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IASCC of stainless steel has been the most important issue for internals BFBs. The inspection data analysis indicates that there is a closed relation between irradiation fluence and cracked BFBs distribution. Then the nanoindentation and 3DAP tests were carried out to study the hardening and radiation induced segregation (RIS) behaviors of the reactor internals stainless steel specimens irradiated with 6 MeV Xe ions at room temperature. It is indicated that higher irradiation damage will cause more significant hardening and RIS and consequently increase the IASCC susceptibility.

We recently published that type 2 diabetes promotes cell centrosome amplification via upregulation of Rho-associated protein kinase 1 (ROCK1) and 14-3-3 protein-σ (14-3-3σ). This study further investigates the molecular mechanisms underlying diabetes-associated centrosome amplification. We found that treatment of cells with high glucose, insulin, and palmitic acid levels increased the intracellular and extracellular protein levels of Wingless-type MMTV integration site family member 6 (Wnt6) as well as the cellular level of β-catenin. The treatment also activated β-catenin and promoted its nuclear translocation. Treatment of cells with siRNA species for Wnt6, Frizzled-4 (FZD4), or β-catenin as well as introduction of antibodies against Wnt6 or FZD4 to the cell culture medium could all attenuate the treatment-triggered centrosome amplification. Moreover, we showed that secreted Wnt6-FZD4-β-catenin was the signaling pathway that was upstream of ROCK1 and 14-3-3σ. We found that advanced glycation end products (AGEs) were also able to increase the cellular and extracellular levels of Wnt6, the cellular protein level of β-catenin, and centrosome amplification. Treatment of the cells with siRNA species for Wnt6 or FZD4 as well as introduction of antibodies against Wnt6 or FZD4 to the cell culture could all inhibit the AGEs-elicited centrosome amplification. In colon tissues from a diabetic mouse model, the protein levels of Wnt6 and 14-3-3σ were increased. In conclusion, our results showed that the pathophysiological factors in type 2 diabetes, including AGEs, were able to induce centrosome amplification. It is suggested that secreted Wnt6 binds to FZD4 to activate the canonical Wnt6 signaling pathway, which is upstream of ROCK1 and 14-3-3σ, and that this is the cell signaling pathway underlying diabetes-associated centrosome amplification.

Type 2 diabetes increases the risk various types of cancer and is associated with a poor prognosis therein. There is also evidence that the disease is associated with cancer metastasis. Centrosome amplification can initiate tumorigenesis with metastasis in vivo and increase the invasiveness of cancer cells in vitro. Our previous study reported that type 2 diabetes promotes centrosome amplification via the upregulation and centrosomal translocation of Rho-associated protein kinase 1 (ROCK1), which suggests that centrosome amplification is a candidate biological link between type 2 diabetes and cancer development. In the present study, functional proteomics analysis was used to further investigate the molecular pathways underlying centrosome amplification by targeting ROCK1 binding partners. High glucose, insulin and palmitic acid were used to induce centrosome amplification, and immunofluorescent staining was employed to visualize centrosomal alterations. Combined with immunoprecipitation, mass spectrometry-based proteomics analysis was used to identify ROCK1 binding proteins, and protein complex disruption was achieved by siRNA-knockdown. In total, 1,148 ROCK1 binding proteins were identified, among which 106 proteins were exclusively associated with the treated samples, 193 were only associated with the control samples, and 849 were found in both the control and treated samples. Of the proteins with evidence of centrosomal localization, Dynactin subunit 2 (DCTN2) was confirmed to be localized to the centrosomes. Treating the cells with high glucose, insulin and palmitic acid increased the protein levels of ROCK1 and DCTN2, promoted their binding with each other, and triggered centrosome amplification. Disruption of the protein complex by knocking down ROCK1 or DCTN2 expression partially attenuated centrosome amplification, while simultaneous knockdown of both proteins completely inhibited centrosome amplification. These results suggested ROCK1-DCTN2 binding as a signal for the regulation of centrosome homeostasis, which is key for diabetes-associated centrosome amplification, and enriches our knowledge of centrosome biology. Therefore, the ROCK1-DCTN2 complex may serve as a target for inhibiting centrosome amplification both in research or future therapeutic development.

