Use of ultra-low dose computed tomography versus abdominal plain film for assessment of stone-free rates after shock-wave lithotripsy: implications on emergency room visits, surgical procedures, and cost-effectiveness

The aims of this investigation were: (1) to compare residual stone-fragment (RSF) detection rates of ultra-low dose computed tomography (ULD-CT) and abdominal plain film (KUB) in urolithiasis patients undergoing shock-wave lithotripsy (SWL), and (2) to evaluate the downstream sequelae of utilizing these two disparate imaging pathways of differing diagnostic fidelity. A retrospective chart-review of patients undergoing SWL at two high-volume surgical centers was undertaken (2013-2016). RSF diagnostic rates of ULD-CT and KUB were assessed, and the impact of imaging modality used on subsequent emergency room (ER) visits, unplanned procedures, and cost-effectiveness was investigated. Adjusted analyses examined association between imaging modality used and outcomes, and Markov decision-tree analysis was performed to identify a cost advantageous scenario for ULD-CT over KUB. Of 417 patients studied, 57 (13.7%) underwent ULD-CT while the remaining 360 underwent KUB. The RSF rates were 36.8% and 22.8% in the ULD-CT and KUB groups, respectively (p = 0.019). A 5.6% and 18% of the patients deemed stone-free on ULD-CT and KUB, respectively, returned to the ER (p = 0.040). Similarly, 2.8% and 15.1% needed an unplanned surgery (p = 0.027). These findings were confirmed on multivariable analyses, Odds ratios CT-ULD versus KUB: 0.19 and 0.10, respectively, p \u3c 0.05. With regards to cost-effectiveness, at low ULD-CT charges, the ULD-CT follow-up pathway was economically more favorable, but with increasing ULD-CT charges, the KUB follow-up pathway superseded. ULD-CT seems to provide a more \u27true\u27 estimate of stone-free status, and in consequence mitigates unwanted emergency and operating room visits by reducing untimely stent removals and false patient reassurances. Further, at low ULD-CT costs, it may also be economically more favorable

Managing Urology Consultations During COVID-19 Pandemic: Application of a Structured Care Pathway

OBJECTIVE: To describe and evaluate a risk-stratified triage pathway for inpatient urology consultations during the SARS-CoV-2 (COVID-19) pandemic. This pathway seeks to outline a urology patient care strategy that reduces the transmission risk to both healthcare providers and patients, reduces the healthcare burden, and maintains appropriate patient care. MATERIALS AND METHODS: Consultations to the urology service during a 3-week period (March 16 to April 2, 2020) were triaged and managed via one of 3 pathways: Standard, Telemedicine, or High-Risk. Standard consults were in-person consults with non COVID-19 patients, High-Risk consults were in-person consults with COVID-19 positive/suspected patients, and Telemedicine consults were telephonic consults for low-acuity urologic issues in either group of patients. Patient demographics, consultation parameters and consultation outcomes were compared to consultations from the month of March 2019. Categorical variables were compared using Chi-square test and continuous variables using Mann-Whitney U test. A P value \u3c.05 was considered significant. RESULTS: Between March 16 and April 2, 2020, 53 inpatient consultations were performed. By following our triage pathway, a total of 19/53 consultations (35.8%) were performed via Telemedicine with no in-person exposure, 10/53 consultations (18.9%) were High-Risk, in which we strictly controlled the urology team member in-person contact, and the remainder, 24/53 consultations (45.2%), were performed as Standard in-person encounters. COVID-19 associated consultations represented 18/53 (34.0%) of all consultations during this period, and of these, 8/18 (44.4%) were managed successfully via Telemedicine alone. No team member developed COVID-19 infection. CONCLUSION: During the COVID-19 pandemic, most urology consultations can be managed in a patient and physician safety-conscious manner, by implementing a novel triage pathway

The Volatile Anesthetic Isoflurane Increases Endothelial Adenosine Generation via Microparticle Ecto-5′-Nucleotidase (CD73) Release

