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Purpose: This study assessed the safety and effectiveness of a technical modification that involves adding short gastric artery (SGA) embolization to left gastric artery (LGA) embolization., Material and Methods: This retrospective single-center study analyzed twenty obese patients (median age of 53.5 (30-73)) who were not eligible for bariatric surgery and underwent bariatric embolization with 300-500-µm microspheres in addition to a lifestyle counseling program between March 2021 and July 2022. Eight patients had LGA + SGA embolization, and twelve had LGA embolization alone. The primary outcome measure was total body weight loss (TBWL) at 6 months in the SGA + LGA and the LGA-only cohorts. Safety was assessed, defined as the 30-day adverse events rate according to the SIR classification., Results: The mean 6-month post-embolization TBWL in the SGA + LGA cohort was 7.3 kg (95%CI 2.1-12.4; p = .01) and 4.1 kg (95%CI 0.4-8.6; p = 0.034) in the LGA-only cohort (mean difference - 3.1 kg ± 2.8; 95%CI (- 9.1-2.8); p = .28). The mean 6-month post-embolization TBWL in the entire cohort was 5.3 kg (p < .01). The rate of complications was similar between the two groups., Conclusion: Combined SGA and LGA embolization is safe and effective to treat obesity. Larger studies are needed to determine whether SGA + LGA embolization results in more significant weight loss than LGA embolization alone., (© 2024. Springer Science+Business Media, LLC, part of Springer Nature and the Cardiovascular and Interventional Radiological Society of Europe (CIRSE).)

The HLA-A10 crossreacting group consists of the A25, A26, A34, A43 and A66 antigens. Here, we report allelic sequences for A43 and for 2 subtypes of both A26 and A34. Combining these results with previously determined sequences for A25, A26 and A66 enables molecular comparison of all the serologically defined A10 antigens. They form a closely related and well-defined group of alleles which may have originated with A*2601. Patterns of serological crossreactivity are correlated with sequence and a public epitope shared by A33 and members of the A10 family is localized to residues R62 and N63. The A*2501, A*4301 and A*6601 alleles appear to have derived from A*2601 by single gene conversion events with other HLA-A alleles. In the case of A*4301, the donor allele was probably an A29 allele as A*4301 has a small element of sequence in the alpha 1 helix (residues L62 and Q63) uniquely shared with A29. The chimaeric structure of A43 explains the reactivity of A43 molecules with both A10 and A29 alloantisera. The rare Oriental variant of A26 (A26v*) is encoded by an allele (A*2602) that differs from A*2601 by a unique nucleotide substitution which changes aspartate to asparagine at position 116 in the floor of the peptide binding groove. Thus A*2602 is a functionally distinct allele that originated by a point mutation. Alleles encoding A34 and A66 antigens are found to have very similar structures, explaining the difficulty in their serological definition.(ABSTRACT TRUNCATED AT 250 WORDS)

The Kaingang and Guarani are culturally and linguistically distinct tribes of southern Brazil. Like all Amerindian groups they show limited HLA polymorphism, which probably reflects the small founder populations that colonized America by overland migration from Asia 11,000-40,000 years ago. We find the nucleotide sequences of HLA-B alleles from the Kaingang and Guarani to be distinct from those characterized in caucasian, oriental and other populations. By comparison, the HLA-A and C alleles are familiar. These results and those reported in the accompanying paper on the Waorani of Ecuador reveal that a marked evolution of HLA-B has occurred since humans first entered South America. New alleles have been formed through recombination between pre-existing alleles, not by point mutation, giving rise to distinctive diversification of HLA-B in different South American Indian tribes.

