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RESULTS: Results of the immunoassay-based MPs and the cRMPs demonstrated good linear correlations for the CS but some significant sample-specific differences were also observed

Albrektsen Humphries
· 3 min read
RESULTS: Results of the immunoassay-based MPs and the cRMPs demonstrated good linear correlations for the CS but some significant sample-specific differences were also observed

vitamin b5 for hair  of the commutability study show that RMs based on unspiked human serum pools can be commutable with CS, whereas human pools spiked with recombinant apo(a) show different behavior compared to CS. CONCLUSIONS: The results of this study show that unspiked human serum pools are the preferred candidate secondary RMs in the future SI-traceable Ordensklinikum Linz Barmherzige Schwestern, Linz, Austria. Standardization of Serum Apolipoprotein (a) Tests. BACKGROUND: Medical results generated by European CE Marking for In Vitro Diagnostic or in-house tests should be traceable to higher order reference measurement systems (RMS), such as International Federation of Clinical Chemistry and Laboratory Medicine (IFCC)-endorsed reference measurement procedures (RMPs) and reference materials. Currently, serum apolipoprotein (a) [apo(a)] is recognized as a novel risk factor for cardiovascular risk assessment and patient management. The former RMS for serum apo(a) is no longer available; consequently, an International System of Units (SI)-traceable, ideally multiplexed, and sustainable RMS for apo(a) is needed.

METHODS: A mass spectrometry (MS)-based candidate RMP (cRMP) for apo(a) was developed using quantitative bottom-up proteomics targeting 3 proteotypic peptides. The method was provisionally validated according to ISO 15193 using a single human serum based calibrator traceable to the former WHO-IFCC RMS. RESULTS: The quantitation of serum apo(a) was by design independent of its size polymorphism, was linear from 8 to 456 nmol/L, and had a lower limit of quantitation for apo(a) of 8 nmol/L using peptide LFLEPTQADIALLK. Interpeptide agreement showed Pearson Rs of 987 and 984 for peptides GISSTVTGR and TPENYPNAGLTR, and method comparison indicated good correspondence (slopes 977, 033, and 085 for LFLEPTQADIALLK, GISSTVTGR, and TPENYPNAGLTR). Average within-laboratory imprecision of the cRMP was 9%, 9%, and 8% for the 3 peptides. CONCLUSIONS: A robust, antibody-independent, MS-based cRMP was developed as higher order RMP and an essential part of the apo(a) traceability chain and future RMS. The cRMP fulfils predefined analytical performance specifications, making it a promising RMP candidate in an SI-traceable MS-based RMS for apo(a).

AIMS: Further investigation on the mechanism of action of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in NSCLC would shed light on the understanding of TRAIL resistance and provide new clues for the counter-strategy. BACKGROUND: Cellular FLICE-inhibitory protein (c-FLIP) is a critical inhibitor of TRAIL-induced apoptosis. Our previous study suggested that glycogen synthase kinase 3β (GSK3β) positively regulated c-FLIP expression in human lung adenocarcinoma cells. Meanwhile, other studies reported that c-FLIP was degraded by HECT-type E3 ligase ITCH (Itchy E3 Ubiquitin Protein Ligase) via the proteasome pathway. OBJECTIVE: We will explore whether ITCH is involved in the expression regulation of c-FLIP positively controlled by GSK3β during the treatment of TRAIL. METHODS: Human lung adenocarcinoma cells were used to stably overexpress and knockdown GSK3β. Quantitative real-time PCR (qRT-PCR) assay was used to test the expressional level of mRNA of genes.

Western blot analysis was employed to detect the expression of proteins at the protein level. si RNA of ITCH was used to knock down its expression. TRAIL treatment was used to cause apoptosis. RESULTS: In the present study, we have confirmed the ITCH protein degradation of c-FLIP and the downregulation of ITCH expression by GSK3β in lung adenocarcinoma cells. Moreover, ITCH silencing reversed the downregulation of c-FLIP protein caused by GSK3β-knockdown in the cells. Accordingly, TRAIL-induced apoptosis facilitated by GSK3β knockdown was blocked by the combined interference of ITCH. CONCLUSION: These results suggested that GSK3β/ITCH axis regulated the stability of c-FLIP and impacting on TRAIL-induced apoptosis.

Taken together, our study revealed a GSK3β/ITCH/c-FLIP axis that counteracts TRAIL-induced apoptosis Schistosomiasis remains a major neglected tropical disease that afflicts over 200 million people globally.  what is pantothenic acid , the aetiological agent of schistosomiasis, are parasitic flatworms that propagate between molluscan and mammalian hosts. Inside the mammalian host, schistosomes rapidly grow over 100-fold in size and develop into a sexually mature male or female that thrives in the bloodstream for several decades. Recent work has identified schistosome stem cells as the source that drives parasite transmission, reproduction and longevity. Moreover, studies have begun to uncover molecular programmes deployed by stem cells that are essential for tissue development and maintenance, parasite survival and immune evasion. Such programmes are reminiscent of neoblast-driven development and regeneration of planarians, the free-living flatworm relative of schistosomes. Over the last few decades, research in planarians has employed modern functional genomic tools that significantly enhanced our understanding of stem cell-driven animal development and regeneration.

In this review, we take a broad stroke overview of major flatworm organ systems at the cellular and molecular levels.