Objective: To describe the strategy and the emergency management and infection control procedure of our radiology department during the COVID-19 outbreak. Methods:We set up emergency management and sensing control teams. The team formulated various measures: reconfiguration of the radiology department, personal protection and training of staff, examination procedures for patients suspected of or confirmed with COVID-19 as well as patients without an exposure history or symptoms. Those with suspected or confirmed COVID-19 infection were scanned in the designated fever-CT unit. people suspected of or confirmed with COVID-19 underwent fever-CT examinations. Including initial examinations and reexaminations, the total number of fever-CT examinations numbered 3,340. As a result of our precautions, none of the staff of the radiology department were infected with COVID-19. Conclusion:Strategic planning and adequate protections can help protect patients and staff against a highly infectious disease while maintaining function at a high volume capacity.

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BackgroundSeveral kinds of cancer surgeries with propofol-based total intravenous anesthesia (TIVA) have been shown to have better outcomes than those with sevoflurane-based inhalational anesthesia (INHA). However, the effects of this anesthetic technique have not been investigated in patients with gastric cancer. In this study, the authors retrospectively examined the link between the choice of anesthetic technique and overall survival in patients undergoing gastric cancer resection.MethodsWe conducted a retrospective analysis of the database of all patients undergoing gastric cancer resection for gastric cancer between 2007 and 2012. Patients who received TIVA or INHA were administered patient-controlled intravenous analgesia for 72–120 hours postoperatively. Survival was estimated using the Kaplan–Meier log-rank test, and associations between anesthetic technique and outcomes were analyzed using Cox proportional hazards regressions after propensity matching.ResultsA total of 2,856 anesthetics using INHA or TIVA were delivered in the study period. After propensity matching, 897 patients remained in each group. According to Kaplan–Meier analysis, the use of TIVA was associated with improved survival (P<0.001). TIVA was associated with a hazard ratio (HR) of 0.67 (95% confidence interval [CI]: 0.58–0.77) for death in univariate analysis and 0.65 (95% CI: 0.56–0.75) after a multivariate analysis of known confounders in the matched group. Cancer stage (HR =0.74, 95% CI: 0.64–0.86, P<0.001) and degree of differentiation (HR =1.28, 95% CI: 1.11–1.47, P<0.001) were also associated with survival in the univariate analysis in the matched group. In the multivariable Cox model, cancer stage (HR =0.72, 95% CI: 0.62–0.84, P<0.001) and degree of differentiation (HR =1.23, 95% CI: 1.07–1.42, P<0.001) were associated with survival in the matched group.ConclusionThese results indicate that TIVA may be associated with improved survival in gastric cancer patients who undergo resection.

Highlights d ADORA1 inhibition promotes immune escape by regulating tumor PD-L1 via ATF3 d ADORA1 or ATF3 screening may be used to assess PD-1 mAb therapy efficacy d Combination of an ADORA1 antagonist and a PD-1 mAb provides therapeutic benefit

Prostate cancer is the second leading cause of cancer-related death in men after lung cancer. Immune responses clearly play a critical role in the tumorigenesis and in the efficacy of radiation therapy and chemotherapy in prostate cancer; however, the underlying molecular mechanisms are still poorly understood. Toll-like receptors (TLRs) are a well-known family of pattern recognition receptors that play a key role in host immune system. Recent studies demonstrate that there are links between TLRs and cancer; however, the function and biological importance of TLRs in prostate cancer seems complex. To elucidate the role of TLRs and innate immunity in prostate cancer might provide us with a better understanding of the molecular mechanisms of this disease. Moreover, utilizing the agonists or antagonists of TLRs might represent a promising new strategy against prostate cancer. In this review, we summarize recent advances on the studies of association between TLR signaling and prostate cancer, TLR polymorphisms and prostate cancer risk, and provide some insights about TLRs as potential targets for prostate cancer immunotherapy.

