Racial and Temporal Differences in Fertility-Education Trade-Offs Reveal the Effect of Economic Opportunities on Optimum Family Size in the United States.

Contemporary trends in low fertility can in part be explained by increasing incentives to invest in offspring's embodied capital over offspring quantity in environments where education is a salient source of social mobility. However, studies on this subject have often neglected to empirically examine heterogeneity, missing out on the opportunity to investigate how this relationship is impacted when individuals are excluded from meaningful participation in economic spheres. Using General Social Survey data from the United States, I examine changes in the relationship between number of siblings and college attendance for White and Black respondents throughout the 1900s. Results show that in the early 1900s, White individuals from larger families had a lower chance of completing four years of college education than those from smaller families, whereas the likelihood for Black individuals was more uniform across family sizes. These racial differences mostly converged in the later part of the century. These results may help explain variations in the timing of demographic transitions within different racial groups in the United States and suggest that the benefits of decreasing family size on educational outcomes may be conditional on the specific economic opportunities afforded to a family.

Lifting the Digital Curtain: Utilizing Social Media to Promote Health Content and Engage with Asian Populations.

BACKGROUND/AIMS: To understand how social media can be used to improve Asian subgroup engagement in a research registry. METHODS: A 10-week social media campaign was implemented with the goal of increasing the percentage of Asian participants in the Stanford Research Registry - platforms utilized include Facebook, Instagram, and Twitter through the Stanford Center for Asian Health Research and Education accounts. Participant data was disaggregated by race and ethnicity in order to better understand the diversity among Asian subgroups. RESULTS: The percentage of Asian participants increased from 14.3% at baseline to 23.8% at the end of the campaign (525 Asian identifying individuals to 1,871). The greatest increase occurred during the general outreach phase which utilized all channels of outreach available. Frequencies of some ethnicities, such as Japanese, Korean, and Vietnamese, were higher in the Multi-Ethnic and/or Multi-Racial categories compared to their corresponding monoethnic groups. CONCLUSIONS: Social media is a powerful tool that can be leveraged for targeted recruitment - in this study we see how it can increase diversity amongst research participants and potentially be used as an effective tool for information dissemination. This work can be expanded in the future by examining other social media platforms more targeted toward Asian populations, and more thorough disaggregation to fully understand the diversity present in the Asian population.

Staying alive enhances both women's and men's fitness.

We argue that Benenson et al. need to consider not only sex differences in the effects of care on offspring survival but also in age-specific fertility when predicting how longevity affects fitness. We review evidence that staying alive has important effects on both women's and men's fitness, and encourage consideration of alternative explanations for observed sex differences in threat responses.

Pre- and postsynaptically expressed spike-timing-dependent plasticity contribute differentially to neuronal learning.

A plethora of experimental studies have shown that long-term synaptic plasticity can be expressed pre- or postsynaptically depending on a range of factors such as developmental stage, synapse type, and activity patterns. The functional consequences of this diversity are not clear, although it is understood that whereas postsynaptic expression of plasticity predominantly affects synaptic response amplitude, presynaptic expression alters both synaptic response amplitude and short-term dynamics. In most models of neuronal learning, long-term synaptic plasticity is implemented as changes in connective weights. The consideration of long-term plasticity as a fixed change in amplitude corresponds more closely to post- than to presynaptic expression, which means theoretical outcomes based on this choice of implementation may have a postsynaptic bias. To explore the functional implications of the diversity of expression of long-term synaptic plasticity, we adapted a model of long-term plasticity, more specifically spike-timing-dependent plasticity (STDP), such that it was expressed either independently pre- or postsynaptically, or in a mixture of both ways. We compared pair-based standard STDP models and a biologically tuned triplet STDP model, and investigated the outcomes in a minimal setting, using two different learning schemes: in the first, inputs were triggered at different latencies, and in the second a subset of inputs were temporally correlated. We found that presynaptic changes adjusted the speed of learning, while postsynaptic expression was more efficient at regulating spike timing and frequency. When combining both expression loci, postsynaptic changes amplified the response range, while presynaptic plasticity allowed control over postsynaptic firing rates, potentially providing a form of activity homeostasis. Our findings highlight how the seemingly innocuous choice of implementing synaptic plasticity by single weight modification may unwittingly introduce a postsynaptic bias in modelling outcomes. We conclude that pre- and postsynaptically expressed plasticity are not interchangeable, but enable complimentary functions.

