112 research outputs found
Reno-protective effect of Roflumilast against kidney injury induced by ischemia/reperfusion in rats: Evidence from biochemical and histological investigations
No full textOxidative stress, inflammation, and apoptosis are major contributors to renal ischemia/reperfusion (I/R) injury. This study aimed to investigate the effects of pretreatment with the PDE4 inhibitor roflumilast (Rof) on renal I/R and its underlying mechanisms. Sprague-Dawley rats were subjected to 30 minutes of unilateral renal ischemia followed by 45 minutes of reperfusion. Rof (1.5 and 3 mg/kg) was administered for seven days prior to I/R induction. The findings showed that Rof significantly and dose-dependently attenuated kidney damage by reducing blood urea nitrogen and creatinine levels. Rof also exhibited antioxidant and anti-inflammatory effects, as evidenced by improved glutathione and malondialdehyde levels and decreased proinflammatory cytokines (IL-6 and TNF-α). Furthermore, Rof prevented the downregulation of HO-1 and Nrf2 expression. These results suggest that Rof therapy could protect the kidneys from I/R-induced injury through its antioxidant and anti-inflammatory properties, providing a potential therapeutic approach for the management of renal I/R damage
Identification, Development and Achievement Analysis of Talented and Gifted Children in West Germany
No full text
L-carnitine alleviated acute lung injuries induced by potassium dichromate in rats: involvement of Nrf2/HO-1 signaling pathway
No full textThe activation of the Nrf2/HO-1 signaling pathway regulates cellular antioxidant stress and exerts anti-inflammatory and cytoprotective effects against acute lung injury (ALI). The present study aimed to evaluate the therapeutic role of L-carnitine (LC) against potassium dichromate (PD) - induced acute lung injury in adult male albino rats via modulation of Nrf2/HO-1 signaling pathway. For this purpose, forty rats were randomly allocated into 5 groups (8 rats each). The normal group received intranasal (i.n.) saline, while the ALI group received intranasal instillation of PD as a single dose of 2 mg/kg. The 3d – 5th groups received PD then after 24 h administered L-carnitine (25, 50 and 100 mg/kg; orally) for 3 consecutive days. The therapeutic effect of L-carnitine was evaluated by assessment of serum levels of glutathione (GSH) and malondialdehyde (MDA) along with measurement of lung contents of transforming growth factor β1 (TGFβ1), protein kinase B (AKT), Nuclear factor erythroid-2 related factor 2 (Nrf2), Kelch-like ECH-associated protein 1 (Keap1), heme oxygenase-1 (HO-1), NAD(P)H quinone oxidoreductase 1 enzyme (NQO1) and glutathione cysteine ligase modifier subunit (GCLM) expression. Post-treatment with L-carnitine effectively increased the levels of GSH and AKT, elevated Nrf2 and its target genes and decreased the levels of MDA and TGFβ1 in comparison with PD control rats. Additionally, L-carnitine effectively reduced the number of goblet cell, inhibited the mucus formation in bronchioles and interstitial inflammatory infiltrate as well as alleviated the destruction of alveolar walls, and the congestion of blood vessels in lung tissue induced by PD. Our findings showed that L-carnitine may be a promising therapeutic agent against PD-induced acute lung injury
Photomicrographs of caspase-3 and NFκB p65 immune-stained sections of frontal cortex and hippocampus.
No full text(a-d) Sham-operated group showing negative expression of caspase-3 and NFκB p65. (e-h) OVC/D-gal group showing intense expression of caspase-3 and NFκB p65 among the neuronal cells. AD-model rats’ which treated with AM1241, (i-l) 3mg/kg and (m-p) 6mg/kg showing marked decreased expression of caspase-3 and NFκB p65 in a dose related response. (q and r) image analysis software for quantification of the positive expression of both caspase-3 and NFκB p65 (data were analyzed by using one way ANOVA followed by Tukey’s post hoc test. Values expressed as mean ± SE (n = 5 rats/group). *, #, and ± statistically significant different at P ± statistically significant different comparing with AM1241 (3mg/Kg).</p
Photomicrographs of CD68 and GFAP immune-stained sections of frontal cortex and hippocampus.
