86 research outputs found

    Relationship between tumor markers CEA and CA15-3 and recurrence breast cancer

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    The value of clinical use of tumor markers CEA and CA15-3 for early detection of recurrent breast cancer still is a controversial. This study was investigated relationship between tumor markers CEA and CA15-3 and recurrence breast cancer. Data regarding 147 women who had breast cancer were entered into the study. Patients were reviewed for 120 months after treatment. Maximum time for relapse was considered a 6 months. Results were showed recurrence cancer in 20% of diagnosed patients. All of them in diagnosis time had a higher of normal tumor markers (CA<3, CA15-3<30).These observations indicated that CA15-3 is a sensitive tumor marker for diagnosis especially for recurrent breast cancer.

    Glial Cell Dysfunction in C9orf72-Related Amyotrophic Lateral Sclerosis and Frontotemporal Dementia

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    Since the discovery of the chromosome 9 open reading frame 72 (C9orf72) repeat expansion mutation in 2011 as the most common genetic abnormality in amyotrophic lateral sclerosis (ALS, also known as Lou Gehrig\u27s disease) and frontotemporal dementia (FTD), progress in understanding the signaling pathways related to this mutation can only be described as intriguing. Two major theories have been suggested-(i) loss of function or haploinsufficiency and (ii) toxic gain of function from either C9orf72 repeat RNA or dipeptide repeat proteins (DPRs) generated from repeat-associated non-ATG (RAN) translation. Each theory has provided various signaling pathways that potentially participate in the disease progression. Dysregulation of the immune system, particularly glial cell dysfunction (mainly microglia and astrocytes), is demonstrated to play a pivotal role in both loss and gain of function theories of C9orf72 pathogenesis. In this review, we discuss the pathogenic roles of glial cells in C9orf72 ALS/FTD as evidenced by pre-clinical and clinical studies showing the presence of gliosis in C9orf72 ALS/FTD, pathologic hallmarks in glial cells, including TAR DNA-binding protein 43 (TDP-43) and p62 aggregates, and toxicity of C9orf72 glial cells. A better understanding of these pathways can provide new insights into the development of therapies targeting glial cell abnormalities in C9orf72 ALS/FTD

    Blood particulate analogue fluids: A review

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    Microfluidics has proven to be an extraordinary working platform to mimic and study blood flow phenomena and the dynamics of components of the human microcirculatory system. However, the use of real blood increases the complexity to perform these kinds of in vitro blood experiments due to diverse problems such as coagulation, sample storage, and handling problems. For this reason, interest in the development of fluids with rheological properties similar to those of real blood has grown over the last years. The inclusion of microparticles in blood analogue fluids is essential to reproduce multiphase effects taking place in a microcirculatory system, such as the cell-free layer (CFL) and Fähraeus–Lindqvist effect. In this review, we summarize the progress made in the last twenty years. Size, shape, mechanical properties, and even biological functionalities of microparticles produced/used to mimic red blood cells (RBCs) are critically exposed and analyzed. The methods developed to fabricate these RBC templates are also shown. The dynamic flow/rheology of blood particulate analogue fluids proposed in the literature (with different particle concentrations, in most of the cases, relatively low) is shown and discussed in-depth. Although there have been many advances, the development of a reliable blood particulate analogue fluid, with around 45% by volume of microparticles, continues to be a big challengeThis research was funded by the Spanish Ministry of Science and Education Grant No. PID2019-108278RB-C32 / AEI / 10.13039/501100011033, and Junta de Extremadura (Spain) Grant Nos. GR18175 and IB18005 (partially financed by FEDER funds). The authors also acknowledge the Fundação para a Ciência e a Tecnologia (FCT) for partially financing the research under the strategic grants UIDB/04077/2020, UIDB/00532/2020, and the project NORTE-01-0145-FEDER030171 (PTDC/EME-SIS/30171/2017) funded by COMPETE2020, NORTE 2020, PORTUGAL 2020, Lisb@2020, and FEDE

    Apoptosis inhibition or inflammation: the role of NAIP protein expression in Hodgkin and non-Hodgkin lymphomas compared to non-neoplastic lymph node

