Public hospital data resources have become an important factor of new productivity.Gradually improving the rights and interests allocation mechanism of data assets is the premise of mining value-added,and value release is the core of driving the development of data assets.It is needed to follow the law of data value release,build a classification and classification differentiated configuration mechanism,and realize the dynamic balance between hospital data ownership distribution and value creation;build a data asset value transformation hub with the circulation,integration and sharing of multiple data as the underlying path,the global data intensive governance,the enabling of data elements and the operation of data assets as the central path,and the establishment of a"full coverage"data governance architecture,the improvement of the"multi-dimensional"technology implementation mechanism and the creation of a"multimodal"security management paradigm as the supporting path,systematically improve the data value release efficiency,and help form a new pattern of data driven hospital intelligent transformation and high-quality development.

[Objective] To investigate the infection and characteristics of hepatitis E virus among blood donors in Hangzhou. [Methods] A total of 5 075 blood samples of blood donors from Zhejiang Provincial Blood Center from September to November 2023 were collected, including 5 037 samples with normal ALT and 38 samples with elevated ALT (>50 U/L). Enzyme-linked immunosorbent assay (ELISA) was used to detect anti-HEV IgM, anti-HEV IgG and HEV-Ag. The Fisher test and Chi-square test were used to evaluate the difference in the reactivity rates of anti-HEV IgM and anti-HEV IgG among different levels of ALT. The distribution characteristics of HEV screening in blood donors were analyzed. Univariate and multivariate logistic regression were used to analyze the susceptibility factors of anti-HEV IgM and anti-HEV IgG seropositivity, and the anti-HEV IgM-reactive blood donors were followed up by telephone. [Results] The reactivity rates of anti-HEV IgM, anti-HEV IgG and HEV-Ag in 5 075 blood samples were 0.45%, 22.98% and 0%, respectively. There was no difference in the reactivity rates of anti-HEV IgM and anti-HEV IgG among different levels of ALT (P>0.05), and the results of univariate and multivariate logistic regression analysis showed that age was a risk factor for anti-HEV IgM and anti-HEV IgG reactivity in blood donors (P<0.05), while no difference in the reactivity rates of anti-HEV IgM and anti-HEV IgG among blood donors was noticed in gender, occupation and education level (P>0.05). [Conclusion] There is a potential risk of transfusion-transmitted HEV (TT-HEV) in Hangzhou, and a cost-effective HEV screening strategy needs to be established to continue regular HEV surveillance in Hangzhou to assess the risk of infection.

Public hospital data resources have become an important factor of new productivity.Gradually improving the rights and interests allocation mechanism of data assets is the premise of mining value-added,and value release is the core of driving the development of data assets.It is needed to follow the law of data value release,build a classification and classification differentiated configuration mechanism,and realize the dynamic balance between hospital data ownership distribution and value creation;build a data asset value transformation hub with the circulation,integration and sharing of multiple data as the underlying path,the global data intensive governance,the enabling of data elements and the operation of data assets as the central path,and the establishment of a"full coverage"data governance architecture,the improvement of the"multi-dimensional"technology implementation mechanism and the creation of a"multimodal"security management paradigm as the supporting path,systematically improve the data value release efficiency,and help form a new pattern of data driven hospital intelligent transformation and high-quality development.

Objective:To systematically evaluate the effects of liver and kidney function on the occurrence of thrombocytopenia induced by linezolid and the population pharmacokinetic characteristics of linezolid, so as to provide guidance for the individualization of linezolid in patients with liver and renal insufficiency.Methods:Relevant databases at home and abroad have been searched up to November 2023. The literature about the influence of liver and kidney function on linezolid-induced thrombocytopenia were analyzed using the Rev Man 5.4 statistical software, and the effect sizes were odds ratio ( OR) and standardized mean difference ( SMD) with their 95% confidence interval ( CI) in the meta-analysis. The literature on population pharmacokinetic studies of linezolid were summarized and systematically reviewed. Results:A total of 32 literature were included in the meta-analysis, including 4 112 patients. Among them, 1 458 (35.5%) developed thrombocytopenia and 2 654 (64.5%) did not. The meta-analysis results showed that the risk of linezolid-induced thrombocytopenia in the renal insufficiency patients was higher than that in patients with normal renal function [47.9% (594/1 241) vs. 25.8% (493/1 912), OR=3.24, 95% CI: 2.31-4.53], and the lower baseline creatinine clearance (Ccr) and estimated glomerular filtration rate (eGFR) were associated with the higher risk of linezolid-related thrombocytopenia (all P<0.05); the risk of thrombocytopenia induced by linezolid in patients with liver dysfunction was higher than that in patients with normal liver function [47.6% (119/250) vs. 33.9% (360/1 061), OR=2.36, 95% CI: 1.73-3.22], and the higher baseline total bilirubin (TBil) was associated with the higher risk of linezolid-related thrombocytopenia (all P<0.05). A total of 15 articles were included in the review of population pharmacokinetic study, 11 of which were based on self-built or publicly published population pharmacokinetic models and used Monte Carlo simulation to evaluate the efficacy and safety probabilities in different dosing regimens of linezolid. Among them, there were 5 and 2 articles optimized the dosing regimen of linezolid in patients with renal and liver insufficiency, respectively. Conclusions:Liver and renal insufficiency increases the risk of linezolid-induced thrombocytopenia, and baseline levels of Ccr, eGFR, and TBil can serve as sensitive indicators for predicting the risk. Patients with liver and renal insufficiency can use population pharmacokinetic models for an optimized linezolid regimen before treatment to reduce the risk of linezolid-induced thrombocytopenia.

