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Nonalcoholic fatty liver disease (NAFLD) is an independent risk factor for severe acute pancreatitis (AP). The underlying mechanism remains unclear. We sought to determine how bacterial translocation and cholesterol metabolism in the liver and pancreas affect the severity of AP in NAFLD mice.C57BL/6N mice were fed on a high-fat diet (HFD) to generate the NAFLD model, and mice in the control group were provided with a normal diet (ND). After being anesthetized with ketamine/xylazine, mice got a retrograde infusion of taurocholic acid sodium into the pancreatic duct to induce AP, and sham operation (SO) was used as control. Serum amylase and Schmidt's pathological score system were used to evaluate AP severity. Bacterial loads, total cholesterol level, and cholesterol metabolic-associated molecules [low-density lipoprotein receptor (LDLR) and ATP-binding cassette transporter A1 (ABCA1)] were analyzed in the liver and pancreas.Compared with the ND-AP group, mice in the HFD-AP group had severer pancreatitis, manifested with higher serum amylase levels and higher AP pathologic scores, especially the inflammation and hemorrhage scores. Compared with the HFD-SO group and ND-AP group, bacterial loads in the liver and pancreas were significantly higher in the HFD-AP group. Mice in the HFD-AP group showed a decreased LDLR expression and an increased ABCA1 expression in the pancreas, although there was no significant difference in pancreas total cholesterol between the HFD-AP group and the ND-AP group.NAFLD aggravates AP via increasing bacterial translocation in the liver and pancreas and affecting pancreas cholesterol metabolism in mice.

Tamoxifen (TAM) resistance has indicated a significant challenge during endocrine therapy for hormone-sensitive breast cancer. Thus, it is significant to elucidate the molecular events endowing TAM resistance to endocrine therapy. In this study, we found that epithelial-mesenchymal transition (EMT) was an important event to confer TAM resistance, and attenuating EMT by elevating connexin (Cx) 43 expression could reverse TAM resistance. Specifically, Cx43 overexpression improved TAM sensitivity, while Cx43 depletion facilitated TAM insensitivity by modulating EMT in T47D TAM-resistant and -sensitive cells, and transplanted xenografts. Importantly, we found a novel reciprocal regulation between Cx43 and c-Src/PI3K/Akt pathway contributing to EMT and TAM resistance in breast cancer. Moreover, we identified that Cx43 deficiency was significantly correlated with poor relapse-free survival in patients undergoing TAM treatment. Therefore, Cx43 represents a prognostic marker and an attractive target for breast cancer treatments. Therapeutic strategies designed to increase or maintain Cx43 function may be beneficial to overcome TAM resistance.

Hepatocellular carcinoma (HCC) is one of the most common types of liver cancer and is the second leading cause of cancer mortality with an estimated 745 500 deaths annually (Jemal et al., 2011). Although new therapeutic modalities including novel chemotherapeutic interventions and targeted therapy have been applied, the prognosis of HCC patients remains unsatisfactory due to the high incidence of intrahepatic and distal metastases (Siegel et al., 2018).

Acute kidney injury (AKI) causes over 1 million deaths worldwide every year. AKI is now recognized as a major risk factor in the development and progression of chronic kidney disease (CKD). Diabetes is the main cause of CKD as well. Renal fibrosis and inflammation are hallmarks in kidney diseases. Various cytokines contribute to the progression of renal diseases; thus, many drugs that specifically block cytokine function are designed for disease amelioration. Numerous studies showed IL-20 functions as a pro-inflammatory mediator to regulate cytokine expression in several inflammation-mediated diseases. In this review, we will outline the effects of pro-inflammatory cytokines in the pathogenesis of AKI and CKD. We also discuss the role of IL-20 in kidney diseases and provide a potential therapeutic approach of IL-20 blockade for treating renal diseases.

