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Neonatal form of biotin-thiamine-responsive basal ganglia disease. Clues to diagnosis.

Değerliyurt A, Gündüz M, Ceylaner S, Ünal Ö, Ünal S. Neonatal form of biotin-thiamine-responsive basal ganglia disease. Clues to diagnosis. Turk J Pediatr 2019; 61: 261-266. Biotin-thiamine-responsive basal ganglia disease is characterized by seizures, dystonia and encephalopathy attacks, with an acute-subacute onset in childhood. It causes cerebral damage especially with caudate head and putamen involvement and may lead to severe sequelae and even death if left untreated. We report a patient with the neonatal form of biotin-thiamine-responsive basal ganglia disease who presented with encephalopathy and lactic acidosis in the neonatal period together with the diagnostic magnetic resonance imaging (MRI) clues. MRI in the neonatal period revealed bilateral involvement of the putamen, thalamus, and perirolandic cortical regions. However, MRI obtained at 32 months revealed involvement of the caudate nuclei in addition to the putamen and thalami. The neuroimaging findings of our patient and relevant literature indicate that patients with biotin-thiamine-responsive basal ganglia disease who are symptomatic in the neonatal period have putamen, thalami, and perirolandic cortical involvement. However, these patients do not have caudate involvement, unlike the patients who present in childhood.

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Hearing loss through apoptosis of the spiral ganglion neurons in apolipoprotein E knockout mice fed with a western diet.

Age-related hearing loss (ARHL) is a neurodegenerative disease associated with an aged population. ARHL is influenced by biological factors such as aging, sex difference, and atherosclerosis. The mechanisms of ARHL caused by atherosclerosis have not been previously determined in apolipoprotein E knockout (ApoE KO) male mice. To investigate the onset and cause of the hearing loss, ApoE KO male mice were treated with a western diet (ApoE KO-WD) for 16 weeks. The lipid profile, atherosclerotic plaques throughout the aorta, and auditory brainstem response (ABR) thresholds were measured in the ApoE KO-WD male mice. The expression of S100 calcium-binding protein B (S100B), a neuronal damage biomarker, was also observed. Reactive oxygen species (ROS) and apoptosis rates were detected in the cochlea of the ApoE KO male mice. Atherosclerotic plaques on the aorta and ABR thresholds were significantly increased in the ApoE KO-WD male mice at 24 weeks of age. ABR thresholds had a statistically significant positive correlation with the area of atherosclerotic plaques (r = 0.783, p = 0.013) in male mice at 24 weeks of age. S100B protein expression and the dihydroethidium (DHE) reaction to ROS in the cochlear spiral ganglion neurons (SGNs) were significantly increased in the ApoE KO and ApoE KO-WD male mice. Cells positive for active caspase-3 and terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) in the SGNs were significantly increased in ApoE KO-WD male mice indicating an increased rate of cellular apoptosis. In conclusion, ROS in the SGNs were activated by increased S100B expression in ApoE KO-WD male mice, and this resulted in an increased apoptosis rate. Thus, hearing loss began at 16 weeks in ApoE KO-WD male mice. Our results suggest that the ApoE KO-WD male mice are a suitable animal model for studying ARHL associated with exacerbated atherosclerosis.

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Computational and functional analyses of T2D GWAS SNPs for transcription factor binding.

Genome-wide association studies (GWASs) have successfully identified numerous non-coding genetic variants for type 2 diabetes (T2D), but the functional roles underlying these non-coding variants remain largely unknown. The effects of T2D GWAS lead SNPs on transcriptional factors binding motifs were firstly analyzed via JASPAR, followed by functional validations including dual-luciferase reporter assays, biotin-based DNA pull-down assays, real-time quantitative PCR, and western blotting. The results showed that GWAS SNP rs4430796 conferred T allele specific transcriptional enhancer activity via a PAX6 binding element, and upregulated the expression of HNF1B. GWAS SNP rs4607103 showed a bidirectional modulation of ADAMTS9-AS2 and ADAMTS9 by TCF7L2 in a T allele-specific manner. GWAS SNP rs849135 conferred C allele-specific bidirectional transcriptional enhancer activity via a CREB1 binding element. Our findings have uncovered the functional mechanisms of three T2D GWAS SNPs via affecting the binding of transcription factors, providing new insights into the genetics and molecular pathogenesis of T2D.

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Interference From High-Dose Biotin Intake in Immunoassays for Potentially Time-Critical Analytes by Roche: Evaluation of a Countermeasure for Worst-Case Scenarios.

Immunoassays using the interaction between streptavidin and biotin are used for clinical chemical analytes on platforms by many different manufacturers. The design can be susceptible to interference from high-dose biotin intake in patients, which remains an often-overlooked confounder despite recently increased awareness.

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Versatile 3' Functionalization of CRISPR Single Guide RNA.

Specific applications of CRISPR/Cas genome editing systems benefit from chemical modifications of the sgRNA. Here we describe a versatile and efficient strategy for functionalization of the 3' end of a sgRNA. An exemplary collection of six chemically modified sgRNAs was prepared containing crosslinkers, a fluorophore and biotin. Modification of the sgRNA 3' end was broadly tolerated by S. pyogenes Cas9 in an in vitro DNA cleavage assay. The 3'-biotinylated sgRNA was used as an affinity reagent to identify IGF2BP1, YB1 and hnRNP K as sgRNA-binding proteins present in HEK293T cells. Overall, the modification strategy presented here has the potential to expand on current applications of CRISPR/Cas systems.

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Signature Fragment Ions of Biotinylated Peptides.

