Wheelercraft8651

Forming an impression of another person is an essential aspect of human social cognition linked to medial prefrontal cortex (mPFC) function in adults. The current study examined the neurodevelopmental origins of impression formation by testing the hypothesis that infants rely on processes localized in mPFC when forming impressions about individuals who appear friendly or threatening. Infants' brain responses were measured using functional near-infrared spectroscopy while watching 4 different face identities displaying either smiles or frowns directed toward or away from them (N = 77). This was followed by a looking preference test for these face identities (now displaying a neutral expression) using eyetracking. Our results show that infants' mPFC responses distinguish between smiling and frowning faces when directed at them and that these responses predicted their subsequent person preferences. This suggests that the mPFC is involved in impression formation in human infants, attesting to the early ontogenetic emergence of brain systems supporting person perception and adaptive behavior.Blood-oxygenation-level-dependent (BOLD) signals in magnetic resonance imaging indirectly reflect neural activity in cortex, but they are also detectable in white matter (WM). BOLD signals in WM exhibit strong correlations with those in gray matter (GM) in a resting state, but their interpretation and relationship to GM activity in a task are unclear. We performed a parametric visual object recognition task designed to modulate the BOLD signal response in GM regions engaged in higher order visual processing, and measured corresponding changes in specific WM tracts. Human faces embedded in different levels of random noise have previously been shown to produce graded changes in BOLD activation in for example, the fusiform gyrus, as well as in electrophysiological (N170) evoked potentials. The magnitudes of BOLD responses in both GM regions and selected WM tracts varied monotonically with the stimulus strength (noise level). In addition, the magnitudes and temporal profiles of signals in GM and WM regions involved in the task coupled strongly across different task parameters. These findings reveal the network of WM tracts engaged in object (face) recognition and confirm that WM BOLD signals may be directly affected by neural activity in GM regions to which they connect.Serotonin (5-hydroxytryptamine) is crucial for the proper development of neuronal circuits early in life and their refinement throughout adulthood. Its signaling is tightly regulated by the serotonin transporter (SERT), alterations of which were implicated in various neurological and psychiatric disorders. Animal models lacking a functional SERT variant display diverse phenotypes, including increased anxiety, social communication deficits, and altered cortical development. However, it remains unclear how SERT disruption affects sensory processing and experience-dependent learning in adulthood. It has been previously shown that perceptual experience leads to the development of visual familiarity-evoked theta oscillations in mouse V1. Here, we discovered that familiarity-evoked theta oscillations were longer and less stimulus specific in SERT knockout (KO) compared with wild-type (WT) mice. Interestingly, while the overall visual response properties were similar in naive mice, orientation and spatial frequency processing were significantly impaired in SERT KO compared with WT or SERT heterozygous mice following perceptual experience. Our findings shed more light on the mechanism of familiarity-evoked oscillations and highlight the importance of serotonin signaling in perceptual learning.Producing a tool use gesture is a complex process drawing upon the integration of stored knowledge of tools and their associated actions with sensory-motor mechanisms supporting the planning and control of hand and arm actions. Understanding how sensory-motor systems in parietal cortex interface with semantic representations of actions and objects in the temporal lobe remains a critical issue and is hypothesized to be a key determinant of the severity of limb apraxia, a deficit in producing skilled action after left hemisphere stroke. We used voxel-based and connectome-based lesion-symptom mapping with data from 57 left hemisphere stroke participants to assess the lesion sites and structural disconnection patterns associated with poor tool use gesturing. We found that structural disconnection among the left inferior parietal lobule, lateral and ventral temporal cortices, and middle and superior frontal gyri predicted the severity of tool use gesturing performance. Control analyses demonstrated that reductions in right-hand grip strength were associated with motor system disconnection, largely bypassing regions supporting tool use gesturing. Our findings provide evidence that limb apraxia may arise, in part, from a disconnection between conceptual representations in the temporal lobe and mechanisms enabling skilled action production in the inferior parietal lobule.There has been a systematic and largely unconscious neglect of gender in palliative care research, practice and policy. This is despite significant, although previously uncollated, evidence that gender influences almost all aspects of end-of-life preferences, experiences and care. The social situations of women, transgender people and men often differ from one another while also intersecting in complex ways with sex differences rooted in biology. If palliative care is to meet its aspiration of providing universal benefit, it urgently needs to address a range of gender inequalities currently (re)produced at the level of the laboratory all the way through to government departments. In this call to arms, we spotlight specific instances where gender inequalities have been documented, for example, regarding end-of-life caregiving, end-of-life intervention and palliative care access and benefit. We highlight how gender inequalities intersect with other social determinants of health including ethnicity and economic status to exacerbate situations of marginality. We conclude by offering some practical steps that can be taken to support the discipline to adopt a more critical gender lens to support more equitable research, policy and practice.

