Manipulation of Zinc Oxide with Zirconium Doping for Efficient Inverted Organic Solar Cells.

Solution-processed zinc oxide (ZnO) is one of the widely used electron transporting layers (ETLs) for organic solar cells (OSCs). However, low optical transparency along with thickness-sensitivity of ZnO ETL constrains the improvement of photovoltaic performance and large-scale fabrication compatibility. To resolve these issues, zirconium (Zr) doping is applied to tailor the optoelectronic and morphological properties of ZnO layer. This approach not only improves light transmittance with the suppressed parasitic absorption, but also provides an optimized surface morphology for enhancing charge extraction property and reducing potential of charge trap-assisted recombination. By using ZnO:Zr as ETL in inverted device configuration, the maximum power conversion efficiency (PCE) of PM6:Y6:PC71 BM solar cell devices is up to 17.2%, which makes an enhancement of 9.55% compared to ZnO-based devices (15.7%). As the thickness of ZnO:Zr ETL increases to ≈60 nm, the presence of the lower parasitic absorption together with uniform surface morphology can help photovoltaic performance maintain above 15%, which is beyond the performance of the pristine ZnO-based device achieving only 11.9%. Such superiority of ZnO:Zr ETL is also validated by a series of well-known BHJ systems, where in comparison with the devices based on pristine ZnO ETL, a better photovoltaic performance from ZnO:Zr device can be achieved.

Shikonin Attenuates Concanavalin A-Induced Acute Liver Injury in Mice via Inhibition of the JNK Pathway.

OBJECTIVE: Shikonin possesses anti-inflammatory effects. However, its function in concanavalin A-induced acute liver injury remains uncertain. The aim of the present study was to investigate the functions of shikonin and its mechanism of protection on ConA-induced acute liver injury. MATERIALS AND METHODS: Balb/C mice were exposed to ConA (20 mg/kg) via tail vein injection to establish acute liver injury; shikonin (7.5 mg/kg and 12.5 mg/kg) was intraperitoneally administered 2 h before the ConA injection. The serum liver enzyme levels and the inflammatory cytokine levels were determined at 3, 6, and 24 h after ConA injection. RESULTS: After the injection of ConA, inflammatory cytokines IL-1ß, TNF-α, and IFN-γ were significantly increased. Shikonin significantly ameliorated liver injury and histopathological changes and suppressed the release of inflammatory cytokines. The expressions of Bcl-2 and Bax were markedly affected by shikonin pretreatment. LC3, Beclin-1, and p-JNK expression levels were decreased in the shikonin-pretreated groups compared with the ConA-treated groups. Shikonin attenuated ConA-induced liver injury by reducing apoptosis and autophagy through the inhibition of the JNK pathway. CONCLUSION: Our results indicated that shikonin pretreatment attenuates ConA-induced acute liver injury by inhibiting apoptosis and autophagy through the suppression of the JNK pathway.

Block Proposal Neural Architecture Search.

The existing neural architecture search (NAS) methods usually restrict the search space to the pre-defined types of block for a fixed macro-architecture. However, this strategy will limit the search space and affect architecture flexibility if block proposal search (BPS) is not considered for NAS. As a result, block structure search is the bottleneck in many previous NAS works. In this work, we propose a new evolutionary algorithm referred to as latency EvoNAS (LEvoNAS) for block structure search, and also incorporate it to the NAS framework by developing a novel two-stage framework referred to as Block Proposal NAS (BP-NAS). Comprehensive experimental results on two computer vision tasks demonstrate the superiority of our newly proposed approach over the state-of-the-art lightweight methods. For the classification task on the ImageNet dataset, our BPN-A is better than 1.0-MobileNetV2 with similar latency, and our BPN-B saves 23.7% latency when compared with 1.4-MobileNetV2 with higher top-1 accuracy. Furthermore, for the object detection task on the COCO dataset, our method achieves significant performance improvement than MobileNetV2, which demonstrates the generalization capability of our newly proposed framework.

Metformin and Diammonium Glycyrrhizinate Enteric-Coated Capsule versus Metformin Alone versus Diammonium Glycyrrhizinate Enteric-Coated Capsule Alone in Patients with Nonalcoholic Fatty Liver Disease and Type 2 Diabetes Mellitus.