Objective To investigate nutritional treatment in the intensive care unit (ICU) of the mainland China. Methods A cross-sectional study was conducted in 116 ICUs of 118 mainland hospitals on April 26th, 2017. All patients of these ICUs were investigated at 0 o'clock on April 26th. Demographic and clinical parameters of those patients on April 25th (the investigation day) were recorded, including the dates of hospitalization, ICU admission and nutrition initiation and clinical outcome on 28 days after the investigation day. Results A total of 1953 patients were collected, including 631 females and 1306 males. The mean age was (64.1±19.3) years old (1950 cases). The means of Glasgow Coma Scale (GCS), Sequential Organ Failure Assessment (SOFA) and Acute Physiology and Chronic Health Evaluation Ⅱ (APACHEⅡ) scores were (10.76±4.35)(1749 cases), (5.65±3.52)(1783 cases), (17.14±7.31)(1792 cases), respectively. The outcomes of 28 days after the investigation day were 1483 survivors (75.9%), 312 non-survivors (16.0%) and 158 cases (8.1%) being lost to follow-up. There were no significant differences between the males and the females in age, severity of disease and clinical outcomes of 28 days but in height and weight. There were 73.7%(1440 cases) of patients with normal or mildly injured gastrointestinal function, 10.8%(210 cases) with moderately or severely injured function, 1.7%(33 cases) with gastrointestinal failure and 13.2%(258 cases) without evaluation. To the investigation day, enteral nutrition (EN) had been initiated in 69.4%(1356 cases) of patients and parenteral nutrition (PN) in 36.4%(711 cases) of patients. There were 1720(88.1%) patients with EN administration on the investigation day. The proportion of patients with nausea, vomit/regurgitation, aspiration, abdominal pain, abdominal distention and diarrhea was 4.8%(93 cases), 5.4%(105 cases), 0.9%(17 cases), 8.7%(170 cases), 27.5%(538 cases) and 4.3%(84 cases) respectively, while that of patients using EN was 3.1%(40 cases), 4.25%(54 cases), 0.79%(10 cases), 4.41%(56 cases), 26.85%(341 cases) and 5.43%(69 cases) correspondingly. The proportion of cases starting EN within 24, 48 and 72 hours after ICU entry was 22.4%(437/1953), 38.6%(754/1953) and 46.6%(911/1953), respectively. The proportion of cases receiving ≥80% estimated energy target (=past body weight ×25 kcal/kg.d) within 3, 7 and 14 days after ICU entry was 12.9%(78/607), 18.7%(189/1010) and 23%(305/1325) respectively, while that of cases with EN was 9.9%(60/607), 15.0%(151/1010) and 18.6%(246/1325) correspondingly. Conclusions Nowadays, most of patients in the mainland ICUs receive nutrition therapy and the EN usage rate is much higher than the PN rate. However, the time of EN initiation and the target-reaching rate of energy are suboptimal and an individualized plan of nutrition therapy is still missing. Details of energy delivery still need to be improved. DOI: 10.11855/j.issn.0577-7402.2019.05.05

Sanggenone C, oxyresveratrol, catechin and L-epicatechin exist in Morus and Hulless Barley as natural polyphenols with antityrosinase activity. Little research on their synergistic and structure-function relationships of them has been reported in recent years. In this paper, the inhibition mechanisms of these four plant polyphenols were investigated by enzyme kinetics, HPLC, fluorescence spectra, and molecular docking methods. The results showed that oxyresveratrol (IC50 = 1.096 ± 0.048 μg/mL), sanggenone C (IC50 = 13.360 ± 1.029 μg/mL), L-epicatechin (IC50 = 55.730 ± 1.762 μg/mL), and catechin (IC50 = 148.500 ± 3.355 μg/mL) exhibited tyrosinase inhibition activity. When sangenone C (14 μg/mL) was mixed with L-epicatechin (56 μg/mL) at 4:1 (40 μL + 10 μL), the highest tyrosinase inhibition was achieved. Molecular docking showed that the number and position of phenolic hydroxyls of polyphenols were the key for tyrosinase inhibition activity. This study provided new ideas for the application of these four plant polyphenols from Hulless Barley and Morus as tyrosinase inhibitors in food preservation.

