COVID-19: booster(s) vs. hospitalization and Intensive Care Unit admission.

OBJECTIVE: As the pandemic continues, different vaccine protocols have been implemented to maintain the protection of vaccines and to provide protection against new variants. The aim of this study was to assess hospitalized patients' vaccination status and document the efficacy of boosters. PATIENTS AND METHODS: The patients that were hospitalized due to COVID-19 were enrolled from 28 hospitals in Turkey for five months from September 2021. 5,331 confirmed COVID-19 patients from collaborating centers were randomly enrolled to understand/estimate the distribution of vaccination status in hospitalized patients and to compare the efficacy of vaccination/booster protocols. RESULTS: 2,779 men and 2,552 women of which 2,408 (45.2%) were admitted to Intensive Care Units participated in this study. It was found that the highest risk reduction for all age groups was found in groups that received 4 doses. Four doses of vaccination for every 3.7 people under 50 years of age, for every 5.7 people in the 50-64 age group, and for every 4.3 people over 65 years of age will prevent 1 patient from being admitted to intensive care. Regardless of the type of vaccine, it was found that the risk of ICU hospitalization decreased in those who were vaccinated compared to those who were not vaccinated. Regardless of the type of vaccine, the ICU risk was found to decrease 1.25-fold in those who received 1 or 2 doses of vaccine, 1.18-fold in those who received 3 doses, and 3.26-fold in those who received 4 doses. CONCLUSIONS: The results suggested that the addition of a fourth dose is more effective in preventing intensive unit care even in disadvantaged groups.

[Autophagy Does Not Contribute to TKI Response in a Imatinib-resistant Chronic Myeloid Leukemia Cell Line].

Autophagy is an evolutionarily conserved cellular process in which components of the cytoplasm are delivered to lysosomes for degradation and has been proposed to play a role in imatinib resistance in chronic myeloid leukemia cells. Chronic myeloid leukemia is a clonal myeloproliferative disorder arising from the neoplastic transformation of the hematopoietic stem cell. We used a Bcr-Abl-independent and imatinib-resistant K562 subpopulation (K562-IR) that we generated earlier in our laboratory for this study. We showed that in the presence of imatinib autophagy was triggered via LC3I/II transformation, p62 protein expression and acidic vacuoles accumulation in tyrosine kinase inhibitor-sensitive K562 cells; whereas in the cell line K562-IR which is imatinib-resistant and Bcr-Abl independent, autophagy is not triggered. With ongoing research and trails to combine tyrosine kinase inhibitors with autophagy inhibitors, our results suggest a model of resistance in which treatment with a TKI inhibitor does not increase autophagy, basically because its presence does not cause cellular stress due to Bcr-Abl signaling not being required for survival.

[sFRP1 Expression Induces miRNAs That Modulate Wnt Signaling in Chronic Myeloid Leukemia Cells].

Chronic myeloid leukemia is a clonal hematopoietic stem cell disease characterized by myeloid expansion. The hallmark of the disease is the Philadelphia chromosome, which results in the formation of the BCR-ABL oncogene, a tyrosine kinase that is involved in many signaling pathways including Wnt signaling. The latter has a unique role in chronic myeloid leukemia progression; activated signaling leads to the establishment of an additional leukemic stem cell population derived from granulocyte-macrophage progenitors. sFRP1 is an inhibitor of Wnt signaling and its expression is important for differentiation and maintenance of hematopoietic stem cells. In this study, we aimed to investigate miRNAs that target Wnt signaling by being co-induced along with the expression of sFRP1 in K562 cells. We present a detailed analysis of hsa-mir-221 -3p, hsa-mir-222-3p, hsa-mir-106b-5p, hsa-let-7f-5p, hsa-mir-182-5p, hsa-mir-191-5p, and hsa-mir-183-5p and their target genes and their involvement in Wnt signaling.