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A new Bayes Determination Principle to help Policymakers after a Crisis.
We develop a rapid "stroboscopic" fluorescence induction method, using the fast repetition rate fluorometry (FRRF) technique, to measure changes in the quantum yield of light emission from chlorophyll in oxygenic photosynthesis arising from competition with primary photochemical charge separation (P680* ➔ P680+QA-). This method determines the transit times of electrons that pass through PSII during the successive steps in the catalytic cycle of water oxidation/O2 formation (S states) and plastoquinone reduction in any oxygenic phototroph (in vivo or in vitro). We report the first measurements from intact living cells, illustrated by a eukaryotic alga (Nannochloropsis oceanica). We demonstrate that S state transition times depend strongly on the redox state of the PSII acceptor side, at both QB and the plastoquinone pool which serve as the major locus of regulation of PSII electron flux. We provide evidence for a kinetic intermediate S3' state (lifetime 220 μs) following formation of S3 and prior to the release of O2. We compare the FRRF-detected kinetics to other previous spectroscopic methods (optical absorbance, EPR, and XES) that are applicable only to in vitro samples. V.Apoptotic cell death frequently occurs in human cancer tissues including oral squamous cell carcinoma (SCC), wherein apoptotic tumor cells are phagocytosed not only by macrophages but also by neighboring tumor cells. We previously reported that the engulfment of apoptotic SCC cells by neighboring SCC cells frequently occurs at the invading front. Therefore, we hypothesized that the phagocytosis of these apoptotic cells by tumor cells contributes to disease progression. Herein, using cultured oral SCC cells, we aimed to confirm whether tumor cells actually phagocytose apoptotic cells and to examine whether cellular activities are regulated by the phagocytosis of apoptotic cells. Co-culture experiments showed that living cells could ingest apoptotic cells into phagolysosomes. NSC23766, an inhibitor of Rac1, which is a key regulator of phagocytic cup formation in professional phagocytes, dramatically suppressed the phagocytosis of apoptotic cells by living cells. Additionally, cell migration and the secretion of DKK1, a tumor-promoting protein, were enhanced by co-culture with apoptotic cells, whereas NSC23766 inhibited these effects. These results show that tumor cells can actively phagocytose apoptotic neighbors in a Rac1-dependent manner and that such activity increases their migration. The regulation of apoptotic cell phagocytosis thus represents new directions for therapeutic intervention for oral cancer. OBJECTIVE To indicate neck circumference (NC) cutoff points to identify excess weight at different stages of somatic maturation and evaluate the association between NC and body mass index (BMI). METHODS Cross-sectional study with 1715 adolescents. BMI was classified according to the World Health Organization (WHO) criteria. Somatic maturation was obtained through the peak growth velocity (PGV). To define the cutoff points, curves of the receiver operating characteristic (ROC) model were constructed. check details The agreement between the anthropometric evaluation instruments was analyzed. The association between the variables was verified. RESULTS Of the girls, 93 were in the pre-PGV stage, 266 in the PGV stage, and 481 in the post-PGV stage. Of the boys, 264 were in the pre-PGV stage, 334 in the PGV stage, and 277 in the post-PGV stage. For the pre-PGV group, the cutoff point was 28cm for females and 29cm for males; for the group during PGV, the cutoff points were 30cm for females and 33cm for males; in the post-PGV group the cutoff values were 32cm in females and 35cm in males. The prevalence of excess weight was higher in the pre-PGV stage in males and in the PGV stage in females. The correlation coefficients were higher in the pre-PGV and PGV stages. CONCLUSION The cutoff points for NC found in this study showed good sensitivity and specificity to identify excess weight in Brazilian adolescents and can be used as a reference in epidemiological studies. Malaria is transmitted by Plasmodium parasites through the bite of female Anopheles mosquitoes. One of the most important mosquito vectors in the Greater Mekong Subregion is Anopheles dirus. This study reports RNA sequencing (RNA-Seq) transcriptome analysis of An. dirus at 18 hours and 7 days after a P. vivax-infected blood meal, which represent infection at the ookinete and oocyst parasite developmental stages, respectively. Following infection, 582 An. dirus transcripts were modulated. The 2,408 P. vivax transcripts could be classified into ookinete-specific, two-stage, and oocyst-specific groups. Results were validated by quantitative reverse transcription polymerase chain reaction. Gene ontology analysis of the vector and parasite revealed several biological pathways for both, providing a better understanding of Anopheles-Plasmodium interactions at the ookinete and oocyst stages. Genetic lesions that reduce telomerase activity inhibit stem cell replication and cause a range of incurable diseases, including dyskeratosis congenita (DC) and pulmonary fibrosis (PF). Modalities to restore telomerase in stem cells throughout the body remain unclear. Here, we describe small-molecule PAPD5 inhibitors that demonstrate telomere restoration in vitro, in stem cell models, and in vivo. PAPD5 is a non-canonical polymerase that oligoadenylates and destabilizes telomerase RNA component (TERC). We identified BCH001, a specific PAPD5 inhibitor that restored telomerase activity and telomere length in DC patient induced pluripotent stem cells. When human blood stem cells engineered to carry DC-causing PARN mutations were xenotransplanted into immunodeficient mice, oral treatment with a repurposed PAPD5 inhibitor, the dihydroquinolizinone RG7834, rescued TERC 3' end maturation and telomere length. These findings pave the way for developing systemic telomere therapeutics to counteract stem cell exhaustion in DC, PF, and possibly other aging-related diseases. Marburg virus (MARV) and Ebola virus (EBOV) belong to the family Filoviridae. MARV causes severe disease in humans with high fatality. We previously isolated a large panel of monoclonal antibodies (mAbs) from B cells of a human survivor with previous naturally acquired MARV infection. Here, we characterized functional properties of these mAbs and identified non-neutralizing mAbs targeting the glycoprotein (GP) 2 portion of the mucin-like domain (MLD) of MARV GP, termed the wing region. One mAb targeting the GP2 wing, MR228, showed therapeutic protection in mice and guinea pigs infected with MARV. The protection was mediated by the Fc fragment functions of MR228. Binding of another GP2 wing-specific non-neutralizing mAb, MR235, to MARV GP increased accessibility of epitopes in the receptor-binding site (RBS) for neutralizing mAbs, resulting in enhanced virus neutralization by these mAbs. These findings highlight an important role for non-neutralizing mAbs during natural human MARV infection.
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