Rosette-forming glioneuronal tumors (RGNTs) are rare, low-grade, primary CNS tumors first described in 2002 by Komori et al. RGNTs were initially characterized as a World Health Organization (WHO) grade I tumors typically localized to the fourth ventricle. Although commonly associated with an indolent course, RGNTs have the potential for aggressive behavior.

A comprehensive search of PubMed and Web of Science was performed through November 2019 using the search term "rosette-forming glioneuronal tumor." Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines were followed. English, full-text case reports and series with histopathological confirmation were included. Patient demographics, presentations, MRI features, tumor location, treatment, and follow-up of all 130 cases were extracted.

A 19-year-old man with a history of epilepsy and autism presented with acute hydrocephalus. MRI scans from 2013 to 2016 demonstrated unchanged abnormal areas of cortex in the left temporal lobe with extension into the deep gray-white matter. On presentation to our clinic in 2019, the lesion demonstrated significant progression. The patient's tumor was identified as RGNT, WHO grade I. One hundred thirty patients were identified across 80 studies.

RGNT has potential to transform from an indolent tumor to a tumor with more aggressive behavior. The results of our systematic review provide insight into the natural history and treatment outcomes of these rare tumors.

RGNT has potential to transform from an indolent tumor to a tumor with more aggressive behavior. The results of our systematic review provide insight into the natural history and treatment outcomes of these rare tumors.

The overexpression of (basic)helix-loop-helix ((b)HLH) transcription factors (TFs) is frequent in malignant glioma. We investigated molecular effects upon disruption of the (b)HLH network by a dominant-negative variant of the E47 protein (dnE47). Our goal was to identify novel molecular subgroup-specific therapeutic strategies.

Glioma cell lines LN229, LNZ308, and GS-2/GS-9 were lentivirally transduced. Functional characterization included immunocytochemistry, immunoblots, cytotoxic, and clonogenic survival assays in vitro, and latency until neurological symptoms in vivo. Results of cap analysis gene expression and RNA-sequencing were further validated by immunoblot, flow cytometry, and functional assays in vitro.

The induction of dnE47-RFP led to cytoplasmic sequestration of (b)HLH TFs and antiglioma activity in vitro and in vivo. Downstream molecular events, ie, alterations in transcription start site usage and in the transcriptome revealed enrichment of cancer-relevant pathways, particularly of the DNA damage response (DDR) pathway. Pharmacologic validation of this result using ataxia telangiectasia and Rad3 related (ATR) inhibition led to a significantly enhanced early and late apoptotic effect compared with temozolomide alone.

Gliomas overexpressing (b)HLH TFs are sensitive toward inhibition of the ATR kinase. The combination of ATR inhibition plus temozolomide or radiation therapy in this molecular subgroup are warranted.

Gliomas overexpressing (b)HLH TFs are sensitive toward inhibition of the ATR kinase. The combination of ATR inhibition plus temozolomide or radiation therapy in this molecular subgroup are warranted.

Although mutations in the promoter region of the telomerase reverse transcriptase (

p) gene are the most common alterations in glioblastoma (GBM), their clinical significance remains unclear. Therefore, we investigated the impact of

p status on patient outcome and clinicopathological features in patients with GBM over a long period of follow-up.

We retrospectively analyzed 153 cases of GBM. Six patients with isocitrate dehydrogenase 1 (

) or

gene mutations were excluded from this study. Among the 147 cases of

wild-type GBM, 92 (62.6%) had the

p mutation. Clinical, immunohistochemical, and genetic factors (

,

gene mutation, CD133, ATRX expression,



-methylguanine-DNA methyltransferase [

] promoter methylation) and copy number alterations (CNAs) were investigated.

GBM patients with the

p mutation were older at first diagnosis versus those with

p wild type (66.0 vs. selleck inhibitor 60.0 years, respectively,

= .034), and had shorter progression-free survival (7 vs. 10 months, respectively,

= .015) and overall survival (16 vs. 24 months, respectively,

= .017). Notably, magnetic resonance imaging performed showed that

p-mutant GBM was strongly associated with multifocal/distant lesions (

= .004). According to the CNA analysis,

p mutations were positively correlated with

amp/gain,

deletion, and

deletion; however, these mutations were negatively correlated with

amp/gain,

gain, and

deletion.

p mutations were strongly correlated with multifocal/distant lesions and poor prognosis in patients with

wild-type GBM. Less aggressive GBM with

p wild type may be a distinct clinical and molecular subtype of

wild-type GBM.

TERTp mutations were strongly correlated with multifocal/distant lesions and poor prognosis in patients with IDH wild-type GBM. Less aggressive GBM with TERTp wild type may be a distinct clinical and molecular subtype of IDH wild-type GBM.