In spite of the promising initial treatment responses presented by photodynamic therapy (PDT), 5-year recurrence rates remain high level. Therefore, improvement in the efficacy of PDT is needed. There are reports showing that connexin(Cx) 26-composed gap junctional intercellular communication (GJIC) enhances the intercellular propagation of "death signal", thereby increasing chemotherapeutic cytotoxicity. However, it is unclear whether Cx26-formed GJIC has an effect on PDT phototoxicity. The results in the present study showed that Cx26-composed GJ formation at high density enhances the phototoxicity of Photofrin-PDT. When the Cx26 is not expressed or Cx26 channels are blocked, the phototoxicity in high-density cultures substantially reduces, indicating that the enhanced PDT phototoxicity at high density is mediated by Cx26-composed GJIC. The GJIC-mediated increase in PDT phototoxicity was associated with ROS, calcium and lipid peroxide-mediated stress signaling pathways. The work presents the ability of Cx26-composed GJIC to enhance the sensitivity of malignant cells to PDT, and indicates that maintenance or increase of Cx26-formed GJIC may be a profitable strategy towards the enhancement of PDT therapeutic efficiency. Picture: The survival response of Photofrin-PDT in Dox-treated (Cx26 expressing, GJ-formed) and Dox-untreated cells (Cx26 non-expressing, GJ-unformed) at high-cell density condition.

Background and aim: Glasgow prognostic score is a systemic inflammatory-based score. The aim of this study was to determine whether the Glasgow prognostic score was a useful predictor of short-term outcomes in patients who undergo total proctocolectomy for ulcerative colitis. Methods: eighty ulcerative colitis patients who underwent a total proctocolectomy with ileal pouch-anal anastomosis or permanent end ileostomy from June 2014 to March 2020 were retrospectively analyzed. Patients were divided into a lower Glasgow prognostic score group and a higher Glasgow prognostic score group. Results: postoperative infectious complication occurred more frequently in the higher Glasgow prognostic score group (8.3 % vs 29.5 %, p = 0.018). According to the univariate and multivariate analysis, only a higher Glasgow prognostic score was associated with an increased risk of postoperative infectious complication (OR: 5.478, 95 % CI: 1.236-24.279). Conclusion: Glasgow prognostic score is a simple and useful indicator of postoperative infectious complications.

Adipocyte-macrophage crosstalk plays a critical role to regulate adipose tissue microenvironment and cause chronic inflammation in the pathogenesis of obesity. Interleukin-29 (IL-29), a member of type 3 interferon family, plays a role in host defenses against microbes, however, little is known about its role in metabolic disorders. We explored the function of IL-29 in the pathogenesis of obesity-induced inflammation and insulin resistance. We found that serum IL-29 level was significantly higher in obese patients. IL-29 upregulated IL-1β, IL-8, and monocyte chemoattractant protein-1 (MCP-1) expression and decreased glucose uptake and insulin sensitivity in human Simpson-Golabi-Behmel syndrome (SGBS) adipocytes through reducing glucose transporter 4 (GLUT4) and AKT signals. In addition, IL-29 promoted monocyte/macrophage migration. Inhibition of IL-29 could reduce inflammatory cytokine production in macrophage-adipocyte coculture system, which mimic an obese microenvironment. In vivo, IL-29 reduced insulin sensitivity and increased the number of peritoneal macrophages in high-fat diet (HFD)-induced obese mice. IL-29 increased M1/M2 macrophage ratio and enhanced MCP-1 expression in adipose tissues of HFD mice. Therefore, we have identified a critical role of IL-29 in obesity-induced inflammation and insulin resistance, and we conclude that IL-29 may be a novel candidate target for treating obesity and insulin resistance in patients with metabolic disorders.

It has been reported that the decimation of honey bees was because of pesticides of imidacloprid. The imidacloprid is a wildly used neonicotinoid insecticide. However, whether imidacloprid toxicity interferes with the spatial memory of echolocation bats is still unclear. Thus, we compared the spatial memory of Formosan leaf-nosed bats, Hipposideros terasensis, before and after chronic treatment with a low dose of imidacloprid. We observed that stereotyped flight patterns of echolocation bats that received chronic imidacloprid treatment were quite different from their originally learned paths. We further found that neural apoptosis in hippocampal CA1 and medial entorhinal cortex areas of echolocation bats that received imidacloprid treatment was significantly enhanced in comparison with echolocation bats that received sham treatment. Thus, we suggest that imidacloprid toxicity may interfere with the spatial memory of echolocation bats through neural apoptosis in hippocampal CA1 and medial entorhinal cortex areas. The results provide direct evidence that pesticide toxicity causes a spatial memory disorder in echolocation bats. This implies that agricultural pesticides may pose severe threats to the survival of echolocation bats.