TRAF6 plays a crucial role in the regulation of the innate and adaptive immune responses. Although studies have shown that TRAF6 has oncogenic activity, the role of TRAF6 in melanoma is unclear. Here, we report that TRAF6 is overexpressed in primary as well as metastatic melanoma tumors and melanoma cell lines. Knockdown of TRAF6 with shRNA significantly suppressed malignant phenotypes including cell proliferation, anchorage-independent cell growth and metastasis in vitro and in vivo. Notably, we demonstrated that Basigin (BSG)/CD147, a critical molecule for cancer cell invasion and metastasis, is a novel interacting partner of TRAF6. Furthermore, depletion of TRAF6 by shRNA reduced the recruitment of BSG to the plasma membrane and K63-linked ubiquitination, in turn, which impaired BSG-dependent MMP9 induction. Taken together, our findings indicate that TRAF6 is involved in regulating melanoma invasion and metastasis, suggesting that TRAF6 may be a potential target for therapy or chemo-prevention in melanoma.

The RIP, CLIP, and RNA-seq data in this paper can be download via the following link. (SRA accession number: SRP043638) http://www.ncbi.nlm.nih.gov/Traces/sra/?study=SRP043638 The microarray data can be download via the following link. (GEO accession number: GSE59291) http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE59291

BackgroundRibosomal protein S6 (rpS6), a component of the 40S ribosomal subunit, is involved in multiple cellular bioactivities. However, its clinicopathological significance in non-small cell lung cancer (NSCLC) is poorly understood.MethodsExpressions of total rpS6 (t-rpS6) and phosphorylated rpS6 (Ser235/236, p-rpS6) were detected immunohistochemically in 316 NSCLC tissues and 82 adjacent controls, followed by statistical evaluation of the relationship between proteins expressions and patients’ survivals to identify their prognostic values. Cytological experiments with overexpressing or silencing rpS6 by lentivirus in human bronchial epithelial (HBE) and NSCLC cell lines were performed to explore potential mechanisms by which rpS6 affects the clinical development of NSCLC. Additionally, specific RNA interference for Akt1, Akt2, Akt3, Akt inhibitor and subsequent cellular bioactivity tests were employed as well to investigate the upstream regulation of rpS6.ResultsPositive rates of t-rpS6 and p-rpS6 were both significantly increased in NSCLC tissues, compared with controls (82.91 vs 62.20 % for t-rpS6; 52.22 vs 21.95 % for p-rpS6; both P < 0.001). However, only hyperphosphorylation of rpS6, expressed as either elevated p-rpS6 alone or the ratio of p-rpS6 to t-rpS6 (p-rpS6/t-rpS6) no less than 0.67, was greatly associated with the unfavorable survival of NSCLC patients, especially for cases at stage I (all P < 0.001). The independent adverse prognostic value of hyperphosphorylated rpS6 was confirmed by multivariate Cox regression analysis (hazard ratios for elevated p-rpS6 alone and p-rpS6/t-rpS6 no less than 0.67 were 2.403, 4.311 respectively, both P < 0.001). Overexpression or knockdown of rpS6, along with parallel alterations of p-rpS6, led to increased or decreased cells proliferations respectively, which were dependent on redistributions of cell cycles (all P < 0.05). Cells migration and invasion also changed with rpS6 interference (all P < 0.05). Furthermore, upstream overexpression or knockdown of Akt2 or Akt2 phosphorylation inhibition, rather than Akt1 or Akt3, resulted in striking hyperphosphorylation or dephosphorylation of mTOR, p70S6K and rpS6 (all P < 0.05), without any change in total proteins expressions. Further tests showed markedly accompanied variation of cells proliferation, cell cycle distribution and invasion (all P < 0.05).ConclusionHyperphosphorylation of rpS6, probably regulated by the Akt2/mTOR/p70S6K signaling pathway, is closely relevant to the progression of NSCLC and it might be served as a promising therapeutic target for NSCLC treatment.Electronic supplementary materialThe online version of this article (doi:10.1186/s13046-015-0239-1) contains supplementary material, which is available to authorized users.