Endothelial dysfunction is common in acute and chronic organ injury. Isoflurane is a widely used halogenated volatile anesthetic during the perioperative period and protects against endothelial cell death and inflammation. In this study, we tested whether isoflurane induces endothelial ecto-5′-nucleotidase (CD73) and cytoprotective adenosine generation to protect against endothelial cell injury. Clinically relevant concentrations of isoflurane induced CD73 activity and increased adenosine generation in cultured human umbilical vein or mouse glomerular endothelial cells. Surprisingly, isoflurane-mediated induction of endothelial CD73 activity occurred within 1 hr and without synthesizing new CD73. We determined that isoflurane rapidly increased CD73 containing endothelial microparticles into the cell culture media. Indeed, microparticles isolated from isoflurane-treated endothelial cells had significantly higher CD73 activity as well as increased CD73 protein. In vivo, plasma from mice anesthetized with isoflurane had significantly higher endothelial cell-derived CD144+ CD73+ microparticles and had increased microparticle CD73 activity compared to plasma from pentobarbital-anesthetized mice. Supporting a critical role of CD73 in isoflurane-mediated endothelial protection, a selective CD73 inhibitor (APCP) prevented isoflurane-induced protection against human endothelial cell inflammation and apoptosis. In addition, isoflurane activated endothelial cells Rho kinase evidenced by myosin phosphatase target subunit-1 and myosin light chain phosphorylation. Furthermore, isoflurane-induced release of CD73 containing microparticles was significantly attenuated by a selective Rho kinase inhibitor (Y27632). Taken together, we conclude that the volatile anesthetic isoflurane causes Rho kinase-mediated release of endothelial microparticles containing preformed CD73 and increase adenosine generation to protect against endothelial apoptosis and inflammation

Experimental constraints on the relative stabilities of the two systems monazite-(Ce) - allanite-(Ce) - fluorapatite and xenotime-(Y) - (Y,HREE)-rich epidote - (Y,HREE)-rich fluorapatite, in high Ca and Na-Ca environments under P-T conditions of 200-1000 MPa and 450-750 A degrees C

The relative stabilities of phases within the two systems monazite-(Ce) - fluorapatite - allanite-(Ce) and xenotime-(Y) - (Y,HREE)-rich fluorapatite - (Y,HREE)-rich epidote have been tested experimentally as a function of pressure and temperature in systems roughly replicating granitic to pelitic composition with high and moderate bulk CaO/Na2O ratios over a wide range of P-T conditions from 200 to 1000 MPa and 450 to 750 A degrees C via four sets of experiments. These included (1) monazite-(Ce), labradorite, sanidine, biotite, muscovite, SiO2, CaF2, and 2 M Ca(OH)(2); (2) monazite-(Ce), albite, sanidine, biotite, muscovite, SiO2, CaF2, Na2Si2O5, and H2O; (3) xenotime-(Y), labradorite, sanidine, biotite, muscovite, garnet, SiO2, CaF2, and 2 M Ca(OH)(2); and (4) xenotime-(Y), albite, sanidine, biotite, muscovite, garnet, SiO2, CaF2, Na2Si2O5, and H2O. Monazite-(Ce) breakdown was documented in experimental sets (1) and (2). In experimental set (1), the Ca high activity (estimated bulk CaO/Na2O ratio of 13.3) promoted the formation of REE-rich epidote, allanite-(Ce), REE-rich fluorapatite, and fluorcalciobritholite at the expense of monazite-(Ce). In contrast, a bulk CaO/Na2O ratio of similar to 1.0 in runs in set (2) prevented the formation of REE-rich epidote and allanite-(Ce). The reacted monazite-(Ce) was partially replaced by REE-rich fluorapatite-fluorcalciobritholite in all runs, REE-rich steacyite in experiments at 450 A degrees C, 200-1000 MPa, and 550 A degrees C, 200-600 MPa, and minor cheralite in runs at 650-750 A degrees C, 200-1000 MPa. The experimental results support previous natural observations and thermodynamic modeling of phase equilibria, which demonstrate that an increased CaO bulk content expands the stability field of allanite-(Ce) relative to monazite-(Ce) at higher temperatures indicating that the relative stabilities of monazite-(Ce) and allanite-(Ce) depend on the bulk CaO/Na2O ratio. The experiments also provide new insights into the re-equilibration of monazite-(Ce) via fluid-aided coupled dissolution-reprecipitation, which affects the Th-U-Pb system in runs at 450 A degrees C, 200-1000 MPa, and 550 A degrees C, 200-600 MPa. A lack of compositional alteration in the Th, U, and Pb in monazite-(Ce) at 550 A degrees C, 800-1000 MPa, and in experiments at 650-750 A degrees C, 200-1000 MPa indicates the limited influence of fluid-mediated alteration on volume diffusion under high P-T conditions. Experimental sets (3) and (4) resulted in xenotime-(Y) breakdown and partial replacement by (Y,REE)-rich fluorapatite to Y-rich fluorcalciobritholite. Additionally, (Y,HREE)-rich epidote formed at the expense of xenotime-(Y) in three runs with 2 M Ca(OH)(2) fluid, at 550 A degrees C, 800 MPa; 650 A degrees C, 800 MPa; and 650 A degrees C, 1000 MPa similar to the experiments involving monazite-(Ce). These results confirm that replacement of xenotime-(Y) by (Y,HREE)-rich epidote is induced by a high Ca bulk content with a high CaO/Na2O ratio. These experiments demonstrate also that the relative stabilities of xenotime-(Y) and (Y,HREE)-rich epidote are strongly controlled by pressure

