The Aging Workforce And Their Impact On Workplace Injuries

Workplace safety is critical for any organization. Creating a culture of safe behavior and developing safe surroundings can take a lot of time and effort, so it is important for firms to fully understand their risk exposures and their areas of focus for reducing or eliminating those risks. This analysis focuses on the aging American workforce and the impact on injury frequency rates. The aging workforce has been the focus of many analyses, but this analysis differs in that it focuses solely on their effects, if any, on injuries reported to the Occupation Safety and Health Association (OSHA). Over time, individuals have continued to live longer and longer. Workplace safety must keep up with the aging workforce. Age 55 was once considered retirement age, but with the longevity of life, employees are continuing to work well into their sixties and seventies while still allowing themselves ample time for retirement. The study utilizes age 55 as the comparison cutoff point, allowing for a significant amount of the workforce headcount to be examined in the analysis and accounting for the deterioration of physical capabilities as individuals age. The results ultimately show that workers 55 and over are, in fact, more likely to be injured in the workplace than their younger counterparts. This information can prove valuable to firms looking to implement safety initiatives in the workplace and allow them to better understand the scope of employee impact and focus of attention

Design of the Bastei OS Architecture

In the software world, high complexity of a problem solution comes along with a high risk for bugs and vulnerabilities. This correlation is particular perturbing for todays commodity operating systems with their tremendous complexity. The numerous approaches to increase the user’s confidence in the correct functioning of software comprise exhaustive tests, code auditing, static code analysis, and formal verification. Such quality-assurance measures are either rather shallow or they scale badly with increasing complexity. The operating-system design presented in this paper focuses on the root of the problem by providing means to minimize the underlying system complexity for each security-sensitive application individually. On the other hand, we want to enable multiple applications to execute on the system at the same time whereas each application may have different functional requirements from the operating system. Todays operating systems provide a functional superset of the requirements of all applications and thus, violate the principle of minimalism for each single application. We resolve the conflict between the principle of minimalism and the versatility of the operating system by decomposing the operating system into small components and by providing a way to execute those components isolated and independent from each other. Components can be device drivers, protocol stacks such as file systems and network stacks, native applications, and containers for executing legacy software. Each application depends only on the functionality of a bounded set of components that we call application-specific trusted computing base (TCB). If the TCBs of two applications are executed completely isolated and independent from each other, we consider both TCBs as minimal. In practice however, we want to share physical resources between multiple applications without sacrificing their independence. Therefore, the operating-system design has to enable the assignment of physical resources to each application and its TCB to maintain independence from other applications. Furthermore, rather than living in complete isolation, components require to communicate with each other to cooperate. The operating-system design must enable components to create other components and get them to know each other while maintaining isolation from uninvolved parts of the system. First, we narrow our goals and pose our mayor challenges in Section 1. Section 2 introduces our fundamental concepts and protocols that apply to each component in the system. In Section 3, we present the one component that is mandatory part of each TCB, enables the bootstrapping of the system, and provides abstractions for the lowest-level resources. We exercise the composition of the presented mechanisms by the means of process creation in Section 4

Store-operated Ca2+ entry in primary murine lung fibroblasts is independent of classical transient receptor potential (TRPC) channels and contributes to cell migration

Stromal interaction molecules (STIM1, 2) are acting as sensors for Ca2+ in intracellular stores and activate Orai channels at the plasma membrane for store-operated Ca2+ entry (SOCE), while classical transient receptor potential (TRPC) channel mediate receptor-operated Ca2+ entry (ROCE). Several reports, however, indicate a role for TRPC in SOCE in certain cell types. Here, we analyzed Ca2+ influx and cell function in TRPC1/6-deficient (TRPC1/6(-/-)) and STIM1/2- deficient (STIM1/2(Delta pmLF)) primary murine lung fibroblasts (pmLF). As expected, SOCE was decreased in STIM1/2- deficient pmLF and ROCE was decreased in TRPC1/6(-/-) pmLF compared to control cells. By contrast, SOCE was not significantly different in TRPC1/6(-/-) pmLF and ROCE was similar in STIM1/2-deficient pmLF compared to Wt cells. Most interestingly, cell proliferation, migration and nuclear localization of nuclear factor of activated T-cells (NFATc1 and c3) were decreased after ablation of STIM1/2 proteins in pmLF. In conclusion, TRPC1/6 channels are not involved in SOCE and STIM1/2 deficiency resulted in decreased cell proliferation and migration in pmLF

