Chronic Degradation of Seasonally Dry Tropical Forests Increases the Incidence of Genotoxicity in Birds.

Multiple studies have shown that exposure to pollutants can increase genotoxic damage in different taxa. However, to our knowledge, the effects of environmental stress have been explored little. In certain stressful ecosystems, such as seasonally dry tropical forests, the combined effects of anthropogenic activities and ongoing global changes can cause an increase in environmental stresses, in turn, may trigger physiological and genetic effects on biodiversity. The present aims to assess changes in the prevalence of genotoxic damage in birds within three states of forest degradation in the Tumbesian Region of Western Ecuador. We used blood samples from 50 bird species to determine the frequency of micronucleus and nuclear abnormalities in erythrocytes. Our results revealed a significant impact of forest degradation on the occurrence probability of micronucleus and nuclear abnormalities at the community level. Localities with higher levels of degradation exhibited higher levels of abnormalities. However, when analyzing the dominant species, we found contrasting responses. While Lepidocolaptes souleyetii showed a reduction in the proportion of nuclear abnormalities from the natural to shrub-dominated localities Troglodytes aedon and Polioptila plumbea showed an increase for semi-natural and shrub-dominated respectively. We concluded that the degradation process of these tropical forests increases the stress of bird community generating genotoxic damage. Bird responses seem to be species-specific, which could explain the differences in changes in bird composition reported in other studies.

Effect of the degree of oxidation of graphene oxide on As(III) adsorption.

The study of the interaction between graphene oxide (GO) and arsenic is of great relevance not only in the design of adsorbent materials to remove this contaminant but also in the understanding of its combined nanotoxicity. In this work, we show that As(III) adsorption, primarily H3AsO3, by graphene oxide is affected by its degree of oxidation. Three types of GO with C/O ratios between 1.35 and 1.98 were produced, resulting in important variations in the concentration of COH and COC functional groups. The less oxidized material reached a maximum As(III) adsorption capacity of 123 mg/g, whereas the GO with the highest degree of oxidation reached a value of 288 mg/g at pH 7, the highest reported in the literature. We also show that sulfates and carbonates present in water strongly inhibit As(III) adsorption. The interaction between graphene oxide and As(III) was also studied by Density Functional Theory (DFT) computer models showing that graphene oxide interacts with As(III) primarily through hydrogen bonds, having interaction energies with the hydroxyl and epoxide groups of 1508.6 and 1583.6 kJ/mol, respectively. Finally, cytotoxicity tests showed that the graphene oxide maintained cellular viability of 57% with 50 µg/ml, regardless of its degree of oxidation.

Glomerular damage as a predictor of renal allograft loss

Interstitial fibrosis and tubular atrophy (IF/TA) are the most common cause of renal graft failure. Chronic transplant glomerulopathy (CTG) is present in approximately 1.5-3.0 percent of all renal grafts. We retrospectively studied the contribution of CTG and recurrent post-transplant glomerulopathies (RGN) to graft loss. We analyzed 123 patients with chronic renal allograft dysfunction and divided them into three groups: CTG (N = 37), RGN (N = 21), and IF/TA (N = 65). Demographic data were analyzed and the variables related to graft function identified by statistical methods. CTG had a significantly lower allograft survival than IF/TA. In a multivariate analysis, protective factors for allograft outcomes were: use of angiotensin-converting enzyme inhibitor (ACEI; hazard ratio (HR) = 0.12, P = 0.001), mycophenolate mofetil (MMF; HR = 0.17, P = 0.026), hepatitis C virus (HR = 7.29, P = 0.003), delayed graft function (HR = 5.32, P = 0.016), serum creatinine ≥1.5 mg/dL at the 1st year post-transplant (HR = 0.20, P = 0.011), and proteinuria ≥0.5 g/24 h at the 1st year post-transplant (HR = 0.14, P = 0.004). The presence of glomerular damage is a risk factor for allograft loss (HR = 4.55, P = 0.015). The presence of some degree of chronic glomerular damage in addition to the diagnosis of IF/TA was the most important risk factor associated with allograft loss since it could indicate chronic active antibody-mediated rejection. ACEI and MMF were associated with better outcomes, indicating that they might improve graft survival.

Glomerular damage as a predictor of renal allograft loss.