The use of biotin or biotin-containing reagents is an essential component of many protein purification and labeling technologies. Owing to its small size and high affinity to the avidin family of proteins, biotin is a versatile molecular handle that permits both enrichment and purity that is not easily achieved by other reagents. Traditionally, the use of biotinylation to enrich for proteins has not required the detection of the site of biotinylation. However, newer technologies for discovery of protein-protein interactions, such as APEX and BioID, as well as some of the click chemistry-based labeling approaches have underscored the importance of determining the exact residue that is modified by biotin. Anti-biotin antibody-based enrichment of biotinylated peptides (e.g., BioSITe) coupled to LC-MS/MS permit large-scale detection and localization of sites of biotinylation. As with any chemical modification of peptides, understanding the fragmentation patterns that result from biotin modification is essential to improving its detection by LC-MS/MS. Tandem mass spectra of biotinylated peptides has not yet been studied systematically. Here, we describe the various signature fragment ions generated with collision-induced dissociation of biotinylated peptides. We focused on biotin adducts attached to peptides generated by BioID and APEX experiments, including biotin, isotopically heavy biotin, and biotin-XX-phenol, a nonpermeable variant of biotin-phenol. We also highlight how the detection of biotinylated peptides in high-throughput studies poses certain computational challenges for accurate quantitation which need to be addressed. Our findings about signature fragment ions of biotinylated peptides should be helpful in the confirmation of biotinylation sites.

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Immobilization of Enzymes on Magnetic Beads Through Affinity Interactions.

The development of enzyme immobilization techniques that will not affect catalytic activity and conformation is an important research task. Affinity tags that are present or added at a specific position far from the active site in the structure of the native enzyme could be used to create strong affinity bonds between the protein structure and a surface functionalized with the complementary affinity ligand. These immobilization techniques are based on affinity interactions between biotin and (strept)avidin molecules, lectins and sugars, or metal chelate and histidine tag.Recent developments involve immobilization of tagged enzymes onto magnetic nanoparticles. These supports can improve the performance of immobilized biomolecules in analytical assay because magnetic beads provide a relative large numbers of binding sites for biochemical reactions resulting in faster assay kinetics.This chapter describes immobilization procedures of tagged enzymes onto various magnetic beads.

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Metformin and rapamycin protect cells from vital dye-induced damage in retinal pigment epithelial cells and in vivo.

To evaluate the effect of autophagy inducers on damage caused by vital dye in adult human RPE (ARPE) cells and in a rat model.

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BPTF cooperates with p50 NF-κB to promote COX-2 expression and tumor cell growth in lung cancer.

Cyclooxygenase-2 (COX-2) is overexpressed in most human cancers, but its precise regulatory mechanism in cancer cells remains unclear. The aims of this study are to discover and identify the new regulatory factors which bind to the COX-2 promoter and regulate COX-2 expression and cancer cell growth, and to elucidate the mechanisms of action of these factors in lung cancer. In this study, the COX-2 promoter-binding protein BPTF (bromodomain PHD finger transcription factor) was detected, identified and verified by biotin-streptavidin-agarose pulldown, mass spectrum analysis and chromatin immunoprecipitation (ChIP) in lung cancer cells, respectively. The expressions of COX-2 and BPTF in lung cancer cell lines, mouse tumor tissues and human clinical samples were detected by RT-PCR, Western blot and immunohistochemistry assays. The interaction of BPTF with NF-kB was analyzed by immunoprecipitation and confocal immunofluorescence assays. We discovered and identified BPTF as a new COX-2 promoter-binding protein in human lung cancer cells. Knockdown of BPTF inhibited COX-2 promoter activity and COX-2 expression in lung cancer cells in vitro and in vivo. We also found that BPTF functioned as a transcriptional regulator through its interaction with the p50 subunit of NF-kB. Knockdown of BPTF abrogated the binding of p50 to the COX-2 promoter, while the inhibition of p50 activity abolished the decreased trend of COX-2 expression and lung cancer cell proliferation caused by BPTF silencing. Moreover, we showed that the expressions of BPTF and COX-2 in tumor tissues of lung cancer patients were positively correlated, and high co-expression of BPTF and COX-2 predicted poor prognosis in lung cancer patients. Collectively, our results indicated that BPTF cooperated with p50 NF-κB to regulate COX-2 expression and lung cancer growth, suggesting that the BPTF/p50/COX-2 axis could be a potential therapeutic target for lung cancer.

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AuNPs Amplified Surface Acoustic Wave Sensor for Quantification of Exosomes.

In this study, we report a gold nanoparticles (AuNPs) amplified surface acoustic wave (SAW) sensor for exosomes detection with high sensitivity. The SAW chip was self-assembled with mercapto acetic acid to generate carboxylic groups via Au-S bond. Anti-CD63 was then anchored to the chip by pre-treatment with 1-(3-Dimethylaminopropyl)-3-ethylcarbodiimide hydrochloride (EDC) and N-Hydroxysuccinimide;1-hydroxypyrrolidine-2,5-dione (NHS). Due to existence of membrane protein, CD63, on the exosome surface, exosomes could be bound to the antibody-immobilized SAW chip. To amplify the detection signal, both biotin-conjugated epithelial cell adhesion molecule (EpCAM) antibody as a secondary antibody and AuNPs-labeled streptavidin were applied to the exosomes-bound SAW chip, resulting in AuNPs assembly on the chip through biotin-avidin recognition. The sensor was capable of detecting 1.2×103 particles/mL exosomes, which was about 2 orders of magnitude higher than those detected by the strategy without using signal amplification. The sensor also achieved a satisfactory specificity and could detect the low-abundance exosomes directly in blood samples from cancer patients with minimal disturbance. This makes the SAW sensor useful for early diagnosis of cancer.

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