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Filename: drivers/Session_files_driver.php
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File: /var/www/html/index.php
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Function: require_once
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Filename: Session/Session.php
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File: /var/www/html/index.php
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Function: require_once
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Message: Undefined array key "choices"
Filename: controllers/Detail.php
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Line: 249
Function: _error_handler
File: /var/www/html/index.php
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Function: require_once
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Filename: controllers/Detail.php
Line Number: 249
Backtrace:
File: /var/www/html/application/controllers/Detail.php
Line: 249
Function: _error_handler
File: /var/www/html/index.php
Line: 316
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Message: Trying to access array offset on value of type null
Filename: controllers/Detail.php
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Backtrace:
File: /var/www/html/application/controllers/Detail.php
Line: 249
Function: _error_handler
File: /var/www/html/index.php
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Message: Trying to access array offset on value of type null
Filename: controllers/Detail.php
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Backtrace:
File: /var/www/html/application/controllers/Detail.php
Line: 249
Function: _error_handler
File: /var/www/html/index.php
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Filename: models/Detail_model.php
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File: /var/www/html/application/models/Detail_model.php
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Function: strpos
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Function: insertAPISummary
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Filename: helpers/my_audit_helper.php
Line Number: 8919
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File: /var/www/html/application/helpers/my_audit_helper.php
Line: 8919
Function: str_replace
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Function: formatAIDetailSummary
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Filename: controllers/Detail.php
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Line: 256
Function: _error_handler
File: /var/www/html/index.php
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Filename: controllers/Detail.php
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File: /var/www/html/application/controllers/Detail.php
Line: 256
Function: _error_handler
File: /var/www/html/index.php
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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File: /var/www/html/index.php
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Function: _error_handler
File: /var/www/html/index.php
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Filename: controllers/Detail.php
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File: /var/www/html/application/controllers/Detail.php
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Function: _error_handler
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Message: Trying to access array offset on value of type null
Filename: controllers/Detail.php
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File: /var/www/html/application/controllers/Detail.php
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Fyn kinase phosphorylates tau and exacerbates amyloid beta (Aβ)-mediated synaptic dysfunction. However, Fyn also increases the nonpathological cleavage of amyloid precursor protein (APP), suggesting opposing roles for Fyn in the pathogenesis of Alzheimer's disease (AD). To determine the effect of Fyn on both Aβ and tau pathologies, we crossed homozygous Alzheimer's disease triple transgenic (3×Tg) mice harboring mutations in amyloid precursor protein, presenilin-1, and tau with wild-type or Fyn knockout mice to generate Fyn(+/+)3×Tg(+/-) or Fyn(+/-)3×Tg(+/-) mice. We found that Fyn(+/-)3×Tg(+/-) mice had increased soluble and intracellular Aβ, and these changes were accompanied by impaired performance on the Morris water maze at 18 months. Fyn(+/-)3×Tg(+/-) mice had decreased phosphorylated tau at 15-18 months (as did Fyn knockout mice), but Fyn(+/-)3×Tg(+/-) mice had increased phosphorylated tau by 24 months. In addition, we observed that Fyn(+/-)3×Tg(+/-) males were delayed in developing Aβ pathology compared with females, and displayed better spatial learning performance at 18 months. Overall, these findings suggest that loss of Fyn at early stages of disease increases soluble Aβ accumulation and worsens spatial learning in the absence of changes in tau phosphorylation.
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http://dx.doi.org/10.1016/j.neurobiolaging.2011.05.014 | DOI Listing |
Parasit Vectors
December 2024
INSERM UMR-S-MD 1197, Ministère des Armées et Université Paris Saclay, Villejuif, France.
Background: Leishmania is the causal parasite of leishmaniasis, a neglected tropical disease affecting millions of individuals worldwide, and its dissemination is linked to climate change. Despite the complexity and effectiveness of the immune response, the parasite has developed many strategies to evade it and take control of the host cell to replicate. These evasion strategies start at early stages of infection by hijacking immune receptors to mitigate the cellular response.
View Article and Find Full Text PDFBiochem Pharmacol
December 2024
Department of Pharmacology, School of Medicine, Daegu Catholic University, 33 Duryugongwon-ro 17-gil, Nam-gu, Daegu 42472, Republic of Korea. Electronic address:
Isobavachin, isolated from Psoralea corylifolia L. exhibits therapeutic potential for osteoporosis or skin disease. Here, we evaluated the pharmacological effects of isobavachin on IgE-dependent inflammatory allergic reactions, as well as the underlying mechanisms, in bone marrow-derived mast cells and a mouse model of passive cutaneous anaphylaxis (PCA).
View Article and Find Full Text PDFbioRxiv
November 2024
Section of Nephrology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA.
Common intronic enhancer SNPs in Shroom3 associate with CKD in GWAS, although there is paucity of detailed mechanism. Previously, we reported a role for Shroom3 in mediating crosstalk between TGFβ1- & Wnt/Ctnnb1 pathways promoting renal fibrosis (TIF). However, beneficial roles for Shroom3 in proteinuria have also been reported suggesting pleiotropic effects.
View Article and Find Full Text PDFInt J Mol Sci
November 2024
Department of Immunology, College of Medicine, Konkuk University, Chungju 27478, Republic of Korea.
Although antimicrobial peptides (AMPs) exhibit a range of biological functions, reports on AMPs with therapeutic effects in allergic disorders are limited. In this study, we investigated the anti-allergic effects of Pro10-1D, a 10-meric AMP derived from insect defensin protaetiamycine. Our findings demonstrate that Pro10-1D effectively inhibits antigen-induced degranulation of mast cells (MCs) with IC values of approximately 11.
View Article and Find Full Text PDFJ Gene Med
November 2024
Department of Orthopedics, Changzheng Hospital, Second Military Medical University (Naval Medical University), Shanghai, China.
Osteoporosis manifests through adipocyte accrual and osteoblast diminution within bone marrow. However, the precise mechanisms driving the shift from osteogenesis to adipogenesis in bone marrow mesenchymal stem cells (BMSCs) remain largely undefined. In this study, we harnessed the power of bioinformatic tools to analyze gene expression patterns of BMSCs during adipogenic differentiation and osteoporosis using the data from Gene Expression Omnibus (GEO) repositories (GSE113253 and GSE35956), complemented by in vitro and in vivo experiments to validate the findings.
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