Singular stress field near the edge of interface of bonded dissimilar materials with an interlayer

AbstractFor bonded dissimilar materials, the free-edge stress singularity usually prevails near the intersection of the free-surface and the interface. When two materials are bonded by using an adhesive, an interlayer develops between the two bonded materials. When a ceramic and a metal are bonded, the residual stress develops because of difference in the coefficient of thermal expansion. An interlayer may be inserted between the two materials to defuse the residual stress. Stress field near the intersection of the interface and free-surface in the presence of the interlayer is then very important for evaluating the strength of bonded dissimilar materials.In this study, stress distributions on the interface of bonded dissimilar materials with an interlayer were calculated by using the boundary element method to investigate the effect of the interlayer on the stress distribution. The relation between the free-edge singular stress fields of bonded dissimilar materials with and without an interlayer was investigated numerically. It was found that the influence of the interlayer on the stress distributions was confined within a small area of the order of interlayer thickness around the intersection of the interface and the free-surface when the interlayer was very thin. The stress distribution near the intersection of the interface and the free-surface was controlled by the free-edge stress singularity of the bonded dissimilar materials without the interlayer. In this case, the interlayer can be called free-edge singularity-controlled interlayer. If a stress distribution on the interface is known for one thickness of an interlayer h, stress distributions on the interface for other values of h can be estimated

Allele Loss in MEN 1-associated Pituitary Tumor

We have examined the allele loss of chromosome 11 in a pituitary tumor from a patient with familial multiple endocrine neoplasia type 1 (MEN 1). The extensive loss of chromosome 11, including loci of D11S149, HRAS1 and F2, was detected by the loss of heterozygosity. All of the lost alleles of these loci were transmitted from the unaffected father and not from an affected mother. This is the first evidence of allele loss of chromosome 11 in a pituitary tumor of MEN 1 and supports the idea that similar allelic deletion of MEN1 locus on chromosome 11 is the common genetic basis for tumorigenesis in the pituitary, endocrine pancreas, and parathyroid gland in MEN 1

Acute Exacerbation of Pulmonary Fibrosis in Syndrome of Combined Pulmonary Fibrosis and Emphysema Following Lung Surgery : A Report of Two Cases

We herein report two cases of an acute exacerbation of pulmonary fibrosis in the syndrome of combined pulmonary fibrosis and emphysema (CPFE) following lung surgery, and also review the relevant literature. One is a 76-year-old man, who had been diagnosed with CPFE and lung cancer and undergone lobectomy. He was admitted to our hospital because of aggravation of dyspnea 50 days after lung surgery. The other is a 69-yearold man who had been diagnosed with pulmonary bulla, pulmonary emphysema and idiopathic interstitial pneumonia at 53 years old and was complicated by lung cancer. He underwent right lower lobectomy and presented with slight fever and desaturation 18 days after lung surgery. In both cases, chest computed tomography showed diffuse bilateral ground-glass opacities superimposed on preceding reticular opacities in the lower lung field. They were diagnosed as acute exacerbation of pulmonary fibrosis in CPFE.A strict followup is required, because the prevalence of lung cancer may be higher, and acute exacerbation may occur following lung surgery in CPFE patients. HRCT plays an important role in evaluating the occurrence of lung cancer at an early stage and for determining whether there is an acute exacerbation of pulmonary fibrosis in CPFE patients.Article信州医学雑誌 60(3): 149-156(2012)journal articl

Loss of Heterozygosity in Thyroid Tumors

We analyzed 53 loci on 21 chromosomes other than chromosome 4 to detect possible loss of heterozygosity in 31 thyroid tumors using polymorphic DNA markers that detect allelic deletions at specific chromosomal loci. Loss of heterozygosity on chromosomes 1, 7 and 12 was detected in one follicular thyroid adenoma, and on chromosome 1 in two medullary thyroid carcinomas. However, no loss of heterozygosity was detected at any of the loci examined in papillary thyroid carcinomas. These results suggest that chromosomal loss detected in thyroid adenoma is one of the signals for risk of premalignant transformation, and that inactivation of unknown genes on chromosome 1p contributes to tumorigenesis of medullary thyroid carcinoma. Some genetic changes other than chromosomal losses may participate in the tumorigenesis of papillary thyroid carcinoma

Large Vasopressin in SIADH

A 76-year-old man with small cell lung cancer associated with the syndrome of inappropriate secretion of ADH (SIADH) visited our hospital. The serum Na level was normal on the first visit, but 2 weeks later it decreased to 114 mEq/L with an extremely high plasma vasopressin (VP) level of 1520 pg/ml. Serum Na was normalized after the reduction of the tumor size by chemotherapy, but the plasma VP level remained between 150 to 600 pg/ml. On gel filtration of plasma VP two peaks of immunoreactive VP were eluted at the positions of a larger molecule than authentic VP and authentic VP, and VP in urine gave only one peak compared to that of authentic VP. The dilution curve of plasma VP was almost parallel and that of urine was completely parallel to the standard curve. These findings suggest that a larger VP with low physiological activity was predominantly secreted in the present patient and manifested relatively mild symptoms despite the extremely high plasma VP level

