Taenia solium neurocysticercosis (NCC) represents one of the major public health problems associated with several neurological manifestations worldwide. We previously identified a recombinant 10-kDa protein of T. solium metacestode (CyDA) specific to active NCC. Immunoblottings with sera from active NCC patients and from animals experimentally infected with larval T. solium (pig), T. saginata (pig), T. asiatica (pig), and T. crassiceps (mouse) strongly recognized CyDA, while sera from patients infected only with adult worms did not. Mapping of antigenic sites using deletion mutants revealed that amino acids (aa) residues 30-34, Asn-Met-Thr-Val-Met (NMTVM), reacted only with sera from active stage T. solium cysticercosis cases. Recognition of CyDA aa 30-34 resided almost exclusively in the IgG4 isotype. Competitive immunoprecipitation with synthetic peptides confirmed the specificity of anti-sera for this penta-peptide. These results demonstrated that aa residues NMTVM in CyDA comprise the core sequence for an active stage NCC-related antigenic determinant. ligand binding protein, HLBP; Cyst fluid, CF; Pooled serum of 10 active NCC patients, serum-pool.
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http://dx.doi.org/10.1016/S0014-4894(02)00002-4 | DOI Listing |
Cancer Lett
December 2024
Division of Collaborative Research and Developments, Exploratory Oncology Research & Clinical Trial Center, National Cancer Center, Kashiwa, Japan; Division of Translational Genomics, Exploratory Oncology Research & Clinical Trial Center, National Cancer Center, Kashiwa, Japan. Electronic address:
KRAS inhibitors sotorasib and adagrasib have been approved for the treatment of KRAS-mutant non-small cell lung cancer (NSCLC). However, the efficacy of single-agent treatments is limited, presumably due to multiple resistance mechanisms. To overcome these therapeutic limitations, combination strategies that potentiate the antitumor efficacy of KRAS inhibitors must be developed.
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School of Psychology, University of Wollongong.
Individuals with borderline personality disorder (BPD) often hold pervasive and negative self-views and experience feelings of low connectedness toward others despite effective treatment. This study aimed to identify neural and affective mechanisms of identity disturbance in BPD that contribute to difficulties in relating to others. Participants diagnosed with BPD ( = 34) and nonclinical controls (NCC; = 35) completed a within-subject social feedback task inside a magnetic resonance imaging scanner.
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December 2024
Division of Nephrology and Hypertension, Department of Medicine, Oregon Health and Science University, Portland, Oregon, USA.
The rare disease Familial Hyperkalemic Hypertension (FHHt) is caused by mutations in the genes encoding Cullin 3 (CUL3), Kelch-Like 3 (KLHL3), and two members of the With-No-Lysine [K] (WNK) kinase family, WNK1 and WNK4. In the kidney, these mutations ultimately cause hyperactivation of NCC along the renal distal convoluted tubule. Hypertension results from increased NaCl retention, and hyperkalemia by impaired K secretion by downstream nephron segments.
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December 2024
Division of Genome Analysis Platform Development, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo, 104-0045, Japan.
The KEAP1-NRF2 system plays a crucial role in responding to oxidative and electrophilic stress. Its dysregulation can cause the overexpression of downstream genes, a known cancer hallmark. Understanding and detecting abnormal KEAP1-NRF2 activity is essential for understanding disease mechanisms and identifying therapeutic targets.
View Article and Find Full Text PDFAnal Chem
December 2024
Key Laboratory for Applied Technology of Sophisticated Analytical Instruments of Shandong Province, Shandong Analysis and Test Center, Qilu University of Technology (Shandong Academy of Sciences), Jinan 250014, China.
Ferroptosis, as an iron-dependent cell death mediated by lipid peroxidation, has sparked great interest in the tumor research community. Targeting ferroptosis has been proven to be a new therapeutic opportunity for inhibiting tumor growth. However, it is challenging to precisely characterize the metabolic pattern of ferroptosis in heterogeneous tumors and further identify ferroptosis-associated metabolic vulnerabilities for tumor treatment.
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