Racial/Ethnic Inequality among Older Workers: Focusing on Whites, Blacks, and Latinos within the Cumulative Advantage/Disadvantage Framework

As the number of older workers increases, scholars from variable fields have made an effort to understand what makes the current older generation want to remain in the labor market; however, our knowledge of older minority workers is fragmentary. The experience of older minority workers, defined as Blacks and Latinos in this study, may differ from that of their White counterparts because of persistent racial/ethnic differences among older workers, especially in four domains: 1) financial resources for retirement, 2) health, 3) career patterns, and 4) education. Existing literature has little to offer for older minority workers because of limited methodological approaches and a dearth of appropriate theories. Thus, this study aims to identify factors that explain older Americans’ labor market participation after retirement age and whether there are racial/ethnic differences among those factors. It also presents fragmentary knowledge from existing studies within the framework of the cumulative advantage/disadvantage (CAD) theory. Using the 1,114 pre-retirement aged workers from the 2004 and 2008 datasets of the Health and Retirement Study (HRS), probit analysis was run to estimate the analytic model. Racially separate analyses were performed to treat race as a major indicator for the outcome (workers’ labor market status after age 65) and to systematically compare factors by race. The results showed that, after adjusting for covariates, factors influencing older individuals’ employment after age 65 were conditioned by race. Whereas health and the meaning of work most influence Whites, financial resources (particularly home ownership) most affect Blacks, while health alone most concerns Latinos. Overall, this study suggests that access to the labor market—as opposed to personal preference, financial necessity, or job dissatisfaction—most influences the labor market participation of minorities. These findings of this study highlight the role of race, suggesting that one universal model cannot fully explain older individuals’ labor market participation among different race/ethnic groups. Furthermore, this study’s inclusion of Latinos expanded the scope of the existing literature, finding that both Black and Latino workers experience a lifetime accumulation of disadvantages. However, their employment experiences differ significantly: while class differences potentially exist among Black workers, Latinos can be more disadvantaged as a whole, experiencing substantial barriers related to education level and language in the workplace. This study helps to correct theoretical limitations in studies of older workers by using the more revealing CAD framework to interpret results. Racial/ethnic inequality among older workers should be understood not as sudden occurrences in old age, but as a byproduct of the interplay between the individual’s lifetime experiences in the labor market and the social structures that impose cumulative advantages/disadvantages on the individual. This study also contributes to the field of social work by stressing the importance of both financial and non-financial factors to better comprehend issues surrounding older workers

Resistenz durch Symbiose:Deutsches Fernsehprogramm und Regulierungsmaßnahmen im Globalisierungsprozess

Diese Arbeit beschäftigt sich mit der Veränderung der deutschen Medienlandschaft in den 90er Jahren. Durch die Einführung des dualen Fernsehsystems in der Mitte der 80er Jahre wurde eine umwälzende Veränderung in Gang gesetzt, deren Dynamik sich in den 90er Jahren voll entfaltete. Zu dieser Zeit war es unklar, ob und in welchem Ausmaß sich prognostizierte und kontrovers diskutierte Globalisierungsten-denzen wie Kommerzialisierung, Homogenisierung und „Amerikanisierung“ durchsetzen würden und ob es eher zu einem Verlust der kulturellen Identität oder einer verstärkten Regionalisierung kommen würde. Vor diesem Hintergrund fand eine verstärkte staatliche Förderung auf regionaler, nationaler und europäi-scher Ebene statt, deren Auswirkung auf die Veränderung der Medienlandschaft in dieser Arbeit anhand einer empirischen Untersuchung des Fernsehprogramms in den 90er Jahren untersucht wird

Spindle Checkpoint Regulators in Insulin Signaling

The spindle checkpoint ensures accurate chromosome segregation during mitosis and guards against aneuploidy. Insulin signaling governs metabolic homeostasis and cell growth, and its dysregulation leads to metabolic disorders, such as diabetes. These critical pathways have been extensively investigated, but a link between the two has not been established until recently. Our recent study reveals a critical role of spindle checkpoint regulators in insulin signaling and metabolic homeostasis through regulating endocytosis of the insulin receptor (IR). These findings have linked spindle checkpoint proteins to metabolic regulation, expanding the connection between cell division and metabolism. Here, we briefly review the unexpected roles of spindle checkpoint regulators in vesicle trafficking and insulin signaling

BubR1 acetylation at prometaphase is required for modulating APC/C activity and timing of mitosis

