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MASnI 3 ) PSC yielded device performance with PCE 5-6%, [9,10] but the devices were unstable and lacked reproducibility due to oxidation of Sn 2+ . To suppress that oxidation, much effort has been exerted to improve the enduring stability of the performance of tin-based PSC, [11][12][13][14][15][16] for example, through changing the electronic structure of perovskite, providing a uniform and close-packed film, introducing hydrogen bonding and a hydrophobic shell, and so forth. [12][13][14]17,18] Formamidinium (FA + ) is larger than MA + . FASnI 3 has a greater energy of formation of Sn vacancies because of weaker coupling between Sn and I; [19] FASnI 3 has thereby a smaller p-type conductivity than MASnI 3 and acts as a semiconductor. Wang et al. [18] studied the interaction of both FASnI 3 and MASnI 3 perovskites with water and concluded that these two cations affect the electronic structure of the oxygen-bonded perovskite lattice; FASnI 3 has a smaller rate of oxidation of Sn 2+ than MASnI 3 . They also suggested that stable Sn-based perovskite devices might be realized through an appropriate choice of organic cation to ensure effective protection against water penetration. [18] As a result, organic cation FA + has been used to make a FASnI 3 or hybrid FA + /MA + device with PCE 4-8%. [20] Moreover, applying large hydrophobic ammonium cations such as butylammonium (BA + ) or phenylethylammonium (PEA + ) within FASnI 3 to develop a quasi-2D [21] or hybrid 2D/3D [12,13,15] PSC was reported to make stable devices with PCE as great as 9.0%. [12] Beyond MA + and FA + , organic cation guanidinium (CH 6 N 3 + , GA), of size ≈278 pm [22] that is slightly larger than that of FA + (≈253 pm) [22] but has zero electric-dipolar moment, might be a suitable candidate for a tin-based PSC. [23,24] The empirical Goldschmidt tolerance factor of GASnI 3 is 1.051; GASnI 3 has a hexagonal geometry with crystal structures of two types, both with large bandgaps: 1.9 eV for the 3D hexagonal structure, space group P63/m, and 2.1 eV for the 2D monoclinic structure, space group P21/n, near 296 K. [25] We applied organic cation precursor GAI mixed with FAI in varied proportions with equimolar SnI 2 precursor in the presence of SnF 2 and ethylenediammonium diiodide (EDAI 2 ) as additives to enhance both the photovoltaic performance and the enduring stability of a tin-based perovskite. As demonstrated at the top of Figure 1, we prepared the tin perovskites according to stoichiometric ratios of their precursors; these prepared perovskites conform to a general expression, The stability of a tin-based perovskite solar cell is a major challenge. Here, hybrid tin-based perovskite solar cells in a new series that incorporate a nonpolar organic cation, guanidinium (GA + ), in varied proportions into the formamidinium (FA + ) tin triiodide perovskite (FASnI 3 ) crystal structure in the presence of 1% ethylenediammonium diiodide (EDAI 2 ) as an additive, are reported. The device performance is optimized at a precursor ratio (GAI:FAI) of 20:80 to atta...

Recognition of modified histone species by distinct structural domains within “reader” proteins plays a critical role in the regulation of gene expression. Readers that simultaneously recognize histones with multiple marks allow transduction of complex chromatin modification patterns into specific biological outcomes. Here, we report that chromatin regulator TRIM24 functions as a reader of dual histone marks via tandem Plant Homeodomain (PHD) and Bromodomain (Bromo). The three-dimensional structure of TRIM24 PHD-Bromo revealed a single functional unit for combinatorial recognition of unmodified H3K4 (H3K4me0) and acetylated H3K23 (H3K23ac) within the same histone tail. TRIM24 binds chromatin and estrogen receptor to activate estrogen-dependent genes associated with cellular proliferation and tumor development. Aberrant expression of TRIM24 negatively correlates with survival of breast cancer patients. The PHD-Bromo of TRIM24 provides a structural rationale for chromatin activation via a noncanonical histone signature, establishing a new paradigm by which chromatin readers may influence cancer pathogenesis.

