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Materials for architects and builders
\"This new 6th edition has been completely revised and updated to include the latest developments in materials research, new images, appropriate technologies and relevant legislation. The ecological effects of building construction and lifetime use remain an important focus, and this new edition includes a wide range of energy saving building components.\"--Back cover.
Book
Using Heteroscedasticity to Identify and Estimate Mismeasured and Endogenous Regressor Models
This article proposes a new method of obtaining identification in mismeasured regressor models, triangular systems, and simultaneous equation systems. The method may be used in applications where other sources of identification, such as instrumental variables or repeated measurements, are not available. Associated estimators take the form of two-stage least squares or generalized method of moments. Identification comes from a heteroscedastic covariance restriction that is shown to be a feature of many models of endogeneity or mismeasurement. Identification is also obtained for semiparametric partly linear models, and associated estimators are provided. Set identification bounds are derived for cases where point-identifying assumptions fail to hold. An empirical application estimating Engel curves is provided.
Journal Article
Anyway* : *a story about me with 138 footnotes, 27 exaggerations, and 1 plate of spaghetti
At summer camp, twelve-year-old Max reinvents himself as daring and fearless \"Mad Max,\" and although he regrets some of his behavior among strangers, he tries to keep some of that fearlessness when he returns home to his friends.
Book
Reference Points for Retirement Behavior
This paper studies the large concentration of retirement behavior around statutory retirement ages, a puzzling stylized fact. To investigate this fact, I estimate bunching responses to 644 pension benefit discontinuities, using administrative data on the universe of German retirees. Financial incentives alone cannot explain retirement patterns, but there is a large direct effect of statutory retirement ages. I argue that the framing of statutory ages as reference points for retirement provides a plausible explanation. Simulations based on a model with reference dependence highlight that shifting statutory ages via pension reforms is an effective policy to influence retirement behavior.
Journal Article
The Identification Zoo
Over two dozen different terms for identification appear in the econometrics literature, including set identification, causal identification, local identification, generic identification, weak identification, identification at infinity, and many more. This survey: (i) gives a new framework unifying existing definitions of point identification; (ii) summarizes and compares the zooful of different terms associated with identification that appear in the literature; and (iii) discusses concepts closely related to identification, such as normalizations and the differences in identification between structural models and causal, reduced form models.
Journal Article
Life through time and space
We all had three origins: the origin of our own individual life, the origin of life on Earth, and the origin of our planetary home from a universe that initially had neither stars nor planets. This book tells the stories of these three origins and the evolutionary processes connected with them. It tells the stories in an intertwined way; and it considers the likelihood that intelligent life-forms on other planets exist - indeed are numerous - and had their own versions of these same three origins. The evolutionary story of the universe involves the origins of stars, planets, and life. The evolutionary story of life on Earth involves the origins of cells, animals, and intelligence. The evolutionary story of an intelligent alien living on an exoplanet somewhere in the Milky Way galaxy may have those same three origins, though here we're in the realm of hypothesis. But we come firmly back to Earth for the evolutionary story of the human embryo, which involves the origin of mulberries, sausages, and brains - though the first two of these are metaphorical creatures. These stories are not told in sequence; rather, the book intertwines them. It takes the form of a series of chapter-triplets, in each of which all of the stories feature. So we begin not with the big bang but rather by gazing into the night-time sky and using the constellation of Cassiopeia to locate extra-terrestrial life. And we end not with the rarefied skies of the distant future but with the prospects for human survival - or extinction - and the world-wide clash between intolerance and enlightenment, which may help to decide our ultimate fate.-- Provided by publisher.
Book
Spinal muscular atrophy: why do low levels of survival motor neuron protein make motor neurons sick?
Key Points
Spinal muscular atrophy (SMA) is caused by reduced amounts of the ubiquitously expressed survival motor neuron protein (SMN). SMN functions in RNA metabolism, but the question of which aspect of its function is disrupted to give a motor neuron disease remains unanswered.
SMN functions in the assembly of Sm proteins onto small nuclear RNAs (snRNAs) during pre-mRNA splicing. It has been suggested that SMN might have a role in the assembly of other ribonucleoprotein (RNP) complexes.