Objective. The present study was conducted to compare the efficacy of metformin combined with diammonium glycyrrhizinate enteric-coated capsule (DGEC) versus metformin alone versus DGEC alone for the treatment of nonalcoholic fatty liver disease (NAFLD) in patients with type 2 diabetes mellitus (T2DM). Subjects and Methods. 163 patients with NAFLD and T2DM were enrolled in this 24-week study and were randomized to one of three groups: group 1 was treated with metformin alone; group 2 was treated with DGEC alone; group 3 received metformin plus DGEC combination therapy. Anthropometric parameters, liver function, lipid profile, serum ferritin (SF), metabolic parameters, liver/spleen computed tomography (CT) ratio, and fibroscan value were evaluated at baseline and after 8, 16, and 24 weeks of treatment. Results. After 24 weeks, significant improvements in all measured parameters were observed in three groups (P < 0.05) except for the improvements in low density lipoprotein cholesterol (LDL-C) and metabolic parameters in group 2 which did not reach statistical significance (P > 0.05). Compared with group 1 and group 2, the patients in group 3 had greater reductions in observed parameters apart from CB and TB (P < 0.05). Conclusions. This study showed that metformin plus DGEC was more effective than metformin alone or DGEC alone in reducing liver enzymes, lipid levels, and metabolic parameters and ameliorating the degree of hepatic fibrosis in patients with NAFLD and T2DM.

The protective effects of shikonin on hepatic ischemia/reperfusion injury are mediated by the activation of the PI3K/Akt pathway.

Hepatic ischemia/reperfusion (I/R) injury, which can result in severe liver injury and dysfunction, occurs in a variety of conditions such as liver transplantation, shock, and trauma. Cell death in hepatic I/R injury has been linked to apoptosis and autophagy. Shikonin plays a significant protective role in ischemia/reperfusion injury. The purpose of the present study was to investigate the protective effect of shikonin on hepatic I/R injury and explore the underlying mechanism. Mice were subjected to segmental (70%) hepatic warm ischemia to induce hepatic I/R injury. Two doses of shikonin (7.5 and 12.5 mg/kg) were administered 2 h before surgery. Balb/c mice were randomly divided into four groups: normal control, I/R, and shikonin preconditioning at two doses (7.5 and 12.5 mg/kg). The serum and liver tissues were collected at three time points (3, 6, and 24 h). Shikonin significantly reduced serum AST and ALT levels and improved pathological features. Shikonin affected the expression of Bcl-2, Bax, caspase 3, caspase 9, Beclin-1, and LC3, and upregulated PI3K and p-Akt compared with the levels in the I/R group. Shikonin attenuated hepatic I/R injury by inhibiting apoptosis and autophagy through a mechanism involving the activation of PI3K/Akt signaling.

Protective effect of fucoidan from Fucus vesiculosus on liver fibrosis via the TGF-ß1/Smad pathway-mediated inhibition of extracellular matrix and autophagy.

Liver fibrosis is a dynamic reversible pathological process in the development of chronic liver disease to cirrhosis. However, the current treatments are not administered for a long term due to their various side effects. Autophagy is initiated to decompose damaged or excess organelles, which had been found to alter the progression of liver fibrosis. In this article, we hypothesized that fucoidan from Fucus vesiculosus may attenuate liver fibrosis in mice by inhibition of the extracellular matrix and autophagy in carbon tetrachloride- and bile duct ligation-induced animal models of liver fibrosis. The results were determined using enzyme-linked immunosorbent assay, quantitative real-time polymerase chain reaction, Western blotting, and immunohistochemical staining. Fucoidan from F. vesiculosus could inhibit the activation of hepatic stellate cells and the formation of extracellular matrix and autophagosomes, and its effect may be associated with the downregulation of transforming growth factor beta 1/Smads pathways. Fucoidan, as an autophagy and transforming growth factor beta 1 inhibitor, could be a promising potential therapeutic agent for liver fibrosis.

15d-PGJ2 alleviates ConA-induced acute liver injury in mice by up-regulating HO-1 and reducing hepatic cell autophagy.