Dual metabotropic glutamate receptor signaling enables coordination of astrocyte and neuron activity in developing sensory domains.

Astrocytes play an essential role in the development of neural circuits by positioning transporters and receptors near synapses and secreting factors that promote synaptic maturation. However, the mechanisms that coordinate astrocyte and neural maturation remain poorly understood. Using in vivo imaging in unanesthetized neonatal mice, we show that bursts of neuronal activity passing through nascent sound processing networks reliably induce calcium transients in astrocytes. Astrocyte transients were dependent on intense neuronal activity and constrained to regions near active synapses, ensuring close spatial and temporal coordination of neuron and astrocyte activity. Astrocyte responses were restricted to the pre-hearing period and induced by synergistic activation of two metabotropic glutamate receptors, mGluR5 and mGluR3, which promoted IP3R2-dependent calcium release from intracellular stores. The widespread expression of these receptors by astrocytes during development and the prominence of neuronal burst firing in emerging neural networks may help coordinate the maturation of excitatory synapses.

Purinergic Signaling Controls Spontaneous Activity in the Auditory System throughout Early Development.

Spontaneous bursts of electrical activity in the developing auditory system arise within the cochlea before hearing onset and propagate through future sound-processing circuits of the brain to promote maturation of auditory neurons. Studies in isolated cochleae revealed that this intrinsically generated activity is initiated by ATP release from inner supporting cells (ISCs), resulting in activation of purinergic autoreceptors, K+ efflux, and subsequent depolarization of inner hair cells. However, it is unknown when this activity emerges or whether different mechanisms induce activity during distinct stages of development. Here we show that spontaneous electrical activity in mouse cochlea from both sexes emerges within ISCs during the late embryonic period, preceding the onset of spontaneous correlated activity in inner hair cells and spiral ganglion neurons, which begins at birth and follows a base to apex developmental gradient. At all developmental ages, pharmacological inhibition of P2Y1 purinergic receptors dramatically reduced spontaneous activity in these three cell types. Moreover, in vivo imaging within the inferior colliculus revealed that auditory neurons within future isofrequency zones exhibit coordinated neural activity at birth. The frequency of these discrete bursts increased progressively during the postnatal prehearing period yet remained dependent on P2RY1. Analysis of mice with disrupted cholinergic signaling in the cochlea indicate that this efferent input modulates, rather than initiates, spontaneous activity before hearing onset. Thus, the auditory system uses a consistent mechanism involving ATP release from ISCs and activation of P2RY1 autoreceptors to elicit coordinated excitation of neurons that will process similar frequencies of sound.SIGNIFICANCE STATEMENT In developing sensory systems, groups of neurons that will process information from similar sensory space exhibit highly correlated electrical activity that is critical for proper maturation and circuit refinement. Defining the period when this activity is present, the mechanisms responsible and the features of this activity are crucial for understanding how spontaneous activity influences circuit development. We show that, from birth to hearing onset, the auditory system relies on a consistent mechanism to elicit correlate firing of neurons that will process similar frequencies of sound. Targeted disruption of this activity will increase our understanding of how these early circuits mature and may provide insight into processes responsible for developmental disorders of the auditory system.

Maternal and fetal alkaline ceramidase 2 is required for placental vascular integrity in mice.

