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  1. Blaizot A, Veettil SK, Saidoung P, Moreno-Garcia CF, Wiratunga N, Aceves-Martins M, et al.
    Res Synth Methods, 2022 May;13(3):353-362.
    PMID: 35174972 DOI: 10.1002/jrsm.1553
    The exponential increase in published articles makes a thorough and expedient review of literature increasingly challenging. This review delineated automated tools and platforms that employ artificial intelligence (AI) approaches and evaluated the reported benefits and challenges in using such methods. A search was conducted in 4 databases (Medline, Embase, CDSR, and Epistemonikos) up to April 2021 for systematic reviews and other related reviews implementing AI methods. To be included, the review must use any form of AI method, including machine learning, deep learning, neural network, or any other applications used to enable the full or semi-autonomous performance of one or more stages in the development of evidence synthesis. Twelve reviews were included, using nine different tools to implement 15 different AI methods. Eleven methods were used in the screening stages of the review (73%). The rest were divided: two in data extraction (13%) and two in risk of bias assessment (13%). The ambiguous benefits of the data extractions, combined with the reported advantages from 10 reviews, indicating that AI platforms have taken hold with varying success in evidence synthesis. However, the results are qualified by the reliance on the self-reporting of the review authors. Extensive human validation still appears required at this stage in implementing AI methods, though further evaluation is required to define the overall contribution of such platforms in enhancing efficiency and quality in evidence synthesis.
  2. Roll U, Feldman A, Novosolov M, Allison A, Bauer AM, Bernard R, et al.
    Nat Ecol Evol, 2017 11;1(11):1785.
    PMID: 29046563 DOI: 10.1038/s41559-017-0380-7
    In this Article originally published, owing to a technical error, the author 'Laurent Chirio' was mistakenly designated as a corresponding author in the HTML version, the PDF was correct. This error has now been corrected in the HTML version. Further, in Supplementary Table 3, the authors misspelt the surname of 'Danny Meirte'; this file has now been replaced.
  3. Roll U, Feldman A, Novosolov M, Allison A, Bauer AM, Bernard R, et al.
    Nat Ecol Evol, 2017 Nov;1(11):1677-1682.
    PMID: 28993667 DOI: 10.1038/s41559-017-0332-2
    The distributions of amphibians, birds and mammals have underpinned global and local conservation priorities, and have been fundamental to our understanding of the determinants of global biodiversity. In contrast, the global distributions of reptiles, representing a third of terrestrial vertebrate diversity, have been unavailable. This prevented the incorporation of reptiles into conservation planning and biased our understanding of the underlying processes governing global vertebrate biodiversity. Here, we present and analyse the global distribution of 10,064 reptile species (99% of extant terrestrial species). We show that richness patterns of the other three tetrapod classes are good spatial surrogates for species richness of all reptiles combined and of snakes, but characterize diversity patterns of lizards and turtles poorly. Hotspots of total and endemic lizard richness overlap very little with those of other taxa. Moreover, existing protected areas, sites of biodiversity significance and global conservation schemes represent birds and mammals better than reptiles. We show that additional conservation actions are needed to effectively protect reptiles, particularly lizards and turtles. Adding reptile knowledge to a global complementarity conservation priority scheme identifies many locations that consequently become important. Notably, investing resources in some of the world's arid, grassland and savannah habitats might be necessary to represent all terrestrial vertebrates efficiently.
  4. Hudson J, Cruickshank M, Quinton R, Aucott L, Aceves-Martins M, Gillies K, et al.
    Lancet Healthy Longev, 2022 Jun;3(6):e381-e393.
    PMID: 35711614 DOI: 10.1016/S2666-7568(22)00096-4
    BACKGROUND: Testosterone is the standard treatment for male hypogonadism, but there is uncertainty about its cardiovascular safety due to inconsistent findings. We aimed to provide the most extensive individual participant dataset (IPD) of testosterone trials available, to analyse subtypes of all cardiovascular events observed during treatment, and to investigate the effect of incorporating data from trials that did not provide IPD.

