A Single-center, Retrospective Study of Focal Segmental Glomerulosclerosis after Kidney Transplantation: Evolutive Analysis.

Background: Focal segmental glomerulosclerosis (FSGS) has a high recurrence rate after renal transplantation, which significantly impacts renal graft survival. However, the factors related to recurrence remain unclear. Objective: This study aimed to analyze focal segmental recurrence and evolution of glomerulosclerosis after renal transplantation. Methods: This was a descriptive, retrospective study involving 88 adults who underwent renal transplantation within a 15-year period. Demographic and clinical characteristics, as well as the occurrence of graft loss, were analyzed. Over the study period, 88 patients with a diagnosis of FSGS after transplantation were identified. Results: The mean age of the patients (n=54, males) was 29.1 years. Transplants with deceased donors predominated (60.9%). Calcineurin and prednisone inhibitors were present in 96.4% of the initial immunosuppression regimens. The mean time of onset of proteinuria greater than 0.5 g/g was 20.51 days. At 60 months after transplantation, 44.16% of the patients had partial remission, 25.97% had complete remission, and 29.87% had no remission. However, 50.60% of the patients developed graft loss throughout the analyzed period. Eight patients (9.4%) died within 60 months, of which five (62.5%) were attributed to infection. Conclusion: Our results indicate that FSGS after renal transplantation is a disease of high recurrence that is commonly precocious, and the histological alterations in light microscopy are not simultaneous to the appearance of proteinuria. Hypertension is considered a risk factor causing progression and recurrence. Thus, prospective studies are required to better evaluate progression and recurrence factors.

Lower levels of dehydroepiandrosterone sulfate are associated with more advanced liver fibrosis in chronic hepatitis C.

Chronic infection with the hepatitis C virus induces liver fibrosis, but it is unknown why some patients progress to advanced fibrosis while others remain with mild disease. Recently, an inverse association between serum levels of dehydroepiandrosterone sulphate (DHEA-S) and liver fibrosis in patients with nonalcoholic fatty liver disease was described, and it was postulated that dehydroepiandrosterone (DHEA) has antifibrotic effects. Our aim was to compare serum DHEA-S levels with liver fibrosis in hepatitis C patients. We collected serum samples from hepatitis C patients at the same day they underwent a liver biopsy. S-DHEA was compared to different stages of fibrosis. Binary logistic regression models were applied to evaluate independent variables associated to fibrosis. We included 287 patients (43.9% male). According to fibrosis stages 0, 1, 2, 3 and 4, median serum DHEA-S levels were 103 (26-462), 73 (5-391), 46 (4-425), 35 (6-292) and 28 (2-115) µg/dL, respectively (P < .001). Median serum DHEA-S levels were 74 (5-462) vs 36 (2-425) µg/dL for mild (F0-1) vs significant (F2-4) fibrosis, respectively (P < .001). Median serum DHEA-S levels were 64 (4-462) vs 31 (2-292) µg/dL for non advanced (F0-2) vs advanced fibrosis (F3-4), respectively (P < .001). The same association was found when the subgroup of HCV patients with and without steatosis or steatohepatitis was analysed. The association between lower DHEA-S levels and advanced fibrosis was independent of age, gender, diabetes mellitus, obesity and steatosis. Lower circulating DHEA-S levels are associated with more advanced stages of liver fibrosis in hepatitis C patients.

Phenotypic and genotypic correlations between soybean agronomic traits and path analysis.

The goals of this research were to evaluate the phenotypic and genotypic correlations between agronomic traits, to perform path analysis, having as main character grain yield, and to identify indirect selection criteria for grain yield. The experiment was carried out in an experimental area located at Capim Branco farm, which belongs to Federal University of Uberlândia, during the growing season of 2015/2016.Twenty-four soybean genotypes were evaluated under randomized complete block design with three repetitions, of which agronomic traits and grain yield were measured. There was genetic variability for all traits at 5% probability level through the F-test. Thirty significant phenotypic correlations were also observed with values oscillating from 0.42 to 0.87, which indicated a high level of association between some evaluated traits. Additionally, we verified that phenotypic and genotypic correlations were essential of the same direction, being the genotypic ones of superior magnitudes. Plants with superior vegetative cycle had longer life cycles; this fact could be explained by the significant phenotypic correlations between the number of days to the blooming and number of days to maturity (0.76). Significantly positive phenotypic and genotypic correlations for the total number of pods per plant and grain yield per plant (0.84) were observed. Through the path analysis, the trait that contributed the most over grain yield was the number of pods with three seeds as it showed the highest direct effect on grain yield per plant, as well as a strong indirect effect on the total number of pods. Therefore, the phenotypic and genotypic correlations suggested high correlations between grain yield and number of branched nodes, the number of pods with two and three seeds, and the total number of pods. Also, the path analysis determined the number of pods with three seeds as having the highest favorable effect on grain yield, and thus, being useful for indirect selection toward productive soybean genotypes.