Interstitial fibrosis and tubular atrophy (IF/TA) are the most common cause of renal graft failure. Chronic transplant glomerulopathy (CTG) is present in approximately 1.5-3.0% of all renal grafts. We retrospectively studied the contribution of CTG and recurrent post-transplant glomerulopathies (RGN) to graft loss. We analyzed 123 patients with chronic renal allograft dysfunction and divided them into three groups: CTG (N = 37), RGN (N = 21), and IF/TA (N = 65). Demographic data were analyzed and the variables related to graft function identified by statistical methods. CTG had a significantly lower allograft survival than IF/TA. In a multivariate analysis, protective factors for allograft outcomes were: use of angiotensin-converting enzyme inhibitor (ACEI; hazard ratio (HR) = 0.12, P = 0.001), mycophenolate mofetil (MMF; HR = 0.17, P = 0.026), hepatitis C virus (HR = 7.29, P = 0.003), delayed graft function (HR = 5.32, P = 0.016), serum creatinine > or =1.5 mg/dL at the 1st year post-transplant (HR = 0.20, P = 0.011), and proteinuria > or =0.5 g/24 h at the 1st year post-transplant (HR = 0.14, P = 0.004). The presence of glomerular damage is a risk factor for allograft loss (HR = 4.55, P = 0.015). The presence of some degree of chronic glomerular damage in addition to the diagnosis of IF/TA was the most important risk factor associated with allograft loss since it could indicate chronic active antibody-mediated rejection. ACEI and MMF were associated with better outcomes, indicating that they might improve graft survival.

Establishment of a pediatric liver transplantation program: experience with 100 transplantation procedures.

OBJECTIVE: To analyze the primary factors that influence the development and consolidation of a pediatric liver transplantation program. PATIENTS AND METHODS: This was a retrospective study of 100 liver transplantation procedures performed in 84 pediatric patients between May 1990 and November 2007. The male-female ratio was 40:60. Mean (SD) age was 5 years (40 patients were younger than 2 years); cold ischemia time was 7.10 (3.1) hours; surgery time was 5.2 (2.2) hours; and time on the waiting list for transplantation was 75 (range, 1-1012) days. Indications for transplantation included cholestatic disease (43%), acute hepatic failure (AHF; 34%), metabolic disorders (14%), and cirrhosis (9%). Transplanted organs included 3 split grafts, 29 partial grafts, and 8 living-donor grafts. RESULTS: Mean graft survival was 70.4%, 59.2%, and 58.1% at 1, 3, and 5 years, respectively. Factors that influenced graft outcome were age younger than 2 years; surgery time more than 6 hours; and AHF vs cholestatic disease, metabolic disorders, and cirrhosis. There were no significant differences in long-term (51% vs 59%) and short-term (71% vs 70%) graft survival between procedures performed in 1990-1998 compared with those performed in 1999-2007; however, there was a higher percentage (P = .005) of recipients at high risk (age younger than 2 years or with AHF) in the later period. All data were consistent with those of the European Liver Transplant Registry 2007. CONCLUSIONS: A pediatric liver transplantation program can be established by a group experienced in liver transplantation.

Synergistic effect of mycophenolate mofetil and angiotensin-converting enzyme inhibitor in patients with chronic allograft nephropathy

Experimental data and few clinical non-randomized studies have shown that inhibition of the renin-angiotensin system by angiotensin-converting enzyme (ACE) associated or not with the use of mycophenolate mofetil (MMF) could delay or even halt the progression of chronic allograft nephropathy (CAN). In this retrospective historical study, we investigated whether ACE inhibition (ACEI) associated or not with the use of MMF has the same effect in humans as in experimental studies and what factors are associated with a clinical response. A total of 160 transplant patients with biopsy-proven CAN were enrolled. Eighty-one of them were on ACE therapy (G1) and 80 on ACEI_free therapy (G2). Patients were further stratified for the use of MMF. G1 patients showed a marked decrease in proteinuria and stabilized serum creatinine with time. Five-year graft survival after CAN diagnosis was more frequent in G1 (86.9 vs 67.7 percent; P < 0.05). In patients on ACEI-free therapy, the use of MMF was associated with better graft survival. The use of ACEI therapy protected 79 percent of the patients against graft loss (OR = 0.079, 95 percentCI = 0.015-0.426; P = 0.003). ACEI and MMF or the use of MMF alone after CAN diagnosis conferred protection against graft loss. This finding is well correlated with experimental studies in which ACEI and MMF interrupt the progression of chronic allograft dysfunction and injury. The use of ACEI alone or in combination with MMF significantly reduced proteinuria and stabilized serum creatinine, consequently improving renal allograft survival.

