viral load, and rate of fibrosis progression were determined. Genetic distances of HCV isolates and variations in epitopes of the HCV nonstructural 3 protein (NS3-1393 LIFCHSKKK and NS3-1406 KLVALGINAV) were compared between patients with slow or fast progression of fibrosis. Isolates from transplant patients with fast progression were found to be more divergent (P =.03), had a higher mean value of synonymous (dS) variations (P =.02), and some were differentiated in a phylogenetic tree, compared with isolates from patients with slow progression. The HLA-A2-restricted NS3-1406 epitope was found to be more variable (20 of 21 isolates differed from the prototype) compared with the A3-restricted NS3-1392 epitope (19% vs. 1.25% variation). A shift in the viral peptide was not detected in a subset of transplant patients, but was evident in two of three nontransplant patients with follow-up. There was no correlation noted between a particular amino acid variation and fibrosis progression (slow or fast) in either transplant or nontransplant patients. The results of the current study suggest that 1) there may be different HCV-1b strains in our geographic area, 2) immunosuppression appears to have little effect in amino acid variation at the HCV NS3-1406 epitope, and 3) variations over time might be more frequent in nonimmunosuppressed patients.

Quantification of proinflammatory cytokines in the urine of congestive heart failure patients. Its relationship with plasma levels.

AIMS: Proinflammatory cytokines are important mediators for the development of heart failure and increased plasma levels of these cytokines have been reported in patients with this condition. The purpose of the study was to investigate whether urine, a non-invasively obtained biological sample, was an appropriate medium in which to measure the concentration of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) in patients in the advanced stages of the disease. METHODS AND RESULTS: Thirty consecutive patients who had severe congestive heart failure (NYHA classes III and IV) and 30 matched healthy control subjects were enrolled. Plasma and the first urine of the day were collected and TNF-alpha and IL-6 were quantitatively analyzed by enzyme-linked immunosorbent assays. For every subject there were no differences in the amount of cytokine determined in plasma and urine. Both urine and plasma levels of IL-6 and TNF-alpha were greater in heart failure patients than in controls. CONCLUSION: Our results show that plasmatic and urinary levels of proinflammatory cytokines did not differ significantly. Thus, urine may be a good milieu in which to study these cytokines and may have diagnostic, prognostic and therapeutic implications.