Magnetic properties of thermally aged Fe-Cu alloys with pre-deformation have been evaluated to improve the understanding of using magnetic technology for the nondestructive evaluation (NDE) of irradiation embrittlement in reactor pressure vessel (RPV) steels. Fe-Cu alloys with and without pre-deformation were thermally aged at 500 °C and the changes in microstructure, mechanical properties and magnetic properties were determined. It is found that the strain-induced dislocations recover and the Cu-rich particles precipitate during the aging process, and the magnetic properties variation depends on the combined influence of these two factors. From the point of view of NDE, a fully tempered or annealed microstructure is favorable before RPV is put into service. These results improve the understanding of magnetic property evolution in actual RPV steels and help to develop NDE theory for irradiation embrittlement.

It has been reported recently that type 2 diabetes promotes centrosome amplification via 14-3-3σ/ROCK1 complex. In the present study, 14-3-3σ interacting proteins are characterized and their roles in the centrosome amplification by high glucose, insulin, and palmitic acid are investigated. Co-immunoprecipitation in combination with MS analysis identified 134 proteins that interact with 14-3-3σ, which include heat shock 70 kDa protein 4 (Hsp74). Gene ontology analyses reveal that many of them are enriched in binding activity. Kyoto Encyclopedia of Genes and Genomes analysis shows that the top three enriched pathways are ribosome, carbon metabolism, and biosynthesis of amino acids. Molecular and functional investigations show that the high glucose, insulin, and palmitic acid increase the expression and binding of 14-3-3σ and Hsp74 as well as centrosome amplification, all of which are inhibited by knockdown of 14-3-3σ or Hsp74. Moreover, molecular docking analysis shows that the interaction between the 14-3-3σ and the Hsp74 is mainly through hydrophobic contacts and a lesser degree ionic interactions and hydrogen bond by different amino acids residues. In conclusion, the results suggest that the experimental treatment triggers centrosome amplification via upregulations of expression and binding of 14-3-3σ and Hsp74.

Type2 diabetes is associated with oxidative stress which can cause cell centrosome amplification. The study investigated centrosome amplification in type 2 diabetes and the underlying mechanisms. We found that centrosome amplification was increased in the peripheral blood mononuclear cells (PBMC) from the type 2 diabetic patients, which correlated with the levels of fasting blood glucose and HbA1c. High glucose, insulin and palmitic acid, alone or in combinations, induced ROS production and centrosome amplification. Together, they increased AKT activation as well as the expression, binding and centrosome translation of ROCK1 and 14-3-3σ. Results from further analyses showed that AKT-ROS-dependent upregulations of expression, binding and centrosome translocation of ROCK1 and 14-3-3σ was the molecular pathway underlying the centrosome amplification induced by high glucose, insulin and palmitic acid. Moreover, the increases in AKT activation and ROS production as well as expression, binding and centrosome distribution of ROCK1 and 14-3-3σ were confirmed in the PBMC from the patients with type 2 diabetes. In conclusion, our results show that type 2 diabetes promotes cell centrosome amplification, and suggest that the diabetic pathophysiological factors-activated AKT-ROS-dependent signalling of ROCK1 and 14-3-3σ is the underlying molecular mechanism.

Space attack-defense confrontation is the commanding height in modern warfare. This paper takes space platform as research object and tries to solve problems such as space non-coplanar, large energy consumption of multiple-targets orbit interception and long interception time. Firstly, a design energy-optimal method of orbit interception based on Traversing Points is proposed. Secondly, the optimal design model of orbital interception is established. Finally, we take space platform interception of three targets in low earth orbit as an example and STK simulations analysis is carried out to verify the effectiveness of the proposed method. The research provides a theoretical basis for analysing non-coplanar and multi-targets interception strategy.

The influence of the cathode work function, carriers mobilities and temperature on the short-circuit current of single layer organic solar cells with Schottkey contacts was numerically studied, and the quantitative dependences of the short-circuit current on these quantities were obtained. The results provide the theoretical foundation for experimental study of single layer organic solar cells with Schottkey contacts.

To evaluate whether parvovirus B19, a common human pathogen, was also involved in papillary thyroid carcinoma (PTC), 112 paraffin-embedded thyroid specimens of benign nodules, papillary, medullary and follicular carcinomas, and normal controls were examined for B19 DNA and capsid protein by nested PCR, in situ hybridisation (ISH) and immunohistochemistry (IHC). The expression of the nuclear factor-kappaB (NF-kappaB) was investigated by IHC. The results showed B19 DNA commonly exists in human thyroid tissues; however, there were significant differences between PTC group and normal controls, and between PTC and nonneoplastic adjacent tissues (P0.001). The presence of viral DNA in PTC neoplastic epithelium was confirmed by laser-capture microdissection and sequencing of nested PCR products. B19 capsid protein in PTC group was significantly higher than that of all the control groups and nonneoplastic adjacent tissues (Por=0.001). Compared with control groups, the activation of NF-kappaB in PTC group was significantly increased (Por=0.02), except for medullary carcinomas, and the activation of NF-kappaB was correlated with the viral protein presence (P=0.002). Moreover, NF-kappaB was colocalised with B19 DNA in the neoplastic epithelium of PTC by double staining of IHC and ISH. These results indicate for the first time a possible role of B19 in pathogenesis of PTC.