Synergistic effect of mycophenolate mofetil and angiotensin-converting enzyme inhibitor in patients with chronic allograft nephropathy.

Experimental data and few clinical non-randomized studies have shown that inhibition of the renin-angiotensin system by angiotensin-converting enzyme (ACE) associated or not with the use of mycophenolate mofetil (MMF) could delay or even halt the progression of chronic allograft nephropathy (CAN). In this retrospective historical study, we investigated whether ACE inhibition (ACEI) associated or not with the use of MMF has the same effect in humans as in experimental studies and what factors are associated with a clinical response. A total of 160 transplant patients with biopsy-proven CAN were enrolled. Eighty-one of them were on ACE therapy (G1) and 80 on ACEI_free therapy (G2). Patients were further stratified for the use of MMF. G1 patients showed a marked decrease in proteinuria and stabilized serum creatinine with time. Five-year graft survival after CAN diagnosis was more frequent in G1 (86.9 vs 67.7%; P < 0.05). In patients on ACEI-free therapy, the use of MMF was associated with better graft survival. The use of ACEI therapy protected 79% of the patients against graft loss (OR = 0.079, 95%CI = 0.015-0.426; P = 0.003). ACEI and MMF or the use of MMF alone after CAN diagnosis conferred protection against graft loss. This finding is well correlated with experimental studies in which ACEI and MMF interrupt the progression of chronic allograft dysfunction and injury. The use of ACEI alone or in combination with MMF significantly reduced proteinuria and stabilized serum creatinine, consequently improving renal allograft survival.

Are the current chronic allograft nephropathy grading systems sufficient to predict renal allograft survival?

A major problem in renal transplantation is identifying a grading system that can predict long-term graft survival. The present study determined the extent to which the two existing grading systems (Banff 97 and chronic allograft damage index, CADI) correlate with each other and with graft loss. A total of 161 transplant patient biopsies with chronic allograft nephropathy (CAN) were studied. The samples were coded and evaluated blindly by two pathologists using the two grading systems. Logistic regression analyses were used to evaluate the best predictor index for renal allograft loss. Patients with higher Banff 97 and CADI scores had higher rates of graft loss. Moreover, these measures also correlated with worse renal function and higher proteinuria levels at the time of CAN diagnosis. Logistic regression analyses showed that the use of angiotensin-converting enzyme inhibitor (ACEI), hepatitis C virus (HCV), tubular atrophy, and the use of mycophenolate mofetil (MMF) were associated with graft loss in the CADI, while the use of ACEI, HCV, moderate interstitial fibrosis and tubular atrophy and the use of MMF were associated in the Banff 97 index. Although Banff 97 and CADI analyze different parameters in different renal compartments, only some isolated parameters correlated with graft loss. This suggests that we need to review the CAN grading systems in order to devise a system that includes all parameters able to predict long-term graft survival, including chronic glomerulopathy, glomerular sclerosis, vascular changes, and severity of chronic interstitial fibrosis and tubular atrophy.

Are the current chronic allograft nephropathy grading systems sufficient to predict renal allograft survival?

A major problem in renal transplantation is identifying a grading system that can predict long-term graft survival. The present study determined the extent to which the two existing grading systems (Banff 97 and chronic allograft damage index, CADI) correlate with each other and with graft loss. A total of 161 transplant patient biopsies with chronic allograft nephropathy (CAN) were studied. The samples were coded and evaluated blindly by two pathologists using the two grading systems. Logistic regression analyses were used to evaluate the best predictor index for renal allograft loss. Patients with higher Banff 97 and CADI scores had higher rates of graft loss. Moreover, these measures also correlated with worse renal function and higher proteinuria levels at the time of CAN diagnosis. Logistic regression analyses showed that the use of angiotensin-converting enzyme inhibitor (ACEI), hepatitis C virus (HCV), tubular atrophy, and the use of mycophenolate mofetil (MMF) were associated with graft loss in the CADI, while the use of ACEI, HCV, moderate interstitial fibrosis and tubular atrophy and the use of MMF were associated in the Banff 97 index. Although Banff 97 and CADI analyze different parameters in different renal compartments, only some isolated parameters correlated with graft loss. This suggests that we need to review the CAN grading systems in order to devise a system that includes all parameters able to predict long-term graft survival, including chronic glomerulopathy, glomerular sclerosis, vascular changes, and severity of chronic interstitial fibrosis and tubular atrophy.