Vascular dysfunction in cerebrovascular disease: mechanisms and therapeutic intervention

The endothelium plays a crucial role in the control of vascular homoeostasis through maintaining the synthesis of the vasoprotective molecule NO* (nitric oxide). Endothelial dysfunction of cerebral blood vessels, manifested as diminished NO* bioavailability, is a common feature of several vascular-related diseases, including hypertension, hypercholesterolaemia, stroke, subarachnoid haemorrhage and Alzheimer's disease. Over the past several years an enormous amount of research has been devoted to understanding the mechanisms underlying endothelial dysfunction. As such, it has become apparent that, although the diseases associated with impaired NO* function are diverse, the underlying causes are similar. For example, compelling evidence indicates that oxidative stress might be an important mechanism of diminished NO* signalling in diverse models of cardiovascular 'high-risk' states and cerebrovascular disease. Although there are several sources of vascular ROS (reactive oxygen species), the enzyme NADPH oxidase is emerging as a strong candidate for the excessive ROS production that is thought to lead to vascular oxidative stress. The purpose of the present review is to outline some of the mechanisms thought to contribute to endothelial dysfunction in the cerebral vasculature during disease. More specifically, we will highlight current evidence for the involvement of ROS, inflammation, the RhoA/Rho-kinase pathway and amyloid beta-peptides. In addition, we will discuss currently available therapies for improving endothelial function and highlight future therapeutic strategies

U-Pb and trace element zircon and apatite petrochronology of eclogites from the Scandinavian Caledonides

The petrochronological records of eclogites in the Scandinavian Caledonides are investigated using EPMA and LA-ICPMS of zircon and apatite for U-Pb geochronology, combined with major and trace element characteristics. Metamorphic zircon from two eclogites from the Lofoten-Vesteralen Complex (Lofoten Archipelago region) collectively yielded a Concordia age 427.8 & PLUSMN; 5.7 Ma and an upper intercept U-Pb age 425 & PLUSMN; 30 Ma. Apatites from the same eclogites provided U-Pb lower intercepts at 322 & PLUSMN; 28 Ma and 354 & PLUSMN; 33 Ma, with the latter also yielding a younger age of 227 & PLUSMN; 24 Ma. Two eclogites from the Lower Seve Nappe (Northern Jamtland) demonstrate different zircon and apatite age records. Metamorphic zircon provided Concordia ages of 467.2 & PLUSMN; 5.9 Ma and 444.5 & PLUSMN; 5.5 Ma, which resolve the age of prograde metamorphism and zircon growth during retrogression, respectively. The lower intercept U-Pb ages of apatites from the same eclogites are 436 & PLUSMN; 18 and 415 & PLUSMN; 25 Ma, respectively. In combination with their geochemical characteristics, they suggest two separate stages of exhumation of eclogite bodies in the Lower Seve Nappe. Zircons from an eclogite from the Blaho Nappe (Nordoyane Archipelago) yielded a continuum of concordant U-Pb dates from ca. 435 to 395 Ma, which suggests several cycles of HT metamorphism within short intervals. Distinctive trace element characteristics of apatites from the Blaho Nappe eclogite suggest formation coeval with zircon and garnet during HT metamorphism, but Pb diffusion behaved as an open system until cooling during exhumation of the nappe at 390 & PLUSMN; 12 Ma (lower intercept U-Pb age of apatite). To summarize, this study presents the high potential of coupled zircon and apatite petrochronology of eclogites in resolving their metamorphic evolution, particularly with respect to using trace element characteristics of apatites to constrain the records of their growth, alterations and the meaning of their U-Pb age record