Sphingolipids have been implicated in mammalian placental development and function, but their regulation in the placenta remains unclear. Herein we report that alkaline ceramidase 2 (ACER2) plays a key role in sustaining the integrity of the placental vasculature by regulating the homeostasis of sphingolipids in mice. The mouse alkaline ceramidase 2 gene (Acer2) is highly expressed in the placenta between embryonic day (E) 9.5 and E12.5. Acer2 deficiency in both the mother and fetus decreases the placental levels of sphingolipids, including sphingoid bases (sphingosine and dihydrosphingosine) and sphingoid base-1-phosphates (sphingosine-1-phosphate and dihydrosphingosine-1-phosphate) and results in the in utero death of ≈50% of embryos at E12.5 whereas Acer2 deficiency in either the mother or fetus has no such effects. Acer2 deficiency causes hemorrhages from the maternal vasculature in the junctional and/or labyrinthine zones in E12.5 placentas. Moreover, hemorrhagic but not non-hemorrhagic Acer2-deficient placentas exhibit an expansion of parietal trophoblast giant cells with a concomitant decrease in the area of the fetal blood vessel network in the labyrinthine zone, suggesting that Acer2 deficiency results in embryonic lethality due to the atrophy of the fetal blood vessel network in the placenta. Taken together, these results suggest that ACER2 sustains the integrity of the placental vasculature by controlling the homeostasis of sphingolipids in mice.

AANAT1 functions in astrocytes to regulate sleep homeostasis.

How the brain controls the need and acquisition of recovery sleep after prolonged wakefulness is an important issue in sleep research. The monoamines serotonin and dopamine are key regulators of sleep in mammals and in Drosophila. We found that the enzyme arylalkylamine N-acetyltransferase 1 (AANAT1) is expressed by Drosophila astrocytes and specific subsets of neurons in the adult brain. AANAT1 acetylates monoamines and inactivates them, and we found that AANAT1 limited the accumulation of serotonin and dopamine in the brain upon sleep deprivation (SD). Loss of AANAT1 from astrocytes, but not from neurons, caused flies to increase their daytime recovery sleep following overnight SD. Together, these findings demonstrate a crucial role for AANAT1 and astrocytes in the regulation of monoamine bioavailability and homeostatic sleep.

Sleep is essential for our physical and mental health. A lack of sleep can affect our energy and concentration levels and is often linked to chronic illnesses and mood disorders. Sleep is controlled by an internal clock in our brain that operates on a 24-hour cycle, telling our bodies when we are tired and ready for bed, or fresh and alert to start a new day. In addition, the brain tracks the need for sleep and drives the recovery of sleep after periods of prolonged wakefulness ­ a process known as sleep-wake homeostasis. Chemical messengers in the brain such as dopamine and serotonin also play an important part in regulating our sleep drive. While dopamine keeps us awake, serotonin can both prevent us from and help us falling asleep, depending on the part of the brain in which it is released. Most research has focused on the role of different brain circuits on sleep, but it has been shown that a certain type of brain cell, known as astrocyte, may also be important for sleep regulation. So far, it has been unclear if astrocytes could be involved in regulating the need for recovery sleep after a sleep-deprived night ­ also known as rebound sleep. Now, Davla, Artiushin et al. used sleep-deprived fruit flies to investigate this further. The flies were kept awake over 12 hours (from 6pm to 6am), using intermittent physical agitation. The researchers found that astrocytes in the brains of fruit flies express a molecule called AANAT1, which peaked at the beginning of the night, declined as the night went on and recovered by morning. In sleep deprived flies, it inactivated the chemical messengers and so lowered the amount of dopamine and serotonin in the brain. However, in mutant flies that lacked AANAT1, both dopamine and serotonin levels increased in the brain after sleep deprivation. When AANAT1 was selectively removed from astrocytes only, sleep-deprived flies needed more rebound sleep during the day to make up for lost sleep at night. This shows that both astrocytes and AANAT1 play a crucial role in sleep homeostasis. Molecules belonging to the AANAT family exist in both flies and humans, and these results could have important implications for the science of sleep. The study of Davla, Artiushin et al. paves the way for understanding the mechanisms of sleep homeostasis that are similar in both organisms, and may in the future, help to identify sleep drugs that target astrocytes and the molecules they express.

A Practical Guide to Using CV Analysis for Determining the Locus of Synaptic Plasticity.