Adipocyte-macrophage crosstalk plays a critical role in regulating adipose tissue microenvironment and causes chronic inflammation in the pathogenesis of obesity. Interleukin-29 (IL-29), a member of type 3 interferon family, plays a role in host defenses against microbes. The macrophage is one of the cellular sources of IL-29; however, the role of IL-29 in metabolic disorders is still unclear. We explored the function of IL-29 in the pathogenesis of obesity-induced inflammation and insulin resistance. We found that serum IL-29 level was significantly higher in obese patients. IL-29 upregulated IL-1β, IL-8, and monocyte chemoattractant protein-1 (MCP-1) expression and decreased glucose uptake and insulin sensitivity in human SGBS adipocytes through reducing glucose transporter 4 (GLUT4) and AKT signals. Inhibition of IL-29 could reduce inflammatory cytokine production in the macrophage-adipocyte co-culture system, which mimics an obese microenvironment. In vivo, IL-29 reduced insulin sensitivity and increased the number of peritoneal macrophages in high-fat diet (HFD)-induced obese mice. IL-29 increased M1/M2 macrophage ratio and enhanced MCP-1 expression in adipose tissues of HFD mice. Therefore, we have identified a critical role of IL-29 in obesity-induced inflammation and insulin resistance, and we conclude that IL-29 may be a novel candidate target for inhibiting obesity-induced inflammation and insulin resistance in patients with metabolic disorders.

The aim of the present study was to determine the role of interleukin-6 (IL-6) in the epithelial-mesenchymal transition (EMT) of human intrahepatic biliary epithelial cell (HIBEC) lines in vitro. HIBECs were stimulated with IL-6 at concentrations of 0, 10, 20, 50 and 100 µg/l for 24 h. A wound healing and Transwell assay were performed to determine the migratory and invasive capacity of HIBECs, respectively. Following 24 h of incubation, IL-6 at 10 and 20 µg/l significantly increased the number of migrated and invaded cells (P

Li 0.5 x Mn 0.4 Ni 0.6– x Fe 2+0.5 x O 4 (0.0≤ x ≤0.3) was obtained by calcining oxalates precursor over 600 °C in air. The precursor and its calcined products were characterized by thermogravimetry and differential scanning calorimetry, X-ray powder diffraction, scanning electron microscopy, and vibrating sample magnetometer. A high-crystallized Li 0.5 x Mn 0.4 Ni 0.6– x Fe 2+0.5 x O 4 with a cubic structure was obtained when the precursor was calcined at 600 °C in air for 2 h. The specific saturation magnetization of Li 0.5 x Mn 0.4 Ni 0.6– x Fe 2+0.5 x O 4 depends on the composition and calcination temperature. Li 0.1 Mn 0.4 Ni 0.4 Fe 2.1 O 4 obtained at 600 °C had the highest specific saturation magnetization value, 57.94 emu/g. However, Mn 0.4 Ni 0.6 Fe 2 O 4 obtained at 600 °C had the highest coercivity value, 130.32 Oe.

In order to calibrate the response characteristic of voltage dividers, the article presents a potable high-voltage nanosecond rectangular pulse generator based on the transmission-line theory. The generator consists of DC high-voltage source, pulse forming line (PFL), special high-voltage switch, pulse transmission line (PTL), resistive load and coaxial voltage divider. The compact charging and discharging circuit is developed coaxially and the interference proof performance is excellent. The voltage amplitude and the pulse width can vary from the output of the DC high-voltage source and the length of PFL respectively. In the article the theory of pulse forming process, the design and the key devices of the generator are investigated theoretically and experimentally. The experimental results demonstrate that the generator can meet the measurement demands and export well-defined rectangular pulses with the rise time less than 751.738ps and the voltage amplitude up to 2kV.

Resistive dividers have been widely applied in the field of high voltage pulse measurement because of its simple structure, fast response, large power and low distortion rate [1], but measurement inaccuracy is usually coming when the rise time of pulses is less than 10ns. In the article the effects on the response characteristic are investigated theoretically and experimentally and it puts forward a solution that a mid-electrode is joined to transform the distributed capacitance into the one from high voltage side to mid-electrode and the one from mid-electrode to earth in series connection. A new resistive divider with mid-electrode is designed with high voltage side of 10.2kΩ, low voltage side of 10.01Ω and ratio of 1061.86. It is revealed that the divider has excellent response characteristic with the step response time of less than 1.6ns and the measurement uncertainty of less than 1%.