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    <p>Abstract</p> <p>Background</p> <p>Inhibitors of Apoptosis (IAP) family play a critical role in apoptosis and inflammatory response. Neuronal Apoptosis Inhibitory Protein (NAIP), as a member of both IAPs and NLR families (NOD-Like Receptor), is a unique IAP harboring NOD (Nucleotide Oligomerization Domain) and LLR (Leucine Rich Repeat) motifs. Considering these motifs in NAIP, it has been suggested that the main function of NAIP is distinct from other members of IAPs. As a member of NLR, NAIP mediates the assembly of 'Inflammasome' for inflammatory caspase activation. Pathologic expression of NAIP has been reported not only in some infectious and inflammatory diseases but also in some malignancies. However, there is no report to elucidate NAIP expression in lymphomatic malignancies.</p> <p>Methods</p> <p>In this study, we examined <it>NAIP </it>protein expression in 101 Formalin-Fixed Paraffin-Embedded blocks including samples from 39 Hodgkin Lymphoma and 23 Non Hodgkin Lymphoma cases in comparison with 39 control samples (30 normal and 9 Reactive Lymphoid Hyperplasia (RLH) lymph nodes) using semi-quantitative immuno-flourecent Staining.</p> <p>Results</p> <p>NAIP expression was not statistically different in lymphoma samples neither in HL nor in NHL cases comparing to normal samples. However, we evaluated NAIP expression in normal and RLH lymph nodes. Surprisingly, we have found a statistically significant-difference between the NAIP expression in RLH (M.R of NAIP/GAPDH expression = 0.6365 ± 0.017) and normal lymph node samples (M.R of NAIP/GAPDH expression = 0.5882 ± 0.047) (<it>P </it>< 0.01).</p> <p>Conclusions</p> <p>These findings show that the regulation of apoptosis could not be the main function of NAIP in the cell, so the pathologic expression of NAIP is not involved in lymphoma. But, we concluded that the over expression of NAIP has more effective role in the inflammatory response. Also, this study clarifies the NAIP expression level in lymphoma which is required for IAPs profiling in order to be used in potential translational applications of IAPs.</p

    Infestation rates of Bactrocera oleae (Dip.: Tephritidae) in 22 olive cultivars at Tarom Olive Research Station of Zanjan province, Iran

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    Olive fruit fly, Bactrocera oleae (Rossi), is one of the most injurious pests of the olive in Iran. Since its introduction to Iran, in 2004, it has caused considerable economic loss to the domestic olive industry, especially in the years when the climate is favorable to its activity. In this research, we evaluated the infestation rates of olive fruit fly in 22 imported and native olive cultivars at Tarom Olive Research Station, Zanjan, Iran, from 2005 through 2009. The first sampling was started at hard pitting time and continued until harvesting time in which 20-50 fruits were collected from each tree (replicate). Totally 60-150 fruits, from 3 replications, were carefully examined under stereomicroscope in the laboratory. Using the formula of Sqrt (x + 0.5), the data were transformed and subjected to analysis based on Randomized Complete Block Designs usingsoftware SAS, 9.0. The results revealed that among the four recommended cultivars for the region, the cultivar "Arbequina" showed the lowest rate of infestation, while "Konservolia"," Zard", and "Koroneiki" were the most susceptible cultivars due to their higher rates of infestation in 2005 (11.62%, 13.74% and 7.56%), 2007 (3.23%, 1.01% and 1.49%) and 2009 (10.03%, 34.75% and 15.10%), respectively. The cultivars "Lechin de sevilla" and "Manzanilla cacereña" were found to be unfavorable to olive fruit fly

    A decision support system for evaluating effects of feed-in tariff mechanism: dynamic modeling of Malaysia’s electricity generation mix

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    Malaysia has abundant potentials of renewable energy resources mainly because of its rich agriculture that makes high potential in bio-power and its tropical climate, which provides sufficient sunlight for utilization of solar systems. Feed in Tariff mechanism has been applied since 2011 in Malaysia to expand utilization of renewable energy for electricity generation. In this study, a broad range of data is gathered to develop a comprehensive system dynamics model to evaluate the impacts of Feed in Tariff mechanism on the generation mix of Malaysia during a 20-year period between 2011 and 2030. Results demonstrate that although the policy may lead to a satisfactory level of target achievement but the Malaysian government may face an increasing shortage in its RE fund budget starting around 2019 unless it increases its income sources by rising the surcharges on electricity bills or decreases its expenditures by optimizing the amount of FiT payments in different periods. The sensitivity analysis illustrates that the more funding will not lead to a more sustainable generation mix unless it is paid in the right time and in the right direction. Using this model, policymakers can carry out analysis to determine the amount of money that must be collected from the electricity consumers through the surcharges on electricity bills as well as the amount of feed in tariff to be paid for different renewable resources in different periods

    Determination of economic injury level of Lipaphis erysimi (Hemiptera: Aphididae) on canola var. Hayola 401 in Khuzestan

