Exposure to high-rise buildings negatively influences affect: evidence from real world and 360-degree video

Cities are densifying at a rapid rate, and accordingly, are constructing high-rise buildings to accommodate more people. The aim of this study was to quantify the physiological and psychological impacts of being in the presence of high-rise buildings in Central London, in a real and virtual 360-degree video environment. Using a within-subjects design, participants were exposed to a low-rise and high-rise building. While exposed, participants were monitored for electrodermal activity. They were also administered the Self-Assessment Manikin measure and a cognitive appraisal questionnaire. Participants rated the high-rise building environment to be less open, less friendly and rated themselves to feel less happy and have less sense of control, as compared to low-rise buildings. We found these effects in both the real world (n = 16) and a 360-degree video setting (n = 121). These findings suggest that city environments populated with high-rise buildings can have negative impacts on urban dwellers. Furthermore, this study provides a methodology to examine how individuals respond to the built environment and stand to inform urban design and architectural practices

Combining Path Integration and Remembered Landmarks When Navigating without Vision

This study investigated the interaction between remembered landmark and path integration strategies for estimating current location when walking in an environment without vision. We asked whether observers navigating without vision only rely on path integration information to judge their location, or whether remembered landmarks also influence judgments. Participants estimated their location in a hallway after viewing a target (remembered landmark cue) and then walking blindfolded to the same or a conflicting location (path integration cue). We found that participants averaged remembered landmark and path integration information when they judged that both sources provided congruent information about location, which resulted in more precise estimates compared to estimates made with only path integration. In conclusion, humans integrate remembered landmarks and path integration in a gated fashion, dependent on the congruency of the information. Humans can flexibly combine information about remembered landmarks with path integration cues while navigating without visual information.National Institutes of Health (U.S.) (Grant T32 HD007151)National Institutes of Health (U.S.) (Grant T32 EY07133)National Institutes of Health (U.S.) (Grant F32EY019622)National Institutes of Health (U.S.) (Grant EY02857)National Institutes of Health (U.S.) (Grant EY017835-01)National Institutes of Health (U.S.) (Grant EY015616-03)United States. Department of Education (H133A011903

A Kir6.2 mutation causing severe functional effects in vitro produces neonatal diabetes without the expected neurological complications

AIMS/HYPOTHESIS: Heterozygous activating mutations in the pancreatic ATP-sensitive K+ channel cause permanent neonatal diabetes mellitus (PNDM). This results from a decrease in the ability of ATP to close the channel, which thereby suppresses insulin secretion. PNDM mutations that cause a severe reduction in ATP inhibition may produce additional symptoms such as developmental delay and epilepsy. We identified a heterozygous mutation (L164P) in the pore-forming (Kir6.2) subunit of the channel in three unrelated patients and examined its functional effects. METHODS: The patients (currently aged 2, 8 and 20 years) developed diabetes shortly after birth. The two younger patients attempted transfer to sulfonylurea therapy but were unsuccessful (up to 1.1 mg kg(-1) day(-1)). They remain insulin dependent. None of the patients displayed neurological symptoms. Functional properties of wild-type and mutant channels were examined by electrophysiology in Xenopus oocytes. RESULTS: Heterozygous (het) and homozygous L164P K(ATP) channels showed a marked reduction in channel inhibition by ATP. Consistent with its predicted location within the pore, L164P enhanced the channel open state, which explains the reduction in ATP sensitivity. HetL164P currents exhibited greatly increased whole-cell currents that were unaffected by sulfonylureas. This explains the inability of sulfonylureas to ameliorate the diabetes of affected patients. CONCLUSIONS/INTERPRETATION: Our results provide the first demonstration that mutations such as L164P, which produce a severe reduction in ATP sensitivity, do not inevitably cause developmental delay or neurological problems. However, the neonatal diabetes of these patients is unresponsive to sulfonylurea therapy. Functional analysis of PNDM mutations can predict the sulfonylurea response

Integration of vestibular and proprioceptive signals for spatial updating

Frissen I, Campos JL, Souman JL, Ernst MO. Integration of vestibular and proprioceptive signals for spatial updating. Experimental Brain Research. 2011;212(2):163-176.Spatial updating during self-motion typically involves the appropriate integration of both visual and non-visual cues, including vestibular and proprioceptive information. Here, we investigated how human observers combine these two non-visual cues during full-stride curvilinear walking. To obtain a continuous, real-time estimate of perceived position, observers were asked to continuously point toward a previously viewed target in the absence of vision. They did so while moving on a large circular treadmill under various movement conditions. Two conditions were designed to evaluate spatial updating when information was largely limited to either proprioceptive information (walking in place) or vestibular information (passive movement). A third condition evaluated updating when both sources of information were available (walking through space) and were either congruent or in conflict. During both the passive movement condition and while walking through space, the pattern of pointing behavior demonstrated evidence of accurate egocentric updating. In contrast, when walking in place, perceived self-motion was underestimated and participants always adjusted the pointer at a constant rate, irrespective of changes in the rate at which the participant moved relative to the target. The results are discussed in relation to the maximum likelihood estimation model of sensory integration. They show that when the two cues were congruent, estimates were combined, such that the variance of the adjustments was generally reduced. Results also suggest that when conflicts were introduced between the vestibular and proprioceptive cues, spatial updating was based on a weighted average of the two inputs

Activating mutations in the gene encoding the ATP-sensitive potassium-channel subunit Kir6.2 and permanent neonatal diabetes

Background Patients with permanent neonatal diabetes usually present within the first three months of life and require insulin treatment. In most, the cause is unknown. Because ATP-sensitive potassium (KATP) channels mediate glucose-stimulated insulin secretion from the pancreatic beta cells, we hypothesized that activating mutations in the gene encoding the Kir6.2 subunit of this channel (KCNJ11) cause neonatal diabetes. Methods We sequenced the KCNJ11 gene in 29 patients with permanent neonatal diabetes. The insulin secretory response to intravenous glucagon, glucose, and the sulfonylurea tolbutamide was assessed in patients who had mutations in the gene. Results Six novel, heterozygous missense mutations were identified in 10 of the 29 patients. In two patients the diabetes was familial, and in eight it arose from a spontaneous mutation. Their neonatal diabetes was characterized by ketoacidosis or marked hyperglycemia and was treated with insulin. Patients did not secrete insulin in response to glucose or glucagon but did secrete insulin in response to tolbutamide. Four of the patients also had severe developmental delay and muscle weakness; three of them also had epilepsy and mild dysmorphic features. When the most common mutation in Kir6.2 was coexpressed with sulfonylurea receptor 1 in Xenopus laevis oocytes, the ability of ATP to block mutant KATP channels was greatly reduced. Conclusions Heterozygous activating mutations in the gene encoding Kir6.2 cause permanent neonatal diabetes and may also be associated with developmental delay, muscle weakness, and epilepsy. Identification of the genetic cause of permanent neonatal diabetes may facilitate the treatment of this disease with sulfonylureas