Self-adhesive, conductive, and multifunctional hybrid hydrogel for flexible/wearable electronics based on triboelectric and piezoresistive sensor.

Flexible electronics are highly developed nowadays in human-machine interfaces (HMI). However, challenges such as lack of flexibility, conductivity, and versatility always greatly hindered flexible electronics applications. In this work, a multifunctional hybrid hydrogel (H-hydrogel) was prepared by combining two kinds of 1D polymer chains (polyacrylamide and polydopamine) and two kinds of 2D nanosheets (Ti3C2Tx MXene and graphene oxide nanosheets) as quadruple crosslinkers. The introduced Ti3C2Tx MXene and graphene oxide nanosheets are bonded with the PAM and PDA polymer chains by hydrogen bonds. This unique crosslinking and stable structure endow the H-hydrogel with advantages such as good flexibility, electrical conductivity, self-adhesion, and mechanical robustness. The two kinds of nanosheets not only improved the mechanical strength and conductivity of the H-hydrogel, but also helped to form the double electric layers (DELs) between the nanosheets and the bulk-free water phase inside the H-hydrogel. When utilized as the electrode of a triboelectric nanogenerator (TENG), high electrical output performances were realized due to the dynamic balance of the DELs between the nanosheets and the H-hydrogel's inside water molecules. Moreover, flexible sensors, including triboelectric, and strain/pressure sensors, were achieved for human motion detection at low frequencies. This hydrogel is promising for HMI and e-skin.

Toxic effects of hexavalent chromium (Cr6+) on bioaccumulation, apoptosis, oxidative damage and inflammatory response in Channa asiatica.

The objective of this study was to evaluate the toxic effects of Cr6+ on bioaccumulation, digestion, immunity, oxidative stress, apoptosis and inflammation-related genes in Channa asiatica. The fish was exposed to waterborne Cr6+ concentrations (0, 0.5, 1.0 and 2.0 mg/L) for 28 and 56 days. Our results demonstrated that the accumulation of Cr6+ in tissues increased in a concentration-dependent manner, and the content in tissue was liver > gill > gut > muscle. Meanwhile, Cr6+ exposure led to a remarkable suppression of digestion, immunity and antioxidant capacity in C. asiatica. Inversely, MDA and PC content were positively correlated with Cr6+ exposure concentration. Furthermore, the expression of genes went up with the increase of waterborne Cr6+ concentration. Among them, HSP90, NF-κB and TNF-α have a sharp increase. These results elucidate that waterborne Cr6+ exposure may induce bioaccumulation, inhibit digestion and immunity, promote oxidative stress and up-regulate the expression of apoptosis and inflammation-related genes in C. asiatica.

Somatic Mutation Profiling of Intrahepatic Cholangiocarcinoma: Comparison between Primary and Metastasis Tumor Tissues.

INTRODUCTION: Intrahepatic cholangiocarcinoma (ICC) exhibited increasing incidence and mortality around the world, with a 35% five-year survival rate. In this study, the genetic alteration of primary ICC and metastasis ICC was exhibited to discover novel personalized treatment strategies to improve the clinical prognosis. METHODS: Based on 153 primary and 49 metastasis formalin-fixed paraffin-embedded ICC samples, comprehensive genomic profiling was carried out. RESULTS: In primary tumor samples (PSs) and metastasis tumor samples (MSs), the top alteration genes were TP53 (41.8% vs 36.7%), KRAS (30.7% vs 36.7%), and ARID1A (22.2% vs 14.2%). In the top 20 most frequent alteration genes, BRAF showed lower mutation frequency in MSs as compared to PSs (0 vs 11.1%, P=0.015), while LRP1B exhibited opposed trend (22.4% vs 10.4%, P=0.032). In PSs, patients with MSI-H showed all PDL1 negative, and patients with PDL1 positive exhibited MSS both in PSs and MSs. It was found that the Notch pathway had more alteration genes in MSI-H patients (P=0.027). Furthermore, the patients with mutated immune genes in PSs were more than that in MSs (28.8% vs 8.2%, P=0.003, odd ratio = 0.2). Interestingly, the platinum drug resistance pathway was only enriched by mutated genes of MSs. CONCLUSIONS: In this study, the identification of two meaningful mutated genes, BRAF and LRP1B, highly mutated immune gene harbored by primary ICC patients. Both in PSs and MSs, no patients with MSI-H showed PDL1 positive. The Notch pathway had more alteration genes in patients with MSI-H. And the enrichment of the platinum drug resistance pathway in MSs might offer reference for the novel therapeutic strategy of ICC.

Overexpression of interleukin-32α promotes invasion by modulating VEGF in hepatocellular carcinoma.