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    Canola, an oil seed with high contents of oil, is a major farming in Khuzestan province, where there is an increase over its cultivation year by year. One of the canola key pests is mustard aphid (Lipaphis erysimi Kalt.) in this province. However, there was not available information on the economic injury level (EIL) of the pest that is much vital for correct decision making on pest control. Therefore, a study on EIL was conducted through complete randomized block design with 5 replications and 11 treatments (0, 5, 10, 15, 20, 25, 30, 35, 40, 45, and 50 aphid per central stem of Hayola 401 variety of canola) inside a netted cage. This research was conducted in Behbahan Agricultural Research Station during 2004-2006. The average of seed yield and also the yeild components was analyzed with Duncanâs multiple range tests. The damage of the aphid was estimated by regression equation. The injury level was estimated by Grain threshold method. The results indicated that EIL was 7.53 and 2.49 cm aphid per central stem of canola in Behbahan region in 2004-2005 and 2005-2006, respectively. Economic threshold (ET) was 5.65 and 1.87 cm2 aphid per central stem of canola

    Glial Cell Dysfunction in <i>C9orf72</i>-Related Amyotrophic Lateral Sclerosis and Frontotemporal Dementia

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    Since the discovery of the chromosome 9 open reading frame 72 (C9orf72) repeat expansion mutation in 2011 as the most common genetic abnormality in amyotrophic lateral sclerosis (ALS, also known as Lou Gehrig’s disease) and frontotemporal dementia (FTD), progress in understanding the signaling pathways related to this mutation can only be described as intriguing. Two major theories have been suggested—(i) loss of function or haploinsufficiency and (ii) toxic gain of function from either C9orf72 repeat RNA or dipeptide repeat proteins (DPRs) generated from repeat-associated non-ATG (RAN) translation. Each theory has provided various signaling pathways that potentially participate in the disease progression. Dysregulation of the immune system, particularly glial cell dysfunction (mainly microglia and astrocytes), is demonstrated to play a pivotal role in both loss and gain of function theories of C9orf72 pathogenesis. In this review, we discuss the pathogenic roles of glial cells in C9orf72 ALS/FTD as evidenced by pre-clinical and clinical studies showing the presence of gliosis in C9orf72 ALS/FTD, pathologic hallmarks in glial cells, including TAR DNA-binding protein 43 (TDP-43) and p62 aggregates, and toxicity of C9orf72 glial cells. A better understanding of these pathways can provide new insights into the development of therapies targeting glial cell abnormalities in C9orf72 ALS/FTD

    Glial Cell Dysfunction in C9orf72-Related Amyotrophic Lateral Sclerosis and Frontotemporal Dementia

    No full text
    Since the discovery of the chromosome 9 open reading frame 72 (C9orf72) repeat expansion mutation in 2011 as the most common genetic abnormality in amyotrophic lateral sclerosis (ALS, also known as Lou Gehrig&rsquo;s disease) and frontotemporal dementia (FTD), progress in understanding the signaling pathways related to this mutation can only be described as intriguing. Two major theories have been suggested&mdash;(i) loss of function or haploinsufficiency and (ii) toxic gain of function from either C9orf72 repeat RNA or dipeptide repeat proteins (DPRs) generated from repeat-associated non-ATG (RAN) translation. Each theory has provided various signaling pathways that potentially participate in the disease progression. Dysregulation of the immune system, particularly glial cell dysfunction (mainly microglia and astrocytes), is demonstrated to play a pivotal role in both loss and gain of function theories of C9orf72 pathogenesis. In this review, we discuss the pathogenic roles of glial cells in C9orf72 ALS/FTD as evidenced by pre-clinical and clinical studies showing the presence of gliosis in C9orf72 ALS/FTD, pathologic hallmarks in glial cells, including TAR DNA-binding protein 43 (TDP-43) and p62 aggregates, and toxicity of C9orf72 glial cells. A better understanding of these pathways can provide new insights into the development of therapies targeting glial cell abnormalities in C9orf72 ALS/FTD

    On pricing and bundling decisions for stackelberg games in parallel channels of substitutable composites

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    The paper describes competition within a supply network with parallel distribution channels. Each supply chain in the network is composed of a manufacturer and a retailer. Manufacturers sell two complementary products to the retailers, who then deliver to the end consumers. All players can bundle or not bundle their products assuming that the retail market presents the products in a mixed bundling setting. The motivation of this study is to mainly analyze the impact of cost reduction via manufacturers, on how the whole supply network will behave. We have modeled and solved partly and fully sequential game structures well known as Bertrand and Stackelberg games, where the preceding movers are considered to have more market power. Mathematical and numerical analyses reveal interesting propositions and managerial insights for decision makers who are practicing cost cutting strategies. The combination of different ordinal structures have led to exact mathematical comparisons among 24 games. Results indicate both manufacturers and retailers are better off with simultaneous pricing games. This promotes the concept of coordination through layer and channels of the network. Cost reduction with compensation increases payoffs when applied by the manufacturer whose complementary products’ manufacturing costs are more distanced. It is also shown that retailers enjoy a retail advantage on one product at its best when playing retailer leading Stackelberg games
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