OBJECTIVE: In this study, we confirmed a protective effect of 15d-PGJ2 in concanavalin A (ConA)-induced fulminant hepatitis in mice and investigated the potential mechanism. MATERIALS AND METHODS: Balb/C mice were injected with ConA (25mg/kg) to induce acute fulminant hepatitis, and 15d-PGJ2 (2.5-10µg) was administered 30min after the ConA injection. The histological grade, pro-inflammatory cytokine and ROS levels, apoptosis and autophagy activity, the expression of HO-1, Nrf2, JNK and Bcl-2 activity were determined 2, 4, and 8h after the ConA injection. RESULTS: Following ConA challenge, the expression of cytokines tumor necrosis factor α (TNF-α) and interleukin 1ß (IL-1ß) was up-regulated. Treatment with 15d-PGJ2 reduced the pathological effects of ConA-induced fulminant hepatitis and significantly reduced the levels of TNF-α, IL-1ß and ROS after injection. 15d-PGJ2 inhibited apoptosis and autophagic cell death, facilitated Nrf2 nuclear translocation, increased HO-1 expression and suppressed the JNK activation. CONCLUSION: 15d-PGJ2 alleviates ConA-induced acute liver injury in mice by up-regulating the anti-oxidative stress factor HO-1 and reducing the production of cytokines and ROS, thereby inhibiting hepatic cell autophagy probably induced by ROS.

In vitro and in vivo study of epigallocatechin-3-gallate-induced apoptosis in aerobic glycolytic hepatocellular carcinoma cells involving inhibition of phosphofructokinase activity.

Glycolysis, as an altered cancer cell-intrinsic metabolism, is an essential hallmark of cancer. Phosphofructokinase (PFK) is a metabolic sensor in the glycolytic pathway, and restricting the substrate availability for this enzyme has been researched extensively as a target for chemotherapy. In the present study, we investigated that the effects of epigallocatechin-3-gallate (EGCG), an active component of green tea, on inhibiting cell growth and inducing apoptosis by promoting a metabolic shift away from glycolysis in aerobic glycolytic hepatocellular carcinoma (HCC) cells. EGCG modulated the oligomeric structure of PFK, potentially leading to metabolic stress associated apoptosis and suggesting that EGCG acts by directly suppressing PFK activity. A PFK activity inhibitor enhanced the effect, while the allosteric activator reversed EGCG-induced HCC cell death. PFK siRNA knockdown-induced apoptosis was not reversed by the activator. EGCG enhanced the effect of sorafenib on cell growth inhibition in both aerobic glycolytic HCC cells and in a xenograft mouse model. The present study suggests a potential role for EGCG as an adjuvant in cancer therapy, which merits further investigation at the clinical level.

Cerebral Hemodynamics and Cognitive Function in Cirrhotic Patients with Hepatic Encephalopathy.

Aims. To investigate cerebral hemodynamics in cirrhotic patients with HE and to observe effects of treatment in cerebral hemodynamics and correlations among ammonia, cerebral hemodynamics, and cognitive function. Methods. There were four groups: healthy controls (group 1), cirrhosis without HE (group 2), cirrhosis with MHE (group 3), and cirrhosis with OHE (group 4). Ammonia and cerebral hemodynamics (by TCD) were assessed. Patients in group 3 were subsequently randomized to two subgroups: the control (group A) and the treated (group B, treated with lactulose for two months), and they were retested for ammonia and TCD after treatment. RESULTS: Ammonia, Vm , Vd , PI, and RI were statistically different before treatment, and ammonia, PI, and RI levels paralleled the severity of HE (P < 0.05). In group B, Vd increased and ammonia, PI, and RI declined following treatment (P < 0.05), while there were no differences in group A (P > 0.05). Correlations were found between ammonia and Vd , PI, RI, NCT-A, and DST and also found between Vd , PI, RI, and NCT-A and DST (P < 0.05). Conclusions. This study revealed that cerebral hemodynamics were related to the severity of HE and cerebral autoregulation was impaired. There were tight correlations among ammonia, cerebral hemodynamics, and cognitive function, and, following treatment, cerebral hemodynamics improved.