To investigate the role of nuclear translocation of calcyclin binding protein, also called Siah-1 interacting protein (CacyBP/SIP), in gastric carcinogenesis.The expression of CacyBP/SIP protein in gastric cancer cell lines was detected by Western blot. Immunofluorescence experiments were performed on gastric cancer cell lines that had been either unstimulated or stimulated with gastrin. To confirm the immunofluorescence findings, the relative abundance of CacyBP/SIP in nuclear and cytoplasmic compartments was assessed by Western blot. The effect of nuclear translocation of CacyBP/SIP on cell proliferation was examined using MTT assay. The colony formation assay was used to measure clonogenic cell survival. The effect of CacyBP/SIP nuclear translocation on cell cycle progression was investigated. Two CacyBP/SIP-specific siRNA vectors were designed and constructed to inhibit CacyBP/SIP expression in order to reduce the nuclear translocation of CacyBP/SIP, and the expression of CacyBP/SIP in stably transfected cells was determined by Western blot. The effect of inhibiting CacyBP/SIP nuclear translocation on cell proliferation was then assessed.CacyBP/SIP protein was present in most of gastric cancer cell lines. In unstimulated cells, CacyBP/SIP was distributed throughout the cytoplasm; while in stimulated cells, CacyBP/SIP was found mainly in the perinuclear region. CacyBP/SIP nuclear translocation generated a growth-stimulatory effect on cells. The number of colonies in the CacyBP/SIP nuclear translocation group was significantly higher than that in the control group. The percentage of stimulated cells in G1 phase was significantly lower than that of control cells (69.70% ± 0.46% and 65.80% ± 0.60%, control cells and gastrin-treated SGC7901 cells, P = 0.008; 72.99% ± 0.46% and 69.36% ± 0.51%, control cells and gastrin-treated MKN45 cells, P = 0.022). CacyBP/SIPsi1 effectively down-regulated the expression of CacyBP/SIP, and cells stably transfected by CacyBP/SIPsi1 were then chosen for further cellular assays. In CacyBP/SIPsi1 stably transfected cells, CacyBP/SIP was shown to be distributed throughout the cytoplasm, irregardless of whether they were stimulated or not. After CacyBP/SIP nuclear translocation was reduced, there had no major effect on cell proliferation, as shown by MTT assay. There had no enhanced anchorage-dependent growth upon stimulation, as indicated by colony formation in flat plates. No changes appeared in the percentage of cells in G0-G1 phase in either cell line (71.09% ± 0.16% and 70.86% ± 0.25%, control cells and gastrin-treated SGC7901-CacyBP/SIPsi1 cells, P = 0.101; 74.17% ± 1.04% and 73.07% ± 1.00%, control cells and gastrin-treated MKN45-CacyBP/SIPsi1 cells, P = 0.225).CacyBP/SIP nuclear translocation promotes the proliferation and cell cycle progression of gastric cancer cells.

The main treatment of leukemia is traditional radiochemotherapy, which is associated with serious side effects. In the past twenty years, differentiation was found as an important effective measure to treat leukemia with fewer side effects. Gossypol, a natural compound which has been used as an effective contraceptive drug, has been proposed to be a potent drug to treat leukemia, but the differentiation effect has not been studied. In the present study, we investigated the pro-differentiated effects, in vitro, of gossypol on the classic human myeloid leukemia HL-60 cell line. The effects of gossypol were investigated by using morphological changes, nitroblue tetrazolium (NBT) reduction, surface markers, cell-cycle analysis and Western blot analysis, etc. When HL-60 cells were incubated with low concentrations of gossypol (2-5μM) for 48hr, a prominent G0/G1 arrest was observed. At 96 hr of treatment, 90% of HL-60 cells differentiated, as evidenced by morphological changes, NBT reduction, and increase in cell surface expression of some molecules were detected. This study is the first to identify gossypol’s pro-differentiated effects on the leukemia cell line, and it induced differentiation through the PBK (PDZ-binding kinase)/TOPK (T-LAKcell-originated protein kinase) (PBK/TOPK) pathway. It is concluded that gossypol could induce differentiation in the leukemia HL-60 cells, and it may be a potential therapeutic agent, chemoprevention or chemotherapeutic adjuvant especially in combination drug therapy for leukemia.