Regulation of BubR1 is central to the control of APC/C activity. We have found that BubR1 forms a complex with PCAF and is acetylated at lysine 250. Using mass spectrometry and acetylated BubR1-specific antibodies, we have confirmed that BubR1 acetylation occurs at prometaphase. Importantly, BubR1 acetylation was required for checkpoint function, through the inhibition of ubiquitin-dependent BubR1 degradation. BubR1 degradation began before the onset of anaphase. It was noted that the pre-anaphase degradation was regulated by BubR1 acetylation. Degradation of an acetylation-mimetic form, BubR1–K250Q, was inhibited and chromosome segregation in cells expressing BubR1–K250Q was markedly delayed. By contrast, the acetylation-deficient mutant, BubR1–K250R, was unstable, and mitosis was accelerated in BubR1–K250R-expressing cells. Furthermore, we found that APC/C–Cdc20 was responsible for BubR1 degradation during mitosis. On the basis of our collective results, we propose that the acetylation status of BubR1 is a molecular switch that converts BubR1 from an inhibitor to a substrate of the APC/C complex, thus providing an efficient way to modulate APC/C activity and mitotic timing

Sexual Maturation, Attitudes towards Sexual Maturity, and Body Esteem in Elementary-School Children

PURPOSE: The purpose of this study is to evaluate sexual maturation, attitudes toward sexual maturity, and body esteem in the sexual development of Korean elementary-school boys and girls. METHODS: A descriptive cross-sectional study was conducted with 399 fifth and sixth graders (192 boys and 207 girls). The data were analysed with a χ2 test, t-test, and Pearson correlation coefficients. RESULTS: Among the 207 girls, 70.5% had pubic hair growth, 68.1% had breast development, and 56.0% had a menstrual period. In boys, 59.4% of the 192 subjects experienced the development of external genitalia and 52.6% had pubic hair growth. Sexual maturation was related to grade (boys, t=7.07, p=.008; girls, t=12.76, p < .001), age (t=−2.20, p=.030; t=−4.11, p < .001), height (t=−5.16, p < .001; t=−7.52, p < .001), and weight (t=−2.89, p=.004; t=−5.19, p < .001) in both boys and girls. Girls were more likely to have sexual maturity than boys (χ2=22.29, p < .001). Boys showed more positive attitudes toward sexual maturity (t=2.10, p=.036) and higher body esteem (t=2.12, p=.035) than girls. CONCLUSION: This study shows that sexual maturation, attitude toward sexual maturity, and body esteem in sexual development differ between boys and girls. The findings indicate that it is necessary to develop a tailored sex-education program according to the sex of elementary-school children

Directing ricin-based immunotoxins with targeting affibodies and KDEL signal peptide to cancer cells effectively induces apoptosis and tumor suppression

<jats:title>Abstract</jats:title><jats:p>The plant toxin ricin, especially its cytotoxic A chain (RTA), can be genetically engineered with targeting ligands to develop specific anti-cancer recombinant immunotoxins (RITs). Here, we used affibody molecules targeting two cancer biomarkers, the receptors HER2 and EGFR, along with the KDEL signal peptide to construct two cancer-specific ricin-based RITs, HER2Afb-RTA-KDEL and EGFRAfb-RTA-KDEL. The affibodies successfully provided target-specificity and subsequent receptor-mediated endocytosis and the KDEL signal peptide routed the RITs through the retrograde transport pathway, effectively delivering RTA to the cytosol as well as avoiding the alternate recycling pathway that typical cancer cells frequently have. The in vivo efficacy of RITs was enhanced by introducing the albumin binding domain (AlBD) to construct AlBD/HER2Afb/RTA-KDEL. Systemic administration of AlBD-containing RITs to tumor-bearing mice significantly suppressed tumor growth without any noticeable side-effects. Collectively, combining target-selective affibody molecules, a cytotoxic RTA, and an intracellularly designating peptide, we successfully developed cancer-specific and efficacious ricin-based RITs. This approach can be applied to develop novel protein-based ???magic bullets??? to effectively suppress tumors that are resistant to conventional anti-cancer drugs.</jats:p> <jats:p><jats:bold>Graphical Abstract</jats:bold></jats:p&gt

Leucine-Rich Alpha-2-Glycoprotein 1 is a Systemic Biomarker of Early Brain Injury and Delayed Cerebral Ischemia After Subarachnoid Hemorrhage

BACKGROUND: After subarachnoid hemorrhage (SAH), early brain injury (EBI) and delayed cerebral ischemia (DCI) lead to poor outcomes. Discovery of biomarkers indicative of disease severity and predictive of DCI is important. We tested whether leucine-rich alpha-2-glycoprotein 1 (LRG1) is a marker of severity, DCI, and functional outcomes after SAH. METHODS: We performed untargeted proteomics using mass spectrometry in plasma samples collected at \u3c 48 h of SAH in two independent discovery cohorts (n = 27 and n = 45) and identified LRG1 as a biomarker for DCI. To validate our findings, we used enzyme-linked immunosorbent assay and confirmed this finding in an internal validation cohort of plasma from 72 study participants with SAH (22 DCI and 50 non-DCI). Further, we investigated the relationship between LRG1 and markers of EBI, DCI, and poor functional outcomes (quantified by the modified Rankin Scale). We also measured cerebrospinal fluid (CSF) levels of LRG1 and investigated its relationship to EBI, DCI, and clinical outcomes. RESULTS: Untargeted proteomics revealed higher plasma LRG1 levels across EBI severity and DCI in both discovery cohorts. In the validation cohort, the levels of LRG1 were higher in the DCI group compared with the non-DCI group (mean (SD): 95 [44] vs. 72 [38] pg/ml, p \u3c 0.05, Student\u27s t-test) and in study participants who proceeded to have poor functional outcomes (84 [39.3] vs. 72 [43.2] pg/ml, p \u3c 0.05). Elevated plasma LRG1 levels were also associated with markers of EBI. However, CSF levels of LRG1 were not associated with EBI severity or the occurrence of DCI. CONCLUSIONS: Plasma LRG1 is a biomarker for EBI, DCI, and functional outcomes after SAH. Further studies to elucidate the role of LRG1 in the pathophysiology of SAH are needed

