Quantifying Worsened Glycemic Control During the COVID-19 Pandemic.

AIMS: We hypothesized that glycemic control in outpatients, measured by HbA1c, was worse during the early months of the COVID-19 pandemic than in 2019. We sought to quantify how much worse and to determine if social determinants of health were associated with these differences. MATERIALS AND METHODS: Data were extracted from the electronic medical records of 2 cohorts of patients seen in the family medicine clinic of a southeastern academic health center. Three hundred patients with baseline HbA1c results as well as HbA1c results in May 2019 or May 2020 were evaluated. RESULTS: The groups had similar mean baseline HbA1c (7.65, SD = 1.50 for 2019; 7.61, SD = 1.71 for 2020; P = .85). Mean May HbA1c decreased from baseline in 2019 (7.19, SD = 1.45) but rose in 2020 (7.63, SD = 1.73), a statistically significant difference (P < .01). Controlling for age, gender, race, and insurance status, HbA1c in May 2020 (meanadj = 7.73) was significantly higher than in May 2019 (meanadj = 7.16). CONCLUSIONS: During the early months of the COVID-19 pandemic, glycemic control in our patient population was significantly worse than during the same period in 2019 (mean HbA1c difference = 0.57). Contrary to our expectations, we did not find associations between patient demographic variables and glycemic control, including race.

Physical and genetic mapping of human chromosome 3 loci containing microsatellite repeats.

One hundred and six microsatellite repeat-containing loci, including 59 CA-containing repeats from the CEPH/Genethon collection, were regionally assigned on human chromosome 3 using a somatic cell hybrid mapping panel, diving the chromosome into 14 intervals. The others were dinucleotide and tetranucleotide repeat-containing loci newly developed for human chromosome 3, of which 26 were also localized by means of genetic linkage analysis against selected CEPH microsatellites. The regional assignment of these two marker sets in a common mapping panel facilitates their integration. Incorporation of these highly polymorphic loci into the developing physical and genetic maps should provide useful information for studies of various diseases involving chromosome 3.

Genetic mapping of dinucleotide repeat polymorphisms and von Hippel-Lindau disease on chromosome 3p25-26.

A genetic map of highly polymorphic microsatellite markers spanning the von Hippel-Lindau region (VHL) of 3p25 was constructed using the CEPH reference pedigrees. A greater than 1000:1 odds map of pter-D3S1038-RAF1-D3S651-D3S656-D3S110- D3S1255-cen was found. Genotyping of six multigenerational VHL families showed the region surrounding the D3S1038 marker to be the most likely location for the VHL gene with a peak location score of 10.04 with VHL completely linked to D3S1038. These data provide an initial high resolution genetic map of this region; D3S1038 appears to be a highly polymorphic marker that should prove useful in the future for presymptomatic diagnosis.

Identification of breakpoints in t(8;21) acute myelogenous leukemia and isolation of a fusion transcript, AML1/ETO, with similarity to Drosophila segmentation gene, runt.

We have developed a restriction map of the chromosome 21 breakpoint region involved in t(8;21)(q22;q22.3) acute myelogenous leukemia (AML) and have isolated a genomic junction clone containing chromosome 8 and 21 material. Using probes from these regions, rearrangements have been identified in each of nine cases of t(8;21) AML examined. In addition, we have isolated cDNA clones from a t(8;21) AML cDNA library that contain fused sequences from chromosome 8 and 21. The chromosome 8 component, referred to as ETO (for eight twenty-one), is encoded over a large genomic region, as suggested by the analysis of corresponding yeast artificial chromosomes (YACs). The DNA sequence of the chromosome 21 portion of the fusion transcript is derived from the normal AML1 gene. A striking similarity (67% identity over 387 bp, with a corresponding 69% amino acid identity) was detected between AML1 and the Drosophila segmentation gene, runt. The critical consequence of the translocation is the juxtaposition of 5' sequences of AML1 to 3' sequences of ETO, oriented telomere to centromere on the der(8) chromosome.

Evolution and sequence analysis of a human Y-chromosomal DNA fragment.

A Y-chromosomal DNA fragment has been isolated from a human Y-Charon 21A recombinant library. Evolutionary analysis of 1F5 indicates that the size and sequence of this fragment have been conserved in higher primates. Deletion mapping and in situ hybridization analysis have localized 1F5 to the middle euchromatic portion of the long arm of the human Y chromosome at Yq11.2. Sequence analysis revealed the presence of an atypical Alu element and two regions rich in polypyrimidine-polypurine residues.

A Y-chromosomal DNA fragment is conserved in human and chimpanzee.

A human male-specific Y-chromosomal DNA fragment (lambda YH2D6) has been isolated. By deletion-mapping analysis, 2D6 has been localized to the euchromatic portion of the long arm (Yq11) of the human Y chromosome. Among great apes, this fragment was found to be conserved in male chimpanzee but was lacking in male gorilla and male orangutan. No homologous fragments were detected in females of orangutan, gorilla, chimpanzee, or human. Nucleotide sequence analysis indicated the presence of partial-Alu-elements and of sequences similar to the GATA repeats of the snake Bkm sequence.

Physical mapping of mouse histone gene clusters.

A chicken histone H2A probe has been used to isolate five different clones from a mouse genomic library in lambda Charon 4A. The size of the inserts in these clones ranged from 11 to 16 kb. The full complement of histone genes was not present in any of the five isolated clones. A physical map, for each of the five clones, has been constructed using partial- and double-restriction digests.

Biochemical and immunocytochemical analysis of a histone H1 variant from the mouse testis.

An H1 histone variant, H1a, has been isolated and purified from the mouse testis. Biochemical and amino acid analyses indicate its similarity with the rat testis H1a. Specific antibodies against the purified H1a have been generated in rabbits and used to study its tissue and species distribution using protein blotting procedures. We have also used the immunocytochemical technique to determine in situ distribution of H1a in spermatogenic cells and somatic tissues of the mouse. A non-random distribution of H1a has been noted in the nuclei of certain somatic cell types such as Sertoli cells, Leydig cells and neurons. By contrast, hepatocyte nuclei lacked detectable levels of H1a. In adult seminiferous tubules, the early primary spermatocyte nuclei displayed a greater level of immunoreactivity relative to other cell types. Developmental studies indicate its initial expression in the 7-day-old mouse testis concomitant with the appearance of intermediate and type B spermatogonia.

Histone messenger RNAs of the mouse testis.

A 6-12S RNA fraction has been isolated following sucrose gradient fractionation of mouse testis RNA, and further resolved into poly A+ and poly A- RNA fractions by oligo-(dt)-cellulose chromatography. Polyacrylamide gel electrophoresis of products formed in a reticulocyte lysate-dependent cell-free translation system has enabled identification of histone variants, H1t, H2S, H2A . X, an H4-like protein and a low Mr protein (presumably TP and/or protamine). Cell-free synthesis of a number of these histone variants appears to be directed by poly A+ mRNAs.