Spruitkool in deelbouw : bedrijfseconomische gevolgen van oogst- en oppervlaktevergroting

The farm-economic results of the increase of area and yield of Brussels sprouts grown on a share-cropping basis. Brussels sprouts are grown mainly on a share-cropping basis in the Netherlands. In the last years the costs for the share cropper have risen more than those for the farmer. To achieve an insight into the cost structure the production costs have been calculated. With a yield of 9,250 kg and an area under Brussels sprouts of 1 ha per share cropper the production costs in North Groningen are Dfl. 3,850 per ha. If picking is started a week earlier, the yield is 7 percent higher. Picking is often started too late to obtain the highest possible yield and returns. The average course of prices in the past ten years showed that an earlier start of picking did not reduce the average prices. Yield increase causes a degressive reduction in the number of work hours applied for picking and sorting per kg of product. The resulting decrease in cost price varies from Dfl. 0.31 to Dfl. 0.61 per kg for yield ranging from 5 to 13 tons per ha. Yield increase too hardly reduces the average prices. By increasing the area per share-cropper the labour requirement for picking is reduced linearly. This causes a reduction in the costs per kg of product from Dfl. 0.42 to Dfl. 0.38 per kg in plots varying from 0.5 to 2 ha with a yield of 9,250 kg/ha ; the returns per kg are not reduced. The costs of the share cropper show a greater fall than those of the farmer, the percentage being 28 and 6 respectively. If in North Groningen, Brussels sprouts are picked earlier and the area per share cropper is increased, the costs are reduced, but not the proceeds

Functional impairment of circulating FcεRI+ monocytes and myeloid dendritic cells in hepatocellular carcinoma and cholangiocarcinoma patients

Background Hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA) represent the most common primary liver malignancies whose outcome is influenced by the immune response. Methods In this study, we have functionally characterized, by flow cytometry, circulating myeloid dendritic cells (mDCs) and FcεRI+ monocytes in a group of healthy individuals (n = 10) and in a group of patients with HCC (n = 19) and CCA (n = 8), at the time point of the surgical resection (T0) and once the patient had recovered from surgery (T1). Moreover, we proceeded to a more in depth phenotypic characterization of the FcεRI+ monocyte subpopulation. Results A significant decrease in the frequency of TNFα producing FcεRI+ monocytes and mDCs in HCC and CCA patients when compared to the group of healthy individuals was observed, and a close association between FcεRI+ monocytes and mDCs dysfunction was identified. In addition, the phenotypic characteristics of FcεRI+ monocytes from healthy individuals strongly suggest that this population drives to mDCs, which matches with the fact that both populations are functionally affected. Conclusions The frequency and the function of circulating mDCs and FcεRI+ monocytes are affected in both HCC and CCA patients, and FcεRI+ monocytes could represent those fated to become mDCs.publishe

Efficient Inhibition of Collagen-Induced Platelet Activation and Adhesion by LAIR-2, a Soluble Ig-Like Receptor Family Member

LAIR-1 (Leukocyte Associated Ig-like Receptor -1) is a collagen receptor that functions as an inhibitory receptor on immune cells. It has a soluble family member, LAIR-2, that also binds collagen and can interfere with LAIR-1/collagen interactions. Collagen is a main initiator for platelet adhesion and aggregation. Here, we explored the potential of soluble LAIR proteins to inhibit thrombus formation in vitro. LAIR-2/Fc but not LAIR-1/Fc inhibited collagen-induced platelet aggregation. In addition, LAIR-2/Fc also interfered with platelet adhesion to collagen at low shear rate (300 s−1; IC50 = 18 µg/ml) and high shear rate (1500 s−1; IC50 = 30 µg/ml). Additional experiments revealed that LAIR-2/Fc leaves interactions between collagen and α2β1 unaffected, but efficiently prevents binding of collagen to Glycoprotein VI and von Willebrand factor. Thus, LAIR-2/Fc has the capacity to interfere with platelet-collagen interactions mediated by Glycoprotein VI and the VWF/Glycoprotein Ib axis