Hemolysis is one of the main complications associated with the use of ventricular assist devices. The primary factors influencing hemolysis include the shear stress and exposure time experienced by red blood cells. In addition, factors such as local negative pressure and temperature may also impact hemolysis. The different combinations of hemolysis prediction models and their empirical constants lead to significant variations in prediction results; compared to the power-law model, the OPO model better accounts for the complexity of turbulence. In terms of improving hemolytic performance, research has primarily focused on optimizing blood pump structures, such as adjustments to pump gaps, impellers, and guide vanes. A small number of scholars have studied hemolytic performance through control modes of blood pump speed and the selection of blood-compatible materials. This paper reviews the main factors influencing hemolysis, prediction methods, and improvement strategies for rotary blood pumps, which are currently the most widely used. It also discusses the limitations in current hemolysis research and provides an outlook on future research directions.

BACKGROUND:Cardiac hypertrophy is an adaptive response of the heart to physiological and pathological stimuli such as pressure overload.It is of compensatory significance in the early stage,but if the stimulation continues,it can cause cardiomyopathy leading to heart failure.MicroRNAs are involved in the regulation of cardiac hypertrophy.However,the role of miR-20a in pressure overload-induced cardiac hypertrophy has not been reported. OBJECTIVE:To investigate the role of miR-20a in pressure overload-induced cardiac hypertrophy and the underlying mechanisms. METHODS:Transverse aortic constriction was used to induce cardiac hypertrophy in vivo and angiotensin Ⅱ was used to induce H9c2 cell models of cardiac hypertrophy in vitro.MiR-20a was overexpressed in vivo by intramyocardial injection of miR-20a overexpressing adenovirus and in vitro by transfecting miR-20a mimic into H9c2 cells.Cardiac hypertrophy was assessed by measuring heart weight/body weight ratio,cell surface area,and myocardial fibrosis.The expression levels of atrial natriuretic peptide,brain natriuretic peptide,β-myosin heavy chain and miR-20a were detected by real-time fluorescence quantitative PCR.Mitochondrial fission was detected by MitoTracker.The downstream target genes of miR-20a were predicted by RNAhybrid software. RESULTS AND CONCLUSION:(1)The expression level of miR-20a was significantly decreased in both hypertrophic cardiomyocytes and hearts(P<0.05).(2)At the animal level,overexpression of miR-20a significantly inhibited transverse aortic constriction-induced cardiac hypertrophy,including decreasing the upregulated expression level of hypertrophic marker genes(P<0.05),reduced the enlarged heart volume,reducing the increased heart weight/body weight ratio(P<0.01),reducing the increased myocardial cross-sectional area(P<0.05),and attenuating fibrosis(P<0.01).(3)At the cellular level,overexpression of miR-20a significantly inhibited angiotensin Ⅱ-induced cardiomyocyte hypertrophy,including decreasing the upregulated expression levels of atrial natriuretic peptide(P<0.05),brain natriuretic peptide(P<0.01)and β-myosin heavy chain(P<0.05),reducing the increased protein/DNA ratio(P<0.01),and suppressing the increased cell surface area(P<0.05).(4)Overexpression of miR-20a significantly inhibited angiotensin Ⅱ-induced mitochondrial fission(P<0.05).(5)The results of RNAhybrid software analysis showed that miR-20a and the mRNA 3'untranslated region of cAMP-dependent protein kinase inhibitor alpha were well complementary and the predicted binding sites were highly conserved.(6)In conclusion,miR-20a is significantly down-regulated in pressure overload-induced cardiac hypertrophy.Overexpression of miR-20a inhibits cardiac hypertrophy at both the cellular level and animal level and attenuates angiotensin Ⅱ-induced mitochondrial fission.

Senescence is the major risk factor that promotes development of different stages of chronic liver diseases and is closely related to occurrence of hepatocellular carcinoma.Significant differences consist in clinicopathological features and tumor microenvironment between elderly and young patients with hepatocellular carcinoma.With rapid development of systemic therapy,immune checkpoint inhibitors combined with targeted therapy have greatly improved the prognosis of patients with advanced hepa-tocellular carcinoma.The selection of treatment decisions for elderly patients with hepatocellular carcinoma requires to consider u-nique age-related issues.Adequate communication and necessary evaluation should be carried out before making decisions.Elderly patients with hepatocellular carcinoma are speculated to benefit from combination immunotherapy based on age subgroup analysis of large clinical studies.However,data of effects and security obtained from clinical trials has certain limitations when being ap-plied in elderly populations of real world.The optimal therapeutic strategies for elderly patients with hepatocellular carcinoma still remain to be further explored in large-scale prospective clinical studies.

