catena-Poly[[(dichloridozinc)-μ-4,4′-bis­(1H-imidazol-1-yl)biphenyl-κ2 N 3:N 3′] 0.25-hydrate]

In the title one-dimensional coordination polymer, {[ZnCl2(C18H14N4)]·0.25H2O}n, the ZnII atom is coordinated by two chloride ions and two 4,4′-bis­(1H-imidazol-1-yl)biphenyl ligands, generating a distorted tetra­hedral ZnCl2N2 geometry. The dihedral angle between the benzene rings of the ligand is 51.0 (1)° and the dihedral angles between the benzene rings and their attached imidazole rings are 18.7 (2) and 45.9 (1)°. The bridging ligand leads to [10-1] polymeric chains in the crystal and the disordered water mol­ecule (occupancy 0.25) forms O—H⋯Cl hydrogen bonds

Developing tTA Transgenic Rats for Inducible and Reversible Gene Expression

To develop transgenic lines for conditional expression of desired genes in rats, we generated several lines of the transgenic rats carrying the tetracycline-controlled transactivator (tTA) gene. Using a vigorous, ubiquitous promoter to drive the tTA transgene, we obtained widespread expression of tTA in various tissues. Expression of tTA was sufficient to strongly activate its reporter gene, but was below the toxicity threshold. We examined the dynamics of Doxycycline (Dox)-regulated gene expression in transgenic rats. In the two transmittable lines, tTA-mediated activation of the reporter gene was fully subject to regulation by Dox. Dox dose-dependently suppressed tTA-activated gene expression. The washout time for the effects of Dox was dose-dependent. We tested a complex regime of Dox administration to determine the optimal effectiveness and washout duration. Dox was administered at a high dose (500 μg/ml in drinking water) for two days to reach the effective concentration, and then was given at a low dose (20 μg/ml) to maintain effectiveness. This regimen of Dox administration can achieve a quick switch between ON and OFF statuses of tTA-activated gene expression. In addition, administration of Dox to pregnant rats fully suppressed postnatal tTA-activated gene expression in their offspring. Sufficient levels of Dox are present in mother's milk to produce maximal efficacy in nursing neonates. Administration of Dox to pregnant or nursing rats can provide a continual suppression of tTA-dependent gene expression during embryonic and postnatal development. The tTA transgenic rat allows for inducible and reversible gene expression in the rat; this important tool will be valuable in the development of genetic rat models of human diseases

Dual-Polarized Communication Rectenna Array for Simultaneous Wireless Information and Power Transmission

A dual-polarized communication rectenna array with high isolation and low cross polarization for simultaneous wireless information and power transmission (SWIPT) is presented. It consists of a 2 × 2 element receiving antenna array and a high efficiency rectifier based on voltage doubler topology. The receiving element is corner-fed to achieve high isolation of more than 20 dB between the dual-polarized ports, which guarantees low mutual interference between the communication and the rectifying ports. To receive enough electromagnetic (EM) wave for rectifying and meanwhile meet the communication sensitivity, this 2 × 2 array uses its 2 × 2 vertical polarization ports and 1 × 2 horizontal polarization ports for power rectifying, and the rest 1 × 2 horizontal polarization ports for communication. For the communication port, the measured gain is 10.9 dBi and the cross polarization is less than -20 dB. The performance of the whole communication rectenna array has been measured, where a 2 × 4 circularly-polarized array with a gain of 17.5 dBi, settled 1 meter away is used as the transmitter. Measured results show that the system achieves a peak microwave - direct circuit (mw-dc) conversion efficiency of 74.9 % for the CW signal, and 67 % for the QPSK signal with 10 MHz channel bandwidth on the load of 345 Ω at 2.58 GHz operating frequency

Temporal Expression of Mutant LRRK2 in Adult Rats Impairs Dopamine Reuptake

Parkinson's disease (PD) results from progressive degeneration of dopaminergic neurons. Most PD cases are sporadic, but some have pathogenic mutation in the individual genes. Mutation of the leucine-rich repeat kinase-2 (LRRK2) gene is associated with familial and sporadic PD, as exemplified by G2019S substitution. While constitutive expression of mutant LRRK2 in transgenic mice fails to induce neuron death, transient expression of the disease gene by viral delivery causes a substantial loss of dopaminergic neurons in mice. To further assess LRRK2 pathogenesis, we created inducible transgenic rats expressing human LRRK2 with G2019S substitution. Temporal overexpression of LRRK2G2019S in adult rats impaired dopamine reuptake by dopamine transporter (DAT) and thus enhanced locomotor activity, the phenotypes that were not observed in transgenic rats constitutively expressing the gene throughout life time. Reduced DAT binding activity is an early sign of dopaminergic dysfunction in asymptomatic subjects carrying pathogenic mutation in LRRK2. Our transgenic rats recapitulated the initiation process of dopaminergic dysfunction caused by pathogenic mutation in LRRK2. Inducible transgenic approach uncovered phenotypes that may be obscured by developmental compensation in constitutive transgenic rats. Finding in inducible LRRK2 transgenic rats would guide developing effective strategy in transgenic studies: Inducible expression of transgene may induce greater phenotypes than constitutive gene expression, particularly in rodents with short life time

Coverage Dependent H2_2 Desorption Energy: a Quantitative Explanation Based on Encounter Desorption Mechanism

Recent experiments show that the desorption energy of H$_2$ on a diamond-like carbon (DLC) surface depends on the H$_2$ coverage of the surface. We aim to quantitatively explain the coverage dependent H$_2$ desorption energy measured by the experiments. We derive a math formula to calculate an effective H$_2$ desorption energy based on the encounter desorption mechanism. The effective H$_2$ desorption energy depends on two key parameters, the desorption energy of H$_2$ on H$_2$ substrate and the ratio of H$_2$ diffusion barrier to its desorption energy. The calculated effective H$_2$ desorption energy qualitatively agrees with the coverage dependent H$_2$ desorption energy measured by the experiments if the values of these two parameters in literature are used in the calculations. We argue that the difference between the effective H$_2$ desorption energy and the experimental results is due to the lacking of knowledge about these two parameters. So, we recalculate these two parameters based on experimental data. Good agreement between theoretical and experimental results can be achieved if these two updated parameters are used in the calculations.Comment: 6 pages,6 figures,2 tables, accepted for publication in MNRA

Transgenic Rat Model of Neurodegeneration Caused by Mutation in the \u3ci\u3eTDP\u3c/i\u3e Gene

TDP-43 proteinopathies have been observed in a wide range of neurodegenerative diseases. Mutations in the gene encoding TDP-43 (i.e., TDP) have been identified in amyotrophic lateral sclerosis (ALS) and in frontotemporal lobe degeneration associated with motor neuron disease. To study the consequences of TDP mutation in an intact system, we created transgenic rats expressing normal human TDP or a mutant form of human TDP with a M337V substitution. Overexpression of mutant, but not normal, TDP caused widespread neurodegeneration that predominantly affected the motor system. TDP mutation reproduced ALS phenotypes in transgenic rats, as seen by progressive degeneration of motor neurons and denervation atrophy of skeletal muscles. This robust rat model also recapitulated features of TDP-43 proteinopathies including the formation of TDP-43 inclusions, cytoplasmic localization of phosphorylated TDP-43, and fragmentation of TDP-43 protein. TDP transgenic rats will be useful for deciphering the mechanisms underlying TDP-43– related neurodegenerative diseases