Frequent p53 Accumulation in the Chronically Sun-Exposed Epidermis and Clonal Expansion of p53 Mutant Cells in the Epidermis Adjacent to Basal Cell Carcinoma

p53 expression was studied immunohistochemically to identify a precursor lesion of basal cell carcinoma (BCC) in the epidermis adjacent to BCC. With two different anti-p53 antibodies of CM1 and DO7, p53 expression was frequently detected in the epidermis adjacent to BCCs arising on the face and in the normal epidermis with usual sun exposure. In the epidermis adjacent to BCC, stained cells were occasionally clustered in a small area, but no cluster was found in the normal epidermis with usual sun exposure. The expression was less frequent in the normal epidermis with rare sun exposure. Ten cases of normal skin with usual sun exposure, showing CM1 staining in the epidermis, were screened for p53 gene mutations with polymerase chain reaction-single- strand conformation polymorphism analysis using DNAs obtained from the epidermis. No mutation was detected in exons 2 to 10 of the p53 gene in these 10 cases. The epidermis flanking three BCCs that was stained with CM1, on the other hand, carried a missense mutation of C to G transversIon at a dipyrimidine site of codon 249. This alteration replaced arginine with threonine. The mutation of codon 249 was not detected in the three BCCs. Our results first suggest that ultraviolet light irradiating the skin in a daily life induces p53 accumulation in the epidermis and secondly that the frequent clonal expansion of p53 mutant cells occurs in the epidermis adjacent to BCCs. This clonal expansion of mutant p53 may provide a molecular basis for high risk of developing subsequent new skin cancers in patients with BCC

Allergin-1 on mast cells suppresses house dust mite-induced airway hyperresponsiveness in mice

Although airway hyperresponsiveness (AHR) is a prominent feature of asthma, how it is regulated remains incompletely understood. Allergin-1, an inhibitory immunoglobulin-like receptor containing an immunoreceptor tyrosine-based inhibitory motif (ITIM), is expressed on human and mouse mast cells (MCs) and inhibits high-affinity receptor for IgE (FcεRI)-mediated signaling. Using MC-deficient KitW-sh/W-sh mice and Mas-TRECK mice, which carries a diphtheria toxin (DT)-induced MC deletion system based on il4 enhancer elements, we demonstrate here that MCs are involved in the induction of house dust mite (HDM)-induced AHR. Further, we show that MCs deficient in Allergin-1 exacerbated HDM-induced AHR, but had no effect on airway inflammation. In vitro analysis demonstrated that Allergin-1 inhibited anti-HDM allergen antibody-dependent HDM allergen-mediated degranulation by MCs. Thus, Allergin-1 on MCs plays an important role in the regulation of HDM-induced AHR

New Sequence Variants in HLA Class II/III Region Associated with Susceptibility to Knee Osteoarthritis Identified by Genome-Wide Association Study

Osteoarthritis (OA) is a common disease that has a definite genetic component. Only a few OA susceptibility genes that have definite functional evidence and replication of association have been reported, however. Through a genome-wide association study and a replication using a total of ∼4,800 Japanese subjects, we identified two single nucleotide polymorphisms (SNPs) (rs7775228 and rs10947262) associated with susceptibility to knee OA. The two SNPs were in a region containing HLA class II/III genes and their association reached genome-wide significance (combined P = 2.43×10−8 for rs7775228 and 6.73×10−8 for rs10947262). Our results suggest that immunologic mechanism is implicated in the etiology of OA

Allergin-1 inhibits TLR2-mediated mast cell activation and suppresses dermatitis

TLR2 recognizes cell wall components of Staphylococcus aureus, which colonizes >90% of atopic eczematous skin lesions. The regulatory mechanisms of TLR2 signaling in the skin remain unclear. Allergin-1, an inhibitory immunoglobulin-like receptor containing an ITIM, is expressed on mast cells (MCs) and inhibits IgE-mediated anaphylaxis in mice. Here, we show that Allergin-1 inhibits TLR2-mediated activation of, and inflammatory cytokine production by, MCs in vitro. Compared with wild-type mice, Allergin-1-deficient mice showed enhanced ear swelling with enhanced collagen deposition and greater Ly6G+ neutrophil recruitment after intra-dermal injection of Pam2CSK4 into pinnae. Using Mas–TRECK mice, which is an MC deletion system based on il4 enhancer elements, we also demonstrated that Allergin-1 on MCs is responsible for the Pam2CSK4-induced ear swelling. These results suggest that Allergin-1 on skin MCs suppresses TLR2-induced dermatitis