5-(4-Nitro­benz­yl)-1H-1,2,3,4-tetra­zole

In the title compound, C8H7N5O2, the dihedral angle between the benzene and tetra­zole rings is 63.13 (8)°. The crystal structure exhibits inter­molecular N—H⋯N hydrogen bonds which lead to the formation of one-dimensional chains along the [010] direction

Connexin26 Gap Junction Mediates miRNA Intercellular Genetic Communication in the Cochlea and Is Required for Inner Ear Development

Organ development requires well-established intercellular communication to coordinate cell proliferations and differentiations. MicroRNAs (miRNAs) are small, non-coding RNAs that can broadly regulate gene expression and play a critical role in the organ development. In this study, we found that miRNAs could pass through gap junctions between native cochlear supporting cells to play a role in the cochlear development. Connexin26 (Cx26) and Cx30 are predominant isoforms and co-express in the cochlea. Cx26 deficiency but not Cx30 deficiency can cause cochlear developmental disorders. We found that associated with Cx26 deletion induced the cochlear developmental disorders, deletion of Cx26 but not Cx30 disrupted miRNA intercellular transfer in the cochlea, although inner ear gap junctions still retained permeability after deletion of Cx26. Moreover, we found that deletion of Cx26 but not Cx30 reduced miR-96 expression in the cochlea during postnatal development. The reduction is associated with the cochlear tunnel developmental disorder in Cx26 knockout (KO) mice. These data reveal that Cx26-mediated intercellular communication is required for cochlear development and that deficiency of Cx26 can impair miRNA-mediated intercellular genetic communication in the cochlea, which may lead to cochlear developmental disorders and eventually congenital deafness as previously reported

(E)-3,3′-(Diazene-1,2-di­yl)bis­(1-methyl-1,4,5,6-tetra­hydro­pyrrolo­[3,4-c]pyrazol-5-ium) dinitrate dihydrate

The title compound, C12H18N8 2+·2NO3 −·2H2O, was synthesized unexpectedly from 3-amino-1-methyl-1,4,5,6-tetra­hydro­pyrrolo­[3,4-c]pyrazol-5-ium chloride and cerium(IV) ammonium nitrate. The cation has a crystallographically imposed centre of symmetry. In the crystal, the ions and water mol­ecules are linked via O—H⋯N, N—H⋯O and O—H⋯O hydrogen bonds into a three-dimensional network

Effect of Acorus tatarinowii extract on hyperprolactinemia in rats

Purpose: To determine the mechanism underlying the anti-hyperprolactinemia effect of Acorus tatarinowii extract (ATE) in rats. Methods: Rats were divided into six groups (n =10 each group), viz, healthy control, untreated hyperprolactinemic rats, hyperprolactinemic rats treated with bromocriptine (0.6 mg/kg), and hyperprolactinemic rats treated with ATE (3.2, 6.4, or 12.8 g/kg). After 30 days, the hypothalamic protein levels of dopamine D2 receptor, protein kinase A (PKA), and cyclic adenosine monophosphate (cAMP) were determined. Results: Dopamine D2 receptor levels were lower in untreated hyperprolactinemic rats than in healthy control (p < 0.01), but this decrease was attenuated by ATE (p < 0.05). Elevated PKA levels in untreated hyperprolactinemic rats (0.78 ± 0.03µg/mL, p < 0.01) were decreased by ATE (3.2 g/kg, 0.51 ± 0.02 µg/mL, p < 0.05; 6.4 g/kg, 0.39 ± 0.03 µg/mL, p < 0.01; 12.8 g/kg, 0.24 ± 0.04 µg/mL, p < 0.01). Similarly, elevated cAMP levels in hyperprolactinemic rats (3.1 ± 0.3 ng/mL) were lowered by ATE (3.2 g/kg, 2.2 ± 0.4 ng/mL, p < 0.05; 6.4 g/kg, 1.8 ± 0.3 ng/mL, p < 0.01; 12.8 g/kg, 1.4 ± 0.3 ng/mL, p < 0.01). Conclusion: ATE anti-hyperprolactinemia activity is mediated by dopamine D2 receptor signaling via cAMP/PKA pathway

