Object-based warping: an illusory distortion of space within objects

Visual objects are high-level primitives that are fundamental to numerous perceptual functions, such as guidance of attention. We report that objects warp visual perception of space in such a way that spatial distances within objects appear to be larger than spatial distances in ground regions. When two dots were placed inside a rectangular object, they appeared farther apart from one another than two dots with identical spacing outside of the object. To investigate whether this effect was object based, we measured the distortion while manipulating the structure surrounding the dots. Object displays were constructed with a single object, multiple objects, a partially occluded object, and an illusory object. Nonobject displays were constructed to be comparable to object displays in low-level visual attributes. In all cases, the object displays resulted in a more powerful distortion of spatial perception than comparable non-object-based displays. These results suggest that perception of space within objects is warped.     

Why does ADHD Confer Risk for Cigarette Smoking? A Review of Psychosocial Mechanisms

Research has documented that adolescents and young adults with attention-deficit/hyperactivity disorder (ADHD) are at increased risk for cigarette smoking, but less attention has examined why this risk exists. The current paper reviews the literature on different psychosocial mechanisms [self-medication hypothesis, social factors (social modeling, social impairments), cognitive factors (attitudes, coping skills), and psychological variables (ADHD symptom dimensions, comorbidity)] that might explain this increased smoking risk. Results of the review suggest that, while the self-medication hypothesis has some theoretical merit, it has not been adequately examined among adolescents and young adults with ADHD. Further, cognitive and social factors may be important mechanisms that help to explain the association between ADHD and cigarette smoking, but research in these areas is sparse. Finally, a larger body of literature suggests that different psychological aspects of ADHD (e.g., comorbidity, symptom dimensions) are related to smoking. Interpretation of findings of many of these studies was hindered due to significant methodological problems and the lack of a guiding theoretical orientation. Potential theories that might facilitate future work in this area are discussed. Future research should continue to explore these important psychosocial mechanisms as well as gene–environment interactions in examining the link between ADHD and cigarette smoking.     

Self-coded indirect memory associations and

Indirect memory associations for substance use predict both the concurrent and prospective levels of substance use. These methods assess spontaneous, possibly implicit, and easily accessible associations that predict substance use over direct (explicit) methods of assessment (e.g., outcome expectancies). The present study tested and expanded the application of a coding method for alcohol and marijuana associations on the basis of self-coding of indirect responses (Frigon & Krank, 2009). College students generated free associates to (1) ambiguous words (e.g., draft or weed), (2) situations (e.g., at a party, hanging out with friends), and (3) emotions (having fun, feeling dreamy). Later, participants were shown their responses and were asked to code their responses according to both nonrisk and risk activities, such as alcohol and marijuana use. Self-coded scores were higher than researcher-coded scores, captured the same variance, and improved the prediction of substance use. Self-coding of indirect memory associations provides accurate and efficient prediction of the level of alcohol and marijuana. Self-coding is efficient and may be useful for reducing ambiguities in coding of many different kinds of open-ended responses.     

Predicting preference for items during periods of extended access based on early response allocation

Top‐ranked items were identified during 30‐min free‐operant preference assessments for 9 individuals. Data from each session were analyzed to identify the item (a) that was engaged with first in each session and (b) to which the most responding was allocated after 5 min, 10 min, 15 min, 20 min, and 25 min had elapsed in each session. The results indicated that the first‐engaged item and the 5‐min high‐allocation item predicted the top‐ranked item in 55% and 62% of the sessions, respectively. The results also showed that engagement with the top‐ranked item from the first session decreased across subsequent sessions for 6 of the 9 participants. The implications of the results for brief versus extended stimulus preference assessments are discussed.     

Angiotensin II differentially affects hippocampal glial inflammatory markers in young adult male and female mice

Hypertension is a risk factor for neurodegenerative disorders involving inflammation and inflammatory cytokine-producing brain cells (microglia and astrocytes) in the hippocampus and medial prefrontal cortex (mPFC). Here we investigated the effect of slow-pressor angiotensin II (AngII) on gliosis in the hippocampus and mPFC of young adult (2-mo-old) male and female mice. In males, AngII induced hypertension, and this resulted in an increase in the density of the astrocyte marker glial fibrillary acidic protein (GFAP) in the subgranular hilus and a decrease in the density of the microglial marker ionized calcium binding adapter molecule (Iba-1) in the CA1 region. Females infused with AngII did not show hypertension but, significantly, showed alterations in hippocampal glial activation. Compared with vehicle, AngII-infused female mice had an increased density of Iba-1 in the dentate gyrus and CA2/3a region. Like males, females infused with AngII exhibited decreased Iba-1 in the CA1 region. Neither male nor female mice showed differences in GFAP or Iba-1 in the mPFC following AngII infusion. These results demonstrate that the hippocampus is particularly vulnerable to AngII in young adulthood. Differences in gonadal hormones or the sensitivity to AngII hypertension may account for divergences in GFAP and Iba-1 in males and females.

