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This paper investigates the impacts of stringent environmental regulation of firm‐level upstreamness in the global value chains (GVCs). Specifically, we use the non‐uniform promulgation of local water pollution control regulations across cities and over time after the 11th Five‐Year Plan as a quasi‐natural experiment in China, in which firms are forced to adopt cleaner technologies or equipment to reduce pollution after enforcing tighter environmental standards. Using highly disaggregated firm‐level data between 2008 and 2014, we find that firms in cities with stricter water pollution regulations tend to move to more upstream sectors in the GVCs. We find that this effect is more prominent for low‐productivity firms, high‐polluting firms, and firms with a high dependence on water in production. This paper sheds new light on the GVC upgrading of firms in response to environmental regulation changes. [ABSTRACT FROM AUTHOR]

Keywords: blood group genomics; hematology - red cells; immunohematology EN blood group genomics hematology - red cells immunohematology E43 E44 2 08/16/23 20230801 NES 230801 Abbreviation B3GALNT1 3- -N-acetyl galactosaminyl-transferase gene INTRODUCTION GLOB (ISBT 028) blood group system has three antigens, including P, PX2, and ExtB.[[1]] These antigens are synthesized by the globotriaosyl-ceramide 3- - I N i -acetyl galactosaminyl-transferase gene ( I B3GALNT1 i ), which encodes a globoside synthase ( 3GalNAc-T1).[[1]] However, I B3GALNT1 i variants (null alleles) can abolish the globoside synthase function, forming P SB 1 sb SP k sp or P SB 2 sb SP k sp phenotype in the GLOB blood group system.[[1], [3]] The individuals with P SB 1 sb SP k sp or P SB 2 sb SP k sp phenotype are notably scarce in the population.[[1], [3]] To date, 13 I B3GALNT1 i variants have been identified in individuals with P SB 1 sb SP k sp or P SB 2 sb SP k sp phenotypes, representing the rare globoside-deficient null phenotypes in the GLOB blood group system (https://www.isbtweb.org/resource/028glob.html). The red blood cells of the proband were not agglutinated with the serum from an individual with P SB 1 sb SP k sp phenotype in A blood group but did agglutinate with human anti-PP1P SP k sp from an individual with p phenotype in A blood group. [Extracted from the article]

I ABO i blood group genotyping methods have been used to identify and differentiate individuals with the ABO subgroup phenotype in some blood group laboratories.[[1]] Currently, the techniques for I ABO i blood group genotyping include polymerase chain reaction (PCR) sequence-specific primers, PCR sequencing-based typing (Sanger method), real-time PCR, DNA chip, next-generation sequencing, and so on. The sequences for Exons 1 to 7 of the I ABO i gene were amplified by PCR, and the amplicons were sequenced according to our previous reports.[[3], [5]] For further confirmation, the haplotypes of the I ABO i gene in the proband were determined using the respective B and O allele-specific primer sequencing methods according to our in-house method. Furthermore, a novel B allele and an AB0*O.01.01 allele were found in the proband with the B and O allele specific primer sequencing methods. [Extracted from the article]

The article presents a case study of a novel B allele which was characterized by a nucleotide deletion in exon 1 of the ABO gene identified in a Chinese individual with B subtype. Topics include ABO blood group antigens which play an important role in the fields of both transfusion and transplantation medicine; ABO phenotypes which were determined by hemagglutination tests and serologic diagnostic classification; and therefore was identified to carry the novel B allele through forward typing.

Background: As is well documented, the para-Bombay phenotype is typically characterized by the reduction or absence of ABH antigens on red blood cells but the presence of corresponding antigens in saliva. Herein, the underlying molecular mechanism of an individual with para-Bombay AB phenotype combined with two novel variants of the FUT1 gene was investigated., Materials and Methods: ABH antigens and antibodies were detected in the serum of the proband using conventional serological methods. The coding region nucleotides of the ABO, FUT1, and FUT2 genes were directly sequenced by polymerase chain reaction. Moreover, the FUT1 haploid type in the proband was analyzed by TA clone sequencing. The 3D structure of wild-type and mutant fucosyltransferases were simulated and analyzed using Phyre2 and Pymol software. Lastly, the effect of missense substitution on the function of fucosyltransferase was predicted by the Polymorphism Phenotyping algorithm (PolyPhen-2) and MutationTaster., Results: ABH antigens were noted to be absent on the surface of red blood cells of the proband. The ABO genotype was ABO*A1.02/ABO*B.01, while the FUT2 genotype was FUT2*01/FUT2*c.357T. Interestingly, two novel missense variants (c.289G>A, p.Ala97Thr and c.575G>C, p.Arg192Pro) and one synonymous SNP (c.840G>A) were identified in the FUT1 gene. Furthermore, c.289G>A was detected in one haploid type, whereas c.575G>C and c.840G>A were discovered in another haploid type. Meanwhile, in silico analysis revealed that amino acid substitution caused by missense variants altered the partial spatial structure of the a-helices where residues 97 and 298 were located using 3D homology modeling software. Finally, both missense variants were defined as probably damaging based on PolyPhen-2 prediction., Discussion: Two novel FUT1 variants were identified in a Chinese individual with para-Bombay AB phenotype, which can expand our understanding of the molecular mechanism underlying the para-Bombay phenotype and contribute to improving the safety of blood transfusion.