Long-term synaptic plasticity is widely believed to underlie learning and memory in the brain. Whether plasticity is primarily expressed pre- or postsynaptically has been the subject of considerable debate for many decades. More recently, it is generally agreed that the locus of plasticity depends on a number of factors, such as developmental stage, induction protocol, and synapse type. Since presynaptic expression alters not just the gain but also the short-term dynamics of a synapse, whereas postsynaptic expression only modifies the gain, the locus has fundamental implications for circuits dynamics and computations in the brain. It therefore remains crucial for our understanding of neuronal circuits to know the locus of expression of long-term plasticity. One classical method for elucidating whether plasticity is pre- or postsynaptically expressed is based on analysis of the coefficient of variation (CV), which serves as a measure of noise levels of synaptic neurotransmission. Here, we provide a practical guide to using CV analysis for the purposes of exploring the locus of expression of long-term plasticity, primarily aimed at beginners in the field. We provide relatively simple intuitive background to an otherwise theoretically complex approach as well as simple mathematical derivations for key parametric relationships. We list important pitfalls of the method, accompanied by accessible computer simulations to better illustrate the problems (downloadable from GitHub), and we provide straightforward solutions for these issues.

Nuclear factor-kappaB regulates multiple steps of gliogenesis in the developing murine cerebral cortex.

Nuclear factor-kappaB (NF-κB) is activated in neural progenitor cells in the developing murine cerebral cortex during the neurogenic phase, when it acts to prevent premature neuronal differentiation. Here we show that NF-κB activation continues in mouse neocortical neural progenitor cells during the neurogenic-to-gliogenic switch. Blockade of endogenous NF-κB activity during neocortical gliogenesis leads to the formation of supernumerary committed gliogenic progenitors and premature glial cell differentiation. Conversely, forced NF-κB activation during the neocortical neurogenic-to-gliogenic transition causes delayed gliogenic commitment and decreased astroglial gene expression. NF-κB activation continues in neocortical gliogenic progenitors following commitment and is important to inhibit the differentiation of oligodendrocyte precursor cells and to maintain persistent expression of glial fibrillary acidic protein in maturing astrocytes. These results reveal a number of previously uncharacterized roles for NF-κB during different phases of neocortical gliogenesis and identify NF-κB as an inhibitor of early oligodendrocyte development in the cerebral cortex.

Homeostatic Control of Spontaneous Activity in the Developing Auditory System.

Neurons in the developing auditory system exhibit spontaneous bursts of activity before hearing onset. How this intrinsically generated activity influences development remains uncertain, because few mechanistic studies have been performed in vivo. We show using macroscopic calcium imaging in unanesthetized mice that neurons responsible for processing similar frequencies of sound exhibit highly synchronized activity throughout the auditory system during this critical phase of development. Spontaneous activity normally requires synaptic excitation of spiral ganglion neurons (SGNs). Unexpectedly, tonotopic spontaneous activity was preserved in a mouse model of deafness in which glutamate release from hair cells is abolished. SGNs in these mice exhibited enhanced excitability, enabling direct neuronal excitation by supporting cell-induced potassium transients. These results indicate that homeostatic mechanisms maintain spontaneous activity in the pre-hearing period, with significant implications for both circuit development and therapeutic approaches aimed at treating congenital forms of deafness arising through mutations in key sensory transduction components.

Ihog and Boi elicit Hh signaling via Ptc but do not aid Ptc in sequestering the Hh ligand.

