Alternating offers protocols for multilateral negotiation

This paper presents a general framework for multilateral turn-taking protocols and two fully specified protocols namely Stacked Alternating Offers Protocol (SAOP) and Alternating Multiple Offers Protocol (AMOP). In SAOP, agents can make a bid, accept the most recent bid or walk way (i.e., end the negotiation without an agreement) when it is their turn. AMOP has two different phases: bidding and voting. The agents make their bid in the bidding phase and vote the underlying bids in the voting phase. Unlike SAOP, AMOP does not support walking away option. In both protocols, negotiation ends when the negotiating agents reach a joint agreement or some deadline criterion applies. The protocols have been evaluated empirically, showing that SAOP outperforms AMOP with the same type of conceder agents in a time-based deadline setting. SAOP was used in the ANAC 2015 competition for automated negotiating agents.ITE

Mesenchymal Stem Cells from Rats with Chronic Kidney Disease Exhibit Premature Senescence and Loss of Regenerative Potential

<div><p>Mesenchymal stem cell (MSC) transplantation has the potential for organ repair. Nevertheless, some factors might lessen the regenerative potential of MSCs, e.g. donor age or systemic disease. It is thus important to carefully assess the patient's suitability for autologous MSC transplantation. Here we investigated the effects of chronic kidney disease (CKD) on MSC function. We isolated bone marrow MSCs from remnant kidney rats (RK) with CKD (CKD-RK-MSC) and found signs of premature senescence: spontaneous adipogenesis, reduced proliferation capacity, active senescence-associated-β-galactosidase, accumulation of actin and a modulated secretion profile. The functionality of CKD-RK-MSCs <i>in vivo</i> was tested in rats with acute anti-Thy1.1-nephritis, where healthy MSCs have been shown to be beneficial. Rats received healthy MSCs, CKD-RK-MSC or medium by injection into the left renal artery. Kidneys receiving healthy MSCs exhibited accelerated healing of glomerular lesions, whereas CKD-RK-MSC or medium exerted no benefit. The negative influence of advanced CKD/uremia on MSCs was confirmed in a second model of CKD, adenine nephropathy (AD). MSCs from rats with adenine nephropathy (CKD-AD-MSC) also exhibited cellular modifications and functional deficits <i>in vivo</i>. We conclude that CKD leads to a sustained loss of <i>in vitro</i> and <i>in vivo</i> functionality in MSCs, possibly due to premature cellular senescence. Considering autologous MSC therapy in human renal disease, studies identifying uremia-associated mechanisms that account for altered MSC function are urgently needed.</p></div

Analysis of renal function and histology on Day 4 and Day 6 of anti-Thy1.1-nephritis.

<p>(A) Experimental design. (B–D) Comparison of rats that had anti-Thy1.1-nephritis and received H-MSC (“Healthy”, n = 7), TG-MSC (“TG”, n = 8), CKDmod-RK-MSC (“CKDmod-RK”, n = 6) or control DMEM (“Medium”, n = 10) injected into the left renal artery on Day 2 after disease induction and were analysed on Day 4. (E) Experimental design. (F–H) Comparison of rats that had anti-Thy1.1-nephritis and received H-MSC (“Healthy”, n = 7), TG-MSC (“TG”, n = 7), CKDmod-RK-MSC (“CKDmod-RK”, n = 6) or control DMEM (“Medium”, n = 9) injected into the left renal artery on Day 2 after disease induction and were analysed on Day 6. * p<0.05; ** p<0.01; *** p<0.001. All data: mean ± SD.</p