An ultrasound and histomorphological analysis of experimental liver cirrhosis in rats.

We investigated whether liver injury by dual exposure to ethanol and carbon tetrachloride (EtOH + CCl4) for 15 weeks would persist after hepatotoxic agents were removed (EtOH + CCl4/8wR). After 15 weeks of hepatic injury with ethanol (5.5%, m/v) and carbon tetrachloride (0.05, mL/kg, ip), 5 of 11 female Wistar rats were sacrificed. The other 6 rats were maintained for an additional 8 weeks without hepatotoxic agents. Ultrasonography showed increased liver echogenicity and dilation of portal vein caliber in both groups (EtOH + CCl4: 0.22 +/- 0.01 cm, P < 0.001; EtOH + CCl4/8wR: 0.21 +/- 0.02 cm, P < 0.01) vs control (0.16 +/- 0.02 cm). Histopathology showed regenerative nodules in both experimental groups. Histomorphometry revealed increased fibrosis content in both groups (EtOH + CCl4: 12.6 +/- 2.64%, P < 0.001; EtOH + CCl4/8wR: 10.4 +/- 1.36%, P < 0.05) vs control (2.2 +/- 1.21%). Collagen types I and III were increased in groups EtOH + CCl4 (collagen I: 2.5 +/- 1.3%, P < 0.01; collagen III: 1.3 +/- 0.2%, P < 0.05) and EtOH + CCl4/8wR (collagen I: 1.8 +/- 0.06%, P < 0.05; collagen III: 1.5 +/- 0.8%, P < 0.01) vs control (collagen I: 0.38 +/- 0.11%; collagen III: 0.25 +/- 0.06%). Tissue transglutaminase increased in both groups (EtOH + CCl4: 66.4 +/- 8%, P < 0.01; EtOH + CCl4/8wR: 58.8 +/- 21%, P < 0.01) vs control (7.9 +/- 0.8%). Cirrhosis caused by the association of CCl4-EtOH remained for at least 8 weeks after removal of these hepatotoxic agents. Ultrasound images can be a useful tool to evaluate advanced hepatic alterations.

Bone marrow cell transplant does not prevent or reverse murine liver cirrhosis.

We tested the effect of bone marrow cell (BMC) transplantation in either preventing or reversing cirrhosis on an experimental model of chronic liver disease. Female Wistar rats were fed a liquid alcohol diet and received intraperitoneal injections of carbon tetrachloride (CCl4) over 15 weeks. Ten animals (cell-treated group) received five injections of BMCs during the cirrhosis induction protocol (on the 4th, 6th, 8th, 10th, and 12th weeks) and four animals received the cells after liver injury was established through tail vein. Nine animals (nontreated group) were submitted to the previously described protocols; however, they received vehicle injections. Analyses were performed to verify whether the infusion of cells was effective in preventing the development of cirrhosis in our model of induction, and if the cells could reverse cirrhosis once it was established. Hepatic architecture and fibrotic septa were analyzed in liver slices stained with hematoxilin & eosin and Sirius red, respectively. Fibrosis quantification was measured by Sirius red histomorphometry. Indirect immunofluorescence was performed to detect the amount of tissue transglutaminase 2. Blood analyses were performed to assess liver injury and function by the assessment of alanine aminotransferase and albumin. Ultrasound was performed to analyze the portal vein caliber and presence of ascitis. Cirrhosis features (regenerative nodules and fibrous septa) were observed in histopathology after 15 weeks of continuous hepatic injury in nontreated and cell-treated groups. Collagen content, immunofluorescence analysis, and biochemical and ultrasound parameters were similar in nontreated and cell-treated groups; however, both groups showed significant differences compared to a normal control group. Cell infusions with bone marrow-derived cells seem to be ineffective in improving morphofunctional parameters of the liver when applied to chronic cases either during or after establishment of the hepatic lesion.