Liver segmentation is a prerequisite for liver cancer CAD, and the result of it affects the accuracy rate of feature extraction and recognition of liver cancer directly. Euclidean distance transformation is one of the main methods in medical image segmentation. However, simply using Euclidean distance transformation will lead to some problems, such as over-segmentation and excessively high cost of calculation. Therefore, this paper puts forward a new method of liver segmentation, which combines High-speed complete Euclidean distance transformation with statistical analysis. The effectiveness of this method has been verified after we apply it to the liver segmentation of abdominal liver CT images.

Parvovirus B19 is a common human pathogen, which has been linked to autoimmune diseases recently. The aim of the study is to evaluate whether B19 is involved in adult Hashimoto's thyroiditis (HT).Eighty-six thyroid tissues from the adult patients with a spectrum of thyroid disorders were examined for B19 DNA and capsid protein by nested PCR, in-situ hybridization and immunohistochemistry. The presence of viral DNA in HT epithelium was studied by laser-capture microdissection and sequencing of PCR products. The expressions of nuclear factor-kappaB (NF-kappaB) and interleukin-6 were investigated by immunohistochemistry.B19 DNA was significantly present in HT tissues by both PCR (29/32, 90.6%) and in-situ hybridization (23/32, 71.9%, all p0.01) compared with normal thyroid tissue (7/16, 43.8%; 2/16, 12.5%). Laser-capture microdissection further confirmed this difference. B19 capsid protein in HT group was significantly higher than that in all the control groups (p0.01), and the expression of NF-kappaB and interleukin-6 in HT tissues was up-regulated. NF-kappaB was well co-localized with B19 protein in thyroid epithelia by double-labeling immunofluorescence and confocal microscopy.The presence of B19 nuclear acid and viral protein was significantly common in HT tissues and it suggested a possible role of B19 in adult HT.

Although Kikuchi-Fujimoto disease (KFD) has a higher prevalence among Asian countries, it is a well-defined entity throughout the world. However, its etiology and pathogenesis remain undetermined. To study whether B19 infection is associated with idiopathic KFD (iKFD), we examined the presence of the viral genome and proteins in paraffin-embedded tissues of lymph nodes retrospectively from 33 iKFD patients and 16 age- and sex-matched control subjects by nested PCR (nPCR), in situ hybridization (ISH), and immunohistochemistry (IHC). B19 was detected in 87.1, 69.7, and 57.6% of iKFD specimens by nPCR, ISH, and IHC, respectively, whereas the virus was positive in only 56.3, 31.3, and 25.0% of control tissues by the respective methods (nPCR: p = 0.029; ISH: p = 0.011; IHC: p = 0.032). The IHC-ISH double-staining assay demonstrated that B19-infected cells were mainly lymphocytes and a small number of histiocytes. These results showed for the first time a high frequency of localized persistence of B19 in lymph nodes from iKFD patients, suggesting that B19 might play an important role in the pathogenesis of iKFD.

To establish the bone marrow stem cells (MSC) model which could highly express the insulin-like growth factor 1 (IGF-1) transfected by dog's IGF-1 gene.pIRES2-EGFP-IGF-1 was transfected into MSC by lipofectamine. Positive clones were selected with G418. The expression of IGF-1 protein in the MSC was determined by immunohistochemistry and Western blot analysis. The IGF-1 in the supernatant of the transfected MSC was detected by sandwich-in ELISA. The periodontal ligament cells (PDLC) were cultured in the supernatant of the transfected MSC. The changes of PDLC' proliferation were observed by MTT.IGF-1-transfected MSC could apparently express IGF-1. The IGF-1 protein in the supernatant of the transfected MSC was confirmed by sandwich-in ELISA. IGF-1 could promote the PDLC' proliferation.The MSC transfected by dog's IGF-1 gene can highly express IGF-1, which may lay the foundation for further study on periodontal regeneration.