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Background Neoadjuvant chemotherapy combined with radical gastrectomy is the standard treatment for resectable gastric cancer, but whether these patients can benefit from adjuvant chemotherapy remains unclear. Methods A total of 732 patients with initially diagnosed non-metastatic resectable gastric cancer between 2004 and 2016 were screened using the Surveillance, Epidemiology, and Results database of the National Cancer Institute of the United States and retrospectively analyzed. Among them, 366 patients received postoperative chemotherapy and 506 patients did not. The propensity score matching was used to balance the two groups of confounding factors, the Kaplan–Meier method was used for survival analysis, and the logrank test was used to compare the differences between the survival curves. The Cox proportional hazards regression model was used to screen independent prognostic factors and establish a nomogram survival prediction model. The patients were divided into high-, moderate-, and low-risk groups according to the overall survival prediction score generated by X-tile software based on the nomogram. Results Multivariate analysis showed that the independent prognostic factors of gastric cancer in the group not receiving chemotherapy were history, ypT stage, ypN stage, and examined lymph node count, which were included in the nomogram prediction model. The C-index for the model was 0.727 (95% confidence interval, 0.65056–0.80344). The patients were divided into three different risk level groups based on the nomogram prediction score. Low- and moderate-risk patients did not benefit from adjuvant chemotherapy, while high-risk patients did. Conclusion The nomogram model in the present study can effectively evaluate the prognosis of patients with resectable gastric cancer. In addition, postoperative chemotherapy can be recommended for high-risk patients, but not for low-risk patients.

The purpose of this paper is to identify the medical risk of applying big data technology and to build a medical big data risk (MBDR) control process and manage medical big data risk (MBDR) from a systematic perspective. In this process, we firstly used systematic literature reviews (SLRs) method to systematically search 322 papers in web of science with the topics of “medical risk” and “big data risk” to build a dimensional system of medical big data risk (MBDR) from the theoretical level. Based on a case study of a hospital in Shanghai, we explored the formation mechanism and interaction effect of medical big data risk (MBDR) by using Bayesian belief networks (BBNs) method, and built a systematic risk control process. This paper finally finds that: the dimensional system of medical big data risk (MBDR) includes 24 subdimensions and 5 major categories of dimensions, which helps to explore the medical application of big data technology from a risk perspective. In addition, the medical big data risk (MBDR) control process constructed in this paper includes: risk prediction, reverse reasoning, risk control, and risk prevention in 4 aspects, which is important for hospitals to actually carry out medical big data risk (MBDR) control.

Accruing research shows the implications of long non-coding RNAs (lncRNAs) in the progression of various autoimmune diseases including systemic lupus erythematosus (SLE). The present study aimed to identify the expression pattern of LINC00176 in SLE and to explore its effects on CD4+T cell adhesion in this context. The biological functions of LINC00176, WIF1 and WNT5a on CD4+T cells in SLE were evaluated via gain- and loss-of-function experiments, following delivery of pcDNA3-LINC00176, siRNA-LINC00176, pcDNA3-WIF1 and WNT-sFRP5 (an inhibitor for the WNT5a signaling pathway). High LINC00176 expression was evident in the CD4+T cells of SLE patients. Additionally, WIF1 was identified as a potential target gene of LINC00176, and was negatively regulated by LINC00176. The overexpression of LINC00176 could promote proliferation and adhesion of CD4+T cells in SLE. Such alternations were reversed following up-regulation of WIF1 or inhibition of the WNT5a signaling pathway. Taken together, the key findings of our study highlight the ability of LINC00176 to potentially promote the proliferation and adhesion of CD4+T cells in SLE by down-regulating WIF1 and activating the WNT5a signaling pathway, providing new insight and a theoretical basis for translation in SLE therapy.

The intelligent poly N,N-dimethylacrylamide hydrogel material system with high mechanical strength and the 3D printable property was prepared via in situ free radical polymerization under vacuum successfully. With the increase in nanofibrillated cellulose (NFC) content, stress and strain of hydrogels increased gradually. As the effective reinforcement, NFC enhanced the crosslinking density, which realized the controllable regulation of rheology behaviors including viscosity, storage modulus, and loss modulus of hydrogels. Combined with the swelling rate and the existence of the gel–sol transition point, a hydrogel with 10 mg/mL NFC was treated as the 3D printing ink of hydrogel actuators. Variation of printing parameters significantly affected self-driven deformations. The hydrogel actuators with 90°/0° and 45°/135° configurations owned bending and spiral deformations, respectively. Actuators with a larger length–width ratio owned a lower pitch value. The precise anisotropic swelling property of the printed bilayer structure was the self-driven deformation mechanism of hydrogel actuators, which provided material candidates for the preparation of soft robots and actuators.