An ultrasound and histomorphological analysis of experimental liver cirrhosis in rats

We investigated whether liver injury by dual exposure to ethanol and carbon tetrachloride (EtOH + CCl4) for 15 weeks would persist after hepatotoxic agents were removed (EtOH + CCl4/8wR). After 15 weeks of hepatic injury with ethanol (5.5 percent, m/v) and carbon tetrachloride (0.05, mL/kg, ip), 5 of 11 female Wistar rats were sacrificed. The other 6 rats were maintained for an additional 8 weeks without hepatotoxic agents. Ultrasonography showed increased liver echogenicity and dilation of portal vein caliber in both groups (EtOH + CCl4: 0.22 ± 0.01 cm, P < 0.001; EtOH + CCl4/8wR: 0.21 ± 0.02 cm, P < 0.01) vs control (0.16 ± 0.02 cm). Histopathology showed regenerative nodules in both experimental groups. Histomorphometry revealed increased fibrosis content in both groups (EtOH + CCl4: 12.6 ± 2.64 percent, P < 0.001; EtOH + CCl4/8wR: 10.4 ± 1.36 percent, P < 0.05) vs control (2.2 ± 1.21 percent). Collagen types I and III were increased in groups EtOH + CCl4 (collagen I: 2.5 ± 1.3 percent, P < 0.01; collagen III: 1.3 ± 0.2 percent, P < 0.05) and EtOH + CCl4/8wR (collagen I: 1.8 ± 0.06 percent, P < 0.05; collagen III: 1.5 ± 0.8 percent, P < 0.01) vs control (collagen I: 0.38 ± 0.11 percent; collagen III: 0.25 ± 0.06 percent). Tissue transglutaminase increased in both groups (EtOH + CCl4: 66.4 ± 8 percent, P < 0.01; EtOH + CCl4/8wR: 58.8 ± 21 percent, P < 0.01) vs control (7.9 ± 0.8 percent). Cirrhosis caused by the association of CCl4-EtOH remained for at least 8 weeks after removal of these hepatotoxic agents. Ultrasound images can be a useful tool to evaluate advanced hepatic alterations.

On the production of neutrons in laminated barriers for 10 MV medical accelerator rooms.

When space limitations are primary constraints, laminated barriers with metals can be an option to provide sufficient shielding for a radiotherapy treatment room. However, if a photon clinical beam with end point energy of 10 MeV or higher interacts with the metal inside the barriers neutrons are ejected and can result in an exposure problem inside and outside the vault. The empirical formulae existing in the literature to estimate neutron dose equivalents beyond laminated barriers do not take into account neutron production for spectra below 15 MV. In this work, the Monte Carlo code MCNP was used to simulate the production and transport of photoneutrons across primary barriers of 10 MV accelerator treatment rooms containing lead or steel, in order to obtain the ambient dose equivalents produced by these particles outside the room and in the patient plane. It was found that the neutron doses produced are insignificant when steel is present in the primary barriers of 10 MV medical accelerators. On the other hand, the results show that, in all cases where lead sheets are positioned in the primary barriers, the neutron ambient dose equivalents outside the room generally exceed the shielding design goal of 20 microSv/week for uncontrolled areas, even when the lead sheets are positioned inside the treatment room. Moreover, for laminated barriers, the photoneutrons produced in the metals are summed with the particles generated in the accelerator head shielding and can represent a significant component of additional dose to the patients. In this work, it was found that once lead sheets are positioned inside the room, the neutron ambient dose equivalents can reach the value of 75 microSv per Gray of photon absorbed dose at the isocenter. However, for all simulated cases, a tendency in the reduction of neutron doses with increasing lead thickness can be observed. This trend can imply in higher neutron ambient dose equivalents outside the room for thinner lead sheets. Therefore, when a medical accelerator treatment room is designed with laminated barriers to receive equipment with an end point energy equal to or higher than 10 MeV, not only the required shielding thickness for photon radiation attenuation should be considered, but also the dose due to photoneutrons produced in the metal, which may involve an increase of the lead thickness or even the use of neutron shielding.