Automated peritoneal dialysis as a lifesaving therapy in an emergency room: report of four cases.

The present article describes four cases of patients with chronic kidney disease who arrived at the emergency room in critical condition, needing acute dialysis for severe hyperkalemia and metabolic acidosis. These four patients were treated acutely with automated peritoneal dialysis (APD) using a Tenckhoff catheter placed percutaneously at the bedside in the emergency room. All patients were discharged in good condition and with APD as their chronic renal replacement therapy (RRT). APD is a RRT, that may be considered a frontline acute therapy option for renal failure patients in an emergency room. Coordinated teamwork between emergency and nephrology medical and nursing staff is the key to a successful outcome in these life threatening situations.

Nanostructures of crystalline molybdenum trioxide grown by condensation in a carrier gas.

Molybdenum trioxide nanostructures were grown by direct evaporation of MoO3 from a tungsten boat resistively heated in the presence of hydrogen or helium as carrier gas at pressures from 100 to 600 Pa. Crystalline structures such as, nanoribbons, nanofibers, nanoneedles and nanoparticles were obtained at source temperatures below 900 degrees C. On the other hand, at source temperatures above 1000 degrees C, nanoporous structures were obtained. The latter were found more often when hydrogen was used as carrier gas.

Single dose of Rituximab plus plasmapheresis in an HIV patient with acute humoral kidney transplant rejection: a case report.

Before the highly active antiretroviral therapy (HAART) era, kidney transplantation was not considered an option for patients infected with human immunodeficiency virus (HIV) because of its poor outcome. However, recent studies have demonstrated results comparable to those of recipients without HIV infections. They have shown that HIV-positive patients maintained on HAART mount an immune response. Immunosuppressive agents are chosen to minimize aggravation of HIV infection, bearing in mind the potential side effects of the combination of HAART and immunosuppressive drugs. Herein we have reported the case of a 43-year-old HIV- and hepatitis C virus-infected woman with preserved immune function who received a cadaveric kidney transplant and developed an acute humoral rejection, which was successfully treated with Rituximab.

Impact of therapeutic changes on renal graft survival with posttransplant glomerulonephritis.

INTRODUCTION: Posttransplant glomerulonephritis (GN) is the third cause of graft loss after 1 year of transplant follow-up; few approaches have been efficient in reversing this outcome. The aim of this study was to evaluate whether the modification of the immunosuppressive therapy for treating posttransplant GN had an impact on allograft survival. PATIENTS AND METHODS: Forty-nine patients who underwent renal transplantation and developed posttransplant GN were divided into two groups: group 1, 22 patients with modified immunosuppressive treatment (72.3%, pulse of methylprednisolone; 13.6%, high-dose oral corticosteroid), and group 2, where it was maintained. Additionally, the impact of the concomitant use of drugs that promote the renin-angiotensin-aldosterone system blockade (RAASB) was analyzed in terms of graft survival. RESULTS: We established the diagnosis of GN at 17.9 months (range, 0.57 to 153.4) after transplantation, when serum creatinine (Cr) was 2.2 mg/dL (range, 0.8 to 12.5) and proteinuria 3.2 g/L (range, 0.2 to 24.2). Graft survivals at 1 and 3 years after diagnosis were 69.2% and 52.9%, respectively. The patients of group 1 showed a lower prevalence of graft loss (27.2% versus 48.1%, P = .40) and better survival at the end of 1 year (73.2% versus 60.4%) and 3 years (62.5% versus 38.0%, P = .26), but the differences were not significant. RAASB showed a positive impact on survival at the end of 3 years in both groups: for group 1, 83.8% with RAASB, 41.4% without RAASB; and for group 2, 75% with RAASB and 14.8% without RAASB (P < .001). CONCLUSION: Although treatment of posttransplant GN with modification of immunosuppression seemed to improve graft survival in the first 3 years after diagnosis, RAASB improved this effect.

Initial response to immunosuppressive and renoprotective treatment in posttransplant glomerulonephritis.

