The NASTRAN Error Correction Information System (ECIS)

A data management procedure, called Error Correction Information System (ECIS), is described. The purpose of this system is to implement the rapid transmittal of error information between the NASTRAN Systems Management Office (NSMO) and the NASTRAN user community. The features of ECIS and its operational status are summarized. The mode of operation for ECIS is compared to the previous error correction procedures. It is shown how the user community can have access to error information much more rapidly when using ECIS. Flow charts and time tables characterize the convenience and time saving features of ECIS

Perfluoro (Imidoylamidine) diamidines

Perfluoroether triazine elastomers having improved properties are prepared from oligomeric imidoylamidines that were in turn, prepared by the process of: (1) reacting a perfluorodinitrile with liquid ammonia to yield a perfluorodiamidine, (2) isolating the perfluorodiamidine, (3) reacting the isolated diamidine with a perfluorodinitrile to yield a perfluoro(imidoylamidine) dinitrile, and then repeating the steps to sequentially grow an oligomer of desired molecular size. The isolated amidine and nitrile intermediates are also disclosed. The elastomers can be fashioned into seals, gaskets, and sealing components and the like

Process for preparing perfluorotriazine elastomers and precursors thereof

Perfluoroether triazine elastomers having improved properties and utility in seals, gaskets, sealing components and the like are prepared from oligomeric imidoylamidines that have, in turn, been prepared by the process of (1) reacting a perfluorodinitrile with liquid ammonia to yield a perfluorodiamidine, (2) isolating the perfluorodiamidine, (3) reacting the isolated diamidine with a perfluorodinitrile to yield a perfluoror(imidoylamidine) dinitrile, and then repeating step (1), (2), and (3) to sequentially grow an oligomer of desired molecular size. The isolated amidine and nitrile intermediates are also described

A clinical update on the significance of the gut microbiota in systemic autoimmunity

Systemic lupus erythematosus (SLE) is a complex autoimmune disease where a loss of tolerance to nuclear antigens leads to inflammation in multiple organ systems. The cause of SLE remains ill defined, although it is known that a complex interplay between genes and environment is necessary for disease development. In recent years, case studies have reported that the incidence of SLE in the USA, for example, has increased by approximately 3 fold. Although the reason for this is likely to be multifactorial, it has been hypothesized that the increasing incidence of autoimmune disease is due to considerable shifts in the bacterial communities resident the gut, collectively known as the gut microbiota, following a change in diet and the widespread introduction of antibiotics. Furthermore, a growing body of evidence suggests that the gut microbiota plays a role in the development of a range of autoimmune diseases including inflammatory bowel disease, multiple sclerosis, type one diabetes and rheumatoid arthritis. In this review, we summarize how advances in DNA-based sequencing technologies have been critical in providing baseline information concerning the gut microbiota in health and how variation amongst individuals in controlled by multiples factors including age, genetics, environment and the diet. We also discuss the importance of the gut microbiota in the development of a healthy immune system and how changes in particular bacterial phyla have been associated with immune abnormalities in animal models of autoimmune disease. Finally, in order to place the data in a clinical context, we highlight recent findings showing that abnormalities in the gut microbiota can be detected in patients with SLE, which provides the rationale for greater investigation into whether microbiota-targeted therapies could be used for the treatment/prevention of disease

The emerging field of regulatory B cell immunometabolism

B cells are well known as critical mediators of humoral immune responses via the production of antibodies. However, numerous studies have also identified populations of B cells that are characterized by their anti-inflammatory properties. These “regulatory B cells” restrain excessive inflammatory responses in a wide range of health conditions. A significant knowledge gap remains concerning the nature of the signals that determine whether a B cell exerts a pro-inflammatory or anti-inflammatory function. In this perspective, we explore the concept that in addition to the cytokine microenvironment, intracellular and extracellular metabolic signals play a pivotal role in controlling the balance between regulatory and antibody-producing B cell subsets. Determining the metabolites and tissue-specific signals that influence B cell fate could establish novel therapeutic targets for the treatment of diseases where abnormal B cell responses contribute to pathogenesis

Regulatory B Cells in Experimental Mouse Models of Arthritis

Regulatory B cells (Breg) have been shown to have a role in the suppression of a wide variety of immune responses, yet they are deficient or defective in autoimmune diseases such as rheumatoid arthritis. For the study of autoimmune inflammation, experimental models of arthritis have acted as a valuable tool in understanding the development of Bregs and their role in maintaining immune homeostasis. In this chapter, we will focus on the study of transitional-2 marginal zone precursor (T2-MZP) Bregs in the context of two experimental arthritis models: antigen-induced arthritis (AIA) and collagen-induced arthritis (CIA). We will specifically focus on how to induce arthritis, as well as on methods for the isolation and functional study of Bregs both in vitro and in vivo

Electrons in the Earth's Outer Radiation Zone

Electrons in the earths outer radiation bel