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To assess the utility of infrared thermography (IRT), to map skin temperature, in the detection of femoral arterial (FA) thrombosis after cardiac catheterization.

Ultrasound is a validated method for thrombus detection but is generally reserved as a confirmatory test for clinical suspicion due to various constraints.

Prospective study of infants and children undergoing cardiac catheterization via FA access, comparing IRT and pulse examination. The thermograms, displayed in a color map with each pixel representing a temperature, were examined by qualitative assessment of symmetry in thermal patterns and quantitative image analysis with abnormal thermographic asymmetry defined as a difference of >10% between limbs.

In the 20 children enrolled, excellent agreement was found between the two methods with a Kappa value of 0.89. The median thermographic asymmetry in the nine children with pulse loss was 36 (13-76)%. Using receiver operating characteristicanalysis, the asymmetrical pattern of ≥18% between limbs predicted the need for anticoagulation with a sensitivity of 100% and specificity of 89%. The area under the curve was 0.97 (95% confidence interval 0.95-1). Children with absent pulse requiring anticoagulation showed a slower recovery in thermal asymmetry compared to those with a reduced pulse. By qualitative IRT assessment, all children with absent pulse requiring anticoagulation were correctly identified by 10 independent assessors.

This pilot study showed that IRT is feasible and reliable as an adjunctive tool for thrombus detection postcatheterization and treatment monitoring. Specific advantages of IRT include portability, affordability, and contactless image acquisition.

This pilot study showed that IRT is feasible and reliable as an adjunctive tool for thrombus detection postcatheterization and treatment monitoring. Specific advantages of IRT include portability, affordability, and contactless image acquisition.The catalysed ring opening copolymerizations (ROCOP) of carbon dioxide/epoxide or anhydride/epoxide are controlled polymerizations that access useful polycarbonates and polyesters. Here, a systematic investigation of a series of heterodinuclear Mg(II)M(II) complexes reveals which metal combinations are most effective. The complexes combine different first row transition metals (M(II)) from Cr(II) to Zn(II), with Mg(II); all complexes are coordinated by the same macrocyclic ancillary ligand and by two acetate co-ligands. The complex syntheses and characterization data, as well as the polymerization data, for both carbon dioxide/cyclohexene oxide (CHO) and endo-norbornene anhydride (NA)/cyclohexene oxide, are reported. The fastest catalyst for both polymerizations is Mg(II)Co(II) which shows propagation rate constants (kp ) of 34.7 mM-1  s-1 (CO2 ) and 75.3 mM-1  s-1 (NA) (100 °C). The Mg(II)Fe(II) catalyst also shows excellent performances with equivalent rates for CO2 /CHO ROCOP (kp =34.7 mM-1  s-1 ) and may be preferable in terms of metallic abundance, low cost and low toxicity. PIK-90 nmr Polymerization kinetics analyses reveal that the two lead catalysts show overall second order rate laws, with zeroth order dependencies in CO2 or anhydride concentrations and first order dependencies in both catalyst and epoxide concentrations. Compared to the homodinuclear Mg(II)Mg(II) complex, nearly all the transition metal heterodinuclear complexes show synergic rate enhancements whilst maintaining high selectivity and polymerization control. These findings are relevant to the future design and optimization of copolymerization catalysts and should stimulate broader investigations of synergic heterodinuclear main group/transition metal catalysts.Donation after circulatory death (DCD) represents a promising opportunity to overcome the relative shortage of donors for heart transplantation. However, the necessary period of warm ischemia is a concern. This study aims to determine the critical warm ischemia time based on in vivo biochemical changes. Sixteen DCD non-cardiac donors, without cardiovascular disease, underwent serial endomyocardial biopsies immediately before withdrawal of life-sustaining therapy (WLST), at circulatory arrest (CA) and every 2 min thereafter. Samples were processed into representative pools to assess calcium homeostasis, mitochondrial function and cellular viability. Compared to baseline, no significant deterioration was observed in any studied parameter at the time of CA (median 9 min; IQR 7-13 min; range 4-19 min). Ten min after CA, phosphorylation of cAMP-dependent protein kinase-A on Thr197 and SERCA2 decreased markedly; and parallelly, mitochondrial complex II and IV activities decreased, and caspase 3/7 activity raised significantly. These results did not differ when donors with higher WLST to CA times (≥9 min) were analyzed separately. In human cardiomyocytes, the period from WLST to CA and the first 10 min after CA were not associated with a significant compromise in cellular function or viability. These findings may help to incorporate DCD into heart transplant programs.

There are no data on the effect of low-dose anticoagulation as secondary prophylaxis for venous thromboembolism (VTE) in cancer patients. We assessed the efficacy and safety of low-dose apixaban for 30months, after initial 6months of full-dose treatment.

We included 298 patients with cancer and any type of VTE in a single arm interventional clinical trial. All patients were treated with full-dose apixaban (5mg twice daily) for 6months. Total 196 patients with active cancer after 6months treatment continued with apixaban 2.5mg twice daily for another 30months. The main endpoints were recurrent VTE, major bleeding and clinically relevant non-major bleeding.

