VIKOR Method for Interval Neutrosophic Multiple Attribute Group Decision-Making

In this paper, we will extend the VIKOR (VIsekriterijumska optimizacija i KOmpromisno Resenje) method to multiple attribute group decision-making (MAGDM) with interval neutrosophic numbers (INNs). Firstly, the basic concepts of INNs are briefly presented. The method first aggregates all individual decision-makers’ assessment information based on an interval neutrosophic weighted averaging (INWA) operator, and then employs the extended classical VIKOR method to solve MAGDM problems with INNs. The validity and stability of this method are verified by example analysis and sensitivity analysis, and its superiority is illustrated by a comparison with the existing methods.</div

DataSheet1_Comparative effectiveness of tenofovir versus entecavir in patients with hepatitis B virus-related cirrhosis in Taiwan: a retrospective cohort study.PDF

Background: Tenofovir and entecavir demonstrated substantial effectiveness in the reversion of fibrosis and reversed cirrhosis in patients with hepatitis B virus (HBV)-related cirrhosis. However, there has not been a definitive conclusion regarding the association between entecavir and tenofovir on the risk of cirrhosis-related complications. Therefore, this study aimed to investigate the comparative effectiveness between tenofovir and entecavir in HBV-related cirrhosis patients.Methods: This was a retrospective study using Taiwan’s Health Insurance Research Database. We enrolled newly diagnosed HBV-related cirrhosis patients who initiated entecavir and tenofovir between 2011 and 2019. Treatment groups were determined by the initial HBV antiviral medication prescribed. The primary composite outcome was the development of hepatocellular carcinoma (HCC), death from any causes, and liver transplantation. The secondary outcomes included all the individual components of the primary outcome. The incidence rate was calculated for each outcome for both treatment groups using the Fine–Gray subdistribution hazard models. Propensity score adjustment was used to balance treatment groups.Results: A total of 7,316 propensity score-matched treatment-naïve patients and 3,524 propensity score-matched treatment-experienced patients were included. Within treatment-naïve patients, those receiving tenofovir showed significantly lower hazards of developing the composite outcome (HR, 0.79; p Conclusion: Tenofovir presented a significantly lower incidence of cirrhosis-related complications than entecavir in patients with hepatitis B virus-related cirrhosis. However, no statistically significant difference in death and liver transplantation was seen in treatment-experienced patients.</p

Data_Sheet_1_Effects of Septin-14 Gene Deletion on Adult Cognitive/Emotional Behavior.docx

While various septin GTPases have been reported for their physiological functions, their roles in orchestrating complex cognitive/emotional functions in adult mammals remained scarcely explored. A comprehensive behavioral test battery was administered to two sexes of 12-week-old Septin-14 (SEPT14) knockout (KO) and wild-type (WT) mice. The sexually dimorphic effects of brain SEPT14 KO on inhibitory avoidance (IA) and hippocampal mGluR5 expression were noticed with greater IA latency and elevated mGluR5 level exclusively in male KO mice. Moreover, SEPT14 KO appeared to be associated with stress-provoked anxiety increase in a stress-related navigation task regardless of animals’ sexes. While male and female WT mice demonstrated comparable cell proliferation in the dorsal and ventral hippocampal dentate gyrus (DG), both sexes of SEPT14 KO mice had increased cell proliferation in the ventral DG. Finally, male and female SEPT14 KO mice displayed dampened observational fear conditioning magnitude and learning-provoked corticosterone secretion as compared to their same-sex WT mice. These results, taken together, prompt us to conclude that male, but not female, mice lacking the Septin-14 gene may exhibit increased aversive emotion-related learning and dorsal/ventral hippocampal mGluR5 expressions. Moreover, deletion of SEPT14 may be associated with elevated ventral hippocampal DG cell proliferation and stress-provoked anxiety-like behavior, while dampening vicarious fear conditioning magnitudes.</p

Src-FAK signaling blockade reduced IL-6/sIL-6R-induced SV-LEC migration.

<p>SV-LECs were starved in DMEM medium without FBS for 16 h. After starvation, cells were pretreated with PP2 (A) or NSC 667249 (B) at indicated concentrations followed by the stimulation with IL-6 plus sIL6R (20 ng/ml) for another 24 h. Cell migration was determined as described in the ‘‘Materials and methods” section. Each column represents the mean ± S.E.M. of five independent experiments * p<0.05, compared to the control group; ^# p<0.05, compared to the vehicle-treated group in the presence of IL-6 plus sIL6R.</p

Transfection efficiency in SV-LECs.

SV-LECs were transfected with control vector (pcDNA) or a green fluorescence protein expression vector pEGFP as described in the “Materials and methods” section. After transfection, cells were harvested and resuspended in PBS. Green fluorescence derived from successful transfected cells were determined by flow-cytometric analysis with FACScan and Cellquest program (Becton Dickinson). Transfection efficiency is defined as the percentage of cells expressing green fluorescence (GF). The compiled results show a transfection rate is approximately 40% (N = 3). (PDF)</p

STAT3 siRNA suppressed IL-6/sIL-6R-induced VEGF-C expression in SV-LECs.

