Physical-chemical characterization of a galvanic sludge and its inertization by vitrification using container glass

Several industrial processes produce large amounts of heavy metals-rich wastes, which could be considered as "trash-can raw materials". The incorporation in ceramic systems can be regarded as a key process to permanently incorporate hazardous heavy metals in stable matrixes. In particular the aim of this work is to prepare and evaluate environmental risk assessment of coloured glass and glass-ceramic with the addition of chromium(III) galvanic sludge having a high content of Cr2O3 (15.91 wt%). Trivalent chromium compounds generally have low toxicity while hexavalent chromium is recognized by the International Agency for Research on Cancer and by the US Toxicology Program as a pulmonary carcinogen. The sludge has been characterized by ICP -AES chemical analysis, powder XRD diffraction, DTA, SEM, leaching test after different thermal treatments ranging from 400°C to 1200°C. Batch compositions were prepared by mixing this sludge with glass containers. The glass container composition is rich in SiO2 (69.89 wt%), Na 2O (12.32 wt%) and CaO (11.03 wt%), while the sludge has a high amount of CaO (42.90 wt%) and Cr2O3 (15.91 wt%). The vitrification was carried out at 1450°C in an electrical melting furnace for 2 h followed by quenching in water or on graphite mould. Chromium incorporation mechanisms, vitrification processability, effect of initial Cr oxidation state, and product performance were investigated. In particular toxic characterization by leaching procedure and chemical durability studies of the glasses and glass-ceramics were used to evaluate the leaching of heavy metals (in particular of Cr). The results indicate that all the glasses obtained were inert and the heavy metals were immobilized

Preparation of low-cost nano and microcomposites from chicken eggshell, nano-silica and rice husk ash and their utilisations as additives for producing geopolymer cements

This work aims to prepare low-cost nanocomposite and microcomposite with lower molar ratio CaO/SiO2 (0.4). Nano-silica, rice husk ash and calcined chicken eggshell have been used as silica and calcium sources. Metakaolin has been separately replaced by 0, 10 and 20 wt% of each composite in order to study their behavior on the properties of geopolymers. The hardener used is sodium waterglass from rice husk ash. The surface area of nano-silica and rice husk ash was 54.40 and 4.08 m2/g, respectively. The cumulative volumes of the control geopolymer, the ones containing 10 wt% of microcomposite and nanocomposite are 119.71, 89.92 and 110.49 mm3/g, respectively. The compressive strength of the control specimen is around 64.02 MPa. The one using 10 wt% of microcomposite was 68.97 MPa. It drops to 42.88 MPa when metakaolin was replaced by 20 wt % of microcomposite. Whereas the one using 10 wt% of nanocomposite was 30.03 MPa and it decreases to 26.05 MPa when metakaolin was substituted by 20 wt% of nanocomposite. It can be concluded that 10 wt% of microcomposite could be mixed to metakaolin for strength development and nanocomposite does not recommend to use as an additive for producing high strength of geopolymer cements. © 2020, © 2020 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group

Recombinant Alkaline Phosphatase Prevents Acute on Chronic Liver Failure

The lipopolysaccharide (LPS)– toll-like receptor-4 (TLR4) pathway plays an important role in liver failure. Recombinant alkaline phosphatase (recAP) deactivates LPS. The aim of this study was to determine whether recAP prevents the progression of acute and acute-on-chronic liver failure (ACLF). Eight groups of rats were studied 4-weeks after sham surgery or bile duct ligation and were injected with saline or LPS to mimic ACLF. Acute liver failure was induced with Galactosamine-LPS and in both models animals were treated with recAP prior to LPS administration. In the ACLF model, the severity of liver dysfunction and brain edema was attenuated by recAP, associated with reduction in cytokines, chemokines, liver cell death, and brain water. The activity of LPS was reduced by recAP. The treatment was not effective in acute liver failure. Hepatic TLR4 expression was reduced by recAP in ACLF but not acute liver failure. Increased sensitivity to endotoxins in cirrhosis is associated with upregulation of hepatic TLR4, which explains susceptibility to development of ACLF whereas acute liver failure is likely due to direct hepatoxicity. RecAP prevents multiple organ injury by reducing receptor expression and is a potential novel treatment option for prevention of ACLF but not acute liver failure