Objective:To systematically evaluate the effects of liver and kidney function on the occurrence of thrombocytopenia induced by linezolid and the population pharmacokinetic characteristics of linezolid, so as to provide guidance for the individualization of linezolid in patients with liver and renal insufficiency.Methods:Relevant databases at home and abroad have been searched up to November 2023. The literature about the influence of liver and kidney function on linezolid-induced thrombocytopenia were analyzed using the Rev Man 5.4 statistical software, and the effect sizes were odds ratio ( OR) and standardized mean difference ( SMD) with their 95% confidence interval ( CI) in the meta-analysis. The literature on population pharmacokinetic studies of linezolid were summarized and systematically reviewed. Results:A total of 32 literature were included in the meta-analysis, including 4 112 patients. Among them, 1 458 (35.5%) developed thrombocytopenia and 2 654 (64.5%) did not. The meta-analysis results showed that the risk of linezolid-induced thrombocytopenia in the renal insufficiency patients was higher than that in patients with normal renal function [47.9% (594/1 241) vs. 25.8% (493/1 912), OR=3.24, 95% CI: 2.31-4.53], and the lower baseline creatinine clearance (Ccr) and estimated glomerular filtration rate (eGFR) were associated with the higher risk of linezolid-related thrombocytopenia (all P<0.05); the risk of thrombocytopenia induced by linezolid in patients with liver dysfunction was higher than that in patients with normal liver function [47.6% (119/250) vs. 33.9% (360/1 061), OR=2.36, 95% CI: 1.73-3.22], and the higher baseline total bilirubin (TBil) was associated with the higher risk of linezolid-related thrombocytopenia (all P<0.05). A total of 15 articles were included in the review of population pharmacokinetic study, 11 of which were based on self-built or publicly published population pharmacokinetic models and used Monte Carlo simulation to evaluate the efficacy and safety probabilities in different dosing regimens of linezolid. Among them, there were 5 and 2 articles optimized the dosing regimen of linezolid in patients with renal and liver insufficiency, respectively. Conclusions:Liver and renal insufficiency increases the risk of linezolid-induced thrombocytopenia, and baseline levels of Ccr, eGFR, and TBil can serve as sensitive indicators for predicting the risk. Patients with liver and renal insufficiency can use population pharmacokinetic models for an optimized linezolid regimen before treatment to reduce the risk of linezolid-induced thrombocytopenia.

Aim To investigate the effect of 4-Amino- 2-Trifluoromethyl-Phenyl Retinate on human breast cancer cells MDA-MB-231 and the possible mecha-nisms. Method Human breast cancer MDA-MB-231 cells were incubated with different concentrations of ATPR in vitro. MTT assay was performed to measure the proliferation of MDA-MB-231 . Cell growth curves were made by counting cells and morphologic changes were observed by Wright-Giemsa staining. The differ-entiation marker mucin-1 ( MUC-1 ) was measured by enzyme linked immunosorbent assay ( ELISA ) . Cell cycle was examined by Flow cytometry ( FCM ) . The expression of retinoic acid receptors ( RARs) and reti-noid X receptors ( RXRs ) were detected by Western blot and Quantitative real-time PCR (q-RT-PCR),re-spectively. Results Compared with solvent group, ATPR could inhibit the proliferation of MDA-MB-231 cells in a time-and dose dependent manner and induce the maturing and normality of morphology. The express of MUC-1 was significantly decreased, and the progres of cell cycle was blocked in the G0/G1-phase. The ex-pression of RARγ was decreased. Conclusions AT-PR could inhibit proliferation and induce differention of MDA-MB-231cells, it′s associated with RARγ.

Aim To observe the effect of BAPTA-AM on extracellular acid-induced autophagy in rat articular chondrocytes and its possible mechanisms.Methods Rat articular chondrocytes were isolated from Sprague-Dawley rats and incubated with different pH medium. The states of autophagy were examined by acridine or-ange (AO ) staining .Moreover,the expressions of LC3 ,Beclin-1 ,ULK1 ,CaMKKβ,AMPK and mTOR were detected using Western blot or quantitative real-time PCR (qRT-PCR ). Intracellular calcium ([Ca2+]i )was analyzed by a Ca2+-imaging method. Results Compared with pH 6.0 group,BAPTA-AM could significantly decrease the activation of autophagyinduced by acid exposure,and the expressions of autophagy markers including LC3 Ⅱ,Beclin1 and ULK1were also decreased,accompanied with reduced acidinduced [Ca2 +]i influx,decreased proteins expressionof CaMKKβand phosphorylatedAMPK,and increasedphosphorylation of mTOR.Conclusion BAPTAAMcan significantly restrain acidinduced autophagy in ratarticular chondrocytes,the mechanism of which may beassociated with decreased Ca2 + influx.

AIM: To construct prokaryotic expression vector of His-tagged human IP-10 for further study of its biological function in the inflammatory response. METHODS: The coding sequence of IP-10 lacking signal peptide was amplified from human lung cDNA library by polymerase chain reaction (PCR) and the fragment was cloned into pET-14b plasmid for the construction of His-tagged fusion protein expressing vector, pET-14b/IP-10. After being identified by enzyme digestion and sequencing, the recombinant vector was transformed into a strain of E. coli, BL21 (DE_3). The expression of His-tagged fusion protein was induced with IPTG and purified with Ni+-NTA affinity chromatography. Then the chemotactic activity of IP-10 was determined by transwell migration assay on THP-1 cells. RESULTS: The construction of pET-14b/IP-10 recombinant vector was proved by enzyme digestion and sequencing. The fusion protein IP-10, which was purified by a routine Ni+ affinity method, had an activity on the induction of cell migration of THP-1. CONCLUSION: We successfully construct IP-10 fusion protein expressing vector and get the fusion protein with high bioactivity, which provides essential materials for the future studies on IP-10.