41 research outputs found

    Search for gravitational waves associated with gamma-ray bursts detected by Fermi and Swift during the LIGO–Virgo run O3b

    Get PDF
    We search for gravitational-wave signals associated with gamma-ray bursts (GRBs) detected by the Fermi and Swift satellites during the second half of the third observing run of Advanced LIGO and Advanced Virgo (2019 November 1 15:00 UTC–2020 March 27 17:00 UTC). We conduct two independent searches: a generic gravitational-wave transients search to analyze 86 GRBs and an analysis to target binary mergers with at least one neutron star as short GRB progenitors for 17 events. We find no significant evidence for gravitational-wave signals associated with any of these GRBs. A weighted binomial test of the combined results finds no evidence for subthreshold gravitational-wave signals associated with this GRB ensemble either. We use several source types and signal morphologies during the searches, resulting in lower bounds on the estimated distance to each GRB. Finally, we constrain the population of low-luminosity short GRBs using results from the first to the third observing runs of Advanced LIGO and Advanced Virgo. The resulting population is in accordance with the local binary neutron star merger rate

    Early corneal epithelial complications of combined trans-epithelial and accelerated collagen cross-linking in treatment of keratoconus

    No full text
    PosterESCRS: 10-14 September and Euretina: 8-11 SeptemberPURPOSE: Trans-epithelial collagen crosslinking (CXL) benefits conventional epithelium off CXL by its ability to avoid epithelial defect or complications related to epithelium healing. In our study, we combine trans-epithelial CXL with an accelerated irradiation protocol (18 mW/cm2 for 5 min) in order to shorten the time of irradiation. The purpose of this study is to report any early corneal epithelial complications after combined trans-epithelial and accelerated CXL in treating keratoconus. By far, trans-epithelial CXL with conventional irradiation settings (3 mW/cm2 for 30 minutes) have not yet reported any epithelial related complications. SETTING: Department of Ophthalmology, Queen Mary Hospital, Hong Kong. METHODS: 7 patients and 11 eyes with topography evidence of progressive keratoconus were included. All patients underwent the combined trans-epithelial technique with an accelerated collagen crosslinking. Solution containing 0.25% riboflavin, 1.2 % HPMC and 0.01 % Benzalkoniumchloride were instilled every 2 minutes for 30 minutes, followed by 18 mW/cm2 UVA irradiation for 5 minutes at a working distance of 5cm (with continued application of the solution every 2 min). Complications of treatment were reported. RESULTS: A total of 7 eyes (64%) developed early corneal epithelial complications. 5 eyes (45%) developed large epithelial defect as large as the size of the irradiated area within the first week of operation. The other 2 eyes from the same patient resulted in diffuse punctate epithelial erosions. 1 eye with epithelial defect developed dendritic ulcer shortly after healing of the epithelial defect, which resolved after a course of topical acyclovir treatment. The early corneal stromal haze was seen only in those eyes with post-operative epithelial defects, but not in other eyes in which the epithelium remained intact. CONCLUSIONS: 64% of patients developed epithelial complications after combined trans-epithelial and accelerated CXL protocol. We propose the result to be due to increased intensity of UVA irradiation, which might have loosened tight junctions in the corneal epithelium, thus leading to epithelial defects. As a result, the main advantage of trans-epithelial technique in preserving the epithelium has been defeated. This study concludes that combined trans-epithelial and accelerated CXL protocol has no additional benefit in the treatment of keratoconus, hence we propose to continue with conventional UVA irradiation protocol if trans-epithelial technique is to be used

    C-Type Natriuretic peptide (CNP) release does not contribute to endothelium-derived hyperpolarizing factor (EDHF) mediated relaxation in porcine coronary artery

    No full text
    Objective: The release of CNP accounts for EDHF-mediated relaxations in the rat mesenteric artery1 and is Gi protein dependent2. EDHF-mediated relaxations in the porcine coronary artery are not Gi dependent3. This study investigates whether or not CNP release accounts for EDHF-responses in this artery. Methods: (1) CNP concentration was measured by enzyme immunoassay in bathing solution containing porcine coronary arterial rings where EDHF response was initiated by bradykinin (100 nM). (2) EDHF-mediated relaxations induced by SFLLRN were compared with those to exogenous CNP in the presence of phosphoramidon (10 µM; known to potentiate CNP induced relaxations). Results: There was no significant difference in the CNP concentrations between chambers containing rings that did or did not exhibit a EDHF-mediated response. Relaxations induced by CNP alone were potentiated by phosphoramidon (maximal relaxation 60.7 ± 7.7 % vs 84.1 ± 7.5 %, control vs phosphoramidon, P<0.05) but the EDHF-mediated responses to SFLLRN were not (maximal relaxation 69.9 ± 9.1 % vs 72.8 ± 9.9 %, control vs phosphoramidon) Conclusions: Unlike in the mesenteric artery and the heart of the rat, CNP release does not contribute to EDHF-mediated relaxations in the porcine coronary artery. FOOTNOTES Support: HKU CRCG (No. 21374077) REFERENCES Villar , et al. Cardiovasc Res 2007914.3 Chauhan , et al. PNAS 2003914.3 Ng , et al. J Vasc Res 200512 S201

