Single Nuclear Spin Cavity QED

We constructed a cavity QED system with a diamagnetic atom of 171Yb and performed projective measurements on a single nuclear spin. Since Yb has no electronic spin and has 1/2 nuclear spin, the procedure of spin polarization and state verification can be dramatically simplified compared with the pseudo spin-1/2 system. By enhancing the photon emission rate of the 1S0-3P1 transition, projective measurement is implemented for an atom with the measurement time of T_meas = 30us. Unwanted spin flip as well as dark counts of the detector lead to systematic error when the present technique is applied for the determination of diagonal elements of an unknown spin state, which is delta|beta|^2 < 2 * 10^-2. Fast measurement on a long-lived qubit is key to the realization of large-scale one-way quantum computing.Comment: 5 pages, 5 figure

Corrigendum: Retrospective cohort study to determine the effect of preinjury antiplatelet or anticoagulant therapy on mortality in patients with major trauma

OBJECTIVE: This study aimed to compare outcomes among patients who sustained major trauma from injury with and without receiving antiplatelet therapy (APT) or anticoagulant therapy (ACT) to test the hypothesis that APT does not increase the risk of mortality. However, ACT increases the mortality risk in the acute phase of trauma. METHODS: Patients registered in the Japanese Observational body for Coagulation and Thrombolysis in Early Trauma 2 between April 2017 and March 2018 who had sustained a severe injury in any anatomic region of the body, as determined using an injury severity score (ISS) ≥ 16 were included in this retrospective cohort study. We analyzed the mortality within 24 h from the arrival using a multivariable linear regression analysis adjusted for several confounding variables. RESULTS: We identified 1,186 eligible participants who met the inclusion criteria for this study: 105 in the APT (cases), 1,081 in the non-antiplatelet therapy (nAPT) group (controls), 65 in the ACT (cases), and 1,121 in the non-anticoagulant therapy (nACT) group (controls). The mortality within 24 h in the ACT group was significantly higher than in the nACT group (odds ratio 4.5; 95%CI: 1.2–16.79; p = 0.025); however, there was no significant difference between the two groups with or without the antiplatelet drug (odds ratio 0.32; 95%CI: 0.04–2.79; p = 0.3) administration. Other outcomes, like the 28-day mortality, mortality at discharge, and surgery for hemostasis, were not significantly different between regular users and non-users of either antiplatelet or anticoagulant drugs. CONCLUSION: Regular antiplatelet medications did not increase mortality within 24 h, 28 days, or at discharge in patients with major trauma, suggesting that standard treatment, including surgery, is sufficient

The identification of novel small extracellular vesicle (sEV) production modulators using luciferase‐based sEV quantification method

Abstract Small extracellular vesicles (sEVs) are nano‐sized vesicles secreted from various cells that contain bioactive metabolites and function as key regulators for intercellular communication. sEVs modulate diverse biological and pathological processes in the body, and the amount of circulating sEVs has been reported to correlate with certain disease progression. Therefore, the identification of small molecular compounds that can control sEV production may become a novel therapeutic strategy. In this study, a rapid, highly sensitive sEV quantification method utilizing fusion proteins consisting of Gaussia luciferase (gLuc) reporter protein and sEV markers (CD63 and CD82) was developed. A total of 480 compounds were screened to identify potent inducers and inhibitors of gLuc activity. Two novel compounds, KPYC08425 and KPYC12163, showed significant and dose‐dependent changes in gLuc activity with minimal cytotoxicity based on the LDH assay. The efficacy of these two compounds was further evaluated by protein quantification of the isolated sEVs. Further evaluation of KPYC12163 suggested that the autolysosomal pathway may be involved in its inhibitory effect on sEV production

Atypical drug-induced hypersensitivity syndrome with multiple organ failure rescued by combined acute blood purification therapy: a case report