Most of the existing chemotherapeutic drugs have plenty of side effects. Chinese herbal medicine has been used for pharmaceutical and dietary therapy for thousands of years with more effective and fewer side effects.Cestrum nocturnum(CN) has long been used to treat digestive diseases for centuries in China. Our previous study first proved that the n-butanol part isolated from the flowers of CN produced an inhibitory effect on the proliferation of malignant cells. However, the fractions responsible for the antiproliferation effect of n-butanol part from CN flowers and related mechanisms remain unknown. Thus, in this study, we extracted fractions C4 and C5 from n-butanol part of CN flowers and investigated their immune toxicity and antitumor activities. It was found that fractions C4 and C5 exhibited great cytotoxicity to cancer cell lines but had low immune toxicity towards T and B lymphocytes in vitro. The tested fractions also attenuated proliferation and induced apoptosis at G0/G1and G2/M phases in Bel-7404 cells through inducing DNA damage and inhibiting topoisomerase II relaxation activity. These results suggest that fractions C4 and C5 may represent important sources of potential antitumor agents due to their pronounced antitumor effects and low immune toxicity.

Four high-purity germanium 4-fold segmented Clover detectors have been applied in the experiment of neutron-rich nucleus 21N. The performance of those four Clovers have been tested with radioactive sources and in-beam experiments, and the main results including energy resolution, peak-to-total ratios, the variation of the hit pattern distribution in different crystals of one Clover detector with the energy of γ ray, and absolute full energy peak detection efficiency curve, were presented.

The β-delayed neutron and γ energy spectra taken from the decay of neutron-rich nucleus 21N were measured by using the β–γ and β – n coincidence detection method. Thirteen new neutron groups ranging from 0.28MeV to 4.98MeV and with a total branching ratio of 88.7 ± 4.2% were observed and presented. One γ transition with an energy of 1222keV emitted from the excited state of 21O, and four γ transitions with energies of 1674, 2397, 2780, and 3175keV emitted from the excited states of 20O were identified in the β decay chain of 21N. The β decay half-life for 21N is determined to be 82.9 ± 1.9 ms. The uncertainty of half-life is much smaller than the previous result.

Our study investigated whether microRNA-122 (miR-122) played important roles in the proliferation, invasion and apoptosis of human cholangiocarcinoma (CC) cells. QBC939 and RBE cells lines were chosen and divided into five groups: miR-122 mimic group, anti-miR-122 group, negative control (NC) group, mock group and blank group. MiR-122 expression was measured by qRT-PCR. Roles of miR-122 in cell proliferation, apoptosis and invasion were investigated using MTT assay, flow cytometer and Transwell invasion assay, respectively. MiR-122 expression was lower in CC tissues and QBC939 cell than that in normal bile duct tissues, HCCC-9810 and RBE cells. In both QBC939 and RBE cells lines, miR-122 expression was higher in miR-122 mimic group than that in NC group, mock group and blank group; opposite results were found in anti-miR-122 group. Cell proliferation and invasion were remarkably inhibited in miR-122 mimic group after 48 h/72 h transfection, while apoptotic cells numbers were much greater in miR-122 mimic group; the opposite results were obtained from anti-miR-122 group (all P

The LPT (Lanzhou Penning Trap) is under construction and its task is to perform direct mass measurement of fusion-evaporation residues and if possible for heavy isotopes. Detailed simulations have been done for a good understanding to the ion's movement and mechanics in the trap. The optimization of the LPT is also performed based on the simulation. With a scale of 0.5 mm per grid used in the simulation and many other limitations a highest mass resolution has been achieved to be 1.9 × 10−5. An unexpected behaviour in the simulation related to magnetron motion has been found.

To study the clinicopathological significance of p53 and mdm2 protein expression in human pancreatic cancer.To investigate the expression of p53 and mdm2 in pancreatic cancer by immunohistochemistry, and the relationships between the p53 and mdm2 protein expression and clinicopathological parameters in pancreatic cancer.The positive expression of p53 protein was found in 40 of 59 patients (67.8%) and that of mdm2 protein in 17 of 59 patients (28.8%). No obvious relationships were found between p53 as well as mdm2 expression and sex, tumor site, TNM staging and histological differentiation. p53 expression was increased in patients younger than 65 years old, while mdm2 had no relationship with age. The survival time of the patients with the positive expression of p53 and mdm2 proteins was obviously shorter than the other groups.Both p53 and mdm2 presented relatively high expression in human pancreatic cancer. The overexpression of p53 and mdm2 might reflect the malignant proliferation of pancreatic cancer and their co-expression might be helpful to evaluate the prognosis of the patients with pancreatic cancer.