A New Photocatalytic System Using Steel Mesh and Cold Cathode Fluorescent Light for the Decolorization of Azo Dye Orange G

High color and organic composition, the effluents from the textile dyeing and finishing industry, can be treated by photocatalytic oxidation with UV/TiO2. The objective of this study was to prepare a new photocatalytic system by coating nanosized TiO2 particles on steel mesh support and using cold cathode fluorescent light (CCFL) irradiation at 365 nm in a closed reactor for the oxidation of azo dye C.I. Orange G (OG). Various factors such as reaction time, coating temperature, TiO2 dosage, pH, initial dye concentration, and service duration were studied. Results showed efficient color removal of the OG azo dye by the photocatalytic system with TiO2-coated temperature at 150°C. The optimal TiO2 dosage for color removal was 60 g m−2. An acidic pH of 2.0 was sufficient for photocatalytic oxidation whereas basic condition was not. The rate of color removal decreased with increase in the initial dye concentration. The TiO2-coated steel mesh can be used repeatedly over 10 times without losing the photocatalytic efficiency. Results of FTIR and IC indicated the breakage of N=N bonds, with sulfate as the major and nitrite and nitrate as the minor products, which implied degradation of dye molecules

A novel deep intronic variant strongly associates with Alkaptonuria.

Alkaptonuria is a rare autosomal recessive inherited disorder of tyrosine metabolism, which causes ochronosis, arthropathy, cardiac valvular calcification, and urolithiasis. The epidemiology of alkaptonuria in East Asia is not clear. In this study, patients diagnosed with alkaptonuria from January 2010 to June 2020 were reviewed. Their clinical and molecular features were further compared with those of patients from other countries. Three patients were found to have alkaptonuria. Mutation analyses of the homogentisate 1,2-dioxygenase gene (HGD) showed four novel variants c.16-2063 A > C, p.(Thr196Ile), p.(Gly344AspfsTer25), and p.(Gly362Arg) in six mutated alleles (83.3%). RNA sequencing revealed that c.16-2063 A > C activates a cryptic exon, causing protein truncation p.(Tyr5_Ile6insValTer17). A literature search identified another 6 patients with alkaptonuria in East Asia; including our cases, 13 of the 18 mutated alleles have not been reported elsewhere in the world. Alkaptonuria is rare in Taiwan and East Asia, with HGD variants being mostly novel and private

A novel strategy for sibship determination in trio sibling model

Aim To use a virtually simulated population, generated from published allele frequencies based on 15 short tandem repeats (STR), to evaluate the efficacy of trio sibship testing and sibling assignment for forensic purposes. Methods Virtual populations were generated using 15 STR loci to create a large number of related and unrelated genotypes (10 000 trio combinations). Using these virtual populations, the probability of related and unrelated profiles can be compared to determine the chance of inclusions of being siblings if they are true siblings and the chance of inclusion if they are unrelated. Two specific relationships were tested – two reference siblings were compared to a third true sibling (3S trio, sibling trio) and two reference siblings were compared to an unrelated individual (2S1U trio, non-sibling trio). Results When the likelihood ratio was greater than 1, 99.87% of siblings in the 3S trio population were considered as siblings (sensitivity); 99.88% of non-siblings in the 2S1U trio population were considered as non-siblings (specificity); 99.9% of both populations were identified correctly as siblings and non-siblings; and the accuracy of the test was 99.88%. Conclusions The high sensitivity and specificity figures when using two known siblings compared to a putative sibling are significantly greater than when using only one known relative. The data also support the use of increasing number of loci allowing for greater confidence in genetic identification. The system established in this study could be used as the model for evaluating and simulating the cases with multiple relatives

The risk of false inclusion of a relative in parentage testing – an in silico population study

Aim To investigate the potential of false inclusion of a close genetic relative in paternity testing by using computer generated families. Methods 10 000 computer-simulated families over three generations were generated based on genotypes using 15 short tandem repeat loci. These data were used in assessing the probability of inclusion or exclusion of paternity when the father is actually a sibling, grandparent, uncle, half sibling, cousin, or a random male. Further, we considered a duo case where the mother’s DNA type was not available and a trio case including the mother’s profile. Results The data showed that the duo scenario had the highest and lowest false inclusion rates when considering a sibling (19.03 ± 0.77%) and a cousin (0.51 ± 0.14%) as the father, respectively; and the rate when considering a random male was much lower (0.04 ± 0.04%). The situation altered slightly with a trio case where the highest rate (0.56 ± 0.15%) occurred when a paternal uncle was considered as the father, and the lowest rate (0.03 ± 0.03%) occurred when a cousin was considered as the father. We also report on the distribution of the numbers for non-conformity (non-matching loci) where the father is a close genetic relative. Conclusions The results highlight the risk of false inclusion in parentage testing. These data provide a valuable reference when incorporating either a mutation in the father’s DNA type or if a close relative is included as being the father; particularly when there are varying numbers of non-matching loci