During the 30months of treatment with low-dose apixaban 14 (7.6%; 95% confidence interval (CI) 4.0%-11.7%) patients experienced recurrent VTE, six (3.1%; 95% CI 1.1%-6.5%) experienced major bleeding and 16 (8.1%, 95% CI 4.7%-12.8%) experienced clinically relevant non-major bleeding. The incidence rate per person month of recurrent VTE was 0.8% (95% CI 0.41-1.6) at 2-6months with full-dose apixaban, and 1.0% (95% CI 0.5-1.9) at 7-12months with low-dose apixaban. The incidence rate of major bleeding was 1.1% (95% CI 0.6-2.0) at 2-6months, and 0.3% (95% CI 0.1-1.0) at 7-12months. Between 12 and 36months the incidence rate of recurrent VTE and major bleedings remained low.

Dose reduction of apixaban to 2.5mg twice daily seems safe after 6months of full-dose treatment. After 12months the incidence rate of recurrent VTE and major bleeding remained low.

Dose reduction of apixaban to 2.5 mg twice daily seems safe after 6 months of full-dose treatment. After 12 months the incidence rate of recurrent VTE and major bleeding remained low.CCR5 KO kidney transplant (KTx) recipients are extraordinarily high alloantibody producers and develop pathology that mimics human antibody-mediated rejection (AMR). C57BL/6 and CCR5 KO mice (H-2b ) were transplanted with A/J kidneys (H-2a ); select cohorts received adoptive cell therapy (ACT) with alloprimed CXCR5+ CD8+ T cells (or control cells) on day 5 after KTx. ACT efficacy was evaluated by measuring posttransplant alloantibody, pathology, and allograft survival. Recipients were assessed for the quantity of CXCR5+ CD8+ T cells and CD8-mediated cytotoxicity to alloprimed IgG+ B cells. Alloantibody titer in CCR5 KO recipients was four-fold higher than in C57BL/6 recipients. The proportion of alloprimed CXCR5+ CD8+ T cells 7 days after KTx in peripheral blood, lymph node, and spleen was substantially lower in CCR5 KO compared to C57BL/6 recipients. In vivo cytotoxicity towards alloprimed IgG+ B cells was also reduced six-fold in CCR5 KO recipients. ACT with alloprimed CXCR5+ CD8+ T cells (but not alloprimed CXCR5- CD8+ or third-party primed CXCR5+ CD8+ T cells) substantially reduced alloantibody titer, ameliorated AMR pathology, and prolonged allograft survival. These results indicate that a deficiency in quantity and function of alloprimed CXCR5+ CD8+ T cells contributes to high alloantibody and AMR in CCR5 KO recipient mice, which can be rescued with ACT.Equity, diversity, and inclusion (EDI) have become essential considerations in different academic fields in recent years, attracting an increasing number of voices and perspectives from different groups. There is a need for an intersectionality framework that is inclusive of both the local and global diversity of researchers. Here, we present an intersectionality framework called KLOB which structures barriers to academic success into four components knowledge exchange (K), language (L), obligations (O), and biases (B), and thus helps to think about the cumulative effect of multiple barriers that individuals from different backgrounds encounter to succeed in academic activities such as scientific publishing, which is the primary currency of academic success in our current system. This framework highlights both local and global disparities in socioeconomic, linguistic, and discriminatory factors that determine the opportunity of individual researchers to succeed in academia. We emphasise that individual researchers have no control over most barriers they face because of where and how they were born. Implementing solutions to address barriers associated with KLOB requires a multiscale vision and initiatives that tackle local and global inequities.Cardiovascular diseases (CVDs) contribute to the leading cause of death worldwide. Despite significant improvements in CVDs diagnosis and treatment, a continued effort to explore novel therapeutic strategies is urgently need. N6-methyladenosine (m6 A) RNA methylation, well known as the most prevalent type of RNA modifications, involved in RNA stability, nuclear exports, translation, and decoy, plays a crucial role in the pathogenesis of a variety of diseases, including CVDs, cancer, and drug resistance. Here, our article summarizes cellular functions of m6 A modulators and recent research progress concerning the functions and mechanisms of m6 A methylation in CVDs, in hope of providing references for exploring novel therapeutic approaches and potential biomarkers in the treatment of CVDs.Composite photocatalyst-adsorbents such as TiO2 /Fe2 O3 are promising materials for the one-step treatment of arsenite contaminated water. However, no previous study has investigated how coupling TiO2 with Fe2 O3 influences the photocatalytic oxidation of arsenic(III). Herein, we develop new hybrid experiment/modelling approaches to study light absorption, charge carrier behaviour and changes in the rate law of the TiO2 /Fe2 O3 system, using UV-Vis spectroscopy, transient absorption spectroscopy (TAS), and kinetic analysis. Whilst coupling TiO2 with Fe2 O3 improves total arsenic removal by adsorption, oxidation rates significantly decrease (up to a factor of 60), primarily due to the parasitic absorption of light by Fe2 O3 (88 % of photons at 368 nm) and secondly due to changes in the rate law from disguised zero-order kinetics to first-order kinetics. Charge transfer across this TiO2 -Fe2 O3 heterojunction is not observed. Our study demonstrates the first application of a multi-adsorbate surface complexation model (SCM) towards describing As(III) oxidation kinetics which, unlike Langmuir-Hinshelwood kinetics, includes the competitive adsorption of As(V).

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