Strategy-Proof and Anonymous Rule in Queueing Problems: A Relationship between Equity and Efficiency

In this paper, we consider a relationship between equity and efficiency in queueing problems. We show that under strategy-proofness, anonymity in welfare implies queue-efficiency. Furthermore, we also give a characterization of the equally distributed pairwise pivotal rule, as the only rule that satisfies strategy-proofness, anonymity in welfare and budget-balance.Queueing Problems, Strategy-Proofness, Anonymity in welfare, Efficiency

A case of acute myocardial infarction during perioperative period of non-cardiac surgery in a patient with antiphospholipid syndrome and a history of coronary artery bypass surgery

AbstractA 65-year-old woman underwent coronary artery bypass surgery and was diagnosed with antiphospholipid syndrome (APS) at the same time in 1985. She was admitted to our hospital to undergo mastectomy for left breast cancer in 2012. She was put on intravenous infusion of heparin and stopped receiving both antiplatelet agents and warfarin. The operation was performed without complications, and antithrombotic therapy was restarted one day after the operation. On day 6 postoperative, she complained of sudden chest pain and on examination she was diagnosed with acute myocardial infarction. The culprit lesion was in a saphenous vein graft and coronary intervention was performed.<Learning objective: Antithrombotic therapy for patients with APS is complicated because of prolonged baseline activated partial thromboplastin time (aPTT). An effective perioperative antithrombotic therapy for APS patients who have a history of coronary artery disease and have undergone non-cardiac surgery has not yet been established. A safe strategy for such a therapy should therefore be discussed.

Impact of behavioral/developmental disorders comorbid with conduct disorder

Aims: The aim of the present study was to verify the comorbidity of conduct disorder (CD) and behavioral/developmental disorders in children and adolescents, and to examine the traits of CD comorbid with them. Methods: Subjects were 64 children (60 boys, four girls) who were resident at three institutions for delinquent children or who were conduct-disordered outpatients of a university hospital aged under 18 years. A diagnostic interview was carried out by experienced child psychiatrists and the intelligence score and the Adverse Childhood Experiences score were measured by a licensed psychologist. Results: A total of 57 children were diagnosed as having CD, of whom 26 (45.6%) were diagnosed with comorbid attention-deficit-hyperactivity disorder (ADHD), 12 were diagnosed with comorbid pervasive developmental disorder (PDD, 21,1%), and 19 (33.3%) had no comorbidity of either disorder. Six children (18.8% of CD comorbid with ADHD) met the criteria for both ADHD and PDD. The group with comorbid PDD was significantly younger at onset (F = 6.51, P = 0.003) and included unsocialized type more frequently (KH2 = 6.66, P = 0.036) compared with the other two groups. Conclusions: Clinicians should be aware that not only ADHD but also PDD may be comorbid with CD. Establishment of the correct diagnosis is important because recognizing the presence of PDD will enable us to provide appropriate treatment and guidance, which may improve prognosis.ArticlePSYCHIATRY AND CLINICAL NEUROSCIENCES. 63(6):762-768 (2009)journal articl

Cardio-protective effects of pentraxin 3 produced from bone marrow-derived cells against ischemia/reperfusion injury

AbstractBackgroundInflammation is one of major mechanisms contributing to the pathogenesis of myocardial ischemia/reperfusion (I/R) injury. Pentraxin 3 (PTX3), produced in response to inflammatory signals, acts as a humoral arm of the innate immunity. Here we investigated the role of PTX3 produced from bone marrow-derived cells in myocardial I/R injury using PTX3-deficient (PTX3KO) mice.Methods and resultsPTX3KO mice and wild-type littermate (WT) mice were lethally irradiated and injected with bone marrow (BM) cells, generating four types of mice (WTWT-BM, WTPTX3KO-BM, PTX3KOWT-BM and PTX3KOPTX3KO-BM). Six weeks after BM transplantation, the myocardial I/R procedure (45min of left descending coronary artery ligation followed by 48h of reperfusion) was performed. Infarct size was greater in WT and PTX3KO mice with BM from PTX3KO donor (WTPTX3KO-BM and PTX3KOPTX3KO-BM) compared with WT and PTX3KO mice with BM from WT donor (WTWT-BM and PTX3KOWT-BM). Localization of PTX3 was observed in neutrophils and macrophages in WT and PTX3KO mice with BM from WT donor (WTWT-BM and PTX3KOWT-BM), while only in endothelial cells in WT mice with BM from PTX3KO donor (WTPTX3KO-BM). Infiltration of neutrophils and generation of reactive oxygen species (ROS) at ischemic border zones were greater in PTX3KO mice with BM from PTX3KO donor (PTX3KOPTX3KO-BM) than PTX3KO mice with BM from WT donor (PTX3KOWT-BM). Plasma levels and cardiac expressions of interleukin-6 were higher in PTX3KO mice with BM from PTX3KO donor (PTX3KOPTX3KO-BM) than PTX3KO mice with BM from WT donor (PTX3KOWT-BM). However, no significant differences in infarct size, infiltration of neutrophils, generation of ROS and plasma and cardiac levels of interleukin-6 were observed between WT and PTX3KO mice with BM from WT donor and between WT and PTX3KO mice with BM from PTX3KO donor. These results indicated that the lack of PTX3 produced from BM-derived cells, and not from cardiac resident cells, exacerbated myocardial injury after I/R.ConclusionPTX3 produced from bone marrow-derived cells plays a crucial role in cardiac protection against myocardial I/R injury by attenuating infiltration of neutrophils, generation of ROS and inflammatory cytokine

Astrocytic dysfunction induced by ABCA1 deficiency causes optic neuropathy

Astrocyte abnormalities have received great attention for their association with various diseases in the brain but not so much in the eye. Recent independent genome-wide association studies of glaucoma, optic neuropathy characterized by retinal ganglion cell (RGC) degeneration, and vision loss found that single-nucleotide polymorphisms near the ABCA1 locus were common risk factors. Here, we show that Abca1 loss in retinal astrocytes causes glaucoma-like optic neuropathy in aged mice. ABCA1 was highly expressed in retinal astrocytes in mice. Thus, we generated macroglia-specific Abca1-deficient mice (Glia-KO) and found that aged Glia-KO mice had RGC degeneration and ocular dysfunction without affected intraocular pressure, a conventional risk factor for glaucoma. Single-cell RNA sequencing revealed that Abca1 deficiency in aged Glia-KO mice caused astrocyte-triggered inflammation and increased the susceptibility of certain RGC clusters to excitotoxicity. Together, astrocytes play a pivotal role in eye diseases, and loss of ABCA1 in astrocytes causes glaucoma-like neuropathy