Masonry compressive strength prediction using artificial neural networks

The masonry is not only included among the oldest building materials, but it is also the most widely used material due to its simple construction and low cost compared to the other modern building materials. Nevertheless, there is not yet a robust quantitative method, available in the literature, which can reliably predict its strength, based on the geometrical and mechanical characteristics of its components. This limitation is due to the highly nonlinear relation between the compressive strength of masonry and the geometrical and mechanical properties of the components of the masonry. In this paper, the application of artificial neural networks for predicting the compressive strength of masonry has been investigated. Specifically, back-propagation neural network models have been used for predicting the compressive strength of masonry prism based on experimental data available in the literature. The comparison of the derived results with the experimental findings demonstrates the ability of artificial neural networks to approximate the compressive strength of masonry walls in a reliable and robust manner.- (undefined

Nuclear Targeting of IGF-1 Receptor in Orbital Fibroblasts from Graves' Disease: Apparent Role of ADAM17

Insulin-like growth factor-1 receptor (IGF-1R) comprises two subunits, including a ligand binding domain on extra- cellular IGF-1Rα and a tyrosine phosphorylation site located on IGF-1Rβ. IGF-1R is over-expressed by orbital fibroblasts in the autoimmune syndrome, Graves' disease (GD). When activated by IGF-1 or GD-derived IgG (GD-IgG), these fibroblasts produce RANTES and IL-16, while those from healthy donors do not. We now report that IGF-1 and GD-IgG provoke IGF-1R accumulation in the cell nucleus of GD fibroblasts where it co-localizes with chromatin. Nuclear IGF-1R is detected with anti-IGF-1Rα-specific mAb and migrates to approximately 110 kDa, consistent with its identity as an IGF-1R fragment. Nuclear IGF-1R migrating as a 200 kDa protein and consistent with an intact receptor was undetectable when probed with either anti-IGF-1Rα or anti-IGF-1Rβ mAbs. Nuclear redistribution of IGF-1R is absent in control orbital fibroblasts. In GD fibroblasts, it can be abolished by an IGF-1R-blocking mAb, 1H7 and by physiological concentrations of glucocorticoids. When cell-surface IGF-1R is cross-linked with 125I IGF-1, 125I-IGF-1/IGF-1R complexes accumulate in the nuclei of GD fibroblasts. This requires active ADAM17, a membrane associated metalloproteinase, and the phosphorylation of IGF-1R. In contrast, virally encoded IGF-1Rα/GFP fusion protein localizes equivalently in nuclei in both control and GD fibroblasts. This result suggests that generation of IGF-1R fragments may limit the accumulation of nuclear IGF-1R. We thus identify a heretofore-unrecognized behavior of IGF-1R that appears limited to GD-derived fibroblasts. Nuclear IGF-1R may play a role in disease pathogenesis

Skin Metastasis from an Occult Esophageal Adenocarcinoma

Metastases to the skin from carcinoma arising in other organs are uncommon, yet they may be the first presentation of neoplastic disease. They usually originate from primary tumours in the breast, lung or colon. Skin metastases from esophageal adenocarcinoma are extremely rare. A unique case of an otherwise healthy patient who presented with a small, painless, mobile, clinically localized facial skin nodule is reported. A biopsy revealed metastatic adenocarcinoma, and subsequent investigations detected the primary tumour in the esophagus, despite no symptoms

Visfatin/NAMPT/PBCEF and Cytokine Concentration in Multiple Sclerosis Patients Compared to Healthy Subjects