A magnetically actuated microrobot for targeted neural cell delivery and selective connection of neural networks

There has been a great deal of interest in the development of technologies for actively manipulating neural networks in vitro, providing natural but simplified environments in a highly reproducible manner in which to study brain function and related diseases. Platforms for these in vitro neural networks require precise and selective neural connections at the target location, with minimal external influences, and measurement of neural activity to determine how neurons communicate. Here, we report a neuron-loaded microrobot for selective connection of neural networks via precise delivery to a gap between two neural clusters by an external magnetic field. In addition, the extracellular action potential was propagated from one cluster to the other through the neurons on the microrobot. The proposed technique shows the potential for use in experiments to understand how neurons communicate in the neural network by actively connecting neural clusters. Copyright © 2020 The Authors, some rights reserved.1

Lactate oxidase/catalase-displaying nanoparticles efficiently consume lactate in the tumor microenvironment to effectively suppress tumor growth

<jats:title>Abstract</jats:title><jats:p>The aggressive proliferation of tumor cells often requires increased glucose uptake and excessive anaerobic glycolysis, leading to the massive production and secretion of lactate to form a unique tumor microenvironment (TME). Therefore, regulating appropriate lactate levels in the TME would be a promising approach to control tumor cell proliferation and immune suppression. To effectively consume lactate in the TME, lactate oxidase (LOX) and catalase (CAT) were displayed onto <jats:italic>Aquifex aeolicus</jats:italic> lumazine synthase protein nanoparticles (AaLS) to form either AaLS/LOX or AaLS/LOX/CAT. These complexes successfully consumed lactate produced by CT26 murine colon carcinoma cells under both normoxic and hypoxic conditions. Specifically, AaLS/LOX generated a large amount of H<jats:sub>2</jats:sub>O<jats:sub>2</jats:sub> with complete lactate consumption to induce drastic necrotic cell death regardless of culture condition. However, AaLS/LOX/CAT generated residual H<jats:sub>2</jats:sub>O<jats:sub>2</jats:sub>, leading to necrotic cell death only under hypoxic condition similar to the TME. While the local administration of AaLS/LOX to the tumor site resulted in mice death, that of AaLS/LOX/CAT significantly suppressed tumor growth without any severe side effects. AaLS/LOX/CAT effectively consumed lactate to produce adequate amounts of H<jats:sub>2</jats:sub>O<jats:sub>2</jats:sub> which sufficiently suppress tumor growth and adequately modulate the TME, transforming environments that are favorable to tumor suppressive neutrophils but adverse to tumor-supportive tumor-associated macrophages. Collectively, these findings showed that the modular functionalization of protein nanoparticles with multiple metabolic enzymes may offer the opportunity to develop new enzyme complex-based therapeutic tools that can modulate the TME by controlling cancer metabolism.</jats:p> <jats:p><jats:bold>Graphical Abstract</jats:bold></jats:p&gt

A Magnetically Controlled Soft Microrobot Steering a Guidewire in a Three-Dimensional Phantom Vascular Network

Magnetically actuated soft robots may improve the treatment of disseminated intravascular coagulation. Significant progress has been made in the development of soft robotic systems that steer catheters. A more challenging task, however, is the development of systems that steer sub-millimeter-diameter guidewires during intravascular treatments; a novel microrobotic approach is required for steering. In this article, we develop a novel, magnetically actuated, soft microrobotic system, increasing the steerability of a conventional guidewire. The soft microrobot is attached to the tip of the guidewire, and it is magnetically steered by changing the direction and intensity of an external magnetic field. The microrobot is fabricated via replica molding and features a soft body made of polydimethylsiloxane, two permanent magnets, and a microspring. We developed a mathematical model mapping deformation of the soft microrobot using a feed-forward approach toward steering. Then, we used the model to steer a guidewire. The angulation of the microrobot can be controlled from 21.1° to 132.7° by using a magnetic field of an intensity of 15 mT. Steerability was confirmed by two-dimensional in vitro tracking. Finally, a guidewire with the soft microrobot was tested by using a three-dimensional (3D) phantom of the coronary artery to verify steerability in 3D space