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We aimed to assess an impact of instantaneous wave-free ratio (iFR) on a graft failure after coronary artery bypass grafting (CABG).

A total of 131 coronary arteries from 88 patients who underwent invasive coronary angiography, intracoronary pressure measurements, CABG, and scheduled follow-up coronary computed tomography angiography within one year were investigated. All studied arteries had FFR<0.80. The rate of graft failure was significantly higher in vessels with negative iFR (>0.89) than in those with positive iFR (<0.89) (25.7% vs. 7.3%, p=0.012). selleck chemicals llc The graft failure rates increased as the preoperative iFR values rose (iFR<0.80, 3.3%; iFR 0.80-0.84, 5.6%; iFR 0.85-0.89, 16.0%; iFR 0.90-0.94, 28.0%; and iFR 0.95-1.00, 50.0%; p=0.002). A cut-off value of iFR to predict graft failures was determined as 0.84 by receiver-operating characteristic curve analysis with sensitivity, specificity, positive predictive value, negative predictive value, and accuracy of 88%, 62%, 25%, 97%, and 66%, respectively.

The risk of graft failure becomes higher, as the preoperative iFR increases. The graft failure is significantly more frequent when a bypass graft is anastomosed on vessels with negative iFR than those with positive iFR.

The risk of graft failure becomes higher, as the preoperative iFR increases. The graft failure is significantly more frequent when a bypass graft is anastomosed on vessels with negative iFR than those with positive iFR.

Inflammation is actively involved in the clinical manifestation of peripheral artery disease (PAD). Sonodynamic therapy (SDT), a novel non-invasive, plaque-based, macrophage-targeted anti-inflammatory regimen for atherosclerosis has the potential to improve walking performance by reducing plaque inflammation.

This phase-2, randomized, sham-controlled, double-blind clinical trial enrolled 32 participants with symptomatic femoropopliteal PAD. The primary outcome was the 30-day change in the target-to-background ratio (TBR) within the most diseased segment (MDS) of the femoropopliteal artery assessed through positron emission tomography/computed tomography (PET/CT). The secondary outcomes were changes in walking performance, limb perfusion, lesional morphology and quality of life measurements.

The mean age was 64.7years and 63% were male. Thirty-one completed follow-up. SDT significantly decreased the MDS TBR by 0.53 (95% CI, -0.70 to -0.36, P<0.001) compared with control. Furthermore, SDT increased peak walking time by 118.6s (95% CI, 74.3 to 163.0, P<0.001), increased ankle-brachial index by 0.11 (95% CI, 0.07 to 0.14, P<0.001), decreased lesional diameter and area stenosis by 7.2% (95% CI, -8.6 to -4.5, P<0.001) and 9.6% (95% CI, -24.5 to -5.3, P=0.005), respectively, and increased the walking speed score of the Walking Impairment Questionnaire by 16.1 (95% CI, 2.6 to 29.5, P=0.021) and the physical functioning score of the 36-item Short-Form Health Survey by 10.0 (95% CI, 5.0 to 20.0, P=0.003) compared with control. These improvements were maintained in the SDT group up to 6-month.

SDT rapidly reduced plaque inflammation and improved walking performance among patients with symptomatic PAD.

Clinical Trials NCT03457662.

Clinical Trials NCT03457662.

Preferred neoadjuvant regimens for early-stage triple-negative breast cancer (TNBC) include anthracycline-cyclophosphamide and taxane-based chemotherapy. IMpassion031 compared efficacy and safety of atezolizumab versus placebo combined with nab-paclitaxel followed by doxorubicin plus cyclophosphamide as neoadjuvant treatment for early-stage TNBC.

This double-blind, randomised, phase 3 study enrolled patients in 75 academic and community sites in 13 countries. Patients aged 18 years or older with previously untreated stage II-III histologically documented TNBC were randomly assigned (11) to receive chemotherapy plus intravenous atezolizumab at 840 mg or placebo every 2 weeks. Chemotherapy comprised of nab-paclitaxel at 125 mg/m

every week for 12 weeks followed by doxorubicin at 60 mg/m

and cyclophosphamide at 600 mg/m

every 2 weeks for 8 weeks, which was then followed by surgery. Stratification was by clinical breast cancer stage and programmed cell death ligand 1 (PD-L1) status. Co-primary endpointsy profile.

F Hoffmann-La Roche/Genentech.

F Hoffmann-La Roche/Genentech.The star fruit (Averrhoa carambola) is consumed in high amounts in Asia and Central/South America. It contains oxalic acid and caramboxin. In some individuals, its ingestion may lead to nephrotoxicity and neurotoxicity. The nephrotoxic effect is due to oxalate deposition in renal tubules resulting in acute tubular necrosis and interstitial nephritis. Although uraemic encephalopathy secondary to acute kidney injury may play a role, a shift to an excitatory state of the central nervous system (CNS) by caramboxin through activation of excitatory neuroreceptors and inhibition of GABA receptors leads to mental confusion, seizures and status epilepticus seen with star fruit intoxication. In this mini-review, we discuss the mechanisms of star fruit-related toxicity.Human respiratory disease associated with influenza virus infection is of significant public health concern. Macrophages, as part of the front line of host innate cellular defence, have been shown to play an important role in controlling viral replication. However, fatal outcomes of infection, as evidenced in patients infected with highly pathogenic viral strains, are often associated with prompt activation and excessive accumulation of macrophages. Activated macrophages can produce a large amount of pro-inflammatory cytokines, which leads to severe symptoms and at times death. However, the mechanism for rapid activation and excessive accumulation of macrophages during infection remains unclear. It has been suggested that the phenomena may arise from complex interactions between macrophages and influenza virus. In this work, we develop a novel mathematical model to study the relationship between the level of macrophage activation and the level of viral load in influenza infection. Our model combines a dynamic model of viral infection, a dynamic model of macrophages and the essential interactions between the virus and macrophages.