No full text(a-d) Sham-operated group showing normal few scattered CD68 positive microglia cells and few scattered small sized GFAP positive astrocytes. (e-h) OVC/D-gal group showing intense expression of both markers denoting hyper-activation of microglia and astrocyte cells. OVC/D-gal rats’ which treated with AM1241, (i-l) 3mg/kg and (m-p) 6mg/kg showing a dose related decreased the immuno-reactivity of CD68 and GFAP. (q and r) image analysis software for quantification of the positive expression of both CD68 and GFAP (data were analyzed by using one way ANOVA followed by Tukey’s post hoc test. Values expressed as mean ± SE (n = 5 rats/group). *, #, and ± statistically significant different at P ± statistically significant different comparing with AM1241 (3mg/Kg).</p
Criminally Incompetent Academic Misinterpretation of Criminal Data-and how the Media Pushed the Fake News
No full textOn 17 Jan 2018 multiple news sources (e.g. see here, here, and here) ran a story about a new research paper that claims to expose both the inaccuracies and racial bias in one of the most common algorithms used by parole boards to predict recidivism (i.e. whether or not a defendant will re-offend). The research paper was written by the world famous computer scientist Hany Farid (along with a student Julia Dressel). But the real story here is that the paper’s accusation of racial bias (specifically that the algorithm is biased against black people) is based on a fundamental misunderstanding of causation and statistics. The algorithm is no more ‘biased’ against black people than it is biased against white single parents, old people, people living in Beattyville Kentucky, or women called ‘Amber’. In fact, as we show in this brief article, if you choose any factor that correlates with poverty you will inevitably replicate the statistical ‘bias’ claimed in the paper. And if you accept the validity of the claims in the paper then you must also accept, for example, that a charity which uses poverty as a factor to identify and help homeless people is being racist because it is biased against white people (and also, interestingly, Indian Americans). The fact that the article was published and that none of the media running the story realise that they are pushing fake news is what is most important here. Depressingly, many similar research studies involving the same kind of misinterpretation of statistics result in popular media articles that push a false narrative of one kind or another
Fig 4 -
No full textH&E stained photomicrographs of frontal cortex and hippocampus, (a-c) Sham-operated group, showing normal histological structure. (d-l) OVC/D-gal group, showing; (d) neuronal cells degenerative changes as shrunken neurons with accentuated dusky cytoplasm, vacuolar degeneration (e) marked neuronophagia (upper corner) with scattered apoptosis, (f) corkscrew appearance of the neuronal apical dendrites (g) variable sizes amyloid plaques (dotted-arrow) which (h) stained positively with Congo red stain, (i) glial nodules with satellatosis around degenerated neuron. (j-l) dorsal hippocampus showing vacuolation and loss of the small pyramidal cells of the dentate gyrus (DG) with degenerated cells in the granular layer as well as in Cornu Ammonis (CA) 1 and 3 subdivisions with (k) different sizes amyloid plaques (dotted-arrow) which (l) stained positively with Congo red stain.</p
Photomicrographs of CREB immune-stained sections of frontal cortex and hippocampus.
No full text(a-b) Sham-operated group showing marked expression of CREB. (c-d) OVC/D-gal group showing diminished CREB expression among the neuronal cells. AD-model rats’ which treated with AM1241, (e-f) 3mg/kg and (g-h) 6mg/kg showing restored boosted expression of CREB. (i) Image analysis software for quantification of the positive expression of CREB (data were analyzed by using one way ANOVA followed by Tukey’s post hoc test. Values expressed as mean ± SE (n = 5 rats/group). *, #, and ± statistically significant different at P ± statistically significant different comparing with AM1241 (3mg/Kg).</p
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