Bis[bis­(1H-pyrazol-1-yl)methane-κ2 N 2,N 2′](formato-κ2 O,O′)copper(II) perchlorate

In the crystal structure of the title compound, [Cu(HCO2)(C7H8N4)2]ClO4, the CuII ion is octa­hedrally coordinated by one bidentate formate ion and two bidentate bis­(1H-pyrazol-1-yl)methane ligands. There are C—H⋯O hydrogen bonds and π–π inter­actions [centroid–centroid distance = 3.487  (3) Å] in the crystal structure. The perchlorate anion is disordered over two positions with an occupancy ratio of 0.628 (9):0.372 (9)

Lusin-type approximation of Sobolev by Lipschitz functions, in Gaussian and RCD(K,∞)RCD(K,\infty) spaces

We establish new approximation results, in the sense of Lusin, of Sobolev functions by Lipschitz ones, in some classes of non-doubling metric measure structures. Our proof technique relies upon estimates for heat semigroups and applies to Gaussian and $RCD(K, \infty)$ spaces. As a consequence, we obtain quantitative stability for regular Lagrangian flows in Gaussian settings

[2,2′-Bis(pyridin-2-ylmeth­oxy)biphenyl-κ4 N,O,O′,N′]bis­(nitrato-κ2 O,O′)cadmium

In the title compound, [Cd(NO3)2(C24H20N2O2)], the CdII ion is eight-coordinated by one ligand and two nitrate ions. There are C—H⋯O hydrogen bonds and C—H⋯π inter­actions and π–π inter­actions [centroid–centroid distance = 3.319 (1) Å] in the crystal structure

Pulmonary alveolar type I cell population consists of two distinct subtypes that differ in cell fate.

Pulmonary alveolar type I (AT1) cells cover more than 95% of alveolar surface and are essential for the air-blood barrier function of lungs. AT1 cells have been shown to retain developmental plasticity during alveolar regeneration. However, the development and heterogeneity of AT1 cells remain largely unknown. Here, we conducted a single-cell RNA-seq analysis to characterize postnatal AT1 cell development and identified insulin-like growth factor-binding protein 2 (Igfbp2) as a genetic marker specifically expressed in postnatal AT1 cells. The portion of AT1 cells expressing Igfbp2 increases during alveologenesis and in post pneumonectomy (PNX) newly formed alveoli. We found that the adult AT1 cell population contains both Hopx+Igfbp2+ and Hopx+Igfbp2- AT1 cells, which have distinct cell fates during alveolar regeneration. Using an Igfbp2-CreER mouse model, we demonstrate that Hopx+Igfbp2+ AT1 cells represent terminally differentiated AT1 cells that are not able to transdifferentiate into AT2 cells during post-PNX alveolar regeneration. Our study provides tools and insights that will guide future investigations into the molecular and cellular mechanism or mechanisms underlying AT1 cell fate during lung development and regeneration

Heat Shock Protein 70 Protects the Heart from Ischemia/Reperfusion Injury through Inhibition of p38 MAPK Signaling.

BackgroundHeat shock protein 70 (Hsp70) has been shown to exert cardioprotection. Intracellular calcium ([Ca2+]i) overload induced by p38 mitogen-activated protein kinase (p38 MAPK) activation contributes to cardiac ischemia/reperfusion (I/R) injury. However, whether Hsp70 interacts with p38 MAPK signaling is unclear. Therefore, this study investigated the regulation of p38 MAPK by Hsp70 in I/R-induced cardiac injury.MethodsNeonatal rat cardiomyocytes were subjected to oxygen-glucose deprivation for 6 h followed by 2 h reoxygenation (OGD/R), and rats underwent left anterior artery ligation for 30 min followed by 30 min of reperfusion. The p38 MAPK inhibitor (SB203580), Hsp70 inhibitor (Quercetin), and Hsp70 short hairpin RNA (shRNA) were used prior to OGD/R or I/R. Cell viability, lactate dehydrogenase (LDH) release, serum cardiac troponin I (cTnI), [Ca2+]i levels, cell apoptosis, myocardial infarct size, mRNA level of IL-1β and IL-6, and protein expression of Hsp70, phosphorylated p38 MAPK (p-p38 MAPK), sarcoplasmic/endoplasmic reticulum Ca2+-ATPase2 (SERCA2), phosphorylated signal transducer and activator of transcription3 (p-STAT3), and cleaved caspase3 were assessed.ResultsPretreatment with a p38 MAPK inhibitor, SB203580, significantly attenuated OGD/R-induced cell injury or I/R-induced myocardial injury, as evidenced by improved cell viability and lower LDH release, resulted in lower serum cTnI and myocardial infarct size, alleviation of [Ca2+]i overload and cell apoptosis, inhibition of IL-1β and IL-6, and modulation of protein expressions of p-p38 MAPK, SERCA2, p-STAT3, and cleaved-caspase3. Knockdown of Hsp70 by shRNA exacerbated OGD/R-induced cell injury, which was effectively abolished by SB203580. Moreover, inhibition of Hsp70 by quercetin enhanced I/R-induced myocardial injury, while SB203580 pretreatment reversed the harmful effects caused by quercetin.ConclusionsInhibition of Hsp70 aggravates [Ca2+]i overload, inflammation, and apoptosis through regulating p38 MAPK signaling during cardiac I/R injury, which may help provide novel insight into cardioprotective strategies

Threshold quantum cryptograph based on Grover's algorithm

Grover's operator in the two-qubit case can transform a basis into its conjugated basis. A permutation operator can transform a state in the two conjugated bases into its orthogonal state. These properties are included in a threshold quantum protocol. The proposed threshold quantum protocol is secure based the proof that the legitimate participators can only eavesdrop 2 bits of 3 bits operation information on one two-qubit with error probability 3/8. We propose a scheme to detect the Trojan horse attack without destroying the legal qubit.Comment: 7 pages, 1 figure

Diaqua­(5-methyl­pyrazine-2-carboxyl­ato-κ2 N 1,O)iron(II)

In the neutral title complex, [Fe(C6H5N2O2)2(H2O)2], the coordination geometry aound the FeII atom, which lies on an inversion centre, is distorted octa­hedral comprising two N atoms and two O atoms from two 5-methyl­pyrazine-2-carboxyl­ate ligands, and two water mol­ecules. The crystal structure is stabilized by a network of O—H⋯O hydrogen bonds, resulting in a two-dimensional supra­molecular structure