Hedgehog (Hh) proteins are secreted molecules essential for tissue development in vertebrates and invertebrates. Hh reception via the 12-pass transmembrane protein Patched (Ptc) elicits intracellular signaling through Smoothened (Smo). Hh binding to Ptc is also proposed to sequester the ligand, limiting its spatial range of activity. In Drosophila, Interference hedgehog (Ihog) and Brother of ihog (Boi) are two conserved and redundant transmembrane proteins that are essential for Hh pathway activation. How Ihog and Boi activate signaling in response to Hh remains unknown; each can bind both Hh and Ptc and so it has been proposed that they are essential for both Hh reception and sequestration. Using genetic epistasis we established here that Ihog and Boi, and their orthologs in mice, act upstream or at the level of Ptc to allow Hh signal transduction. In the Drosophila developing wing model we found that it is through Hh pathway activation that Ihog and Boi maintain the boundary between the anterior and posterior compartments. We dissociated the contributions of Ptc from those of Ihog/Boi and, surprisingly, found that cells expressing Ptc can retain and sequester the Hh ligand without Ihog and Boi, but that Ihog and Boi cannot do so without Ptc. Together, these results reinforce the central role for Ptc in Hh binding in vivo and demonstrate that, although Ihog and Boi are dispensable for Hh sequestration, they are essential for pathway activation because they allow Hh to inhibit Ptc and thereby relieve its repression of Smo.

From waste to functional additive: toughening epoxy resin with lignin.

A novel approach to toughen epoxy resin with lignin, a common waste material from the pulp and paper industry, is presented in this article. First, carboxylic acid-functionalized alkali lignin (AL-COOH) was prepared and subsequently incorporated into anhydride-cured epoxy networks via a one-pot method. The results of mechanical tests show that covalent incorporation of rigid AL-COOH into epoxy networks can significantly toughen the epoxy matrix without deteriorating its tensile strength and modulus. The addition of 1.0 wt % AL-COOH gives increases of 68 and 164% in the critical stress intensity factor (K(IC)) and critical strain energy release rate (G(IC)), respectively, relative to that of neat epoxy. This article opens up the possibility of utilizing low-cost and renewable lignin feedstocks as effective toughening agents for thermoset polymers.

Dendrite architecture organized by transcriptional control of the F-actin nucleator Spire.

The architectures of dendritic trees are crucial for the wiring and function of neuronal circuits because they determine coverage of receptive territories, as well as the nature and strength of sensory or synaptic inputs. Here, we describe a cell-intrinsic pathway sculpting dendritic arborization (da) neurons in Drosophila that requires Longitudinals Lacking (Lola), a BTB/POZ transcription factor, and its control of the F-actin cytoskeleton through Spire (Spir), an actin nucleation protein. Loss of Lola from da neurons reduced the overall length of dendritic arbors, increased the expression of Spir, and produced inappropriate F-actin-rich dendrites at positions too near the cell soma. Selective removal of Lola from only class IV da neurons decreased the evasive responses of larvae to nociception. The increased Spir expression contributed to the abnormal F-actin-rich dendrites and the decreased nocifensive responses because both were suppressed by reduced dose of Spir. Thus, an important role of Lola is to limit expression of Spir to appropriate levels within da neurons. We found Spir to be expressed in dendritic arbors and to be important for their development. Removal of Spir from class IV da neurons reduced F-actin levels and total branch number, shifted the position of greatest branch density away from the cell soma, and compromised nocifensive behavior. We conclude that the Lola-Spir pathway is crucial for the spatial arrangement of branches within dendritic trees and for neural circuit function because it provides balanced control of the F-actin cytoskeleton.

Development and validation of perceived rehabilitation require questionnaires for caregivers of people with schizophrenia.

OBJECTIVE: This study aimed at developing and validating the Perceived Rehabilitation Needs Questionnaires for Caregivers (PRNQ-Cs) of people with schizophrenia. METHODS: The items of PRNQ-C were generated based on focus group discussion and literature review. A validation study was conducted to examine its psychometric properties among 98 caregivers who were recruited via convenience sampling. RESULTS: Through the use of direct oblique rotation, exploratory factor analysis yielded an eight-factor solution which accounted for 64.39% of the total variance. Its internal consistency and test-retest reliability were satisfactory. CONCLUSION: Through cross-cultural validation, the PRNQ-C is applicable in other Chinese communities with huge population of schizophrenia.

The perceived rehabilitation needs of people with schizophrenia in Hong Kong: perspectives from consumers and care-givers.

