Single sheet tester having open magnetic path for measurement of magnetostriction of electrical steel sheet

A single sheet tester having closed magnetic path (a closed type of SST) has a problem that measurement accuracy of magnetostriction is considerably affected by electromagnetic force between specimen and yoke. Therefore, an open type has been developed. In order to get uniform flux distribution in a sufficiently large region, a compensating magnetizing winding is installed, and a method of waveform control is investigated, in which applied voltages to main and compensating windings are adjusted individually. The effectiveness of the newly developed open type is demonstrated by measuring magnetostrictions of thin amorphous sheet as well as highly grain-oriented silicon steel sheet</p

Measuring System of Magnetostriction Under AC Excitation Using Optical Methods

A measuring system for magnetostriction of silicon steel sheet using optical methods and a single sheet tester has been developed to establish a standard test method for IEC and JIS. Various factors affecting measurement accuracy and reproducibility of the developed system are examined. Two optical instruments, such as a laser Doppler vibrometer and a heterodyne displacement meter, are compared. 3-D characteristics of magnetostriction under ac excitation in the rolling direction are measured up to 2.0 T </p

Measuring system for magnetostriction of silicon steel sheet under AC excitation using optical methods

A measuring system for magnetostriction of silicon steel sheet using optical methods and a single sheet tester has been developed to establish a standard test method for IEC and JIS. Various factors affecting measurement accuracy and reproducibility of the developed system are examined. Two optical instruments, such as a laser Doppler vibrometer and a heterodyne displacement meter, are compared. 3-D characteristics of magnetostriction under ac excitation in the rolling direction are measured up to 2.0 T </p

The Phagocytic Function of Macrophage-Enforcing Innate Immunity and Tissue Homeostasis

Macrophages are effector cells of the innate immune system that phagocytose bacteria and secrete both pro-inflammatory and antimicrobial mediators. In addition, macrophages play an important role in eliminating diseased and damaged cells through their programmed cell death. Generally, macrophages ingest and degrade dead cells, debris, tumor cells, and foreign materials. They promote homeostasis by responding to internal and external changes within the body, not only as phagocytes, but also through trophic, regulatory, and repair functions. Recent studies demonstrated that macrophages differentiate from hematopoietic stem cell-derived monocytes and embryonic yolk sac macrophages. The latter mainly give rise to tissue macrophages. Macrophages exist in all vertebrate tissues and have dual functions in host protection and tissue injury, which are maintained at a fine balance. Tissue macrophages have heterogeneous phenotypes in different tissue environments. In this review, we focused on the phagocytic function of macrophage-enforcing innate immunity and tissue homeostasis for a better understanding of the role of tissue macrophages in several pathological conditions

Is Osteopontin a Friend or Foe of Cell Apoptosis in Inflammatory Gastrointestinal and Liver Diseases?

Osteopontin (OPN) is involved in a variety of biological processes, including bone remodeling, innate immunity, acute and chronic inflammation, and cancer. The expression of OPN occurs in various tissues and cells, including intestinal epithelial cells and immune cells such as macrophages, dendritic cells, and T lymphocytes. OPN plays an important role in the efficient development of T helper 1 immune responses and cell survival by inhibiting apoptosis. The association of OPN with apoptosis has been investigated. In this review, we described the role of OPN in inflammatory gastrointestinal and liver diseases, focusing on the association of OPN with apoptosis. OPN changes its association with apoptosis depending on the type of disease and the phase of disease activity, acting as a promoter or a suppressor of inflammation and inflammatory carcinogenesis. It is essential that the roles of OPN in those diseases are elucidated, and treatments based on its mechanism are developed

The Etiology of Pancreatic Manifestations in Patients with Inflammatory Bowel Disease

Inflammatory bowel disease (IBD) is an idiopathic chronic and recurrent condition that comprises Crohn&rsquo;s disease and ulcerative colitis. A pancreatic lesion is one of the extraintestinal lesions in patients with IBD. Acute pancreatitis is the representative manifestation, and various causes of pancreatitis have been reported, including those involving adverse effects of drug therapies such as 5-aminosalicylic acid and thiopurines, gall stones, gastrointestinal lesions on the duodenum, iatrogenic harm accompanying endoscopic procedures such as balloon endoscopy, and autoimmunity. Of these potential causes, autoimmune pancreatitis (AIP) is a relatively newly recognized disease and is being increasingly diagnosed in IBD. AIP cases can be divided into type 1 cases involving lymphocytes and IgG4-positive plasma cells, and type 2 cases primarily involving neutrophils; the majority of AIP cases complicating IBD are type 2. The association between IBD and chronic pancreatitis, exocrine pancreatic insufficiency, pancreatic cancer, etc. has also been suggested; however, studies with high-quality level evidence are limited, and much remains unknown. In this review, we provide an overview of the etiology of pancreatic manifestation in patients with IBD

Impact of Autophagy of Innate Immune Cells on Inflammatory Bowel Disease

Autophagy, an intracellular degradation mechanism, has many immunological functions and is a constitutive process necessary for maintaining cellular homeostasis and organ structure. One of the functions of autophagy is to control the innate immune response. Many studies conducted in recent years have revealed the contribution of autophagy to the innate immune response, and relationships between this process and various diseases have been reported. Inflammatory bowel disease is an intractable disorder with unknown etiology; however, immunological abnormalities in the intestines are known to be involved in the pathology of inflammatory bowel disease, as is dysfunction of autophagy. In Crohn&rsquo;s disease, many associations with autophagy-related genes, such as ATG16L1, IRGM, NOD2, and others, have been reported. Abnormalities in the ATG16L1 gene, in particular, have been reported to cause autophagic dysfunction, resulting in enhanced production of inflammatory cytokines by macrophages as well as abnormal function of Paneth cells, which are important in intestinal innate immunity. In this review, we provide an overview of the autophagy mechanism in innate immune cells in inflammatory bowel disease