Interleukin-32α (IL-32α) was reported to exhibit pluripotent pro-inflammatory properties. Recent studies indicate that it promotes the migration and invasion of cancers. We detected the expression of IL-32 in hepatocellular carcinoma (HCC) tissues and investigated its role in tumor angiogenesis and invasion. IL-32α expression in HCC was evaluated by real-time PCR, western blot analysis and immunohistochemical (IHC) staining. Secreted serum IL-32α and VEGF concentrations were detected using a custom-made sandwich ELISA. Furthermore, IL-32α was knocked down in HCC cell lines using siRNA and the cell migration and invasion abilities were assessed. IHC staining showed that IL32α-positive particles were mainly located in the cytoplasm of cancer cells, and it was significantly upregulated in the tumor tissues compared with that in peritumoral tissues. Notably, IL-32α was strongly expressed in perivascular areas. The mean serum concentration of IL-32α in HCC patients was significantly higher than that in the control group (571.45±102.28 vs. 144.60±51.172 pg/ml; P<0.01). Real-time RT-PCR showed that IL-32α mRNA was significantly overexpressed in HCC tumor tissues (IL-32/ß-actin, 15.59±7.8 vs. 3.37±0.47; P<0.01). The in vitro results indicated that IL-32α knockdown inhibited the activation of VEGF-STAT3 signaling in HCC tumor cell lines. IL-32α expression was correlated with clinical relevance in HCC tumor tissues. It is strongly suggested that IL-32α may be a potential predictor of anti-angiogenesis therapy and prognosis of HCC.

Diagnostic and therapeutic strategies to manage post-pancreaticoduodenectomy hemorrhage.

OBJECTIVE: To explore the causes, diagnosis and treatment of post-pancreaticoduodenectomy hemorrhages (PPHs). METHODS: A database of 703 pancreaticoduodenectomy patients in our institution (January 2008-July 2013) was analyzed retrospectively. RESULTS: PPHs occurred in 62 patients of which, 38 had clear causes and 15 died because of uncontrolled bleeding and multiple organ failure. Pancreatic fistula and abdominal infection rates were significantly higher in the PPH group compared to the group who did not experience hemorrhages (P < 0.05) but did not significantly increase the mortality of PPH patients. Hemostasis was attempted by endotherapy in 7 patients and was successful in 4 (57.1 %). Angioembolization was performed in 12 patients and was successful in 10 (83.3 %) and relaparotomy in 24 patients successful in 13 (54.2 %). All deceased patients belonged to International Study Group of Pancreatic Surgery clinical grade C and sentinel bleeding occurred in 60 % of PPH mortalities (9/15) (P = 0.005). CONCLUSION: Pancreatic fistulae and abdominal infections are associated with PPH. Control of early mild upper gastrointestinal hemorrhages could be attempted by endotherapy, but angiography with intervention or surgical treatments were always required for delayed bleeding. The mortality in cases with sentinel bleedings was obviously increased.

[Refined mapping of heterozygosity loss on chromosome 5p15 in sporadic colorectal cancer].

OBJECTIVE: To refine the loss of heterozygosity (LOH) on chromosome 5p15 and screen new tumor suppressor gene(s) in colorectal tumorigenesis. METHODS: Samples of colorectal cancer and normal tissue of 83 cases were collected in this study. Sixteen polymorphic microsatellite markers were analyzed on chromosome 5 and another 6 markers on chromosome 5p15 by PCR. PCR products were electrophoresed on an ABI 377 DNA sequencer. Genescan 3.1 and Genotype 2.1 software were used for LOH scanning and analysis. RESULTS: Two distinct regions of frequent allelic deletions at D5S416 on 5p15 and D5S428-D5S410 on 5q were detected. Another 6 polymorphic microsatellite markers were applied to 5p15 and the minimal region of frequrent loss of heterozygosity was established on 5p15 spanning the D5S416 locus. CONCLUSION: A critical and precise location of 5p deletions, 5p15.2-5p15.3, has been detected, which may contain one or more unknown tumor suppressor gene(s) related to colorectal cancer.

Refinement of heterozygosity loss on chromosome 5p15 in sporadic colorectal cancer.

AIM: To refine the loss of heterozygosity on chromosome 5p15 and to identify the new tumor suppressor gene (s) in colorectal tumorigenesis. METHODS: Sixteen polymorphic microsatellite markers were analyzed on chromosome 5 and another 6 markers were applied on chromosome 5p15 in 83 cases of colorectal and normal DNA by PCR. PCR products were electrophoresed on an ABI 377 DNA sequencer. Genescan 3.1 and Genotype 2.1 software were used for LOH scanning and analysis. RESULTS: We observed 2 distinct regions of frequent allelic deletions on Chromosome 5, at D5S416 on 5p15 and D5S428-D5S410 on 5q. Another 6 polymorphric microsatellite markers were applied to 5p15 and the minimal region of frequent loss of heterozygosity was established on 5p15 spanning the D5S416 locus. CONCLUSION: Through our detailed deletion mapping studies, we have found a critical and precise location of 5p deletions, 5p15.2-5p15.3, which must contain one or more unknown tumor suppressor gene (s) of colorectal cancer.