Do Citations and Impact Factors Relate to the Real Numbers in Publications? a Case Study of Citation Rates, Impact, and Effect Sizes in Ecology and Evolutionary Biology.

Do citations and impact factors relate to the real numbers in publications? A case study of citation rates, impact, and effect sizes in ecology and evolutionary biology.

Filed under: Drug and Alcohol Rehabilitation

Scientometrics. 2013 Feb; 94(2): 675-682
Lortie CJ, Aarssen LW, Budden AE, Leimu R

Metrics of success or impact in academia may do more harm than good. To explore the value of citations, the reported efficacy of treatments in ecology and evolution from close to 1,500 publications was examined. If citation behavior is rationale, i.e. studies that successfully applied a treatment and detected greater biological effects are cited more frequently, then we predict that larger effect sizes increases study relative citation rates. This prediction was not supported. Citations are likely thus a poor proxy for the quantitative merit of a given treatment in ecology and evolutionary biology-unlike evidence-based medicine wherein the success of a drug or treatment on human health is one of the critical attributes. Impact factor of the journal is a broader metric, as one would expect, but it also unrelated to the mean effect sizes for the respective populations of publications. The interpretation by the authors of the treatment effects within each study differed depending on whether the hypothesis was supported or rejected. Significantly larger effect sizes were associated with rejection of a hypothesis. This suggests that only the most rigorous studies reporting negative results are published or that authors set a higher burden of proof in rejecting a hypothesis. The former is likely true to a major extent since only 29 % of the studies rejected the hypotheses tested. These findings indicate that the use of citations to identify important papers in this specific discipline-at least in terms of designing a new experiment or contrasting treatments-is of limited value.
HubMed – drug

 

Targets of Vascular Protection in Acute Ischemic Stroke Differ in Type 2 Diabetes.

Filed under: Drug and Alcohol Rehabilitation

Am J Physiol Heart Circ Physiol. 2013 Jan 18;
Kelly-Cobbs AI, Prakash R, Li W, Pillai B, Hafez S, Coucha M, Johnson MH, Ogbi SN, Fagan SC, Ergul A

Hemorrhagic transformation (HT) is an important complication of acute ischemic stroke particularly in diabetic patients receiving thrombolytic treatment with tissue plasminogen activator (tPA), the only approved drug for the treatment of acute ischemic stroke (AIS). The objective of the current study was to determine the effects of acute manipulation of potential targets for vascular protection (i.e., NFkB, peroxynitrite, and matrix metalloproteinases) on vascular injury and functional outcome in a diabetic model of cerebral ischemia. Ischemia was induced by middle cerebral artery occlusion in control and type 2 diabetic Goto-Kakizaki rats. Treatment groups received a single dose of peroxynitrite decomposition catalyst FeTPPs,a non-specific NFkB inhibitor curcumin, or a broad-spectrum matrix metalloproteinase (MMP) inhibitor minocycline at reperfusion. Post-stroke infarct volume, edema, hemorrhage, neurological deficits, and MMP-9 activity were evaluated. All acute treatments reduced MMP-9 and HT in diabetic groups. In addition, acute curcumin and minocycline therapy reduced edema in these animals. Improved neurological function was observed in varying degrees with treatment as indicated by beam-walk performance, modified Bederson scores and grip strength; however, infarct size was similar to untreated diabetic animals. In control animals, all treatments reduced MMP-9 activity yet bleeding was not improved. Neuroprotection was only conferred by curcumin and minocycline. Uncovering underlying mechanisms contributing to the success of acute therapy in diabetes will advance tailored stroke therapies.
HubMed – drug

 

Evaluating 5-nitrofurans as trypanocidal agents.

Filed under: Drug and Alcohol Rehabilitation

Antimicrob Agents Chemother. 2013 Jan 18;
Bot C, Hall BS, Alvarez G, Di Maio R, González M, Cerecetto H, Wilkinson SR

The nitroheterocycle nifurtimox, as part of a nifurtimox-eflornithine combination therapy, represents one of a limited number of treatments targeting Trypanosoma brucei, the causative agent of human African trypanosomiasis. The mode of action of this prodrug involves an initial activation reaction catalysed by a type I nitroreductase (NTR), an enzyme found predominantly in prokaryotes, leading to the formation of a cytotoxic unsaturated open chain nitrile metabolite. Here, we evaluate the trypanocidal activity of a library of other 5-nitrofurans against bloodstream form T. brucei as a preliminary step in the identification of additional nitroaromatic compounds that could potentially partner eflornithine. Biochemical screening against purified enzyme revealed that all 5-nitrofurans were effective substrates for TbNTR with the preferred compounds having apparent k(cat)/K(M) values approximately 50-fold greater than nifurtimox. For several compounds, in vitro reduction by this nitroreductase yielded products characterized by mass spectroscopy as either unsaturated or saturated open chain nitriles. When tested against bloodstream form T. brucei, many of the derivatives displayed significant growth inhibitory properties with the most potent compounds generating IC(50) values around 200 nM. The anti-parasitic activity of the most potent agents was demonstrated to be NTR dependent as parasites having reduced levels of the enzyme displayed resistance to the compounds while parasites over expressing TbNTR showed hypersensitivity. We conclude that other members of the 5-nitrofurans class of nitroheterocycles have potential to treat human African trypanosomiasis perhaps as an alternative partner prodrug to nifurtimox in the next generation of eflornithine-based combinational therapies.
HubMed – drug

 

Reduced drug uptake in phenotypically resistant nutrient-starved non-replicating Mycobacterium tuberculosis.

Filed under: Drug and Alcohol Rehabilitation

Antimicrob Agents Chemother. 2013 Jan 18;
Sarathy J, Dartois V, Dick T, Gengenbacher M

During active tuberculosis a spectrum of physiologically different M. tuberculosis bacilli reside in human tissues. Subpopulations of the pathogen survive antibiotic treatment for prolonged time in a dormant state of phenotypic drug resistance, a phenomenon independent from genetic mutations. Here we used an established culture model of nutrient deprivation to shift down M. tuberculosis from growth to non-replicating survival, which is characterized by a drastic loss in drug susceptibility. Liquid chromatography coupled to mass spectrometry techniques were employed to quantify drug penetration in replicating and nutrient-starved non-replicating bacilli. We found that intracellular concentrations of fluoroquinolones, rifamycins, linezolid were lower in non-replicating M. tuberculosis. Studies with pump inhibitors suggest that observed differences were independent from efflux processes. We conclude that decreased drug permeability contributes to phenotypic drug resistance of dormant M. tuberculosis.
HubMed – drug

 

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