A tensor-valued integral theorem for the gradient of a vector field, with a fluid dynamical application

The familiar divergence and Kelvin--Stokes theorem are generalized by a tensor-valued identity that relates the volume integral of the gradient of a vector field to the integral over the bounding surface of the outer product of the vector field with the exterior normal. The importance of this long-established yet little-known result is discussed. In flat two-dimensional space, it reduces to a relationship between an integral over an area and that over its bounding curve, combining the divergence and Kelvin--Stokes theorems together with two related theorems involving the strain, as is shown through a decomposition using a suitable tensor basis. A fluid dynamical application to oceanic observations along the trajectory of a moving platform is given, and potential extensions to geometrically complex surfaces are discussed.Comment: 20 page

A severe defect in CRAC Ca2+ channel activation and altered K+ channel gating in T cells from immunodeficient patients

Engagement of the TCR triggers sustained Ca2+ entry through Ca2+ release-activated Ca2+ (CRAC) channels, which helps drive gene expression underlying the T cell response to pathogens. The identity and activation mechanism of CRAC channels at a molecular level are unknown. We have analyzed ion channel expression and function in T cells from SCID patients which display 1–2% of the normal level of Ca2+ influx and severely impaired T cell activation. The lack of Ca2+ influx is not due to deficient regulation of Ca2+ stores or expression of several genes implicated in controlling Ca2+ entry in lymphocytes (kcna3/Kv1.3, kcnn4/IKCa1, trpc1, trpc3, trpv6, stim1). Instead, electrophysiologic measurements show that the influx defect is due to a nearly complete absence of functional CRAC channels. The lack of CRAC channel activity is correlated with diminished voltage sensitivity and slowed activation kinetics of the voltage-dependent Kv1.3 channel. These results demonstrate that CRAC channels provide the major, if not sole, pathway for Ca2+ entry activated by the TCR in human T cells. They also offer evidence for a functional link between CRAC and Kv1.3 channels, and establish a model system for molecular genetic studies of the CRAC channel

Calpain 2 Controls Turnover of LFA-1 Adhesions on Migrating T Lymphocytes

The immune cells named T lymphocytes circulate around the body fulfilling their role in immunosurveillance by monitoring the tissues for injury or infection. To migrate from the blood into the tissues, they make use of the integrin LFA-1 which is exclusively expressed by immune cells. These highly motile cells attach and migrate on substrates expressing the LFA-1 ligand ICAM-1. The molecular events signaling LFA-1 activation and adhesion are now reasonably well identified, but the process of detaching LFA-1 adhesions is less understood. The cysteine protease calpain is involved in turnover of integrin-mediated adhesions in less motile cell types. In this study we have explored the involvement of calpain in turnover of LFA-1-mediated adhesions of T lymphocytes. Using live cell imaging and immunohistochemistry, we demonstrate that turnover of adhesions depends on the Ca2+-dependent enzyme, calpain 2. Inhibition of calpain activity by means of siRNA silencing or pharmacological inhibition results in inefficient disassembly of LFA-1 adhesions causing T lymphocyte elongation and shedding of LFA-1 clusters behind the migrating T lymphocytes. We show that calpain 2 is distributed throughout the T lymphocyte, but is most active at the trailing edge as detected by expression of its fluorescent substrate CMAC,t-BOC-Leu-Met. Extracellular Ca2+ entry is essential for the activity of calpain 2 that is constantly maintained as the T lymphocytes migrate. Use of T cells from a patient with mutation in ORAI1 revealed that the major calcium-release-activated-calcium channel is not the ion channel delivering the Ca2+. We propose a model whereby Ca2+ influx, potentially through stretch activated channels, is sufficient to activate calpain 2 at the trailing edge of a migrating T cell and this activity is essential for the turnover of LFA-1 adhesions