Objective: To explore the molecular mechanism for an individual with Bweak subtype., Methods: Serological methods were used to identify the proband's phenotype. In vitro enzyme activity test was used to determine the activity of B-glycosyltransferase (GTB) in her serum. The genotype was determined by PCR amplification and direct sequencing of exons 5 to 7 and flanking sequences of the ABO gene. T-A cloning technology was used to isolate the haploids. The primary physical and chemical properties and secondary structure of the protein were analyzed with the ProtParam and PSIPRED software. Three software, including PolyPhen-2, SIFT, and PROVEAN, was used to analyze the effect of missense variant on the protein., Results: Serological results showed that the proband's phenotype was Bweak subtype with anti-B antibodies presented in her serum. In vitro enzyme activity assay showed that the GTB activity of the subject was significantly reduced. Analysis of the haploid sequence revealed a c.398T>C missense variant on the B allele, which resulted in a novel B allele. The 398T>C variant has caused a p.Phe133S substitution at position 133 of the GTB protein. Based on bioinformatic analysis, the amino acid substitution had no obvious effect on the primary and secondary structure of the protein, but the thermodynamic energy of the variant protein has increased to 6.07 kcal/mol, which can severely reduce the protein stability. Meanwhile, bioinformatic analysis also predicted that the missense variant was harmful to the protein function., Conclusion: The weak expression of the Bweak subtype may be attributed to the novel allele of ABO*B.01-398C. Bioinformatic analysis is helpful for predicting the changes in protein structure and function.

Objective: To explore the molecular basis of an individual with Bel variant of the ABO blood group., Methods: The ABO antigen and serum antibody of the individual were detected by serological method. All coding regions and flanking introns of the ABO gene were amplified with PCR and sequenced bidirectionally. The haplotypes of the individual were analyzed by cloning and sequencing. A three dimensional model of the mutant protein was constructed and analyzed., Results: The individual has expressed a very weak B antigen on its red blood cells by absorption and elution testing, which was identified as a Bel variant phenotype. The heterozygous sites in exon 6 (261del/G) and exon 7 (297A/G, 484del/G, 526C/G, 657C/T, 703G/A, 796C/A, 803G/C, 930G/A) of the coding region of the ABO gene were identified by direct sequencing. Haplotype analysis showed that the individual has carried an O01 allele and a novel B allele. The sequence of the novel B allele was identical to B101 except for a del G at nucleotide position 484 (484delG), which was nominated as B120 by the Blood Group Antigen Gene Mutation Database (dbRBC NCBI). The 484delG mutation of the B allele has led to a reading frame shift and created a premature terminal codon for the glycosyltransferase (GT) enzyme. Prediction of the 3D structure suggested that the GT enzyme has become an incomplete protein only with its N-terminal region., Conclusion: The 484delG mutation of the glycosyltransferase B gene has probably abolished or reduced the enzymatic activity and resulted in the Bel variant phenotype.

Objective: To study the serological characteristics and molecular mechanism for a rare Pk phenotype of the P1Pk blood group system., Methods: The blood group of the proband was identified by serological techniques. The coding region and flanking intronic sequences of the β-1,3-N-acetylgalactosyltransferase gene (B3GALANT1) associated with the Pk phenotype were analyzed using polymerase chain reaction sequence-based typing., Results: The proband was identified as having a rare Pk phenotype including anti-P in her serum. The blood group of her daughter and husband showed a P2 phenotype. The nucleotide sequences of the B3GALANT1 gene of her husband and two randomly-chosen individuals were the same as the reference sequence (GenBank AB050855). Nucleotide position 433 C>T homozygous mutation in the B3GALANT1 was found in the proband, which has resulted in a stop codon at amino acid position 145, which may produce a premature protein capable of decreasing or inhibiting the activity of the β -1,3-N-acetylgalactosyltransferase. The nucleotide position 433 C/T heterozygous in the B3GALANT1 was found in her daughter., Conclusion: The Pk phenotype resulted from 433 C>T mutation in the B3GALANT1 gene has been identified.

