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Max's psychotic brother in Stranger Things 2 is the ideal male

Fontaine

Fontaine

Overlord
★★★★★
Joined
Nov 15, 2017
Posts
5,417
In a female's eye and the writers/producers made no attempt to hide it. 

Even normie shows can't hide the blackpill because it would then look too unrealistic.
 
It's not possible.

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Well, anyway. Back to the basics.

Processing speed

Processing speed is thought to be the most common cognitive deficit affecting individuals with prHD (Maroof et al., 2011; Paulsen, 2011). Across all three prHD subgroups (prHDI, prHDII, and prHDIII), as well as postdiagnosis stages of HD (I–III), processing speed exhibits a linear trend in decline. There are likely several reasons for the sensitivity of timed tasks on cognitive performance. First, it has long been known that cognitive processing speed is one of the most sensitive (though nonspecific) cognitive abilities demonstrating decline with cerebral dysfunction (Lezak, 2012). For example, the Digit Symbol subtest of the Wechsler Adult Intelligence Scales has shown that impairments were present in numerous acquired, developmental, and degenerative brain conditions. Next, it is clear that processing speed can be slowed in the presence of psychiatric symptoms, such as depression (Smith et al., 2012), and many participants with prHD have psychiatric symptoms. Third, other subtle components of HD, such as perceptual processing (O'Rourke et al., 2011) and oculomotor scanning (Blekher et al., 2004, 2006), are impacted in prHD and could weaken processing speed (Paulsen, 2011). Despite common deficits in processing speed, persons who have this symptom in prHD do not typically have highly correlated decline in functioning (Duff et al., 2010a). Paulsen and colleagues (2011) attribute this phenomenon to the concept of “effortful processing.” Effortful processing is the notion that the brain is capable of compensating for dysfunctional circuitry for a given period of time, specifically during the HD prodrome, by recruiting surrogate regions of the brain to complete cognitive tasks. This rerouting to alternate areas of the brain results in accurate but slowed processing during prHD. This explanation may be supported by Bonner-Jackson and colleagues (2013), who suggest that processing speed is mediated by cognitive reserve in prHD so that individuals with greater prodromal intellect may show less bradyphrenia than similarly burdened prodromal participants with lower premorbid IQ. Kloppel and colleagues (2015) provide imaging support for this hypothesis.
While evidence to support the decline in processing speed in HD is clear (Paulsen, 2010, 2011; Stout et al., 2011; Harrington et al., 2012), the assessment of objectively measuring processing speed proves challenging due to its direct ties to many other cognitive tasks. O’Rourke and colleagues (2011) conducted a particularly clever research paper suggesting the Trail Making Test (TMT) can be used to separate distinct cognitive processes. These findings indicate that TMT Part A is most sensitive to perceptual processing, visual scanning, motor speed, and attention, whereas TMT Part B is more associated with executive functions (set shifting, response inhibition), cognitive processing speed, and working memory.

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Enough of that for now.

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Genome-wide association studies (GWAS) accessing thousands of DNA samples from cases and control subjects is a powerful tool for identifying common risk factors for complex diseases. However, even apparently highly significant positive findings require replication, preferably in several sample sets from both the same and different ethnic groups. In 2009, Stefansson et al. (1) described a GWAS in schizophrenia. They examined DNA from 7662 schizophrenic cases and 29,053 normal control subjects recruited from eight European locations. They identified seven common risk single nucleotide polymorphisms (SNPs) showing genome-wide significance after correction for multiple testing (rs6913660, rs13219354, rs6932590, rs13211507, rs3131296, rs12807809, and rs9960767, respectively) (1). They then carried out a combined analysis using schizophrenia and control genotypes from the International Schizophrenia Consortium (ISC) and the Molecular Genetics of Schizophrenia GWAS studies (1, 2, 3). A further SNP, rs3130375, also in the major histocompatibility complex (MHC) region, was reported to be highly associated with schizophrenia in Caucasians by the ISC study alone (2). Therefore, in light of these findings, we decided to genotype these eight highly significant SNPs in Han Chinese. We examined DNA from 2496 schizophrenia patients and 5184 normal control subjects drawn from Han Chinese. Unfortunately, on genotyping, we found that four of the eight SNPs, rs6913660, rs13219354, rs13211507, and rs9960767, were not polymorphic in our Chinese samples. Because rs9960767 was the only SNP in the TCF4 gene reported as significant by Stefansson et al. (1), we selected rs2958182, an SNP nearby to rs9960767 on the HapMap Han Chinese in Beijing (HCB) samples provided by the International HapMap Consortium that was polymorphic in our samples. It is the nearest common SNP to rs9960767 in HapMap HCB samples.


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Disregarding the medications I'm on:

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Why did this guy have a Delon pfp lol? Isn’t that Chad worship?
 
Major bluepill was when the sub5 truecel son of the single mom got together with that HTB from season 1.... like comon, even normies knew that was totally horseshit
 
Wrong thread for that, however.

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Increasing evidence supports schizophrenia may be a neurodevelopmental and neurodegenerative disorder. Fluoxetine, a selective serotonin reuptake inhibitor, has been reported to have neuroprotective effects and be effective in treating neurodegenerative disorders including schizophrenia. The objective of the present study was to evaluate the effect and underlying neuroprotective mechanism of fluoxetine on the sensorimotor gating deficit, a schizophrenia-like behavior in a neurodevelopmental schizophrenic mouse model induced by MK-801, an N-methyl-d-aspartate glutamate receptor antagonist. On postnatal day 7, mouse pups were treated with a total seven subcutaneous daily injections of MK-801 (1 mg/kg/day), followed by intraperitoneal injection of fluoxetine (5 or 10 mg/kg/day) starting on postnatal day 14 in the MK-801-injected mice for 4 weeks. The sensorimotor gating deficit in mice was measured by prepulse inhibition (PPI) behavioral test on postnatal day 43. After the behavioral test, the protein expression of brain-derived neurotrophic factor (BDNF) was measured by western blot or ELISA in the frontal cortex of mice. Our results showed fluoxetine attenuated PPI deficit and the decrease of cerebral BDNF expression in the MK-801-injected mice. These results suggest that fluoxetine can be used to treat sensorimotor gating deficit in a neurodevelopmental mouse model of schizophrenia, and the attenuating effect of fluoxetine on sensorimotor gating deficit may be related to fluoxetine’s neuroprotective effect targeting on the modulation of cerebral BDNF.




Background
Treatment of negative symptoms in chronic schizophrenia continues to be a major clinical issue.
Aims
To analyse the efficacy of add-on antidepressants for the treatment of negative symptoms of chronic schizophrenia.
Method
Systematic review and meta-analysis of randomised controlled trials comparing the effect of antidepressants and placebo on the negative symptoms of chronic schizophrenia, measured through standardised rating scales. Outcome was measured as standardised mean difference between end-of-trial and baseline scores of negative symptoms.
Results
There were 23 trials from 22 publications (n = 819). The antidepressants involved were selective serotonin reuptake inhibitors, mirtazapine, reboxetine, mianserin, trazodone and ritanserin; trials on other antidepressants were not available. The overall standardised mean difference was moderate (–0.48) in favour of antidepressants and subgroup analysis revealed significant responses for fluoxetine, trazodone and ritanserin.
Conclusions

Antidepressants along with antipsychotics are more effective in treating the negative symptoms of schizophrenia than antipsychotics alone.

 

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