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AbstractSixty-six dairy farms (as average, 167.0 ± 106.5 milking cows and milk yield of 31.4 ± 5.1) were visited to identify different nutritional approaches adopted in dairy cows diet formulation. Forage, TMR, faecal, and milk samples from lactating herds were collected and diet composition, in vitromethane production, in vivonutrient digestibility, faecal fermentation profile and milk yield and milk quality were characterised. A hierarchical cluster analysis was applied and six nutritional approaches in diet formulation corresponding with six different clusters (CL) were identified. The CL discriminated the farm feeding choices in the following nutritional strategies, based on high use of: (i) high moisture corn (HMC) and legume silage, (ii) compound feed, (iii) corn and soy meals, (iv) HMC and soy meal, (v) corn meal and protein compound feeds, or (vi) HMC and protein compound feed strategies, respectively for CL1 to CL6. The milk yield tended (p = .061) to differ among CL. The greatest (>1.60) feed efficiency was calculated for CL1 and 5, whereas the lowest (<1.45) for CL 2. The CL2 and 5 had the highest feed costs (i.e. 0.24 or 0.22 €/kg of milk, respectively). Interestingly, the high use of HMC or steam flaked corn resulted associated to higher farm performances. Particularly, HMC and legume silage (CL1), HCM and soy meal (CL4) and HCM and protein compound feed (CL6) nutritional strategies resulted more efficient and profitable, having the greatest feed efficiency, protein and starch degradability as well as income over feed costs. Differentiate carbohydrates in dairy cow diets seems highly convenient.HIGHLIGHTSSix different nutritional strategies were identified based on use of single ingredients and a great variability in both economic and feed efficiency was observed for dairy farms clustering into different groupsThe use of high moisture ear corn in substitution of corn meal increased dry matter intake, feed efficiency, milk yield and lactose content of milk, whereas the use of steam flaked corn reduced the faecal fermentationsThe in vitromethane emission potential of diets did not differ among clustered nutritional strategies

The formation of ADAMTS13‐specific circulating immune complexes (CICs) may be a pathophysiologic mechanism in autoimmune thrombotic thrombocytopenic purpura (TTP), but has not been systematically investigated.

The considerable genetic predisposition to deep vein thrombosis (DVT) is only partially accounted for by known genetic risk variants. Rare single‐nucleotide variants (SNVs) of the coding areas of hemostatic genes may explain part of this missing heritability. The ADAMTS13and VWFgenes encode two interconnected proteins with fundamental hemostatic functions, the disruption of which may result in thrombosis.

Summary. Background:Thrombotic thrombocytopenic purpura (TTP) is a rare life‐threatening disease. Of surviving patients, 45% develops an exacerbation or a late recurrence. Severe ADAMTS‐13 deficiency, both during the acute episode and remission, is a well‐established predictor of recurrence. The predictive value of anti‐ADAMTS‐13 antibodies, their inhibitory activity and Ig class subtype for disease recurrence is still to be established.

To cite this article:Mancini I, Valsecchi C, Palla R, Lotta LA, Peyvandi F. Measurement of anti‐ADAMTS13 neutralizing autoantibodies: a comparison between CBA and FRET assays. J Thromb Haemost2012; 10: 1439–42.

In the present study we evaluated B-cell subsets and their functional development in 74 newborns from birth to 6 months of life. Moreover, we evaluated “natural antibody” production in vitro. The results documented a predominance of naiveB-lymphocytes at all time-points evaluated, decreasing from birth to 6 months (p=0.009). The percentages of CD27+IgD+and CD27+IgDnegmemory B-cells were very low at birth and significantly increased only at 6 months (p=0.02 and p<0.001, respectively). We found a significant increase only in in vitrostimulated IgG production at 6 months as compared to birth (p<0.001). Moreover, a lower secretion of anti-Pn IgM antibodies up to 6 months of age, as compared to controls was observed. Our results underline that the susceptibility and severe course of infection in the neonate can be attributed, at least in part, to the lack of pre-existing immunological memory and competent adaptive immunity.

Renal cell carcinoma (RCC) tissue is composed of a mixture of neoplastic and normal cells, which complicate proteome analysis. The aim of our study was to investigate whether it is feasible to establish primary cell cultures of RCC and of renal cortex maintaining the tissue phenotype along with a more homogeneous and enriched cytological material. Fourteen (82.3%) primary cultures from 17 surgical cases were established and characterized by morphology, growth rate, immunocytochemistry, and molecular analysis performed by Real-time PCR, Western blotting, two-dimensional electrophoresis (2-DE), and mass spectrometry. Cultures showed >90% cytokeratine-positive epithelial cells. In primary tumor cultures, the molecular phenotype of manganese superoxide dismutase and heat shock protein 27 was the same as that found in tumor tissues with overexpression and increased number of isoforms. Moreover, 27 out 28 specific proteins and their isoforms, present in spots excised from 2-DE gel of cortex or RCC cultures, corresponded to those identified on the 2-DE tissue cortex reference map, suggesting that these primary cultures retain the proteomic profile of the corresponding tissues. Keywords: renal cell carcinoma • primary cultures • proteome • real-time PCR • two-dimensional gel electrophoresis • mass spectrometry • Western blotting • immunocytochemistry • manganese superoxide dismutase • heat shock protein 27

The abnormal multimeric composition of plasma von Willebrand factor in type IIB von Willebrand's disease is transiently corrected after infusion of 1-deamino-[8-D-arginine]-vasopressin. However, the larger multimers released into the circulation disappear more rapidly in these patients than in type I von Willebrand's disease or normals. We demonstrate that the larger multimers of normal von Willebrand factor transfused into a type IIB patient are cleared from the circulation more slowly than multimers of similar size endogenously released from tissue stores. The rate of disappearance of large von Willebrand factor multimers after infusion of cryoprecipitate is similar in IIB, IIA, and severe homozygous-like von Willebrand's disease. Platelets from the IIB patient exhibited normal ristocetin-induced binding of normal von Willebrand factor. However, like normal platelets, they bound IIB von Willebrand factor at lower ristocetin concentrations than required for normal von Willebrand factor. These findings provide evidence that absence of the larger multimers from IIB plasma is related to a molecular abnormality of von Willebrand factor rather than to enhanced affinity of abnormal tissue or cellular binding sites, as is the case in the recently described “pseud” von Willebrand's disease and “platelet-type” von Willebrand's disease.

The abnormal multimeric composition of plasma von Willebrand factor in type IIB von Willebrand's disease is transiently corrected after infusion of 1-deamino-[8-D-arginine]-vasopressin. However, the larger multimers released into the circulation disappear more rapidly in these patients than in type I von Willebrand's disease or normals. We demonstrate that the larger multimers of normal von Willebrand factor transfused into a type IIB patient are cleared from the circulation more slowly than multimers of similar size endogenously released from tissue stores. The rate of disappearance of large von Willebrand factor multimers after infusion of cryoprecipitate is similar in IIB, IIA, and severe homozygous-like von Willebrand's disease. Platelets from the IIB patient exhibited normal ristocetin-induced binding of normal von Willebrand factor. However, like normal platelets, they bound IIB von Willebrand factor at lower ristocetin concentrations than required for normal von Willebrand factor. These findings provide evidence that absence of the larger multimers from IIB plasma is related to a molecular abnormality of von Willebrand factor rather than to enhanced affinity of abnormal tissue or cellular binding sites, as is the case in the recently described “pseud” von Willebrand's disease and “platelet-type” von Willebrand's disease.