SMA is caused by loss or mutation of
SMN1
and retention of
SMN2
,leading to low SMN levels. Proteins that carry mild missense mutations complement
SMN2
to restore assembly activity and give a mild phenotype.
Loss of SMN in all species results in lethality, indicating that SMN has an essential function. Animal models of SMA can be created by reducing the levels of SMN.
It has been proposed that reduction of SMN levels results in an alteration of the small nuclear ribonucleoprotein (snRNP) profile. This is supported by the correlation between snRNP assembly activity and SMA severity in mice; however, a clear indication of the downstream target genes that are affected is currently lacking.
SMN is found in axons of cultured cells, and a second hypothesis suggests that altered mRNA transport in axons may contribute to SMA. However, a clear indication of what SMN function is disrupted to alter mRNA transport is lacking.
SMN functions in the assembly of RNPs, but it remains unresolved whether it is an axonal or an snRNP component that is disrupted in SMA. Experiments showing a clear suppression of the phenotype by manipulating a particular pathway could be used to demonstrate the crucial pathway in SMA.
How a reduction in the level of a ubiquitously expressed protein, SMN, causes the motor neuron–specific deficits that characterize spinal muscular atrophy is unknown. Burghes and Beattie discuss the function of SMN and the debate concerning the crucial pathways disrupted in SMA.
Many neurogenetic disorders are caused by the mutation of ubiquitously expressed genes. One such disorder, spinal muscular atrophy, is caused by loss or mutation of the survival motor neuron1 gene (
SMN1
), leading to reduced SMN protein levels and a selective dysfunction of motor neurons. SMN, together with partner proteins, functions in the assembly of small nuclear ribonucleoproteins (snRNPs), which are important for pre-mRNA splicing. It has also been suggested that SMN might function in the assembly of other ribonucleoprotein complexes. Two hypotheses have been proposed to explain the molecular dysfunction that gives rise to spinal muscular atrophy (SMA) and its specificity to a particular group of neurons. The first hypothesis states that the loss of SMN's well-known function in snRNP assembly causes an alteration in the splicing of a specific gene (or genes). The second hypothesis proposes that SMN is crucial for the transport of mRNA in neurons and that disruption of this function results in SMA.
Journal Article
Near-infrared deep brain stimulation via upconversion nanoparticle–mediated optogenetics
Noninvasive deep brain stimulation is an important goal in neuroscience and neuroengineering. Optogenetics normally requires the use of a blue laser inserted into the brain. Chen et al. used specialized nanoparticles that can upconvert near-infrared light from outside the brain into the local emission of blue light (see the Perspective by Feliu et al. ). They injected these nanoparticles into the ventral tegmental area of the mouse brain and activated channelrhodopsin expressed in dopaminergic neurons with near-infrared light generated outside the skull at a distance of several millimeters. This technique allowed distant near-infrared light to evoke fast increases in dopamine release. The method was also used successfully to evoke fear memories in the dentate gyrus during fear conditioning. Science , this issue p. 679 ; see also p. 633 Optogenetic experiments can be performed inside the mouse brain by using near-infrared light applied outside the skull. Optogenetics has revolutionized the experimental interrogation of neural circuits and holds promise for the treatment of neurological disorders. It is limited, however, because visible light cannot penetrate deep inside brain tissue. Upconversion nanoparticles (UCNPs) absorb tissue-penetrating near-infrared (NIR) light and emit wavelength-specific visible light. Here, we demonstrate that molecularly tailored UCNPs can serve as optogenetic actuators of transcranial NIR light to stimulate deep brain neurons. Transcranial NIR UCNP-mediated optogenetics evoked dopamine release from genetically tagged neurons in the ventral tegmental area, induced brain oscillations through activation of inhibitory neurons in the medial septum, silenced seizure by inhibition of hippocampal excitatory cells, and triggered memory recall. UCNP technology will enable less-invasive optical neuronal activity manipulation with the potential for remote therapy.
Journal Article