Publications by authors named "Chris Czarnecki"

Skin cancer is the most common type of cancer in the United States and is estimated to affect one in five Americans. Recent advances have demonstrated strong performance on skin cancer detection, as exemplified by state of the art performance in the SIIM-ISIC Melanoma Classification Challenge; however, these solutions leverage ensembles of complex deep neural architectures requiring immense storage and computation costs, and therefore may not be tractable. A recent movement for TinyML applications is integrating Double-Condensing Attention Condensers (DC-AC) into a self-attention neural network backbone architecture to allow for faster and more efficient computation.

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Objective: To determine the associations of KIR3DL1/S1(3DL1/S1) and its epistatic interactions with human leukocyte antigen class I (HLA-I) alleles with resistance and susceptibility to HIV-1.

Design: Despite repeated exposure to HIV-1, a subset of women enrolled in the Pumwani sex worker cohort remain HIV uninfected. Previous studies have shown that specific HLA class I and II alleles were associated with this natural immunity.

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Background: Understanding natural HIV control may lead to new preventative or therapeutic strategies. Several protective major histocompatibility complex (MHC) genotypes were found in humans and rhesus macaques. Here, we report a simian immunodeficiency virus (SIV) controller MHC genotype in Mauritian cynomolgus macaques (MCMs).

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Transplacental passage is a well-known phenomenon in HIV infection and immune responses at the maternal-fetal interface play a critical role in perinatal mother-to-child HIV transmission (MCHT). The high expression of HLA-G at the maternal-fetal interface and its role in mediating immune tolerance suggest that it could play an important role in MCHT. We investigated the role of HLA-G polymorphism in perinatal HIV transmission in 348 ART naïve mother-child pairs enrolled in a mother-child HIV transmission cohort, established in Nairobi, Kenya in 1986.

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CD4+ T cells orchestrate immunity against viral infections, but their importance in HIV infection remains controversial. Nevertheless, comprehensive studies have associated increase in breadth and functional characteristics of HIV-specific CD4+ T cells with decreased viral load. A major challenge for the identification of HIV-specific CD4+ T cells targeting broadly reactive epitopes in populations with diverse ethnic background stems from the vast genomic variation of HIV and the diversity of the host cellular immune system.

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Background: Infection by the pandemic influenza A (H1N1/09) virus resulted in significant pathology among specific ethnic groups worldwide. Natural Killer (NK) cells are important in early innate immune responses to viral infections. Activation of NK cells, in part, depend on killer-cell immunoglobulin-like receptors (KIR) and HLA class I ligand interactions.

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HLA-G*01:17 was discovered in a woman of Kenyan descent who was enrolled in a mother-to-child HIV-1 transmission cohort. The new allele was identical to HLA-G*01:06 at exons 2, 3, and 4 with the exception of a base pair substitution at codon 169 (CAC → CGC) resulting in a coding change from histidine to arginine and codon 171 (TAC → CAC), resulting in turn in a coding change from tyrosine to histidine. The World Health Organization (WHO) Nomenclature Committee has named this allele HLA-G*01:17.

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We report four novel KIR2DL2 alleles and two novel KIR2DL3 alleles identified from an East African population using sequence-based typing. Sequencing and molecular cloning of exon 4 confirmed that the new 2DL2 alleles were identical to 2DL2*003, except for the following nucleotide differences: 2DL2*00601 had a difference at codon 16 (CGC→CCC), resulting in a coding change from arginine to proline; 2DL2*00602 also had this difference at codon 16, as well as a synonymous difference (GAT→GAC) at codon 31; 2DL2*00303 had a synonymous difference (AAA→AAG) at codon 61; and 2DL2*00304 had a synonymous difference (GGG→GGA) at codon 75. 2DL3*017 was identical to 2DL3*005 except at codon 11 (CGG→CTG, arginine→leucine) and exon 9, codons 297 (CAC→CGC, histidine→arginine) and 321 (TGA→AGA, stop codon→arginine).

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DPA1*020107 was identified from a woman of Ugandan origin by a taxonomy-based sequence analysis of human leukocyte antigen DPA1. The new allele was confirmed by cloning and sequencing of the polymerase chain reaction products. It is identical to DPA1*020101 with the exception of a single nucleotide synonymous substitution at codon 58 (GGC-->GGT).

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