Academic Rights Press (United Kingdom)

Abstract Background Changes in climate and vegetation, in combination with fire exclusion, are altering and homogenizing fire regime attributes compared to historical conditions. Fire regime changes are commonly quantified using departure metrics based on differences in measures of central tendency (i.e., means) between time periods. These metrics can mischaracterize complex changes to fire regime attributes because the distributions underlying these attributes are often not well described by parameters. Results We developed a non-parametric index of fire regime departure that quantifies distributional changes to fire regime attributes between time periods using the Earth Mover’s Distance. We used this departure metric to compare fire frequency and burn severity between historical (~1600–1880) and contemporary (1985–2021) time periods in western US forests. In addition, we compared the proposed metrics with a standard suite of measures of central tendency. Departure metrics based on measures of central tendency reported lower relative departures within frequent fire forests and higher relative departures within infrequent fire forests than the EMD-based method. We found that 89% of western US forests are experiencing less frequent and more severe wildfires than historical baselines. Large departures are associated with increased human land-use intensity, and landscapes prioritized by the Wildfire Crisis Mitigation plan are on average, more departed than non-priority landscapes. Conclusions This proposed method captures facets of fire regime departures that metrics based on measures of central tendency cannot. These new metrics can aid the evaluation and targeting of treatments to restore historical fire regimes and manage the resilience of fire-prone landscapes.

Background Atherosclerotic cardiovascular disease (ASCVD) is a leading cause of morbidity and mortality. Semaglutide 2.4 mg (Wegovy) has demonstrated improved outcomes in patients with overweight or obesity (ov/ob) and ASCVD, but its impact on medical costs and healthcare resource utilization (HCRU) remains unknown. Aims To compare all-cause medical costs and HCRU among patients with ov/ob and ASCVD treated with semaglutide 2.4 mg versus semaglutide-untreated controls. Materials and Methods This observational cohort study utilized Komodo’s Healthcare Map and included patients with ov/ob and ≥1 diagnosis of ASCVD during the baseline period with ≥12 months of insurance coverage before and after the index date. Patients in the semaglutide 2.4 mg cohort initiated treatment after 4 June 2021 and stayed adherent. Semaglutide-untreated controls were randomly selected and 1:4 propensity score matched based on baseline demographics, clinical characteristics, medical costs, and HCRU. Medical costs and HCRU were compared using generalized linear models. Results 770 semaglutide 2.4 mg-treated patients and 3,080 controls were included. In the year following treatment initiation, semaglutide 2.4 mg was associated with 22% lower mean medical costs versus controls (−$4,639 per patient per year [PPPY]; cost ratio = 0.78, 95% confidence interval [CI] 0.67, 0.89). This difference is mainly due to lower inpatient costs with semaglutide 2.4 mg, which were 65% lower than controls (−$3,593; cost ratio = 0.35 [95% CI 0.21, 0.49]), along with a 48% lower inpatient visit rate (0.08 vs. 0.15; rate ratio = 0.52 [95% CI 0.34, 0.70]). Limitations Limitations inherent to retrospective claims analyses apply to this study. Conclusions This real-world analysis shows significantly lower annual medical costs and HCRU with semaglutide 2.4 mg versus no semaglutide 2.4 mg treatment in patients with ov/ob and ASCVD. Improving outcomes with semaglutide 2.4 mg combined with lower costs and HCRU may help slow the growing burden of ASCVD in this population.

I read the articles about physician associates (PAs) with great sadness.PAs are being sold to us as the answer to the ever-growing pressure of workload and demands that GPs are facing, and also as a substitute for the drop in numbers entering general practice.Even extremely well-trained and highly experienced nurse practitioners are stressed and find themselves taking on too many responsibilities.However, when they are faced with tricky or difficult decisions they naturally refer this back to the GP and the responsibility once again falls back to the GP.I feel that PAs will be an added confusion for patients who want to see fully-qualified doctors who take the responsibility for their care.Even now quite a few patients think that our nurse practitioner is a female doctor.The introduction of physician associates is short sighted and simply a gap-filler: in the long run we need to focus on more trained GPs instead.

In the field of photocatalysis the batch-nature of the typical benchmarking experiment makes it very laborious to obtain good kinetic data as a function of parameters such as illumination wavelength, irradiance, catalyst temperature, reactant composition, etc. Microreactors with on-line mass spectrometry, on the other hand, allow fast and automated acquisition of quantitative kinetic data. [1,2] As an example, we show how microreactor experiments on water splitting using Pt- or Rh-loaded GaN:ZnO photocatalysts quickly rank different catalysts according to their activity for gas-phase water splitting - but also how the activity scales with relative humidity and the crucial role of CrOx "capping" of the Pt- or Rh-co catalyst in order to prevent the loss of H2/O2 product via backward reaction on the precious metal. [3,4] The data suggests that protons transfer via the catalyst surface between the oxygen-evolving sites and the hydrogen evolving co-catalyst sites. Recently, the microreactor experimental platform is being developed to support in-situ UV-VIS-IR spectroscopy [5] and even the introduction of liquid aqueous electrolyte and electrodes - all while retaining high sensitivity time resolved mass spectrometric product detection. [6] [1] Vesborg et al. Chemical Engineering Journal, 160, p. 738-741 (2010) [2] Vesborg et al. J. Phys. Chem. C, 114, p. 11162-11168 (2010) [3] Dionigi et al. Energy & Env. Sci., 4, p. 2937-2942 (2011) [4] Dionigi et al. J. Catal., 292, p. 26-31 (2012) [5] Dionigi et al. Rev. Sci. Instr., 84, p. 103910 (2013) [6] Bøndergaard et al. "Fast and sensitive method for detecting volatile species in liquids", submitted

Tianeptine is an antidepressant affecting the glutamatergic system. In spite of its proven clinical efficacy, molecular effects of tianeptine are not entirely clear. Tianeptine modulates cytokine expression in the CNS and protects the hippocampus from chronic stress effects. HIV infection is associated with inflammation and neuronal loss, causing HIV-associated dementia (HAD). The human immunodeficiency virus type-1 glycoprotein gp120 has been proposed as a likely aetiological agent of HAD. In this study, we determined whether tianeptine protects astroglial cells from the neurodegenerative effects of gp120. Human astroglial cells were treated with gp120 and tianeptine, and viability and apoptosis was monitored by TUNEL, annexin V, and activated caspase-3 staining and flow cytometry. Protein levels of glutamine synthase (GS), inducible and constitutive nitric oxide synthases (iNOS, cNOS) and nuclear factor κB (NF-κB) pathway were determined by Western blot analysis. The respective activities were assessed indirectly by measuring glutamine and nitrite concentrations or by luciferase reporter assays. Tianeptine showed an anti-apoptotic effect and prevented caspase-3 activation by gp120. The mechanism of tianeptine's action involved GS and cNOS stabilization and iNOS suppression. Moreover, tianeptine increased IκB-α levels in the absence of gp120 and blocked its degradation in response to gp120. This correlated with the suppression of basal and gp120-induced NF-κB transcriptional activity. Tianeptine clearly exerts neuroprotective effects in vitro by suppressing the molecular pro-inflammatory effects of gp120. Studies in animal models should be performed to evaluate the potential of tianeptine as a treatment for HAD.