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Cardoso, B.

Publications and source records attributed to Cardoso, B..

2 recordsLinked to original sources

The impact of the ABO/Rh blood group on susceptibility and severity among COVID-19 patients in Luanda, Angola

SARS-CoV-2 is a public health concern worldwide. Identification of biological factors that could influence transmission and worsen the disease has been the subject of extensive investigation. Herein, we investigate the impact of the ABO/Rh blood group on susceptibility and severity among COVID-19 patients in Luanda, Angola. This was a multicentric cohort study conducted with 101 COVID-19 patients. Chi-square and logistic regression were calculated to check factors related to the worsening of the disease and deemed significant when p<0.05. Blood type O (51.5%) and Rh-positive (93.1%) were the most frequent. Patients from blood type O had a high risk to severe disease [OR: 1.33 (95% CI: 0.42 - 4.18), p=0.630] and hospitalization [OR: 2.59 (95% CI: 0.84 - 8.00), p=0.099]. Also, Rh-positive blood type presented a high risk for severe disease (OR: 10.6, p=0.007) and hospitalization (OR: 6.04, p=0.026). We find a high susceptibility, severity, hospitalization, and mortality, respectively, among blood group O and Rh-positive patients, while blood group AB presented a low susceptibility, severity, hospitalization, and mortality, respectively. Our findings add to the body of evidence suggesting that ABO/Rh blood groups play an important role in the course of SARS-CoV-2 infection.

genetics↗

Asymmetric post-translational modifications regulate the intracellular distribution of unstimulated STAT3 dimers

Signal Transducer and Activator of Transcription 3 (STAT3) is a ubiquitous and pleiotropic transcription factor that plays essential roles in normal development, immunity, response to tissue damage and cancer. We have developed a Venus-STAT3 bimolecular fluorescence complementation (BiFC) assay that allows the visualization and study of STAT3 dimerization and protein-protein interactions in living cells. Inactivating mutations on residues susceptible to post-translational modifications (K49R, K140R, K685R, Y705F and S727A) did not alter the basal dimerization of unstimulated STAT3, but changed significantly the intracellular distribution of STAT3 dimers. Surprisingly, the distribution of specific asymmetric STAT3 dimers (i.e. the STAT3 molecules carry different mutations) was different from symmetric dimers. Our results indicate that asymmetric post-translational modifications on STAT3 dimers could constitute a new level of regulation of STAT3 signaling. This set of Venus-STAT3 BiFC constructs provides yet unexplored means to advance our understanding of STAT3 behavior and function in cancer and beyond.

cell biology↗