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6 ± 7.7 nm.Long-term cocaine use is associated with a variety of neural and behavioral deficits that impact daily function. This study was conducted to examine the effects of chronic cocaine self-administration on resting-state functional connectivity of the dorsal anterior cingulate (dACC) and putamen-two brain regions involved in cognitive function and motoric behavior-identified in a whole brain analysis. Six adult male squirrel monkeys self-administered cocaine (0.32 mg/kg/inj) over 140 sessions. Six additional monkeys that had not received any drug treatment for ~1.5 years served as drug-free controls. Resting-state fMRI imaging sessions at 9.4 Tesla were conducted under isoflurane anesthesia. Functional connectivity maps were derived using seed regions placed in the left dACC or putamen. Results show that cocaine maintained robust self-administration with an average total intake of 367 mg/kg (range 299-424 mg/kg). In the cocaine group, functional connectivity between the dACC seed and regions primarily involved in motoric behavior was weaker, whereas connectivity between the dACC seed and areas implicated in reward and cognitive processing was stronger. PH797804 In the putamen seed, weaker widespread connectivity was found between the putamen and other motor regions as well as with prefrontal areas that regulate higher-order executive function; stronger connectivity was found with reward-related regions. dACC connectivity was associated with total cocaine intake. These data indicate that functional connectivity between regions involved in motor, reward, and cognitive processing differed between subjects with recent histories of cocaine self-administration and controls; in dACC, connectivity appears to be related to cumulative cocaine dosage during chronic exposure.Medulloblastoma (MB) is the most common malignant pediatric brain tumor that can be categorized into four major molecular subgroups. Group 3 MB with MYC amplification (MYCamp-G3-MB) has been shown to be highly aggressive and exhibited worst prognosis, indicating the need for novel effective therapy most urgently. A few epigenetic targeted therapeutic strategies have recently been proven to effectively treat preclinical models of MYCamp-G3-MB, including BET inhibition, HDAC inhibition and SETD8 inhibition, unveiling a promising direction for further investigation. In this study, we carried out systemic bioinformatic analyses of public-available MB datasets as well as functional genomic screening datasets of primary MYCamp-G3-MB lines to search for other potential therapeutic targets within epigenetic modulators. We identified SSRP1, a subunit of histone-chaperone FACT complex, to be the top drug target candidate as it is highly cancer-dependent in whole-genome CRISPR-Cas9 screening across multiple MYCamp-G3-MBMYCamp-G3-MB, presenting another promising epigenetic-targeted therapeutic strategy against the most devastating form of MB.Efficient oxygen evolution reaction (OER) electrocatalysts are pivotal for sustainable fuel production, where the Ni-Fe oxyhydroxide (OOH) is among the most active catalysts for alkaline OER. Electrolyte alkali metal cations have been shown to modify the activity and reaction intermediates, however, the exact mechanism is at question due to unexplained deviations from the cation size trend. Our X-ray absorption spectroelectrochemical results show that bigger cations shift the Ni2+/(3+δ)+ redox peak and OER activity to lower potentials (however, with typical discrepancies), following the order CsOH > NaOH ≈ KOH > RbOH > LiOH. Here, we find that the OER activity follows the variations in electrolyte pH rather than a specific cation, which accounts for differences both in basicity of the alkali hydroxides and other contributing anomalies. Our density functional theory-derived reactivity descriptors confirm that cations impose negligible effect on the Lewis acidity of Ni, Fe, and O lattice sites, thus strengthening the conclusions of an indirect pH effect.Acute myeloid leukemia (AML) is the most common hematological malignancy in the world. Long noncoding RNAs (lncRNAs) play an important role in the development of physiology and pathology. Many reports have shown that lncRNA HOXA cluster antisense RNA 2 (HOXA-AS2) is a carcinogen and plays an important role in many tumors, but little is known about its role in AML. The aim of this study was to explore the potential mechanism and role of HOXA-AS2 in AML. HOXA-AS2 was upregulated in AML cell lines and tissues, and the overexpression of HOXA-AS2 is negatively correlated with the survival of patients. Silencing HOXA-AS2 can inhibit the proliferation and induce differentiation of AML cells in vitro and in vivo. Overexpressing HOXA-AS2 showed the opposite result. Moreover, more in-depth mechanism studies showed that carcinogenicity of HOXA-AS2 exerted mainly through binding with the epigenetic inhibitor Enhancer of zeste homolog 2 (EZH2) and then inhibiting the expression of Large Tumor Suppressor 2 (LATS2). Taken together, our findings highlight the important role of HOXA-AS2 in AML, suggesting that HOXA-AS2 may be an effective therapeutic target for patients with AML.The cellular and molecular basis to understand the relationship between Chagas disease (CD), a infection caused by Trypanosoma cruzi, and depression, a common psychiatric comorbidity in CD patients, is largely unknown. Clinical studies show an association between CD and depression and preclinical evidence suggests that depressive-like behaviors in T. cruzi infected mice are due, at least partially, to immune dysregulation. However, mechanistic studies regarding this issue are still lacking. Herein, we present and discuss the state of art of data on CD and depression, and revise the mechanisms that may explain the development of depression in CD. We also discuss how the knowledge generated by current and future data may contribute to the discovery of new mechanisms underlying depressive symptoms associated with CD and, hence, to the identification of new therapeutic targets, which ultimately may change the way we see and treat CD and its psychiatric comorbidities.
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