Nucleus accumbens corticotropin-releasing factor increases cue-triggered motivation for sucrose reward: paradoxical positive incentive effects in stress?-1

<p><b>Copyright information:</b></p><p>Taken from "Nucleus accumbens corticotropin-releasing factor increases cue-triggered motivation for sucrose reward: paradoxical positive incentive effects in stress?"</p><p>BMC Biology 2006;4():8-8.</p><p>Published online 13 Apr 2006</p><p>PMCID:PMC1459217.</p><p>Copyright © 2006 Peciña et al; licensee BioMed Central Ltd.</p>os plume as colored symbol in medial shell of nucleus accumbens. Color depicts magnification effect of CRF (500 ng) microinjection at that site on peaks of lever pressing triggered by a 30 sec auditory CS+ previously associated with sucrose reward (within-subject percentage elevation of CRF versus vehicle in the same rat; 100%=vehicle). Size of central symbol depicts radius of intense Fos elevation; size of surrounding halos depict outer radius of moderate Fos elevation. For the sagittal map, bilateral accumbens sites from left and right sides of each rat brain are collapsed together into one combined sagittal map of accumbens for simplicity. Maps adapted from Paxinos and Watson [46]

Nucleus accumbens corticotropin-releasing factor increases cue-triggered motivation for sucrose reward: paradoxical positive incentive effects in stress?-0

<p><b>Copyright information:</b></p><p>Taken from "Nucleus accumbens corticotropin-releasing factor increases cue-triggered motivation for sucrose reward: paradoxical positive incentive effects in stress?"</p><p>BMC Biology 2006;4():8-8.</p><p>Published online 13 Apr 2006</p><p>PMCID:PMC1459217.</p><p>Copyright © 2006 Peciña et al; licensee BioMed Central Ltd.</p>w elevation of Fos compared to normal virgin tissue. Radial arms extending from center show sampling points for Fos measurement (125 μm × 125 μm blocks; 5× magnification). B. CRF microinjection induces intense elevation over normal tissue levels (depicted by color: 10× elevation over normal denoted by yellow, 5× = dark orange; 2× = light orange). CRF also causes elevation compared to vehicle microinjection levels at equivalent points (depicted by dotted lines; 3× relative increase over vehicle-levels denoted by thick dotted line, 5× = thin dotted line; upper right; plume from CRF 500 ng dose in 0.2 μl microinjection volume)

Obstetric practice patterns in pregnancies complicated by fetal trisomy 13 or 18

<p><b>Purpose:</b> Describe practice patterns among obstetrician/gynecologists (OB/GYNs) when caring for women with pregnancy complicated by fetal trisomy 13 (T13) or 18 (T18) and compare these between maternal–fetal medicine (MFM) and non-MFM providers.</p> <p><b>Materials and methods:</b> We conducted an electronic survey using the American College of Obstetricians and Gynecologists database. Using simple statistics, we describe demographics and practice patterns among respondents and compare those of MFM practitioners with non-MFM providers.</p> <p><b>Results:</b> The survey was sent to 300 individuals, 161 individuals verified email receipt, and 105 had complete response and were included. The median age was 58 (IQR 53,62). Sixty percent were female, 69% were private practice, and 38% were MFM. All providers were more likely to offer than to recommend antenatal and intrapartum interventions. MFMs were more likely to offer growth ultrasounds and neonatal hospice consults (53% vs. 29%, <i>p</i> = .02; 88% vs. 60%, <i>p</i> < .01). During labor, MFMs were more likely offer no fetal heart rate monitoring, (90% vs. 52%, <i>p</i> < .01), 60% of all providers offer breech vaginal delivery; 32% offer cesarean delivery for fetal distress.</p> <p><b>Conclusion:</b> Many providers offer antepartum and intrapartum interventions for pregnancies complicated by T13/18. We recommend that providers elicit each woman’s goals for pregnancies complicated by T13/18 and tailor management options to meet these goals.</p

Includes 30 genes associated with brain disorders included in the current study that overlap with the 142 marker genes used to differentially distinguish the MTG cell types in Hodge and colleagues [15].

These genes form a highly differentially stable group, indicating strong cell type specificity, several uniquely associated with a disease. (CSV)</p

Cell type profile of autism, bipolar, and schizophrenia in human MTG.