HLA haplotypes containing the HLA-B46 allele react with both anti-Cw1 and anti-Cw3 alloantisera, a pattern of reactivity defined as the Cw11 antigen and postulated to involve either a distinctive Cw11 allele or a duplicated HLA-C locus. From serological characterization of CIR cells transfected with B46 cDNA we now demonstrate that the anti-Cw3 reactivity with these haplotypes is solely due to the B46 molecule and not to an HLA-C molecule. Furthermore, isolation and characterization of HLA-C mRNA from cells expressing B46 strongly suggest that anti-Cw1 reactions are directed against the product of a conventional Cw1 allele. The antigenic cross-reactivities of B46 with B62 and Cw3 correlate with its chimaeric primary structure, which is identical to that of B62, except in the alpha 1 helix where it is identical to both Cw3 and Cw1. The structure, distribution and genetic linkage of B46 indicate it is of recent, Asian origin and is the result of a gene conversion, involving Cw1 as the donor gene and B62 as the recipient. These results demonstrate that the Cw11 antigen neither corresponds to a novel HLA-C allele nor a duplicated HLA-C locus, but to a combination of epitopes contributed by linked Cw1 and B46 alleles. The nucleotide sequence we previously and erroneously attributed to a distinct Cw11 allele is now demonstrated to encode Cw8. Isolation of the cDNA clone with this sequence from a library made from a cell homozygous for the B46 haplotype was probably an artefact of contamination.

The HLA class I sequences included in this compilation are taken from publications listed in the accompanying paper, Nomenclature for factors of the HLA system, 1990 (Bodmer et al., 1991), and also in Nomenclature for factors of the HLA system, 1989 (Bodmer et al., 1990). Where discrepancies have arisen between reported sequences the original authors have been contacted where possible, and necessary amendments to published sequences have been incorporated into this alignment. Future sequencing may identify errors in this list and we would welcome any evidence that helps to maintain the accuracy of this compilation. In the sequence alignments identity between residues is indicated by a hyphen (-). An unavailable sequence is indicated by a full point (.). Gaps in the sequence are inserted to maintain the alignment between different alleles showing variation in amino acid number.

Adrenal 21-hydroxylase deficiency is strongly associated with HLA-Bw47. This rare HLA allele and the HLA-B13 allele are both found in positive genetic linkage disequilibrium with HLA-A3, -Cw6, -DR7 and also display serological cross-reactivity. To investigate the relationship between these two alleles at the structural level, the nucleotide sequences of the HLA-B13 and HLA-Bw47 genes have been determined. They differ by 28 nucleotides, resulting in 14 amino acid substitutions: 5 in the alpha 1 domain, 8 in the alpha 2 domain, and 1 in the transmembrane region. Comparison of HLA-Bw47 nucleotide sequence with other HLA-B sequences shows a segment of 228 bp identical with B44 in the alpha 1 domain and a segment of 218 bp identical with B27 in the alpha 2 domain, but only a 91 bp segment of identity with B13 in the alpha 1 domain. The complex pattern of substitutions and their degree of divergence indicate that HLA-B13 and HLA-Bw47 alleles are not related by a simple mutational event.

A simple and reliable complement-dependent liposome lysis test for the detection of anti-ganglioside antibodies is described. For sera raised in rabbits against the monosialoganglioside NG-GM3, the sensitivity and specificity of antibody detection was compared with that of the HRBC hemagglutination-inhibition test: the liposome lysis test appears more sensitive. A difference in antigen presentation was also demonstrated.

Differentiation of spleen prothymocytes into Thy-1.2+ cells under the influence of thymosin requires transcription of DNA and translation of RNA, as demonstrated by the effects of inhibitors of DNA, RNA and protein synthesis. The lifespan of the induction message for this T cell differentiation appeared to be relatively short (30 to 60 min) in the presence of a reversible inhibitor of protein synthesis. When anisomycin, a protein synthesis inhibitor, was first introduced into the cell suspension, induction was suppressed but it was restored when actinomycin D, a RNA synthesis inhibitor, was added following anisomycin. By flow cytometry, the RNA content was slightly increased in the presence of thymosin and this increase was enhanced by the simultaneous addition of RNA and protein synthesis inhibitors.