Contribution of Chondroitin Sulfate A to the Binding of Complement Proteins to Activated Platelets

Exposure of chondroitin sulfate A (CS-A) on the surface of activated platelets is well established. The aim of the present study was to investigate to what extent CS-A contributes to the binding of the complement recognition molecule C1q and the complement regulators C1 inhibitor (C1INH), C4b-binding protein (C4BP), and factor H to platelets.Human blood serum was passed over Sepharose conjugated with CS-A, and CS-A-specific binding proteins were identified by Western blotting and mass spectrometric analysis. C1q was shown to be the main protein that specifically bound to CS-A, but C4BP and factor H were also shown to interact. Binding of C1INH was dependent of the presence of C1q and then not bound to CS-A from C1q-depleted serum. The specific interactions observed of these proteins with CS-A were subsequently confirmed by surface plasmon resonance analysis using purified proteins. Importantly, C1q, C4BP, and factor H were also shown to bind to activated platelets and this interaction was inhibited by a CS-A-specific monoclonal antibody, thereby linking the binding of C1q, C4BP, and factor H to exposure of CS-A on activated platelets. CS-A-bound C1q was also shown to amplify the binding of model immune complexes to both microtiter plate-bound CS-A and to activated platelets.This study supports the concept that CS-A contributes to the binding of C1q, C4BP, and factor H to platelets, thereby adding CS-A to the previously reported binding sites for these proteins on the platelet surface. CS-A-bound C1q also seems to amplify the binding of immune complexes to activated platelets, suggesting a role for this molecule in immune complex diseases

The Flip-Flop Trail and Fragile Globalisation

The flip-flop trail is an object biography. It follows the translocal journeys of a pair of plastic sandals, unpacking the lives and landscapes hidden in the plastic. An important shoe-infrastructure enabling human mobility, flip-flops work as an offbeat proxy for globalization too. They proffer empirical footings in translocally-connected worlds in which people and the social textures and terrains of their everyday lives come to the fore, in place of economic processes and commodity chains favoured in hegemonic versions of globalization. These reduce globalization’s complex social forms to the grand narratives of the logics of capital accumulation, implicitly naturalizing it, if critically, as inevitable, entrenched and robust. From the vantage point of the flip- flop trail, globalization looks rather different. It is more fragile and shifting, generating multiple forms of uncertainty in the lives and landscapes it simultaneously sustains and undermines

Abnormal pancreatic enzymes and their prognostic role after acute paraquat poisoning

Ingestion of paraquat causes multi-organ failure. Prognosis is best estimated through measurement of blood paraquat concentrations but this facility is not available in most hospitals. We studied the prognostic significance of abnormal pancreatic enzymes for survival. Patients with acute paraquat poisoning were recruited. An extensive series of blood tests including serum amylase were serially checked. Patients were sorted according to their serum amylase activity (normal [<220 U/L], mildly elevated [220 to 660 U/L], elevated [>660 U/L]), and survival compared between groups. 177 patients were enrolled to the study, of whom 67 died and 110 survived. 122 (70.62%), 27 (15.25%) and 25 (14.13%) patients were in the normal, mildly elevated and elevated amylase activity groups, respectively. The case fatality in the elevated group was 100% compared to 17% in the normal group (P < 0.001). We found four independent factors for paraquat death prediction: amylase, PaCO(2), leukocyte number, and neutrophil percentage. Models using pancreatic enzyme activity showed good prediction power. We have found that abnormal pancreatic enzymes are useful prognostic marker of death after acute paraquat poisoning. Including serum amylase activity into a prognostic model provides a good prognostication

Diagnosis of Etiology in Acute Pancreatitis

The correct identification of etiology in patients with acute pancreatitis is crucial for the outcome of the patient in clinical practice. Biliary acute pancreatitis is the predominant form of the disease, and it is characterized by a transient elevation of transaminases. Other etiologies, such as alcohol consumption, hypertriglyceridemia, drugs, parenchymal, and ductal abnormalities/lesions, need to be excluded in patients with normal transminases before considering the acute pancreatitis as idiopathic. Genetic testing may be considered in selected patients. The aim of the present chapter is to propose a bedside algorithm for clinical practice