Am I missing something here?
Why does it seem like being an IT poster is incompatible with human dignity?
Am I missing something here?
Reddit humor.
Reddit was a mistake
Because they are all cuckolds.
"They're incompatible"
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"All humans have positive and negative variants, so we must match them correctly"
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"Adhering to the pattern, we continue. We must note that most SNPs are common"
"Oh...I didn't note SNP frequencies"
Ooh, is this brain study stuff, @Intellau_Celistic
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Why are you still browsing IT in 2024?
"We look more closely"
"Wait"
Versus
post is from 2018
"Now...matching the studies appropriately, intelligence itself remains"
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I agree Intellau
Researchers have found that there are three driving forces behind schadenfreude – aggression, rivalry, and justice.[4]
Self-esteem has a negative relationship with the frequency and intensity of schadenfreude experienced by an individual; individuals with lower self-esteem tend to experience schadenfreude more frequently and intensely.[5]
Self-esteem has a negative relationship with the frequency and intensity of schadenfreude experienced by an individual; individuals with lower self-esteem tend to experience schadenfreude more frequently and intensely.[5]
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The Psychiatric Risk Gene Transcription Factor 4 (TCF4) Regulates Neurodevelopmental Pathways Associated With Schizophrenia, Autism, and Intellectual Disability
Genetic variants in and around the transcription factor 4 (TCF4) gene are associated with range of disorders that are frequently associated with cognitive dysfunction.1–3 The most recent schizophrenia GWAS reported three independent single nucleotide polymorphisms (SNPs) in TCF4 that surpassed the threshold for genome wide significance.4 Intriguingly, rare TCF4 single nucleotide variants (SNVs) have also been described in schizophrenia patients, although their impact on the function of the protein has not been established.5,6 In addition to the genetic studies in schizophrenia, TCF4 variants are associated with early information processing and cognitive markers, some of which are schizophrenia endophenotypes.7–10 Damaging TCF4 mutations have also been described in large-scale genotyping studies in patients with ID, neurodevelopmental disorders, and most recently ASD.11–15 Haploinsufficiency of TCF4 causes Pitt–Hopkins syndrome (PTHS); a rare form intellectual disability (ID) associated with characteristic facial features, autonomic dysfunction, and behavioral traits that resemble autism spectrum disorder (ASD).16–19 Collectively, these studies implicate TCF4 in a range of neurodevelopmental disorders.CF4 is a member of the basic helix-loop-helix (bHLH) family of proteins.20–22 For the purposes of disambiguation, it should be noted that TCF4 (Gene ID: 6925) described herein should not be confused with T-cell factor 4 (Gene ID: 6934, official gene symbol, TCF7L2) since they can share the same acronym. TCF4 and its paralogues, collectively known as E-proteins, interact with other bHLH proteins to regulate DNA binding specificity and transcriptional activity at promoters and enhancers that contain E-boxes (5′-CANNTG).2,20,23 The human TCF4 gene encodes multiple protein isoforms of which only the major isoforms TCF4-A and TCF4-B have been characterized in detail.24 In neurons, TCF4 regulates the intrinsic excitability of pyramidal cells of the prefrontal cortex and has been shown to attenuate neurite branching.25,26 Furthermore, haploinsufficiency of Tcf4 in mice affects gene expression and DNA methylation in the brain, leading to enhanced long-term potentiation, learning and memory deficits, and autistic-like behavior.22,25,26 By contrast, mice over-expressing Tcf4 in the brain display deficits in sensorimotor gating, fear conditioning, and circadian processes as well as impairments in attentional and behavioral anticipation.7,27
Converging evidence for a pseudoautosomal cytokine receptor gene locus in schizophrenia
Schizophrenia is a strongly heritable disorder, and identification of potential candidate genes has accelerated in recent years. Genomewide scans have identified multiple large linkage regions across the genome, with fine-mapping studies and other investigations of biologically plausible targets demonstrating several promising candidate genes of modest effect. The recent introduction of technological platforms for whole-genome association (WGA) studies can provide an opportunity to rapidly identify novel targets, although no WGA studies have been reported in the psychiatric literature to date. We report results of a case-control WGA study in schizophrenia, examining approximately 500 000 markers, which revealed a strong effect (P=3.7 x 10(-7)) of a novel locus (rs4129148) near the CSF2RA (colony stimulating factor, receptor 2 alpha) gene in the pseudoautosomal region. Sequencing of CSF2RA and its neighbor, IL3RA (interleukin 3 receptor alpha) in an independent case-control cohort revealed both common intronic haplotypes and several novel, rare missense variants associated with schizophrenia. The presence of cytokine receptor abnormalities in schizophrenia may help explain prior epidemiologic data relating the risk for this illness to altered rates of autoimmune disorders, prenatal infection and familial leukemia.
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