<p>(A) Cells were transiently transfected with negative control siRNA or STAT3 siRNA for 48 h. After transfection, cells were treated with IL-6 plus sIL6R (20 ng/ml) for another 6 h. The extent of VEGF-C mRNA was analyzed by RT-PCR as described in the “Materials and Methods” section. Each column represents the mean ± S.E.M. of five independent experiments. *p<0.05, compared to the control group; ^# p<0.05, compared to the vehicle-treated group in the presence of IL-6 plus sIL6R. (B) Cells were transiently transfected with negative control siRNA or STAT3 siRNA for 48 h. After transfection, cells were treated with IL-6 plus sIL6R (20 ng/ml) for another 24 h. The VEGF-C protein level was then determined by immunoblotting. Each column represents the mean ± S.E.M. of four independent experiments. * p<0.05, compared to the control group; ^# p<0.05, compared to the vehicle-treated group in the presence of IL-6 plus sIL6R. (C) Cells were pretreated with the vehicle, PP2 (1 μM) or NSC 667249 (0.3 μM) for 30 min followed by treatment with IL-6 plus sIL6R (20 ng/ml) for another 4 h. The ChIP assay was performed as described in the ‘‘Materials and methods” section. Typical traces representative of three independent experiments with similar results are shown. The VEGF-C promoter region (-367/-198) was detected in the cross-linked chromatin sample before immunoprecipitation (bottom panels of the chart, Input, positive control).</p

Schematic summary of IL-6-induced VEGF-C expression in SV-LECs.

<p>IL-6/sIL-6R activates the Src-FAK signaling cascade, leading to STAT3, C/EBPβ or NF-κB activation and subsequent VEGF-C expression SV-LECs.</p

Src-FAK signaling blockade suppressed IL-6/sIL-6R-induced tube formation of SV-LECs.

<p>(A) SV-LECs were seeded on Matrigel in the presence of VEGF-C (50 ng/ml) or IL-6 plus sIL6R (20 ng/ml) with or without PP2. Cells were then photographed under phase-contrast after 3 h. A representative microscopic phenotype of the formed tubes is shown (N = 3). (B) Total tube length of the formed capillary-like tube under different treatments as described in (A) was also measured using pen type digital meter. Each column represents the mean ± S.E.M. of three independent experiments. (C) SV-LECs were seeded on Matrigel in the presence of IL-6 plus sIL6R (20 ng/ml) with or without NSC 667249. Cells were then photographed under phase-contrast after 3 h. Total tube length of the formed capillary-like tube under different treatments was measured using pen type digital meter. Each column represents the mean ± S.E.M. of three independent experiments. * p<0.05, compared to the control group; ^# p<0.05, compared to the vehicle-treated group in the presence of IL-6 plus sIL6R.</p

FAK contributed to IL-6/sIL-6R-induced VEGF-C expression in SV-LECs.

<p>(A) Cells were pretreated with the vehicle or NSC 667249 (0.3 μM) for 30 min before treatment with IL-6 plus sIL6R (20 ng/ml) for another 24 h. The VEGF-C level and was then determined by immunoblotting. Each column represents the mean ± S.E.M. of eight independent experiments. (B) After treatment as described in (A), cell culture media were collected and VEGF-C in the media was quantified using a ELISA kit. Each column represents the mean ± S.E.M. of four independent experiments. (C) Cells were transiently transfected with VEGF-C promoter-luc-370 and renilla-luc for 48 h. After transfection, cells were treated with vehicle or NSC 667249 (0.3 μM) for 30 min, followed by treatment with IL-6 plus sIL6R (20 ng/ml) for another 24 h. Luciferase activity was then determined as described in the “Materials and Methods” section. Data represent the mean ± S.E.M. of three independent experiments performed in duplicate. (D). Cells were pretreated with the vehicle or NSC 667249 (0.3 μM) for 30min followed by treatment with IL-6 plus sIL6R (20 ng/ml) for another 30 min. The extent of FAK phosphorylation was then determined by immunoblotting. Each column represents the mean ± S.E.M. of four independent experiments. *p<0.05, compared to the control group; ^# p<0.05, compared to the vehicle-treated group in the presence of IL-6 plus sIL6R.</p

FAK mediated IL-6/sIL-6R-induced ERK1/2 and p38MAPK phosphorylation in SV-LECs.

<p>Cells were pretreated with the vehicle or NSC 667249 (0.3 μM) for 30min followed by treatment with IL-6 plus sIL6R (20 ng/ml) for another 30 min. The extent of ERK1/2 (A), p38MAPK (B) or Src (C) phosphorylation was then determined by immunoblotting. Each column represents the mean ± S.E.M. of five independent experiments. *p<0.05, compared to the control group; ^# p<0.05, compared to the vehicle-treated group in the presence of IL-6 plus sIL6R.</p