It was previously confirmed that the apoptotic and necrotic neurons are found during the acute post-traumatic period, suggesting the induction of apoptosis after traumatic brain injury (TBI). To further explore the involvement of apoptotic factors in TBI, an apoptosis antibody array was conducted to measure the alterations of apoptotic factors in rat brain cortex after TBI. As a result, the Neurological Severity Scale (NSS) scores after TBI were increased, and the cell morphology of the brain cortex was destructed with increased neuronal apoptosis. Furthermore, the caspase-3 activity was increased, and the apoptotic-related factors TNF-α and p53 were up-regulated in the brain cortex. More importantly, in vitro experiments demonstrated that down-regulation of TNF-α in oxygen-glucose deprivation/reoxygenation (OGD/R) cells increased cell viability and decreased apoptosis and the p53 expression. These results suggested the involvement of TNF-α-induced apoptotic signalling pathway by activating p53 in the molecular mechanism of neurological injury. © 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.The ongoing COVID-19 pandemic is an exceptional challenge for the health systems throughout the world. So far, no causative therapy nor protective vaccines are available. In several countries, the capacities for intensive care and for support in case of acute respiratory distress syndrome (ARDS) are overstretched, and the mortality is considerable. In this situation, useful prognostic parameters and targeted supportive treatment are urgently needed. This article is protected by copyright. All rights reserved.BACKGROUND/AIM It is crucial to store an avulsed tooth appropriately to preserve the viability of the periodontal ligament cells prior to replantation. The aim of this systematic review was to identify the best available evidence for the effectiveness of any technique available to laypeople for storing an avulsed tooth compared with storage in milk or saliva. METHODS The following databases were searched (September 2019) Cochrane Library, MEDLINE and Embase. Two reviewers independently considered trial eligibility, then extracted and analyzed data and assessed the risk of bias. The certainty of the body of evidence was appraised according to the GRADE methodology. RESULTS Out of 4118 references, 33 studies were included and reported on 23 comparisons of which 10 were synthesized in a meta-analysis. The limited evidence available favors storing an avulsed tooth in Hank's Balanced Salt Solution (pooled SMD 2.47, 95%CI [1.59;3.34], p less then 0.00001), propolis solution (pooled SMD 1.73, 95%CI [1.12;2.33], p leis protected by copyright. All rights reserved.We read and studied with great anticipation the article by Gojkovic et al. (1) and the accompanying editorial by Nikinmaa (2) in the present issue reporting on a new mouse model of high altitude pulmonary edema (HAPE). For investigators in the field, particularly those of us researching and treating HAPE in humans, an animal model for HAPE has been a quest for the holy grail for 60 years (3). A good small animal model would permit more extensive and high throughput experiments to better understand the pathophysiology and screen for preventative and therapeutic medications or non-pharmacologic strategies. For an animal model to serve in this role, however, it must closely reproduce the human pathophysiology. HAPE in humans only develops with the hypoxia of high altitude exposure. In most individuals, the rise in pulmonary artery pressure from hypoxic pulmonary vasoconstriction (HPV) is exaggerated and leads to high enough pressures in the microvasculature to cause pulmonary edema. This article is protected by copyright. All rights reserved.CRISPR/Cas9 (clustered regularly interspaced short palindromic repeats/CRISPR-associated protein9) may be viewed as an adaptive bacterial immune system. When a virus infects a bacterium, a fragment of the virus genome is inserted into the CRISPR sequence of the bacterial genome as a memory. When the bacterium becomes infected again with the same virus, an RNA molecule that is a transcript of the memory sequence, directs Cas9, an endonuclease, to the complementary region of the virus genome, and Cas9 disables the virus by a double-strand break. In recent years, studies have shown that by designing synthetic RNA molecules and delivering them along with Cas9 into eukaryotic cells, different regions of the cell's genome can be targeted and manipulated. These findings have drawn much attention to this new technology and it has been shown that CRISPR/Cas9 gene editing can be used to treat some human diseases. These include infectious diseases and autoimmune diseases. In this review article, in addition to a brief overview of the biology of the CRISPR/Cas9 system, we collected the most recent findings on the applications of CRISPR/Cas9 technology for better investigation of the pathogenesis and treatment of viral infections (human immunodeficiency virus infection, hepatitis virus infections, and onco-virus infections), non-viral infections (parasitic, fungal, and bacterial infections), and autoimmune diseases.  https://www.selleckchem.com/products/rg-7112.html  © 2020 International Union of Biochemistry and Molecular Biology.Inhibition of nodule development is one of the main adverse effects of phosphate (Pi) deficiency in legumes. Despite all the efforts made over the last decades to understand how root nodules cope with Pi deficiency, the molecular mechanisms leading to the reduction in nodule number under Pi deficiency remain elusive. In this study, we provide experimental evidence that Pi deficiency activates the Autoregulation of Nodulation (AON) pathway, leading to a reduction in nodule numbers in both common bean and soybean. A transcriptional profile analysis revealed that the expression of the AON-related genes PvNIN, PvRIC1, PvRIC2, and PvTML is upregulated under Pi deficiency conditions. The downregulation of the MYB transcription factor PvPHR1 in common bean roots significantly reduced the expression of these four AON-related genes. Physiological analyses indicated that Pi deficiency does not affect the establishment of the root nodule symbiosis in the supernodulation mutant lines Pvnark and Gmnark. Reciprocal grafting and split-roots analyses determined that the activation of the AON pathway was required for the inhibitory effect of Pi deficiency.