    METHODS: We did a systematic review and meta-analysis of randomised controlled trials including IPD. We searched MEDLINE, MEDLINE In-Process & Other Non-Indexed Citations, MEDLINE Epub Ahead of Print, Embase, Science Citation Index, the Cochrane Controlled Trials Register, Cochrane Database of Systematic Reviews, and Database of Abstracts of Review of Effects for literature from 1992 onwards (date of search, Aug 27, 2018). The following inclusion criteria were applied: (1) men aged 18 years and older with a screening testosterone concentration of 12 nmol/L (350 ng/dL) or less; (2) the intervention of interest was treatment with any testosterone formulation, dose frequency, and route of administration, for a minimum duration of 3 months; (3) a comparator of placebo treatment; and (4) studies assessing the pre-specified primary or secondary outcomes of interest. Details of study design, interventions, participants, and outcome measures were extracted from published articles and anonymised IPD was requested from investigators of all identified trials. Primary outcomes were mortality, cardiovascular, and cerebrovascular events at any time during follow-up. The risk of bias was assessed using the Cochrane Risk of Bias tool. We did a one-stage meta-analysis using IPD, and a two-stage meta-analysis integrating IPD with data from studies not providing IPD. The study is registered with PROSPERO, CRD42018111005.

    FINDINGS: 9871 citations were identified through database searches and after exclusion of duplicates and of irrelevant citations, 225 study reports were retrieved for full-text screening. 116 studies were subsequently excluded for not meeting the inclusion criteria in terms of study design and characteristics of intervention, and 35 primary studies (5601 participants, mean age 65 years, [SD 11]) reported in 109 peer-reviewed publications were deemed suitable for inclusion. Of these, 17 studies (49%) provided IPD (3431 participants, mean duration 9·5 months) from nine different countries while 18 did not provide IPD data. Risk of bias was judged to be low in most IPD studies (71%). Fewer deaths occurred with testosterone treatment (six [0·4%] of 1621) than placebo (12 [0·8%] of 1537) without significant differences between groups (odds ratio [OR] 0·46 [95% CI 0·17-1·24]; p=0·13). Cardiovascular risk was similar during testosterone treatment (120 [7·5%] of 1601 events) and placebo treatment (110 [7·2%] of 1519 events; OR 1·07 [95% CI 0·81-1·42]; p=0·62). Frequently occurring cardiovascular events included arrhythmia (52 of 166 vs 47 of 176), coronary heart disease (33 of 166 vs 33 of 176), heart failure (22 of 166 vs 28 of 176), and myocardial infarction (10 of 166 vs 16 of 176). Overall, patient age (interaction 0·97 [99% CI 0·92-1·03]; p=0·17), baseline testosterone (interaction 0·97 [0·82-1·15]; p=0·69), smoking status (interaction 1·68 [0·41-6·88]; p=0.35), or diabetes status (interaction 2·08 [0·89-4·82; p=0·025) were not associated with cardiovascular risk.

    INTERPRETATION: We found no evidence that testosterone increased short-term to medium-term cardiovascular risks in men with hypogonadism, but there is a paucity of data evaluating its long-term safety. Long-term data are needed to fully evaluate the safety of testosterone.

    FUNDING: National Institute for Health Research Health Technology Assessment Programme.

  5. Hudson J, Cruickshank M, Quinton R, Aucott L, Wu F, Grossmann M, et al.
    Lancet Healthy Longev, 2023 Oct;4(10):e561-e572.
    PMID: 37804846 DOI: 10.1016/S2666-7568(23)00169-1
    BACKGROUND: Testosterone replacement therapy is known to improve sexual function in men younger than 40 years with pathological hypogonadism. However, the extent to which testosterone alleviates sexual dysfunction in older men and men with obesity is unclear, despite the fact that testosterone is being increasingly prescribed to these patient populations. We aimed to evaluate whether subgroups of men with low testosterone derive any symptomatic benefit from testosterone treatment.

    METHODS: We did a systematic review and meta-analysis to evaluate characteristics associated with symptomatic benefit of testosterone treatment versus placebo in men aged 18 years and older with a baseline serum total testosterone concentration of less than 12 nmol/L. We searched major electronic databases (MEDLINE, Embase, Science Citation Index, and the Cochrane Central Register of Controlled Trials) and clinical trial registries for reports published in English between Jan 1, 1992, and Aug 27, 2018. Anonymised individual participant data were requested from the investigators of all identified trials. Primary (cardiovascular) outcomes from this analysis have been published previously. In this report, we present the secondary outcomes of sexual function, quality of life, and psychological outcomes at 12 months. We did a one-stage individual participant data meta-analysis with a random-effects linear regression model, and a two-stage meta-analysis integrating individual participant data with aggregated data from studies that did not provide individual participant data. This study is registered with PROSPERO, CRD42018111005.