Accruing research shows the implications of long non-coding RNAs (lncRNAs) in the progression of various autoimmune diseases including systemic lupus erythematosus (SLE). The present study aimed to identify the expression pattern of LINC00176 in SLE and to explore its effects on CD4

Activation of nuclear factor erythroid 2-related factor 2 (NRF2) has been found to ameliorate diabetic testicular damage (DTD) in rodents. However, it was unclear whether NRF2 is required for these approaches in DTD. Epigallocatechin gallate (EGCG) is a potent activator of NRF2 and has shown beneficial effects on multiple diabetic complications. However, the effect of EGCG has not been studied in DTD. The present study aims to explore the role of NRF2 in both self and EGCG protection against DTD. Therefore, streptozotocin-induced diabetic C57BL/6 wild type (WT) and Nrf2 knockout (KO) mice were treated in the presence or absence of EGCG, for 24 weeks. The Nrf2 KO mice exhibited more significant diabetes-induced loss in testicular weight and spermatozoa count, and increase in testicular apoptotic cell death, as compared with the WT mice. EGCG activated NRF2 expression and function, preserved testicular weight and spermatozoa count, and attenuated testicular apoptotic cell death, endoplasmic reticulum stress, inflammation, and oxidative damage in the WT diabetic mice, but not the Nrf2 KO diabetic mice. The present study demonstrated for the first time that NRF2 plays a critical role in both self and EGCG protection against DTD.

As one of the most promising intelligent materials, polymeric hydrogel actuators could produce reversible shape change upon external stimuli. Although complex shape deformation from 2D to 3D have been achieved, the realization of actuating behavior from 3D to 3D is still a significant challenge. Herein, an effective strategy to develop a novel bilayer hollow spherical hydrogel actuator is proposed. Through immersing a Ca2+ incorporated gelatin core into alginate solution, an ionic-strength-responsive alginate layer will be formed along the gelatin core via alginate-Ca2+ crosslinks, and then another thermo-responsive alginate-poly(2-(dimethylamino)ethyl methacrylate)(Alg-PDMAEMA) layer is introduced to achieve a bilayer hydrogel with ionic strength and temperature dual responsiveness. A hollow hydrogel capsule could be obtained if a spherical gelatin core is applied, and it could produce complex shape deformations from 3D to 3D upon the trigger of ionic strength and temperatures changes. The present work may offer new inspirations for the development of novel intelligent polymeric hydrogel actuators.

Endothelial dysfunction contributes to diabetic macrovascular complications. Sirtuin 1 (SIRT1) protects against diabetic vasculopathy. SRT2104 is a novel SIRT1 activator and was not previously studied for its effects on diabetes-induced aortic endothelial dysfunction. Additionally, whether or to what extent deacetylation of P53, a substrate of SIRT1, is required for the effects of SIRT1 activation was unclear, given the fact that SIRT1 has multiple targets. Moreover, little was known about the pathogenic role of P53 in diabetes-induced aortic injury. To these ends, diabetes was induced by streptozotocin in C57BL/6 mice. The diabetic mice developed enhanced aortic contractility, oxidative stress, inflammation, P53 hyperacetylation and a remarkable decrease in SIRT1 protein, the effects of which were rescued by SRT2104. In HG-treated endothelial cells (ECs),P53siRNA and SRT2104 produced similar effects on the induction of SIRT1 and the inhibition of P53 acetylation, oxidative stress and inflammation. Interestingly, SRT2104 failed to further enhance these effects in the presence ofP53siRNA. Moreover, P53 activation by nutlin3a completely abolished SRT2104’s protection against HG-induced oxidative stress and inflammation. Further, forced activation of P53 by nutlin3a increased aortic contractility in the healthy mice and generated endothelial oxidative stress and inflammation in both the normal glucose-cultured ECs and the aortas of the healthy mice. Collectively, the present study demonstrates that P53 deacetylation predominantly mediates SRT2104’s protection against diabetes-induced aortic endothelial dysfunction and highlights the pathogenic role of P53 in aortic endothelial dysfunction.