UNLABELLED: The current studies on posttransplant glomerulonephritis (PTxGN) do not establish when, how, or how long we must treat these patients. This study sought to compare the initial response to immunosuppressive treatment and renoprotection in PTxGN. PATIENTS AND METHODS: This prospective study was performed in 23 patients with a histological diagnosis of PTxGN. RESULTS: Mean follow-up was 12 months (3-18); 91% received immunosuppressants, and 56.5% just renoprotective drugs. The best results (reduction of serum creatinine [SCr] and proteinuria) with immunosuppression were observed in patients with recurrent membranous PTxGN using the scheme of Ponticelli (IV + PO corticosteroid [CS] + PO cyclophosphamide [CPP]). A similar response was also seen in subjects with recurrent or de novo focal glomerulosclerosis treated with PO CS or CPP, except when the initial SCr > 2.5 mg/dL. In de novo IgA nephropathy, reduction of proteinuria occurred with use of PO CS, with or without CPP, but without improvement in SCr. Patients with recurrent or de novo crescentic PTxGN used renoprotective drugs and always immunosuppressants. In this group, good results were seen with IV + PO CS, with or without CPP, when there was less than 50% of glomeruli with crescents, or more than 50% with crescents but an initial SCr < 2.5 mg/dL. CONCLUSION: Immunosuppression seemed to give a better initial response than renoprotection in cases of membranous, IgA, and focal segmental glomulerulosclerosis PTxGN. Patients with an initial SCr > or = 2.5 mg/dL displayed worse outcomes.

Adjuvant chemotherapy for prevention of recurrence of invasive hepatocellular carcinoma after orthotopic liver transplantation.

UNLABELLED: Orthotopic liver transplantation (OLT) is the best treatment for nonresectable hepatocellular carcinoma (HCC), but tumor recurrence reduces long-term and medium-term survival. The effectiveness of adjuvant chemotherapy to prevent tumor recurrence has not been fully established. METHODS: Three hundred eighty-seven consecutive patients, including 43 with HCC superimposed on liver cirrhosis, underwent OLT. Twelve patients with one or more prognostic criteria for HCC recurrence were entered into a prospective prophylaxis protocol with monthly cycles of cisplatin (60 mg/m(2)) and adriamycin (30 mg/m(2)), beginning the fourth week post-OLT for a maximum of seven sessions. RESULTS: The 5-year survival of the non-HCC patients was 65.7% and that of the HCC patients was 60.46% (P = NS). Chemotherapy was reasonably well tolerated, but the 9 patients with hepatitis C- or B-associated cirrhosis showed viral and histological recurrence of the primary disease. A high proportion of patients (7 of 12) developed tumor recurrence during the first year after OLT. Six of these patients died, all but one due to HCC relapse. Five patients remain healthy and tumor free at 58 to 130 months. Post-OLT adjuvant chemotherapy does not avoid tumor recurrence and its fatal consequences but may contribute to prolonged tumor-free survival among a significant proportion of patients with high-risk HCC. However, the uncertain implications on viral recurrence and the lack of control groups do not allow post-OLT chemotherapy to be recommended outside controlled clinical trials, which are clearly warranted.

Cns distribution of members of the two-pore-domain (KCNK) potassium channel family.

Two-pore-domain potassium (K(+)) channels are substrates for resting K(+) currents in neurons. They are major targets for endogenous modulators, as well as for clinically important compounds such as volatile anesthetics. In the current study, we report on the CNS distribution in the rat and mouse of mRNA encoding seven two-pore-domain K(+) channel family members: TASK-1 (KCNK3), TASK-2 (KCNK5), TASK-3 (KCNK9), TREK-1 (KCNK2), TREK-2 (KCNK10), TRAAK (KCNK4), and TWIK-1 (KCNK1). All of these genes were expressed in dorsal root ganglia, and for all of the genes except TASK-2, there was a differential distribution in the CNS. For TASK-1, highest mRNA accumulation was seen in the cerebellum and somatic motoneurons. TASK-3 was much more widely distributed, with robust expression in all brain regions, with particularly high expression in somatic motoneurons, cerebellar granule neurons, the locus ceruleus, and raphe nuclei and in various nuclei of the hypothalamus. TREK-1 was highest in the striatum and in parts of the cortex (layer IV) and hippocampus (CA2 pyramidal neurons). mRNA for TRAAK also was highest in the cortex, whereas expression of TREK-2 was primarily restricted to the cerebellar granule cell layer. There was widespread distribution of TWIK-1, with highest levels in the cerebellar granule cell layer, thalamic reticular nucleus, and piriform cortex. The differential expression of each of these genes likely contributes to characteristic excitability properties in distinct populations of neurons, as well as to diversity in their susceptibility to modulation.