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The lipid A component of meningococcal lipopolysaccharide was structurally characterized by using chemical modification methods, methylation analysis, 31P nuclear magnetic resonance, and laser desorption mass spectroscopy. It was shown that Neisseria meningitidis lipid A consists of a 1,4'-bisphosphorylated 1(1'-+6)-linked D-glucosamine disaccharide (lipid A backbone), both phosphate groups being largely replaced by O-phosphorylethanolamine. This disaccharide harbors two nonsubstituted hydroxyl groups at positions 4 and 6', the latter representing the attachment site of the oligosaccharide portion in lipopolysaccharide. In addition, it is substituted by up to six fatty acid residues. In the major lipid A component, representing a hexaacyl species, the hydroxyl groups at positions 3 and 3' carry (R)-3-hydroxydodecanoic acid [12:0(3-OH)], whereas the amino groups at positions 2 and 2' are substituted by (R)-3-(dodecanoyloxy)tetradecanoic acid Meningococcal infections represent a serious problem for small children and young adults in many parts of the world, the lethality being high even in developed countries (1, 5, 6). The causative agent, Neisseria meningitidis, like other gramnegative bacteria, possesses an endotoxin complex located in the bacterial outer cell membrane. Endotoxin (lipopolysaccharide [LPS]) is known to cause or to contribute to the severe symptoms of meningitis, culminating in irreversible shock (37). Meningococci vary in the ability to release endotoxin-containing outer membrane vesicles into the surroundings, both in vitro and in vivo (7). Recent studies performed with N. meningitidis isolates from the nasopharynx of carriers and from cerebrospinal fluid and blood samples from patients with meningococcal infection demonstrated that overproduction and liberation of endotoxin are strongly associated with pathogenicity, regardless of the serological group or serotype of the strain (8, 9).Lipid A represents the principal structural component responsible for the harmful biological activities of LPS (32). To understand the structural parameters required for the expression of endotoxic activity, it appears important to know the precise chemical structure of the lipid A component of pathogenic gram-negative bacteria such as N. meningitidis. The present paper elucidates the primary structure of the lipid A component of N. meningitidis isolated from a strain (M986-NCV1) expressing the serogroup B LPS. It will be shown that this lipid A shares certain structural features with the well-studied enterobacterial lipid A but that it differs significantly in the substitution of the hydrophobic backbone and in the nature and locations of acyl chains. * Corresponding author. MATERIALS AND METHODSMicroorganism and LPS. N. meningitidis M986-NCV1, a nonencapsulated variant of the group B strain M986, was obtained from the culture collection of the Center for Biologics Evaluation and Research. This strain was grown overnight in tryptic soy broth (Difco Laboratories, Detroit, Mich.) in 2.8 liters of baffled Fernbach ...

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Alcohol-based bifunctional ammonium cations, 2-hydroxyethylammonium (HEA+), HO­(CH2)2NH3 +, were introduced into formamidinium (FA+) tin-based perovskites (HEA x FA1–x SnI3; x = 0–1) to absorb light in carbon-based mesoscopic solar cells. We found that HEA+ cations play a key role to control the crystal structures, the lattice structures altered from orthorhombic (x = 0) to rhombohedral (x = 0.2–0.4) with greater symmetry. When x was increased to 0.6–1.0, tin and iodide vacancies were formed to generate 3D-vacant perovskites (HEA x FA1–x Sn0.67I2.33, x ≥ 0.6) with a tetragonal structure. Tin-based perovskites in this series were fabricated into mesoporous solar cells using one-step drop-cast (DC), two-step solvent-extraction (SE), and SE + 3% ethylenediammonium diiodide (EDAI2) as an additive. After optimization of device performance with the SE + 3% EDAI2 approach, the HEA0.4FA0.6SnI3 (HEAI = 40%) device gave the best photovoltaic performance with J SC = 18.52 mA cm–2, V OC = 371 mV, FF = 0.562, and overall efficiency η = 3.9% after the device was stored for a period of 340 h.

Compelling evidence supports vascular contributions to cognitive impairment and dementia (VCID) including Alzheimer’s disease (AD), but the underlying pathogenic mechanisms and treatments are not fully understood. Cis P-tau is an early driver of neurodegeneration resulting from traumatic brain injury, but its role in VCID remains unclear. Here, we found robust cis P-tau despite no tau tangles in patients with VCID and in mice modeling key aspects of clinical VCID, likely because of the inhibition of its isomerase Pin1 by DAPK1. Elimination of cis P-tau in VCID mice using cis-targeted immunotherapy, brain-specific Pin1 overexpression, or DAPK1 knockout effectively rescues VCID-like neurodegeneration and cognitive impairment in executive function. Cis mAb also prevents and ameliorates progression of AD-like neurodegeneration and memory loss in mice. Furthermore, single-cell RNA sequencing revealed that young VCID mice display diverse cortical cell type–specific transcriptomic changes resembling old patients with AD, and the vast majority of these global changes were recovered by cis-targeted immunotherapy. Moreover, purified soluble cis P-tau was sufficient to induce progressive neurodegeneration and brain dysfunction by causing axonopathy and conserved transcriptomic signature found in VCID mice and patients with AD with early pathology. Thus, cis P-tau might play a major role in mediating VCID and AD, and antibody targeting it may be useful for early diagnosis, prevention, and treatment of cognitive impairment and dementia after neurovascular insults and in AD.