(A) Significant cell type-specific covariation of gene expression across MTG for 3 major psychiatric disorders (Methods). All 75 cell types from [15] with magnification of 24 excitatory types shown in (B), color coded by disease combinations. Autism (Aut, cyan), bipolar disorder (Bip, purple), and schizophrenia (Scz, yellow) show interactions unique to these diseases, Aut-Bip (blue), Aut-Scz (green), and Bip-Scz (red) unique to pairs, Aut-Bip-Scz (black) for all. Excitatory cell types (IT, ET,NP, CT, L6b) and dendrogram taxonomy from [15]. (C) Cell type-specific genes unique to excitatory interactions (Aut, Bip, Scz) from (B) and representative enriched biological processes and pathways. NN = non-neuronal. Underlying data for Fig 4 can be found in S1 and S7 Tables, and the data from S1 Data/Three_psychiatric_disorders. Raw data available at https://portal.brain-map.org/atlases-and-data/rnaseq under MTG SMART-seq(2018). Code available as a notebook at https://github.com/yasharz/human-brain-disease-transcriptomics. MTG, middle temporal gyrus.</p

Includes a list of genes unique to autism, bipolar disorder, and schizophrenia, their corresponding enriched biological processes and pathways based on the functional enrichment analysis results (similar to the S2 Table) and select terms for their corresponding interactions network.

Includes a list of genes unique to autism, bipolar disorder, and schizophrenia, their corresponding enriched biological processes and pathways based on the functional enrichment analysis results (similar to the S2 Table) and select terms for their corresponding interactions network.</p

Disease-based cell type expression in mouse and human.

(A) Alignment of transcriptomic cell types obtained in [15] of human MTG to 2 distinct mouse cortical areas, primary visual cortex (V1) and a premotor area, the ALM cortex, each square represents a mouse (orange) or human (blue) cell type cluster mapped to the homologous consensus cell type. (B) Histogram of mouse and human EWCE values [74] over subclass level of 20 aligned cell types. K-S goodness of fit test (Methods) shows that the distributions are marginally distinct (D = 0.091, p = 0.035). (C) Simultaneous clustering of mouse and human using EWCE disease signatures at subclass level 6 inhibitory, 9 excitatory, 5 non-neuronal (orange: mouse, blue: human) shows similarity of most diseases between species. (D) Similar clustering of mouse and human using average expression levels shows species-specific expression profiles while retaining GBD disease associations. Annotation top major cell classes, side disease GBD phenotype and ADG membership. Underlying data for Fig 5 can be found in S1 Table and the data from S1 Data (using EWCE_subclass as well as Cell_subclass expression files). Raw data available at https://portal.brain-map.org/atlases-and-data/rnaseq under MTG SMART-seq (2018). Code for EWCE available through https://github.com/NathanSkene/EWCE. Code available as a notebook at https://github.com/yasharz/human-brain-disease-transcriptomics. ALM, anterior lateral motor; EWCE, expression-weighted cell type enrichment; GBD, Global Burden of Disease; MTG, middle temporal gyrus.</p

Supporting Figures: Fig A in S1 Text.

Genes associated with risk for brain disease exhibit characteristic expression patterns that reflect both anatomical and cell type relationships. Brain-wide transcriptomic patterns of disease risk genes provide a molecular-based signature, based on differential co-expression, that is often unique to that disease. Brain diseases can be compared and aggregated based on the similarity of their signatures which often associates diseases from diverse phenotypic classes. Analysis of 40 common human brain diseases identifies 5 major transcriptional patterns, representing tumor-related, neurodegenerative, psychiatric and substance abuse, and 2 mixed groups of diseases affecting basal ganglia and hypothalamus. Further, for diseases with enriched expression in cortex, single-nucleus data in the middle temporal gyrus (MTG) exhibits a cell type expression gradient separating neurodegenerative, psychiatric, and substance abuse diseases, with unique excitatory cell type expression differentiating psychiatric diseases. Through mapping of homologous cell types between mouse and human, most disease risk genes are found to act in common cell types, while having species-specific expression in those types and preserving similar phenotypic classification within species. These results describe structural and cellular transcriptomic relationships of disease risk genes in the adult brain and provide a molecular-based strategy for classifying and comparing diseases, potentially identifying novel disease relationships.</div

Data accompanying our Jupyter notebook code to produce the main and supplementary figures in the manuscript, the data should be copied in a folder called input and the path should be added to the notebook file.

Data accompanying our Jupyter notebook code to produce the main and supplementary figures in the manuscript, the data should be copied in a folder called input and the path should be added to the notebook file.</p

Includes the aggregated transcriptomic disease profile for each disorder.

Each sheet includes the aggregated gene expression for genes associated with a given disease across the brain structures listed in S3 Table. (XLSX)</p