A novel strategy for sibship determination in trio sibling model

Aim To use a virtually simulated population, generated from published allele frequencies based on 15 short tandem repeats (STR), to evaluate the efficacy of trio sibship testing and sibling assignment for forensic purposes. Methods Virtual populations were generated using 15 STR loci to create a large number of related and unrelated genotypes (10 000 trio combinations). Using these virtual populations, the probability of related and unrelated profiles can be compared to determine the chance of inclusions of being siblings if they are true siblings and the chance of inclusion if they are unrelated. Two specific relationships were tested – two reference siblings were compared to a third true sibling (3S trio, sibling trio) and two reference siblings were compared to an unrelated individual (2S1U trio, non-sibling trio). Results When the likelihood ratio was greater than 1, 99.87% of siblings in the 3S trio population were considered as siblings (sensitivity); 99.88% of non-siblings in the 2S1U trio population were considered as non-siblings (specificity); 99.9% of both populations were identified correctly as siblings and non-siblings; and the accuracy of the test was 99.88%. Conclusions The high sensitivity and specificity figures when using two known siblings compared to a putative sibling are significantly greater than when using only one known relative. The data also support the use of increasing number of loci allowing for greater confidence in genetic identification. The system established in this study could be used as the model for evaluating and simulating the cases with multiple relatives

HDAC1 modulates OGG1-initiated oxidative DNA damage repair in the aging brain and Alzheimer’s disease

DNA damage contributes to brain aging and neurodegenerative diseases. However, the factors stimulating DNA repair to stave off functional decline remain obscure. We show that HDAC1 modulates OGG1-initated 8-oxoguanine (8-oxoG) repair in the brain. HDAC1-deficient mice display age-associated DNA damage accumulation and cognitive impairment. HDAC1 stimulates OGG1, a DNA glycosylase known to remove 8-oxoG lesions that are associated with transcriptional repression. HDAC1 deficiency causes impaired OGG1 activity, 8-oxoG accumulation at the promoters of genes critical for brain function, and transcriptional repression. Moreover, we observe elevated 8-oxoG along with reduced HDAC1 activity and downregulation of a similar gene set in the 5XFAD mouse model of Alzheimer’s disease. Notably, pharmacological activation of HDAC1 alleviates the deleterious effects of 8-oxoG in aged wild-type and 5XFAD mice. Our work uncovers important roles for HDAC1 in 8-oxoG repair and highlights the therapeutic potential of HDAC1 activation to counter functional decline in brain aging and neurodegeneration

HDAC1 modulates OGG1-initiated oxidative DNA damage repair in the aging brain and Alzheimer’s disease

DNA damage contributes to brain aging and neurodegenerative diseases. However, the factors stimulating DNA repair to stave off functional decline remain obscure. We show that HDAC1 modulates OGG1-initated 8-oxoguanine (8-oxoG) repair in the brain. HDAC1-deficient mice display age-associated DNA damage accumulation and cognitive impairment. HDAC1 stimulates OGG1, a DNA glycosylase known to remove 8-oxoG lesions that are associated with transcriptional repression. HDAC1 deficiency causes impaired OGG1 activity, 8-oxoG accumulation at the promoters of genes critical for brain function, and transcriptional repression. Moreover, we observe elevated 8-oxoG along with reduced HDAC1 activity and downregulation of a similar gene set in the 5XFAD mouse model of Alzheimer’s disease. Notably, pharmacological activation of HDAC1 alleviates the deleterious effects of 8-oxoG in aged wild-type and 5XFAD mice. Our work uncovers important roles for HDAC1 in 8-oxoG repair and highlights the therapeutic potential of HDAC1 activation to counter functional decline in brain aging and neurodegeneration

The risk of false inclusion of a relative in parentage testing - an in silico population study FORENSIC SCIENCE

Aim To investigate the potential of false inclusion of a close genetic relative in paternity testing by using computer generated families. Methods 10 000 computer-simulated families over three generations were generated based on genotypes using 15 short tandem repeat loci. These data were used in assessing the probability of inclusion or exclusion of paternity when the father is actually a sibling, grandparent, uncle, half sibling, cousin, or a random male. Further, we considered a duo case where the mother's DNA type was not available and a trio case including the mother's profile. Results The data showed that the duo scenario had the highest and lowest false inclusion rates when considering a sibling (19.03 ± 0.77%) and a cousin (0.51 ± 0.14%) as the father, respectively; and the rate when considering a random male was much lower (0.04 ± 0.04%). The situation altered slightly with a trio case where the highest rate (0.56 ± 0.15%) occurred when a paternal uncle was considered as the father, and the lowest rate (0.03 ± 0.03%) occurred when a cousin was considered as the father. We also report on the distribution of the numbers for non-conformity (non-matching loci) where the father is a close genetic relative. Conclusions The results highlight the risk of false inclusion in parentage testing. These data provide a valuable reference when incorporating either a mutation in the father's DNA type or if a close relative is included as being the father; particularly when there are varying numbers of non-matching loci