Objective: To explore the molecular basis for an individual with rare p phenotype in the P1Pk blood group system., Methods: Erythrocyte blood group antigens and antibodies in serum were identified in the proband and five family members with a serological method. Coding regions and flanking untranslated regions of the α1,4-galactosyltransferase gene (A4GALT) encoding P1Pk antigens were amplified with polymerase chain reaction and directly sequenced. The haplotypes of A4GALT in the parents of the proband were also analyzed by cloning sequencing., Results: The proband was found with a rare p phenotype with anti-Tja antibody in his serum by serological method. The other family members all had a common P2 phenotype. The results of DNA sequencing showed that a cytosine was inserted at nucleotide position 1026 to 1029 (1026_1029insC) of both alleles of the A4GALT gene in the proband. The mutation has caused a reading frame shift and formed a mutant protein by extending 92 amino acid residues. The other family members were either heterozygous for the insertion or of the wild type at above position., Conclusion: The 1026_1029insC mutation of the A4GALT gene is probably responsible for the p phenotype identified for the first time in Chinese population. The individual with the p phenotype possesses anti-Tja antibody.

Background: The relationship between CD36 expression level in platelets and polymorphism of the CD36 gene still needs to be explored. Here, we investigated polymorphisms of the CD36 gene and CD36 expression level in platelets in the Chinese Han population., Materials and Methods: A total of 477 samples were sequenced for exons 2 to 14 of the CD36 gene using a polymerase chain reaction sequence-based typing method. In 192 of these individuals the expression levels of CD36 antigen were analysed by flow cytometry. The genotype-phenotype relationship in platelets was analysed., Results: A total of 22 variants of the CD36 gene were identified, of which five variants (111 A>T, 681 C>A, 1172-1183 del12b, 1236 delT and 1395 A>C) were novel variations, and nine were also found in single nucleotide polymorphism database (dbSNP) but had not been confirmed in individuals with CD36 deficiency. Two variants (329-332 delAC and 1228-1239 del12bp) in the coding region are the most frequent mutations in the Chinese population. Type II CD36 deficiency was identified in seven of 192 individuals, giving a frequency of 3.6%. Individuals with CD36 variations or wild-type genotypes both showed CD36 antigen negative, low-level and high-level expression patterns in platelets. The frequency of the nt-132 A>C polymorphism in the 5'-UTR is relatively high in the Chinese population (0.3516): the expression of CD36 was lower in individuals with nt-132 A>C than in those with the wild-type genotype., Discussion: The distribution of CD36 gene variants in the Chinese population is different from that previously reported. The levels of expression of CD36 antigen in platelets are not determined directly by the genotypes of the CD36 coding region. This suggests that the molecular basis of type II CD36 deficiency may be derived from combined effects of coding region and potential cis-regulatory elements in the 5'-UTR of the CD36 gene.

Objective: To analyze specific expression of blood group genes using nucleated erythroid cells cultured from un-mobilized peripheral stem cells in vitro., Methods: Hematopoietic stem cells(HSC) bearing the CD34 antigen were isolated from peripheral blood by centrifugation and magnetic beads sorting, followed by suspension culture in vitro. Cells were collected from medium on various stages and analyzed by immunofluorescence. The RNA transcription of RH and ABO blood group genes was analyzed using culture cells on day 12., Results: A total of(3.19±0.13) ×10 (4) CD34+cells were isolated from about 50 mL peripheral blood with a recovery rate of 67.3%±2.7%. The cells amount in erythroid-lineage culture system on day 9 reached a plateau of a 237.1±15.5-fold amplification of the initial cell input. The stem cell-specific CD34 antigen was dropped off, while the erythroid-specific CD235a and CD240D antigens were increased in culture period. RHD/CE and ABO genes can be amplified using RNA extracted from culture cells on day 12, and genotypes of Rh and ABO systems by DNA sequencing were consistent with their serologic phenotypes., Conclusion: A method was established to analyze the gene expression of erythroid blood group derived from un-mobilized peripheral stem cells cultured in vitro. It can be used to study the expression of various erythroid-specific genes.

Objective: To delineate serological features and genetic basis for a rare p phenotype of P1Pk blood group system found in a Chinese individual., Methods: Serological assaying was carried out for a proband with unexpected antibody found in his serum using specific antibodies and panel cells. Coding regions and flanking introns of α 1,4-galactosyltransferase gene (A4GALT) associated with the p phenotype were screened with polymerase chain reaction and DNA sequencing., Results: A rare p phenotype of the P1Pk blood group system has been identified with red blood cells from the proband, whose serum contained anti-Tja antibody which can agglutinate and hemolyze with other common red blood cells. Other members of the proband's family were all normal with P1 or P2 phenotype. DNA sequencing has identified in the proband a homozygous 26 bp deletion at position 972 to 997 of the A4GALT gene. The deletion has caused a shift of the reading frame, resulting in a variant polypeptide chain with additional 83 amino acid residues compared with the wild-type protein. Other family members were either heterozygous for above deletion or non-deleted., Conclusion: A 26 bp deletion at position 972 to 997 of the A4GALT gene has been identified in a Chinese individual with p phenotype.