Notes

The outcome of water steam for the Oh yeah reactivity towards CH3CHO from ultra-low temps (21 years old.7-135.Zero Okay): Findings as well as concept.
Examining linkages among multiple sustainable development outcomes is key for understanding sustainability transitions. Yet rigorous evidence on social and environmental outcomes of sustainable development policies remains scarce. We conduct a national-level analysis of Brazil's flagship social protection program, Zero Hunger (ZH), which aims to reduce food insecurity and poverty. Using data from rural municipalities across Brazil and quasi-experimental causal inference techniques, we assess relationships between social protection investment and outcomes related to sustainable development goals (SDGs) "no poverty" (SDG 1), "zero hunger" (SDG 2), and "health and well being" (SDG 3). We also assess potential perverse outcomes arising from agricultural development impacting "climate action" (SDG 13) and "life on land" (SDG 15) via clearance of natural vegetation. Despite increasing daily per capita protein and kilocalorie production, summed ZH investment did not alleviate child malnutrition or infant mortality and negligibly influenced multidimensional poverty. Higher investment increased natural vegetation cover in some biomes but increased losses in the Cerrado and especially the Pampa. Effects varied substantially across subprograms. Conditional cash transfer (Bolsa Familia [BF]) was mainly associated with nonbeneficial impacts but increased protein production and improved educational participation in some states. The National Program to Strengthen Family Farming (PRONAF) was typically associated with increased food production (protein and calories), multidimensional poverty alleviation, and changes in natural vegetation. Our results inform policy development by highlighting successful elements of Brazil's ZH program, variable outcomes across divergent food security dimensions, and synergies and trade-offs between sustainable development goals, including environmental protection.Temperate bacteriophages can enter one of two life cycles following infection of a sensitive host the lysogenic or the lytic life cycle. The choice between the two alternative life cycles is dependent upon a tight regulation of promoters and their cognate regulatory proteins within the phage genome. We investigated the genetic switch of TP901-1, a bacteriophage of Lactococcus lactis, controlled by the CI repressor and the modulator of repression (MOR) antirepressor and their interactions with DNA. We determined the solution structure of MOR, and we solved the crystal structure of MOR in complex with the N-terminal domain of CI, revealing the structural basis of MOR inhibition of CI binding to the DNA operator sites. 15N NMR Carr-Purcell-Meiboom-Gill (CPMG) relaxation dispersion and rotating frame R1ρ measurements demonstrate that MOR displays molecular recognition dynamics on two different time scales involving a repacking of aromatic residues at the interface with CI. Mutations in the CIMOR binding interface impair complex formation in vitro, and when introduced in vivo, the bacteriophage switch is unable to choose the lytic life cycle showing that the CIMOR complex is essential for proper functioning of the genetic switch. On the basis of sequence alignments, we show that the structural features of the MORCI complex are likely conserved among a larger family of bacteriophages from human pathogens implicated in transfer of antibiotic resistance.Profilin2 (PFN2) is a target of the embryonic stem cell (ESC)-enriched miR-290 family of microRNAs (miRNAs) and an actin/dynamin-binding protein implicated in endocytosis. Here we show that the miR-290-PFN2 pathway regulates many aspects of ESC biology. In the absence of miRNAs, PFN2 is up-regulated in ESCs, with a resulting decrease in endocytosis. Reintroduction of miR-290, knockout of Pfn2, or disruption of the PFN2-dynamin interaction domain in miRNA-deficient cells reverses the endocytosis defect. The reduced endocytosis is associated with impaired extracellular signal-regulated kinase (ERK) signaling, delayed ESC cell cycle progression, and repressed ESC differentiation. Mutagenesis of the single canonical conserved 3' UTR miR-290-binding site of Pfn2 or overexpression of the Pfn2 open reading frame alone in otherwise wild-type cells largely recapitulates these phenotypes. Taken together, these findings define an axis of posttranscriptional control, endocytosis, and signal transduction that is important for ESC proliferation and differentiation.Bacterial flagella differ in their number and spatial arrangement. In many species, the MinD-type ATPase FlhG (also YlxH/FleN) is central to the numerical control of bacterial flagella, and its deletion in polarly flagellated bacteria typically leads to hyperflagellation. The molecular mechanism underlying this numerical control, however, remains enigmatic. Using the model species Shewanella putrefaciens, we show that FlhG links assembly of the flagellar C ring with the action of the master transcriptional regulator FlrA (named FleQ in other species). While FlrA and the flagellar C-ring protein FliM have an overlapping binding site on FlhG, their binding depends on the ATP-dependent dimerization state of FlhG. see more FliM interacts with FlhG independent of nucleotide binding, while FlrA exclusively interacts with the ATP-dependent FlhG dimer and stimulates FlhG ATPase activity. Our in vivo analysis of FlhG partner switching between FliM and FlrA reveals its mechanism in the numerical restriction of flagella, in which the transcriptional activity of FlrA is down-regulated through a negative feedback loop. Our study demonstrates another level of regulatory complexity underlying the spationumerical regulation of flagellar biogenesis and implies that flagellar assembly transcriptionally regulates the production of more initial building blocks.Transcription factor fusions (TFFs) are present in ∼30% of soft-tissue sarcomas. TFFs are not readily "druggable" in a direct pharmacologic manner and thus have proven difficult to target in the clinic. A prime example is the CIC-DUX4 oncoprotein, which fuses Capicua (CIC) to the double homeobox 4 gene, DUX4. CIC-DUX4 sarcoma is a highly aggressive and lethal subtype of small round cell sarcoma found predominantly in adolescents and young adults. To identify new therapeutic targets in CIC-DUX4 sarcoma, we performed chromatin immunoprecipitation sequencing analysis using patient-derived CIC-DUX4 cells. We uncovered multiple CIC-DUX4 targets that negatively regulate MAPK-ERK signaling. Mechanistically, CIC-DUX4 transcriptionally up-regulates these negative regulators of MAPK to dampen ERK activity, leading to sustained CIC-DUX4 expression. Genetic and pharmacologic MAPK-ERK activation through DUSP6 inhibition leads to CIC-DUX4 degradation and apoptotic induction. Collectively, we reveal a mechanism-based approach to therapeutically degrade the CIC-DUX4 oncoprotein and provide a precision-based strategy to combat this lethal cancer.
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