Sensitive high-resolution ion microprobe analysis of zircon reequilibrated by late magmatic fl uids in a hybridized pluton

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Phenolic acids improve the antioxidant activity of ceruloplasmin isolated from plasma of healthy volunteers and atherosclerotic patients

The aim of the present study was to estimate the ability of individual phenolic acids to eliminate Fe(II) ions from the solution. Moreover, the influence of phenolic acids on the ferroxidase activity of ceruloplasmin (Cp) isolated from blood plasma of healthy volunteers (CpC) and patients with atherosclerosis obliterans (CpAO) was established in vitro. Phenolic acids demonstrated a ferroxidase-like activity, i.e. the ability to eliminate Fe(II) ions, within the studied concentration range of 2.0-17.0 mol 10-5 dm-3, in the following order of decreasing effectiveness: caffeic acid (CA)>ellagic acid (EA)>chlorogenic acid (ChA)>ferulic acid (FA) ≈ p-coumaric acid (PcA) = sinapic acid (SA). The study showed that the ability of phenolic acids to eliminate Fe(II) ions by oxidation or chelation was related to the structure of the former, to the presence of orto -OH groups, especially. Furthermore, the effect of the molar ratio of phenolic acid to Fe(II) ion was observed. EA and ChA, both containing two orto-OH groups and the highest number of –OH groups (4 and 5, respectively), demonstrated the greatest ability to eliminate Fe(II) ions, especially at the Fe(II) to phenolic acid molar ratio of 6:1. Phenolic acids added to samples with a constant amount of Cp caused decrease in the concentration of Fe(II) ions. Therefore, it may be assumed that the addition of phenolic acids to CpC and CpAO, even in low concentrations, caused a significant decrease in the concentration of Fe(II) ions

Mechanisms of augmented vasoconstriction induced by 5-hydroxytryptamine in aortic rings from spontaneously hypertensive rats

Background and purpose: To test whether development of enhanced vasoconstriction to 5-hydroxytryptamine (5-HT; serotonin) in SHR was temporally related to hypertension, elevated vascular superoxide (O2) levels, decreased NO bioavailability, or increased contractile effects of cyclooxygenase or rho-kinase and/or PKC. Experimental approach: We examined systolic blood pressure (SBP), vascular O2, and 5-HT-induced contractile responses of aortic segments from 4- and 8-week-old WKY and SHR. Key results: SBP was 35% higher in SHR than WKY at 4 weeks and 60% higher at 8 weeks. Contractile responses to 5-HT were similar in WKY and SHR at 4 weeks, but were markedly augmented in SHR at 8 weeks. The NO synthase inhibitor, L-NAME, enhanced contractile responses to 5-HT markedly in both strains at 4 weeks and in WKY at 8 weeks, but only very modestly in SHR at 8 weeks. These functional differences were associated with higher O2 levels in SHR versus WKY at 8 weeks, but not at 4 weeks. The rho-kinase inhibitor, Y-27632, and the PKC inhibitor, Ro 31-8220, each only modestly attenuated contractions in WKY and SHR in each age group, and their effects in each strain were more pronounced at 8 weeks. The cyclooxygenase inhibitor, indomethacin, had no effect on contractile responses. Conclusions and implications: Development of augmented vascular contractile responses to 5-HT in SHR is preceded by hypertension. It is associated with increased vascular O2 levels and reduced modulatory effects of NO, and is unlikely to be due to enhanced activity of rho-kinase, PKC or cyclooxygenase