The aim of the study is to measure IL-1 β, TNF-α, hs-CRP levels and Nampt/visfatin/PBCEF concentrations in patients with multiple sclerosis and to compare them with those of healthy control subjects. In a case-control study a total number of 192 people were recruited. Ninety-six of them were suffering from multiple sclerosis, age 34.80±8.75 years (mean±SD), who were referred form the Iranian Multiple Sclerosis Society. They included relapsing remitting (82 subjects) and both primary and secondary progressive (14 subjects) types of MS. The diagnosis was made according to the diagnostic criteria by a neurology consultant. Ninety-six healthy individuals were recruited from the Iranian Multicenter Osteoporosis Study (IMOS) as the control group. Following an overnight fasting, peripheral blood was taken from all subjects and centrifuged in order to separate serum for measurement of serum visfatin, Interleukin-1beta (IL-1β), TNF-α, and hs-CRP concentrations. Fat tissue mass was measured using DXA. Levels of visfatin, TNF-α and hs-CRP were significantly higher in MS patients. Besides, significant correlation was found between visfatin levels and those of TNF-α, IL-1β, hs-CRP in MS patients. Regarding the control group, significant correlation was found between visfatin levels and levels of TNF-α. However, we did not find any significant correlation between fat tissue mass and visfatin, TNF-α, IL-1β or hs-CRP levels in the MS group. However, there was a significant correlation between fat tissue mass and TNF-α level in the study population. Our findings demonstrated that proinflammatory factor levels were, although not significantly, higher in RRMS patients compared to PPMS and SPMS patients. The results suggest that levels of visfatin and pro-inflammatory cytokines are higher in MS patients compared to healthy subjects. Their higher levels may be, in part, attributable to the MS phenotypes independent of fat mass in patients. We believe that these results may shed some light on a potentially novel source of visfatin as well as explaining its regulating role in the inflammation process

Comparison of the Bone Turn-over Markers in Patients with Multiple Sclerosis and Healthy Control Subjects

One of the major concerns for patients with multiple sclerosis (MS) is developing osteoporosis, especially when corticosteroid treatment is used. The aim of the present study is to compare the bone turnover markers in patients with multiple sclerosis and healthy control subjects. A total of 176 subjects were enrolled in this case-control. Ninety-one MS patients with mean age of 35.26 ± 8.76 yrs were randomly selected from the Committee on Multiple Sclerosis Registry. The control group was composed of 85 healthy subjects who were recruited from the Iranian Multicenter Osteoporosis Study (IMOS). Fasting serum levels of parathyroid hormone (PTH), 25 (OH) D3, osteocalcin and cross laps were measured in two groups. Hip and spine BMD were measured using DXA. Our findings showed significant differences in hip BMD and its T-score and Z-score values between MS patients and the control group. Osteoporosis prevalence at hip area of the MS patients was almost 5 times higher than the control group [OR=4.66, (95% CI 0.97 to 22.27), RR=4.29, (95% CI 0.95 to l9.32), p value=0.03]. No significant difference was found in BMD L2-L4, BMD T-score and BMD Z-score of lumbar area between two groups. The PTH and cross laps serum concentrations in MS patients were significantly higher than the control group. We did not find significant difference in serum osteocalcin level between the two groups. We concluded that in our study the serum levels of bone resorbtion markers in MS patients were significantly higher than the healthy control group. This may explain, at least in part, the elevated susceptibility of MS patients for developing osteoporosis

Hepatitis C virus alternative reading frame protein (ARFP): Production, features, and pathogenesis

Earlier observation suggests that hepatitis C virus (HCV) is a single-stranded RNA virus which encodes at least 10 viral proteins. F protein is a novel protein which has been discovered recently. These studies suggest three mechanisms for the production of this protein concerning ribosomal frameshift at codon 10, initial translation at codons 26 and 85 or 87. In this study, the association between protein F and chronicity of hepatocellular carcinoma (HCC) has been reviewed. Evidence suggests that humoral immune system can recognize this protein and produce antibodies against it. By detecting antibodies in infected people, investigators found that F protein might have a role in HCV infection causing chronic cirrhosis and HCC as higher prevalence was found in patients with mentioned complications. The increment of CD4+, CD25+, and FoxP3+ T cells, along with CD8+ T cells with low expression of granzyme B, also leads to weaker responses of the immune system which helps the infection to become chronic. Moreover, it contributes to the survival of the virus in the body through affecting the production of interferon. F protein also might play roles in the disease development, resulting in HCC. The existence of F protein affects cellular pathways through upregulating p53, c-myc, cyclin D1, and phosphorylating Rb. This review will summarize these effects on immune system and related mechanisms in cellular pathways. © 2020 Wiley Periodicals LL