Early Functional and Cognitive Declines Measured by Auditory-Evoked Cortical Potentials in Mice With Alzheimer’s Disease

Alzheimer’s disease (AD) is characterized by a progressive loss of memory and cognitive decline. However, the assessment of AD-associated functional and cognitive changes is still a big challenge. Auditory-evoked cortical potential (AECP) is an event-related potential reflecting not only neural activation in the auditory cortex (AC) but also cognitive activity in the brain. In this study, we used the subdermal needle electrodes with the same electrode setting as the auditory brainstem response (ABR) recording and recorded AECP in normal aging CBA/CaJ mice and APP/PS1 AD mice. AECP in mice usually appeared as three positive peaks, i.e., P1, P2, and P3, and three corresponding negative peaks, i.e., N1, N2, and N3. In normal aging CBA mice, the early sensory peaks P1, N1, and P2 were reduced as age increased, whereas the later cognitive peaks N2, P3, and N3 were increased or had no changes with aging. Moreover, the latency of the P1 peak was increased as age increased, although the latencies of later peaks had a significant reduction with aging. In AD mice, peak P1 was significantly reduced in comparison with wild-type (WT) littermates at young ages, proceeding AD phenotype presentation. In particular, the later cognitive peak P3 was diminished after 3 months old, different from the normal aging effect. However, the latencies of AECP peaks in AD mice generally had no significant delay or changes with aging. Finally, consistent with AECP changes, the accumulation of amyloid precursor protein (APP) at the AC was visible in AD mice as early as 2 months old. These data suggest that AECP could serve as an early, non-invasive, and objective biomarker for detecting AD and AD-related dementia (ADRD)

Effects of losses in the hybrid atom-light interferometer

Enhanced Raman scattering can be obtained by injecting a seeded light field which is correlated with the initially prepared collective atomic excitation. This Raman amplification process can be used to realize atom-light hybrid interferometer. We numerically calculate the phase sensitivities and the signal-to-noise ratios of this interferometer with the method of homodyne detection and intensity detection, and give their differences between this two methods. In the presence of loss of light field and atomic decoherence the measure precision will be reduced which can be explained by the break of the intermode decorrelation conditions of output modesComment: 9 pages, 7 figure

Investigation of the interaction between indigotin and two serum albumins by spectroscopic approaches

AbstractThe binding characteristics of indigotin with human serum albumin (HSA) and bovine serum albumin (BSA) have been investigated by various spectroscopic techniques. Spectroscopic analysis revealed that the quenching mechanism between indigotin and HSA/BSA belonged to the static quenching. The displacement experiments suggested that indigotin primarily bound to tryptophan residues on proteins within site I. The thermodynamic parameters indicated that the binding of indigotin–HSA/BSA mainly depended on the hydrophobic interaction. The binding distance of indigotin to HSA/BSA was evaluated. The results by synchronous fluorescence, three-dimensional fluorescence, Fourier Transform Infrared spectroscopy (FT-IR) and circular dichroism (CD) spectra showed that the conformation of proteins altered in the presence of indigotin

4-Chloro-5-[(5,5-dimethyl-4,5-dihydro­isoxazol-3-yl)sulfonyl­meth­yl]-3-methyl-1-(2,2,2-trifluoro­ethyl)-1H-pyrazole

The mol­ecule of the title compound, C12H15ClF3N3O3S, is twisted, as indicated by the C—S—C—C torsion angle of 66.00 (18)° for the atoms linking the ring systems. An intra­molecular C—H⋯F short contact occurs. In the crystal, non-classical C—H⋯O inter­actions, one of which has a short H⋯O contact of 2.28 Å, link the mol­ecules