Dynamic changes in carbonate chemistry in the microenvironment around single marine phytoplankton cells

Photosynthesis by marine diatoms plays a major role in the global carbon cycle, although the precise mechanisms of dissolved inorganic carbon (DIC) uptake remain unclear. A lack of direct measurements of carbonate chemistry at the cell surface has led to uncertainty over the underlying membrane transport processes and the role of external carbonic anhydrase (eCA). Here we identify rapid and substantial photosynthesis-driven increases in pH and [CO32−] primarily due to the activity of eCA at the cell surface of the large diatom Odontella sinensis using direct simultaneous microelectrode measurements of pH and CO32− along with modelling of cell surface inorganic carbonate chemistry. Our results show that eCA acts to maintain cell surface CO2 concentrations, making a major contribution to DIC supply in O. sinensis. Carbonate chemistry at the cell surface is therefore highly dynamic and strongly dependent on cell size, morphology and the carbonate chemistry of the bulk seawater

Abnormal platelet adhesion on abdominal vessels in asymptomatic patients with paroxysmal nocturnal hemoglobinuria

Platelet kinetic studies were performed in eight patients with paroxysmal nocturnal hemoglobinuria (PNH) but without symptoms or signs related to thrombosis. Indium-111 tropolonate labeled autologous platelets were used to determine mean platelet life and platelet production rate; total body images were also acquired. Three of seven patients with a thrombocytopenia showed a shortened mean platelet life, and the other five demonstrated a (nearly) normal platelet survival. Four of the seven patients with thrombocytopenia showed a decreased platelet production rate, but bone marrow cellularity was normo- to hypercellular. These observations suggest ineffective thrombopoiesis in 57% of the patients with PNH and thrombocytopenia. Total body imaging was performed during the platelet kinetic study in order to study organ uptake. Imaging of the abdominal vessels was demonstrated in all patients, suggesting enhanced adherence of platelets to the endothelium in patients with PNH. Since thrombosis of especially the abdominal vessels is a major cause of morbidity and mortality, the use of antithrombotic drugs might be considered despite the absence of abdominal complaints

Portal hypertension as presenting feature of a myeloproliferative disorder: Diagnosis and therapeutic dilemmas

In some patients presenting with complications of portal hypertension, thrombosis of hepatic or portal veins is identified as the cause. Hepatic or portal vein thrombosis may be secondary to recognized etiologies like infection or malignancy. When no etiology for the thrombosis is found, it is likely that a 'latent' myeloproliferative disorder (MPD) is the underlying abnormality. We present seven patients referred to us between 1988 and 1993 with complications of portal hypertension due to hepatic or portal vein thrombosis, in whom a 'latent', and in one patient overt, MPD was identified as the underlying disorder. Problems relating to the diagnosis of (latent) MPD in this subset of patients are discussed. The importance of in vitro 'endogenous' erythroid colony formation indicating the presence of MPD is emphasized. Also, a therapeutic strategy, with special emphasis on anticoagulation therapy, is suggested