A quantitative survey was conducted to investigate the perceived rehabilitation needs based on people with schizophrenia and their caregivers. A total of 194 persons with schizophrenia and 83 caregivers were recruited by convenience sampling to complete the two newly developed questionnaires for this purpose which included the Perceived Rehabilitation Needs Questionnaire for People with Schizophrenia and the Perceived Rehabilitation Needs Questionnaire for Caregivers towards People with Schizophrenia respectively. The findings deepened the understanding of this area. Some policy and service development suggestions for mental health strategies in Hong Kong and the Asian-Pacific region were made.

Development and initial validation of Perceived Rehabilitation Needs Questionnaire for people with schizophrenia.

PURPOSE: The Perceived Rehabilitation Needs Questionnaires for people with schizophrenia (PRNQ-S), a culturally relevant and multi-faceted assessment tool for measuring perceived needs of people with schizophrenia, was developed and initially validated. METHODS: A total of 43 participants including people with schizophrenia, their caregivers, and mental health professionals were recruited for six rounds of focus group discussion to identify issues pertaining to rehabilitation needs of schizophrenia. Results were then used to develop PRNQ-S. An initial validation study among a convenience sample consisting of 219 people with schizophrenia was conducted to examine its psychometric properties. RESULTS: Exploratory Factor Analysis yielded a seventeen-factor solution accounting for 70.7% of the total variance which resulted in a 75-item PRNQ-S. The instrument had excellent internal consistencies and intra-rater reliability. CONCLUSIONS: The PRNQ-S has been developed and psychometrically tested in Hong Kong. It can be used to assess perceived rehabilitation needs for individuals with schizophrenia in Hong Kong. Upon further validations, it may be applied in other Chinese societies such as Singapore and the mainland. Similar research methodology can also be used for assessing needs in other types of psychiatric disability groups.

Three year follow-up study of an integrated supported employment for individuals with severe mental illness.

OBJECTIVES: The aim of the present study was to examine and compare the long-term effectiveness of the Integrated Supported Employment (ISE) programme, which consists of individual placement and support (IPS) and work-related social skills training, with the IPS programme on the vocational and non-vocational outcomes among individuals with severe mental illness (SMI) over a period of 3 years. METHOD: One hundred and eighty-nine participants with SMI were recruited from two non-government organizations and three day hospitals in Hong Kong and randomly assigned into the ISE (n = 58), IPS (n = 65) and traditional vocational rehabilitation (TVR) (n = 66) groups. Vocational and non-vocational outcomes of the ISE and IPS participants were collected by a blind and independent assessor at 7 11, 15, 21, 27, 33 and 39 months after their admission, whereas the TVR groups were assessed only up to the 15th month follow up. RESULTS: After 39 months of service provision, ISE participants obtained higher employment rate (82.8% vs 61.5%) and longer job tenure (46.94 weeks vs 36.17 weeks) than the IPS participants. Only 6.1% of TVR participants were able to obtain employment before the 15th month follow up. Fewer interpersonal conflicts at the workplace were reported for the ISE participants. Advantages of the ISE participants over IPS participants on non-vocational outcomes were not conclusive. CONCLUSION: The long-term effectiveness of the ISE programme in enhancing employment rates and job tenures among individuals with SMI was demonstrated by this randomized controlled trial.

Case report of integrated supported employment for a person with severe mental illness.

OBJECTIVE: We illustrate the implementation of an integrated supported employment (ISE) program that augments the individual placement and support model with social skills training in helping people with severe mental illness (SMI) achieve and maintain employment. METHOD: A case illustration demonstrates how ISE helped a 41-year-old woman with SMI to get and keep a job with support from an employment specialist. An independent, blinded assessor conducted data collection of employment information, including self-efficacy and quality of life, at pretreatment and at 3-month, 7-month, 11-month, and 15-month follow-up assessments. RESULTS: The participant eventually stayed in a job for 8 months and reported improved self-efficacy and quality of life. CONCLUSION: The case report suggests that ISE could improve the employment outcomes of people with SMI. Moreover, changes in the participant's self-efficacy and quality of life were shown to be driven by the successful employment experience.