37 research outputs found

    ISOLATION AND CHARACTERIZATION OF CLONES OF A HUMAN LEUKEMIA CELL LINE (HL-60 CELLS) RESISTANT TO 1α,25-DIHYDROXYVITAMIN D3 AND DIMETHYL SULFOXIDE

    Get PDF
    We have previously demonstrated that HL-60 cells pretreated with 1α,25-dihydroxyvitaminD3 at the stage of commitment were induced to differentiate into macrophage-like cells by dimethyl sulfoxide (OMSO) at the stage of promotion (15). Toinvestigate the effect of OMSO on the differentiation of HL-60 cells induced by1α,25-dihydroxyvitamin D3, three variant clones (ORHL-1, ORHL-2 and ORHL-3cells) resistant to 1α,25-dihydroxyvitamin D3 were iso1α,ted from a OMSO-resistantcell clone (ORHL) ofHL-60 cells. These variant clones were insusceptible to 1α,25-dihydroxyvitamin D3 or OMSO, when based on the criteria of cell growth, expressionof antigens for human monocyte specific (OKMS) or human granulocyte specific(80H5) monoclona1α,ntibodies, NBT-reducing activity, phagocytosis, nonspecificesterase activity, and cathepsin Band 1α,ctivities. The variant clones, ORHL-1and ORHL-3, which were insusceptible to 1α,25-dihydroxyvitamin D3 or OMSOalone, were induced to differentiate into macrophage-like cells on simultaneoustreatment with 1α,25-dihydroxyvitamin D3 and OMSO. Furthermore, ORHL-1 butnot ORHL-3 differentiated into macrophage-like cells on I-day treatment with1α,,25-dihydroxyvitamin D3 followed by 3-day treatment with OMSO. The othervariant, ORHL-2, did not differentiate with any combination of 1α,25-dihydroxyvitaminD3 and OMSO. These results suggest that OMSO promotes the differentiationof HL-60 cells initiated by 1α,,25-dihydroxyvitamin D3 into macrophages atvarious stages of differentiation

    Does Genetic Predisposition Contribute to the Exacerbation of COVID-19 Symptoms in Individuals with Comorbidities and Explain the Huge Mortality Disparity between the East and the West?

    No full text
    The elderly and patients with several comorbidities experience more severe cases of coronavirus disease 2019 (COVID-19) than healthy patients without underlying medical conditions. However, it is unclear why these people are prone to developing alveolar pneumonia, rapid exacerbations, and death. Therefore, we hypothesized that people with comorbidities may have a genetic predisposition that makes them more vulnerable to various factors; for example, they are likely to become more severely ill when infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). To test this hypothesis, we searched the literature extensively. Polymorphisms of genes, such as those that encode angiotensin-converting enzyme 1 (ACE1), have been associated with numerous comorbidities, such as cardiovascular disease, hypertension, diabetes, chronic kidney disease, and obesity, and there are potential mechanisms to explain these associations (e.g., DD-type carriers have greater ACE1 activity, and patients with a genetic alpha-1 anti-trypsin (AAT) deficiency lack control over inflammatory mediators). Since comorbidities are associated with chronic inflammation and are closely related to the renin–angiotensin–aldosterone system (RAAS), these individuals may already have a mild ACE1/ACE2 imbalance before viral infection, which increases their risk for developing severe cases of COVID-19. However, there is still much debate about the association between ACE1 D/I polymorphism and comorbidities. The best explanation for this discrepancy could be that the D allele and DD subtypes are associated with comorbidities, but the DD genotype alone does not have an exceptionally large effect. This is also expected since the ACE1 D/I polymorphism is only an intron marker. We also discuss how polymorphisms of AAT and other genes are involved in comorbidities and the severity of SARS-CoV-2 infection. Presumably, a combination of multiple genes and non-genetic factors is involved in the establishment of comorbidities and aggravation of COVID-19

    Field Surveys on Cape Ryugu, East Antarctica in 1977-1978

    No full text
    The summer field party of the 19th Japanese Antarctic Research Expedition (JARE-19) camped at Cape Ryugu 220 km east-northeast of Japanese Antarctic Station, Syowa, from December 30th, 1977 to January 14th, 1978. Dr. KAMINUMA of the National Institute of Polar Research, Japan, led the six-man party which contained three geologists, one biologist, one surveyor and one geophysicist. Cape Ryugu located at 67°58'S and 44°01'E, has an ice-free area of 10 km length in the east-west direction with a breadth of 2 km. The survey was the first ground one by the Japanese field party. Therefore, the principal scientific aims of the party were topographic and geological mapping. Other scientific goals were biological and geophysical surveys. The party succeeded in establishing ten topographic control points, one astronomical station, and six gravity stations. Fundamental geological and biological surveys were made throughout the Cape Ryugu ice-free area. Successful air transport to 177 km north from Cape Ryugu was made by two helicopters. A report on the logistics of the field party and a summary of the field survey are also given in this paper
    corecore