Hypertension is a significant risk factor for neurological disorders such as Alzheimer''s disease (AD) that are associated with neurodegeneration and cognitive decline (Daugherty 2021). Hypertension can develop during the life span yet is often studied at middle and late life. There is emerging evidence that hypertension is becoming more common in late adolescence and early adulthood (Azegami et al. 2021; Hamrahian and Falkner 2022). In addition, there is increasing awareness that the duration of hypertension can impact the onset of neural degeneration (Schaare et al. 2019; Yang et al. 2021) and cognitive dysfunction (Yaffe et al. 2014, 2021; Mahinrad et al. 2020; Zhou et al. 2022). Although the age of onset of hypertension may influence the trajectory of degenerative disease in later life, the effect of hypertension on brain health in young adult subjects is relatively underinvestigated.Hippocampal and medial prefrontal cortical pathology are commonly present in neurodegenerative diseases like AD (Belonwu et al. 2021). Structurally and functionally, both the hippocampus and mPFC also are compromised during hypertension (Raz et al. 2007; Gonzalez et al. 2015; Bu et al. 2018). In the hippocampus, hypertension is known to disrupt cerebrovascular function, promote inflammatory processes, and contribute to neuronal impairment and cognitive decline (Iulita et al. 2018). Although less studied than the hippocampus, the PFC is also compromised by hypertension (Raz et al. 2007; Bu et al. 2018; Wang et al. 2020).Microglia, the resident macrophages in the brain, have been implicated in inflammatory states, cognitive function (Cornell et al. 2022), and the brain''s response to hypertension (Calvillo et al. 2019; Li et al. 2020). An increase in the density of ionized calcium binding adapter molecule (Iba-1), a protein constitutively expressed in microglia and up-regulated when microglia enter an activated stage (Imai et al. 1996; Sasaki et al. 2001), is commonly reported in models of cognitive and neurodegenerative disorders (Prinz et al. 2021).In addition to microglia, astrocytes also have been implicated in the emergence of hippocampal and cortical dysfunction. Astrocytes play critical roles in blood–brain barrier (BBB) formation; brain metabolic, ion, and water homeostasis; neurotransmitter recycling; synapse formation; and neuroimmune signaling (Matias et al. 2019). In the context of insult, pathogen infection, or neurological disease, astrocytes undergo functionally complex reactive responses (Chiu et al. 2014; Giovannoni and Quintana 2020) that are associated with an increase in glial fibrillary acidic protein (GFAP) gene and protein expression (Crespo-Castrillo et al. 2020; Sofroniew 2020).To better understand the consequences of elevated blood pressure on the young adult brain, we conducted an exploratory investigation of the impact of hypertension on the expression of microglia and astrocyte markers—Iba-1 and GFAP, respectively—in the hippocampus and mPFC of male mice. Mice were exposed to angiotensin II (AngII) using the “slow-pressor” model (Dickinson and Lawrence 1963), which in males mimics the gradual rise in blood pressure and increase in sympathetic activation (Grassi and Ram 2016; Lerman et al. 2019) characteristic of essential hypertension (Lerman et al. 2019). Significantly, there is an important sex dimorphism in the risk for hypertension. Compared with men, women are protected from hypertension before middle age but become increasingly affected as they reach perimenopause, and intact young female rodents show a reduced sensitivity to AngII hypertension (Van Kempen et al. 2016). Similarly, there are sex differences in the incidence, progression, and severity of hypertension-associated neurodegenerative disease (Lopez-Lee et al. 2021). Furthermore, sex differences in glial function have also been documented within the context of neurodegenerative diseases (Kodama and Gan 2019; Biechele et al. 2020). Given this evidence, the effect of AngII on hippocampal and medial prefrontal cortical glial markers also was investigated in young intact female mice.     

LeRoy Walters and Julie Gage Palmer,The Ethics of Human Gene Therapy

Theoretical Medicine and Bioethics -