Diaqua­bis­(2,2′-bi-1H-imidazole)­man­ganese(II) benzene-1,4-di­carboxyl­ate

The asymmetric unit of the title compound, [Mn(C6H6N4)2(H2O)2](C8H4O4), contains one-half each of the centrosymmetric cation and anion. The MnII atom is coordinated by four N atoms [Mn—N = 2.2168 (14) and 2.2407 (14) Å] from two 2,2′-biimidazole ligands and two water mol­ecules [Mn—O = 2.2521 (14) Å] in a distorted octa­hedral geometry. Inter­molecular N—H⋯O and O—H⋯O hydrogen bonds consol­idate the crystal packing, which also exhibits π–π inter­actions between five-membered rings, with a centroid–centroid distance of 3.409 (2) Å

Prevention of Diabetic Complications by Activation of Nrf2: Diabetic Cardiomyopathy and Nephropathy

Diabetic cardiomyopathy and nephropathy are two major causes of death of patients with diabetes. Extra generation of reactive oxygen species (ROS), induced by hyperglycemia, is considered as the main reason for the development of these diabetic complications. Transcription factor, NFE2-related factor 2 (Nrf2), is a master regulator of cellular detoxification response and redox status, and also provides a protective action from various oxidative stresses and damages. Recently we have demonstrated its important role in determining the susceptibility of cells or tissues to diabetes-induced oxidative stress and/or damage. Therefore, this review will specifically summarize the information available regarding the effect of Nrf2 on the diabetic complications with a focus on diabetic cardiomyopathy and nephropathy. Given the feature that Nrf2 is easily induced by several compounds, we also discussed the role of different Nrf2 activators in the prevention or therapy of various diabetic complications. These findings suggest that Nrf2 has a potential application in the clinic setting for diabetic patients in the short future

Prevention of Streptozotocin-Induced Diabetic Nephropathy by MG132: Possible Roles of Nrf2 and I κ

Our previous study showed that proteasomal inhibitor MG132 can prevent diabetic nephropathy (DN) along with upregulation of nuclear factor (erythroid-derived 2)-like 2 (Nrf2). The present study was to investigate whether MG132 can prevent DN in wild-type and Nrf2-KO mice. Type 1 diabetes was induced in wild-type and Nrf2-KO mice by multiple low doses of streptozotocin. Two weeks after streptozotocin injection, both wild-type and Nrf2-KO mice were randomly divided into four groups: control, MG132, DM, and DM/MG132. MG132 (10 μg/kg/day) or vehicle was administered intraperitoneally for 4 months. Renal function, morphology, and biochemical changes were measured after 4-month treatment with MG132. MG132 treatment suppressed proteasomal activity in the two genotypes. In wild-type mice, MG132 attenuated diabetes-induced renal dysfunction, fibrosis, inflammation, and oxidative damage along with increased Nrf2 and IκB expression. Deletion of Nrf2 gene resulted in a partial, but significant attenuation of MG132 renal protection in Nrf2-KO mice compared with wild-type mice. MG132-increased IκB expression was not different between wild-type and Nrf2-KO mice. This work indicates that MG132 inhibits diabetes-increased proteasomal activity, resulting in Nrf2 and IκB upregulation and renal protection, which could be used as a strategy to prevent diabetic nephropathy

Prevention of Diabetic Nephropathy by Sulforaphane: Possible Role of Nrf2 Upregulation and Activation

The present study was to investigate whether sulforaphane (SFN) can prevent diabetic nephropathy in type 1 diabetic mouse model induced by multiple low-dose streptozotocin. Diabetic and age-matched control mice were given SFN at 0.5 mg/kg body weight daily for 3 months. At the end of 3-month SFN treatment, the diabetic nephropathy, shown by renal inflammation, oxidative damage, fibrosis, and dysfunction, was significantly prevented along with an elevation of renal Nrf2 expression and transcription in diabetes/SFN group compared with diabetic group. However, this renal prevention by SFN was not seen when the 3-month SFN-treated diabetic mice were aged for additional 3 months without further SFN treatment. Nrf2-mediated renal protective effects in diabetes were evaluated in human renal tubular HK11 cells transfected with control and Nrf2 siRNA and treated with 27.5 mM mannitol or high glucose plus palmitate (300 μM). Blockade of Nrf2 expression completely abolished SFN prevention of the profibrotic effect induced by high glucose plus palmitate. These results support that renal Nrf2 expression and its transcription play important roles in SFN prevention of diabetes-induced renal damage. However, the SFN preventive effect on diabetes-induced renal pathogeneses is not sustained, suggesting the requirement of continual use of SFN for its sustained effect

Hard superconducting gap in PbTe nanowires

Semiconductor nanowires coupled to a superconductor provide a powerful testbed for quantum device physics such as Majorana zero modes and gate-tunable hybrid qubits. The performance of these quantum devices heavily relies on the quality of the induced superconducting gap. A hard gap, evident as vanishing subgap conductance in tunneling spectroscopy, is both necessary and desired. Previously, a hard gap has been achieved and extensively studied in III-V semiconductor nanowires (InAs and InSb). In this study, we present the observation of a hard superconducting gap in PbTe nanowires coupled to a superconductor Pb. The gap size ($\Delta$) is $\sim$ 1 meV (maximally 1.3 meV in one device). Additionally, subgap Andreev bound states can also be created and controlled through gate tuning. Tuning a device into the open regime can reveal Andreev enhancement of the subgap conductance, suggesting a remarkable transparent superconductor-semiconductor interface, with a transparency of $\sim$ 0.96. These results pave the way for diverse superconducting quantum devices based on PbTe nanowires

Ballistic PbTe Nanowire Devices

Disorder is the primary obstacle in current Majorana nanowire experiments. Reducing disorder or achieving ballistic transport is thus of paramount importance. In clean and ballistic nanowire devices, quantized conductance is expected with plateau quality serving as a benchmark for disorder assessment. Here, we introduce ballistic PbTe nanowire devices grown using the selective-area-growth (SAG) technique. Quantized conductance plateaus in units of $2e^2/h$ are observed at zero magnetic field. This observation represents an advancement in diminishing disorder within SAG nanowires, as none of the previously studied SAG nanowires (InSb or InAs) exhibit zero-field ballistic transport. Notably, the plateau values indicate that the ubiquitous valley degeneracy in PbTe is lifted in nanowire devices. This degeneracy lifting addresses an additional concern in the pursuit of Majorana realization. Moreover, these ballistic PbTe nanowires may enable the search for clean signatures of the spin-orbit helical gap in future devices

Reducing disorder in PbTe nanowires for Majorana research

Material challenges are the key issue in Majorana nanowires where surface disorder constrains device performance. Here, we tackle this challenge by embedding PbTe nanowires within a latticematched crystal, an oxide-free environment. The wire edges are shaped by self-organized growth instead of lithography, resulting in nearly-atomic-flat facets along both cross-sectional and longitudinal directions. Quantized conductance plateaus are observed at zero magnetic field with channel lengths reaching 1.54 $\mu$m, significantly surpassing the state-of-the-art of III-V nanowires (nearly an order-of-magnitude improvement compared to InSb). Coupling PbTe to a Pb film unveils a flat interface spanning microns and a large superconducting gap of 1 meV. Our results meet the stringent low-disorder requirement for the definitive observation of Majoranas

Optimal design, modeling and control of a long stroke 3-PRR compliant parallel manipulator with variable thickness flexure pivots

Optimal design, modeling and control of a long stroke 3-PRR compliant parallel manipulator with variable thickness flexure pivot