    Endothelium-derived hyperpolarizing factor mediated relaxations in pig coronary arteries do not involve Gi/o proteins

    No full text
    Aim: Endothelium-dependent relaxations to certain neurohumoral substances are mediated by pertussis toxin-sensitive Gi/o protein. Our experiments were designed to determine the role, if any, of pertussis toxin-sensitive G-proteins in relaxations attributed to endothelium-derived hyperpolarizing factor (EDHF). Methods: Pig coronary arterial rings with endothelia were suspended in organ chambers flled with Krebs-Ringer bicarbonate solution maintained at 37 °C and continuously aerated with 95%O2 and 5% CO2. Isometric tension was measured during contractions to prostaglandin F2α in the presence of indomethacin and NΩnitro-L-arginine methyl ester (L-NAME). Results: Thrombin, the thrombin receptor-activating peptide SFLLRN, bradykinin, substance P, and calcimycin produced dose-dependent relaxations. These relaxations were not inhibited by prior incubation with pertussis toxin, but were abolished upon the addition of charybdotoxin plus apamin. Relaxations to the α2-adrenergic agonist UK14304 and those to serotonin were abolished in the presence of indomethacin and L-NAME. Conclusion: Unlike nitric oxide-mediated relaxations, EDHF-mediated relaxations of pig coronary arteries do not involve pertussis toxin-sensitive pathways and are Gi/o protein independent.link_to_OA_fulltex

    Low-dose desmopressin improves hypothermia-induced impairment of primary haemostasis in healthy volunteers

    No full text
    Mild hypothermia (34-35 °C) increases peri-operative blood loss. We have previously demonstrated the beneficial effect of in vitro desmopressin on impairment of primary haemostasis associated with hypothermia. This study evaluated subcutaneous desmopressin in 52 healthy volunteers, randomly assigned to receive either normal saline or desmopressin 1.5, 5 or 15 μg (with 13 in each group). Blood samples were collected before and 2 h after drug administration and incubated at 32 and 37 °C. Platelet function analyser PFA-100® closure times were measured. Hypothermia at 32 °C prolonged mean (95% CI) closure times (for adenosine diphosphate/collagen by 11.3% (7.5-15.2%) and for adrenaline/collagen by 16.2% (11.3-21.2%); these changes were reversed by desmopressin. A very small dose was found to be effective (1.5 μg); this dose did not significantly change closure times at 37 °C, but fully prevented its prolongation at 32 °C. Subcutaneous desmopressin prevents the development of hypothermia-induced impairment of primary haemostasis. © 2011 The Authors.link_to_OA_fulltex

    Coagulation, blood loss and platelet activation during isoflurane or sevoflurane anesthesia

    No full text
    INTRODUCTION: Sevoflurane has been shown to inhibit platelet aggregation1,2. This study investigates whether sevoflurane causes different coagulation changes, blood loss and platelet activation compared to isoflurane. METHODS: With IRB approval, patients undergoing elective joint arthroplasty were recruited. Patients discontinued their NSAID and no LMWH were used. They were allocated randomly to receive either sevoflurane (Group S) or isoflurane (Group I) anesthesia. Opioids and femoral blocks were employed at the discretion of the anesthesiologists. Intravenous fluids were prescribed using a strict protocol and red cell transfused if hemoglobin dropped below 8g/dL. All operations were performed by the surgeon authors (WMT & KYC) using a standardized technique. Blood is collected for complete blood count, prothrombin time, activated partial thromboplastin time, thrombelastography (TEG®) and plasma soluble CD40 ligand (sCD40L) concentration before induction and in PACU. Intraoperative and postoperative blood loss was recorded. Native TEG® measurement was performed using the TEG® 5000 (Haemoscope Corp, IL, USA). sCD40L was measured using platelet poor plasma (PPP) with a commercial ELISA kit (R&D Systems, MN, USA). PPP was prepared by centrifugation of EDTA blood at 10,000g, 4 oC for 10 minutes. RESULTS: 20 patients were recruited in each group (M/F = 4/16 and 6/14; age = 65±15 and 64±12, Group S and I). There was no difference in all TEG® or other coagulation parameters between the groups (table1), nor in blood loss, fluid requirement or change in Hb (table2).[table1][table2]No patient required transfusion. However patients in Group S had significantly lower plasma sCD40L concentrations at end of surgery.[figure1]Conclusion Sevoflurane reduces platelet activation without impairing coagulation or increasing blood loss compared to isoflurane. REFERENCES: 1. Anesthesiology 1996;85:1447. 2. Can J Anaesth 1997;44:1157.American Society of Anesthesiologists Annual Meeting, Orlando, Florida, USA, 18-22 Oct 2008, Abstract no. A161
    corecore