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Murine Leukemia-Derived Extracellular Vesicles Bring about Antitumor Immune Result.
SDG may act as a supramolecular binding component and naturally occurring metal chelating agent for metal cations like Cd2+. Therefore, flaxseed lignan-SDG can be used as a therapeutic agent against nephrotoxicity caused by cadmium. However, detailed future studies are needed to know the underlying mechanism of action of SDG against the Cd and other heavy metals induced nephrotoxicity.Purpose Neonatal hypoglycemic brain injury (NHBI) is being increasingly recognized as an important cause of drug resistant childhood epilepsy in low resource settings. We report the electro-clinical spectrum of children with epilepsy secondary to NHBI. Methods This was a retrospective study of children enrolled in the Epilepsy Clinic from January 2009 to August 2019. Data of children who had developed epilepsy after documented symptomatic neonatal hypoglycemia was collected. Details of clinical profile, seizure types, neurodevelopmental co-morbidities, EEG, neuroimaging findings and seizure outcomes were noted. Results One hundred and seventy children were enrolled. The mean age at seizure onset was 10.3 months (SD 0.5 months). The seizures types were epileptic spasms (76.5%), focal with visual auras (11.2%), bilateral tonic clonic (7.1%), myoclonic (3.5%) and atonic seizures (1.8%). The EEG findings included classical hypsarrhythmia (49.4%), hypsarrhythmia variant (27.1%), focal occipital or temporo-occipital spike wave discharges (10.6%), multifocal discharges (4.7%), diffuse slow spike and wave with bursts of fast rhythms (2.4%), continuous spike waves during sleep (1.2%) and normal EEG (4.7%). MRI showed gliosis with or without encephalomalacia in the occipital lobe with or without parietal lobe in 96.5% of the patients. Co-morbidities included global developmental delay (91.2%), cerebral palsy (48.7%), vision impairment (48.2%), microcephaly (38.2%), hearing impairment (19.4%), and behavioural problems (16.5%). Drug resistant childhood epilepsy was seen in 116 (68.2%) patients. Conclusions Our study highlights the varied electroclinical and radiological spectrum and the adverse epilepsy and neurodevelopmental outcomes associated with NHBI.Purpose When performed correctly, hyperventilation (HV) for three minutes provokes absence seizures in virtually all children, a finding suggestive of a diagnosis of childhood absence epilepsy (CAE). Envonalkib Interestingly, some children experience absence seizures while performing HV in the office yet do not experience absences during HV on subsequent routine EEG. In most instances, HV during routine EEG is performed in the supine position, while in the office HV is done with the child sitting-up. Therefore, we hypothesized that the position in which HV is performed may influence its yield in provoking absence seizures. Methods We conducted a randomized multi-center controlled trial among children (4-10 years old) with suspected CAE. During a routine EEG, children were asked to perform HV twice, in the supine and sitting positions. Results Twenty children (four males) diagnosed with CAE were included in the analysis. Seventeen of the 20 patients experienced absence seizures while sitting and 13 experienced seizures during supine HV (p = 0.031). All patients that had absence seizures during supine HV also had seizures during sitting HV. Among patients with absences in both positions, seizure duration was significantly shorter during sitting HV (mean 8.69 seconds) than during supine HV (mean 12 seconds) (p = 0.042). An opposite tendency was seen in the younger age group (4-7 years), with shorter seizures in the supine HV group (5.6 seconds supine, 7.57 seconds sitting, p = 0.019). Conclusions HV in the sitting position may increase the yield of provoking absence seizures during routine EEGs, thereby improving its sensitivity in the diagnosis of CAE.In development and in homeostatic maintenance of tissues, stem cells and progenitor cells are constantly subjected to forces. These forces can lead to significant changes in gene expression and function of stem cells, mediating self-renewal, lineage specification, and even loss of function. One of the ways that has been proposed to mediate these functional changes in stem cells is nuclear mechanotransduction - the process by which forces are converted to signals in the nucleus. The purpose of this review is to discuss the means by which mechanical signals are transduced into the nucleus, through the linker of nucleoskeleton and cytoskeleton (LINC) complex and other nuclear envelope transmembrane (NET) proteins, which connect the cytoskeleton to the nucleus. We discuss how LINC/NETs confers tissue-specific mechanosensitivity to cells and further elucidate how LINC/NETs acts as a control center for nuclear mechanical signals, regulating both gene expression and chromatin organization. Throughout, we primarily focus on stem cell-specific examples, notwithstanding that this is a nascent field. We conclude by highlighting open questions and pointing the way to enhanced research efforts to understand the role nuclear mechanotransduction plays in cell fate choice.Astrocytic glycogen is an important energy reserve in the brain and is believed to supply fuel during energy crisis. However, the pattern of glycogen metabolism in ischemic stroke and its potential therapeutic impact on neurological outcomes are still unknown. Here, we found extensive brain glycogen accumulation after reperfusion in ischemic stroke patients and primates. Glycogenolytic dysfunction in astrocytes is responsible for glycogen accumulation, caused by inactivation of the protein kinase A (PKA)-glycogen phosphorylase kinase (PhK)-glycogen phosphorylase (GP) cascade accompanied by the activation of glycogen synthase kinase-3β (GSK3β). Genetic or pharmacological augmentation of astrocytic GP could promote astrocyte and neuron survival and improve neurological behaviors. In addition, we found that insulin exerted a neuroprotective effect, at least in part by rescuing the PKA-PhK-GP cascade to maintain homeostasis of glycogen metabolism during reperfusion. Together, our findings suggest a promising intervention for undesirable outcomes in ischemic stroke.
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