Abstract Background Drug-induced hypersensitivity syndrome (DIHS), including Stevens-Johnson syndrome (SJS), is a severe rash that often develops 2–6 weeks after the intake of the causative drug; however, its diagnosis is sometimes difficult. This article describes a case in which a patient with DIHS-induced multiple organ failure was successfully treated with blood purification therapy. Case presentation A male patient in his 60s was admitted to our hospital with autoimmune encephalitis. The patient was treated with steroid pulse therapy, acyclovir, levetiracetam, and phenytoin. From the 25th day, he presented with fever (≥ 38 °C) as well as miliary-sized erythema on the extremities and trunk, followed by erosions. DIHS and SJS were suspected; accordingly, levetiracetam, phenytoin, and acyclovir were discontinued. On the 30th day, his condition further deteriorated, and he was admitted to the intensive care unit for ventilatory management. The next day, he developed multi-organ failure and was started on hemodiafiltration (HDF) for acute kidney injury. Although he presented with hepatic dysfunction and the appearance of atypical lymphocytes, he did not meet the diagnostic criteria for DIHS or SJS/toxic epidermal necrolysis. Therefore, he was diagnosed with multi-organ failure caused by severe drug eruption and underwent a 3-day treatment with plasma exchange (PE) in addition to HDF. Accordingly, the patient was diagnosed with atypical DIHS. After being started on blood purification therapy, the skin rash began to disappear; moreover, the organ damage improved, with a gradual increase in urine output. Eventually, the patient was weaned off the ventilator and transferred to the hospital on the 101st day. Conclusions HDF + PE could effectively treat multi-organ failure caused by atypical DIHS, which is difficult to diagnose

Serum syndecan-1 concentration in hemolysis, elevated liver enzymes, and low platelets syndrome: A case report

BackgroundHemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome occurs in pregnant and postpartum individuals. We observed serum syndecan-1 (SDC-1) levels, which is a component of the glycocalyx, in a patient with HELLP syndrome from admission to the postpartum period and examined their association as reflecting the pathophysiology related to endothelial injury.Case presentationA 31-year-old primiparous female patient without a previous medical history at a gestational age of 37 weeks and 6 days was transferred to our hospital the morning after a visit to a previous hospital with headache and nausea. Elevated transaminase, platelet count, and proteinuria were noted. Head magnetic resonance imaging revealed a caudate nucleus hemorrhage and posterior reversible encephalopathy syndrome. After she delivered her newborn through an emergency cesarean section, she was admitted to the intensive care unit. On day 4 post-delivery, the patient’s D-dimer concentration was elevated, and contrast-enhanced computed tomography was performed. The results indicated pulmonary embolism, and heparin administration was initiated. The serum SDC-1 level was highest on day 1 post-delivery and quickly decreased subsequently; however, it remained elevated during the postpartum period. Her condition gradually improved, and she was extubated on day 6 and discharged from the ICU on day 7 post-delivery.ConclusionWe measured SDC-1 concentration in a patient with HELLP syndrome and found that the clinical course correlated with SDC-1 levels, indicating that SDC-1 is elevated immediately before and after pregnancy termination in patients with HELLP syndrome. Therefore, SDC-1 fluctuations, combined with the elevation of the D-dimer level, may be a potential marker for the early detection of HELLP syndrome and estimation of the syndrome’s severity in the future

Synergistic effect of collagen and CXCL12 in the low doses on human platelet activation.

CXCL12, also known as stromal cell-derived factor-1, is a chemokine classified into CXC families, which exerts its function by binding to specific receptors called CXCR4 and CXCR7. Human platelets express CXCR4 and CXCR7 on the plasma membrane. It has been reported that CXCL12 potentiates to induce platelet aggregation in cooperation with agonists including collagen. However, the precise roles and mechanisms of CXCL12 in human platelet activation are not fully elucidated. In the present study, we investigated the effect of simultaneous stimulation with low doses of collagen and CXCL12 on the activation of human platelets. The simultaneous stimulation with collagen and CXCL12 induced the secretion of platelet-derived growth factor (PDGF)-AB and the release of soluble CD40 ligand (sCD40L) from human platelets in addition to their aggregation, despite the fact that the simultaneous stimulation with thrombin receptor-activating peptide (TRAP) or adenosine diphosphate (ADP), and CXCL12 had little effects on the platelet aggregation. The agonist of Glycoprotein (GP) Ⅵ convulxin and CXCL12 also induced platelet aggregation synergistically. The monoclonal antibody against CXCR4 but not CXCR7 suppressed the platelet aggregation induced by simultaneous stimulation with collagen and CXCL12. The phosphorylation of p38 mitogen-activated protein kinase (MAPK), but not p44/p42 MAPK, was induced by the simultaneous stimulation. In addition, the simultaneous stimulation with collagen and CXCL12 induced the phosphorylation of HSP27 and the subsequent release of phosphorylated-HSP27 from human platelets. SB203580, a specific inhibitor of p38 MAPK, attenuated the platelet aggregation, the phosphorylation of p38 MAPK and HSP27, the PDGF-AB secretion, the sCD40L release and the phosphorylated-HSP27 release induced by the simultaneous stimulation with collagen and CXCL12. These results strongly suggest that collagen and CXCL12 in low doses synergistically act to induce PDGF-AB secretion, sCD40L release and phosphorylated-HSP27 release from activated human platelets via p38 MAPK activation