    FINDINGS: 9871 citations were identified through database searches. After exclusion of duplicates and publications not meeting inclusion criteria, 225 full texts were assessed for inclusion, of which 109 publications reporting 35 primary studies (with a total 5601 participants) were included. Of these, 17 trials provided individual participant data (3431 participants; median age 67 years [IQR 60-72]; 3281 [97%] of 3380 aged ≥40 years) Compared with placebo, testosterone treatment increased 15-item International Index of Erectile Function (IIEF-15) total score (mean difference 5·52 [95% CI 3·95-7·10]; τ2=1·17; n=1412) and IIEF-15 erectile function subscore (2·14 [1·40-2·89]; τ2=0·64; n=1436), reaching the minimal clinically important difference for mild erectile dysfunction. These effects were not found to be dependent on participant age, obesity, presence of diabetes, or baseline serum total testosterone. However, absolute IIEF-15 scores reached during testosterone treatment were subject to thresholds in patient age and baseline serum total testosterone. Testosterone significantly improved Aging Males' Symptoms score, and some 12-item or 36-item Short Form Survey quality of life subscores compared with placebo, but it did not significantly improve psychological symptoms (measured by Beck Depression Inventory).

    INTERPRETATION: In men aged 40 years or older with baseline serum testosterone of less than 12 nmol/L, short-to-medium-term testosterone treatment could provide clinically meaningful treatment for mild erectile dysfunction, irrespective of patient age, obesity, or degree of low testosterone. However, due to more severe baseline symptoms, the absolute level of sexual function reached during testosterone treatment might be lower in older men and men with obesity.

    FUNDING: National Institute for Health and Care Research Health Technology Assessment Programme.

  6. Sirunyan AM, Tumasyan A, Adam W, Ambrogi F, Asilar E, Bergauer T, et al.
    Eur Phys J C Part Fields, 2018;78(6):457.
    PMID: 30956548 DOI: 10.1140/epjc/s10052-018-5929-3
    Measurements are presented of the lifetimes of the B 0 , B s 0 , Λ b 0 , and B c + hadrons using the decay channels B 0 → J / ψ K ∗ ( 892 ) 0 , B 0 → J / ψ K S 0 , B s 0 → J / ψ π + π - , B s 0 → J / ψ ϕ ( 1020 ) , Λ b 0 → J / ψ Λ 0 , and B c + → J / ψ π + . The data sample, corresponding to an integrated luminosity of 19.7 fb -1 , was collected by the CMS detector at the LHC in proton-proton collisions at s = 8 TeV . The B 0 lifetime is measured to be 453.0 ± 1.6 (stat) ± 1.8 (syst) μ m in J / ψ K ∗ ( 892 ) 0 and 457.8 ± 2.7 (stat) ± 2.8 (syst) μ m in J / ψ K S 0 , which results in a combined measurement of c τ B 0 = 454.1 ± 1.4 (stat) ± 1.7 (syst) μ m . The effective lifetime of the B s 0 meson is measured in two decay modes, with contributions from different amounts of the heavy and light eigenstates. This results in two different measured lifetimes: c τ B s 0 → J / ψ π + π - = 502.7 ± 10.2 (stat) ± 3.4 (syst) μ m and c τ B s 0 → J / ψ ϕ ( 1020 ) = 443.9 ± 2.0 (stat) ± 1.5 (syst) μ m . The Λ b 0 lifetime is found to be 442.9 ± 8.2 (stat) ± 2.8 (syst) μ m . The precision from each of these channels is as good as or better than previous measurements. The B c + lifetime, measured with respect to the B + to reduce the systematic uncertainty, is 162.3 ± 7.8 (stat) ± 4.2 (syst) ± 0.1 ( τ B + ) μ m . All results are in agreement with current world-average values.
  7. Sirunyan AM, Tumasyan A, Adam W, Ambrogi F, Asilar E, Bergauer T, et al.
    Eur Phys J C Part Fields, 2019;79(2):94.
    PMID: 30872972 DOI: 10.1140/epjc/s10052-019-6562-5
    A search is presented for decays of Z and Higgs bosons to a J / ψ meson and a photon, with the subsequent decay of the J / ψ to μ + μ - . The analysis uses data from proton-proton collisions with an integrated luminosity of 35.9 fb - 1 at s = 13 TeV collected with the CMS detector at the LHC. The observed limit on the Z → J / ψ γ decay branching fraction, assuming that the J / ψ meson is produced unpolarized, is 1.4 × 10 - 6 at 95% confidence level, which corresponds to a rate higher than expected in the standard model by a factor of 15. For extreme-polarization scenarios, the observed limit changes from - 13.6 to + 8.6 % with respect to the unpolarized scenario. The observed upper limit on the branching fraction for H → J / ψ γ where the J / ψ meson is assumed to be transversely polarized is 7.6 × 10 - 4 , a factor of 260 larger than the standard model prediction. The results for the Higgs boson are combined with previous data from proton-proton collisions at s = 8 TeV to produce an observed upper limit on the branching fraction for H → J / ψ γ that is a factor of 220 larger than the standard model value.
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