View source for Genome editing inside Ustilago maydis with all the CRISPRCas system

OVID-19.A connection between gut microbiota and Parkinson's disease (PD) indicates that dysbiosis of the gut microbiota might represent a risk factor for PD. Microbiota-targeted interventions, including probiotic Clostridium butyricum (Cb), have been recently shown to have favorable effects in PD by regulating microbiota-gut-brain axis. However, the potential beneficial roles and its mechanisms of Cb on PD were still unknown. Male C57BL/6 mice were subjected to a PD model-induced by 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) and were treated intragastrically with Cb for 4 weeks. The motor functions were assessed by a series of behavioral tests including pole test, beam walking teat, forced swimming test and open field test. The dopaminergic neuron loss, synaptic plasticity and microglia activation, as well as the levels of colonic glucagon-like peptide-1 (GLP-1), colonic G protein-coupled receptors GPR41/43 and cerebral GLP-1 receptors were assessed. Gut microbial composition was assessed by 16S rRNA sequencing analysis. Our results showed that oral administration of Cb could improve motor deficits, dopaminergic neuron loss, synaptic dysfunction and microglia activation in the MPTP-induced mice. Meanwhile, Cb treatment could reverse the dysbiosis of gut microbiota and the decreased levels of colonic GLP-1, colonic GPR41/43 and cerebral GLP-1 receptor in the MPTP-induced mice. These findings indicated that the neuroprotective mechanism of Cb on PD might be related to the improvement of abnormal gut microbiota-gut-brain axis.<br />Ageing is characterized by a decline in cognitive and bodily functions. Metformin, the most commonly prescribed antidiabetic agent today, has proved to be able to modulate oxidative stress, several inflammatory pathways and cellular senescence to promote anti-ageing. [https://www.selleckchem.com/products/su5402.html SU5402] This review aims to explore and summarize the effects of metformin on ageing.<br />Metformin, a longstanding treatment for diabetes, has been shown to increase lifespan in both vertebrate and mammalian models. This pleiotropic effect is hypothesized to mimic calorie restriction, a currently proven means of slowing ageing, by decreasing insulin and insulin-like growth factor (IGF)-1 levels and improving insulin sensitivity. However, studies have shown that metformin is also able to target several other ageing pathways, thereby inhibiting mammalian target of rapamycin (mTOR), increasing AMPK activity and improving DNA repair. Clinical studies, such as those supported by the UK Clinical Practice Research Datalink service, have reported that diabetes patients treated with metformin live longer than patients without diabetes. Metformin use can also reduce type 2 diabetes mellitus (T2DM) incidence among those at risk, lower cancer incidence, and improve cognitive function, cardiovascular disease (CVD) risk factors and atherosclerosis.<br />Various studies have found that metformin can target several nutrient-sensing, anti-ageing and immune pathways, leading to reductions in oxidative stress, inflammation and DNA damage as well as providing effects similar to those of calorie restriction. However, further trials are still needed to confirm these findings.<br />Various studies have found that metformin can target several nutrient-sensing, anti-ageing and immune pathways, leading to reductions in oxidative stress, inflammation and DNA damage as well as providing effects similar to those of calorie restriction. However, further trials are still needed to confirm these findings.Sleep is a key process in neurodevelopment and essential for the maturation of fundamental brain functions. Premature birth can disturb the initial steps of sleep maturation, which may contribute to the impairment of neurodevelopment. It is thus fundamental to understand the maturation of the various sleep states and the quality of cerebral function in each vigilance state, as well as the development of sleep cyclicity, in at-risk neonatal infants, particularly those born premature. The objective of this review is to provide a precise description of sleep states and cycles and their rhythmic organization in premature and term newborns according to their gestational age. Technical aspects of polysomnography, which requires a high level of expertise in neonates, are also described. Principles of the visual interpretation of polysomnography, including the simultaneous analysis of behavioral (spontaneous motricity and eye movements), polysomnographic parameters (electro-oculogram, electrocardiogram, respiration), and electroencephalography patterns are presented. The neurophysiology of sleep ontogenesis and its interaction with brain maturation are discussed, highlighting the crucial role of sleep states and their duration in premature newborns. In particular, the involvement of myoclonic twitches in functional connectivity in sensorimotor development is discussed. Indeed, sleep quality, determined by combined polysomnographic parameters, reflects either normal or pathological developmental processes during the neonatal period. The fundamental place of neurophysiological explorations in the early detection of sleep disorders is discussed, as well as their potential consequences on neurodevelopmental care to improve the prevention of neurodevelopmental impairment.Papulonecrotic tuberculid represents a hypersensitivity reaction to Mycobacterium tuberculosis or its products that disseminate through hematogenous route to the skin from an internal tuberculous focus. It is characterized by recurrent eruptions of asymptomatic, dusky red papules, which undergo ulceration and crusting, and eventually heal after a few weeks with varioliform scarring. Although it most commonly involves extragenital sites, isolated glans penis involvement has been reported very rarely.<br />Nelumbo nucifera are used in folk medicine for anti-depressant, anti-convulsant, neuroprotective, and many other purposes.<br />The present work evaluated the sleep potentiating effects of water extract from lotus seed in rat, and the neuropharmacological mechanisms underlying these effects.<br />Pentobarbital-induced sleep test and electroencephalogram (EEG) analysis were applied to investigate sleep latency, duration, total sleeping time and sleep quality of Lotus extract. In addition, real-time PCR and HPLC analysis were applied to analyze the signaling pathway.<br />We found that the amounts of the possible active compounds GABA (2.33mg/g) and L-tryptophan (2.00mg/g) were higher than quinidine (0.55mg/g) and neferine (0.16mg/g) in lotus seed extract. High dose (160mg/kg) administration of lotus extract led to a tendency towards decreased sleep latency time and an increase in sleep duration time compared to the control group in a pentobarbital-induced sleep model (p&lt;0.05). After high dose administration, total sleep and NREM were significantly increased compared to control, while wake time and REM were significantly decreased.