The role of RIPK1 mediated cell death in acute on chronic liver failure

Acute-on-chronic liver failure (ACLF) is characterized predominantly by non-apoptotic forms of hepatocyte cell death. Necroptosis is a form of programmed lytic cell death in which receptor interacting protein kinase (RIPK) 1, RIPK3 and phosphorylated mixed lineage kinase domain-like (pMLKL) are key components. This study was performed to determine the role of RIPK1 mediated cell death in ACLF. RIPK3 plasma levels and hepatic expression of RIPK1, RIPK3, and pMLKL were measured in healthy volunteers, stable patients with cirrhosis, and in hospitalized cirrhotic patients with acutely decompensated cirrhosis, with and without ACLF (AD). The role of necroptosis in ACLF was studied in two animal models of ACLF using inhibitors of RIPK1, necrostatin-1 (NEC-1) and SML2100 (RIPA56). Plasma RIPK3 levels predicted the risk of 28- and 90-day mortality (AUROC, 0.653 (95%CI 0.530–0.776), 0.696 (95%CI 0.593–0.799)] and also the progression of patients from no ACLF to ACLF [0.744 (95%CI 0.593–0.895)] and the results were validated in a 2nd patient cohort. This pattern was replicated in a rodent model of ACLF that was induced by administration of lipopolysaccharide (LPS) to bile-duct ligated rats and carbon tetrachloride-induced fibrosis mice administered galactosamine (CCL4/GalN). Suppression of caspase-8 activity in ACLF rodent model was observed suggesting a switch from caspase-dependent cell death to necroptosis. NEC-1 treatment prior to administration of LPS significantly reduced the severity of ACLF manifested by reduced liver, kidney, and brain injury mirrored by reduced hepatic and renal cell death. Similar hepato-protective effects were observed with RIPA56 in a murine model of ACLF induced by CCL4/GalN. These data demonstrate for the first time the importance of RIPK1 mediated cell death in human and rodent ACLF. Inhibition of RIPK1 is a potential novel therapeutic approach to prevent progression of susceptible patients from no ACLF to ACLF

PI3KCA/PTEN deregulation contributes to impaired responses to cetuximab in metastatic colorectal cancer patients

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Giant atypical carcinoid of the liver with vascular metastases and local sinusoidal invasion: a case report

We present the case of a 46 year old woman with a giant, 23-centimeter, atypical carcinoid of the liver. A primary site for this neoplasm could not be identified despite multiple radiographic imaging studies, including a somatostatin scan, and a thorough inspection of the bowel during surgical resection of the lesion. Histologically, the tumor displayed mild cytologic atypia, abundant necrosis, and intravascular metastases, the last feature of which was identified by immunohistochemical markers for chromogranin and synaptophysin. Also described is the unusual sinusoidal infiltration, or "spillage," of tumor cells into the surrounding liver parenchyma, a feature that has not been described as far as we are aware but may suggest an aggressive clinical course. Even though an exact definition of atypia for these lesions apparently does not exist at this point, the multiple atypical features in this case strongly suggest the diagnosis of atypical carcinoid of the liver, thus far an altogether rare and vaguely reported entity. As more cases arise in the medical literature, it may be worthwhile to establish a set of guidelines to define atypical hepatic carcinoids and other gastrointestinal carcinoids, although survivorship data thus far indicates no significant difference in the prognosis between typical versus atypical variants

Toll-like receptor 4 is a therapeutic target for prevention and treatment of liver failure

Background and aims: Toll-like receptor 4 (TLR4) plays an essential role in mediating organ injury in acute liver failure (ALF) and acute-on-chronic liver failure (ACLF). Here we assess whether inhibiting TLR4 signaling can ameliorate liver failure and serve as a potential treatment. / Material and Methods: Circulating TLR4 ligands and hepatic TLR4 expression was measured in plasma samples and liver biopsies from patients with cirrhosis. TAK-242 (TLR4 inhibitor) was tested in vivo with 10mg/Kg, i.p. in rodent models of ACLF (bile duct ligation + lipopolysaccharide (LPS); carbontetrachloride + LPS) and ALF (Galactosamine + LPS) and in vitro on immortalized human monocytes (THP-1) and hepatocytes (HHL5).. The in vivo therapeutic effect was assessed by coma free survival, organ injury and cytokine release and in vitro by measuring IL6, IL1b or cell injury (TUNEL), respectively. / Results: In patients with cirrhosis, hepatic TLR4 expression was upregulated and circulating TLR4 ligands were increased (p<0.001). ACLF in rodents was associated with a switch from apoptotic cell death in ALF to non-apoptotic forms of cell death. TAK-242 reduced LPS induced cytokine secretion and cell death (p=0.002) in hepatocytes and monocytes in vitro. In rodent models of ACLF, TAK-242 administration improved coma free survival, reduced the degree of hepatocyte cell death in liver p<0.001) and kidneys (p=0.048) and reduced circulating cytokine levels (IL1b p<0.001). In a rodent model of ALF TAK-242 prevented organ injury (p<0.001) and systemic inflammation (IL1b p<0.001). / Conclusion: This study shows that TLR4 signaling is a key factor in the development of both ACLF and ALF and its inhibition improves severity of organ injury and outcome. TAK-242 may be of therapeutic relevance in patients with liver failure