Objective To understand the discharge readiness of fathers of preterm infants in the Neonatal Intensive Care Unit(NICU),analyze its influencing factors,and provide a basis for formulating individualized discharge health education plans and continuous care plans.Methods A convenience sampling method was employed to select fathers of preterm infants admitted to the NICU in a tertiary A hospital in Zhejiang Province from March 2022 to June 2022 as the subjects of the study.A general information questionnaire and the Discharge Readiness-Parent Version scale were used for the survey.Multiple linear regression analysis was applied to analyze the factors influencing the discharge readiness of fathers of NICU preterm infants.Results A total of 186 fathers of NICU preterm infants were included in the study.The total score of the Discharge Readiness-Parent Version scale was(179.97±28.20)points;the standardized score was(7.82±1.16)points;33.3％of the fathers of preterm infants had a standardized score of＜7 points.Multiple linear regression analysis results showed that the factors influencing the discharge readiness of fathers of NICU preterm infants included the gestational age at birth,birth weight,length of hospital stay,distance to access healthcare service,as well as the fathers'age,annual family income,and number of children in the family.Conclusion The discharge readiness of fathers of NICU preterm infants is at a moderate level.Nursing staff need to pay attention to the discharge readiness of fathers of preterm infants who have lower gestational age at birth,lower birth weight,longer hospital stays,longer distance to healthcare service,and who are younger,have lower annual family income,and are having their first child.Individualized discharge health education plans and continuous care plans should be formulated for them to improve their caregiving knowledge and skills.

Objective:To investigate the mechanism of Wenjing Decoction in the treatment of hepatic fibrosis through network pharmacological methods, and conducting animal experiments to verify the core targets.Methods:The TCMSP database platform was used to screen the active components and related targets of Wenjing Decoction, and the Uniprot database was used to obtain the target genes corresponding to the active components of Wenjing Decoction. The network diagram of "Chinese materia medica-compound-target" was constructed in Cytoscape 3.7.2, and the GeneCards database was used to search liver fibrosis related targets. String database was used to construct a protein interaction network (PPI) to screen the core components and key targets of liver fibrosis, and GO analysis and KEGG pathway enrichment were performed. Animal experiments were conducted to verify the results of the analysis. 10 mice were selected as the blank group, and the remaining 45 rats were induced with carbon tetrachloride induced liver fibrosis model. After modeling, 40 successfully modeled rats were divided into model group and Wenjing Decoction high, medium-, and low-dosage groups using a random number table method, with 10 rats in each group. Wenjing Decoction high, medium-, and low-dosage groups were orally administered with 1.5×3.18, 3.18, and 0.5×3.18 g/kg Wenjing Decoction, respectively. The blank group was orally administered with equal volume distilled water once a day for 8 consecutive weeks. HE staining was used to observe the histopathological and morphological changes in the liver of rats. The serum GPT and GOT levels of rats were detected using a fully automated biochemical analyzer, and the expressions of TNF, AKT, and IL-6 proteins in rat liver tissue was detected using Western Blot.Results:A total of 188 active components of Wenjing Decoction were obtained, and the active components with higher degree values were β-sitosterol, quercetin, naringenin, etc. 799 liver fibrosis gene targets were collected, and the core target genes of the PPI network were TNF, AKT, IL6, etc. The key anti-hepatic fibrosis related pathways were obtained by GO function and KEGG analysis, including pathway in cancer, TNF, PI3K-Akt and other signalling pathways. Results of animal experiments showed that there were obvious inflammatory infiltration, collagen fibre and pseudo lobe generation in the liver tissue of rats in the model group, and the levels of inflammation and fibrosis in the liver tissue of rats in the Wenjing Decoction high, medium-, and low-dosage groups were improved to different degrees compared with that of the model group; compared with the model group, the levels of serum GPT and GOT decreased ( P<0.05); the protein expressions of TNF, AKT and IL6 in the Wenjing Decoction high, medium-, and low-dosage groups decreased ( P<0.05). Conclusion:Wenjing Decoction may exert anti-liver fibrosis effects by intervening in TNF, AKT, IL6 targets, regulating cancer pathways, TNF, PI3K Akt and other signaling pathways.

Objective:To investigate the clinical and pathological characteristics of breast cancer with HER2 low expression.Methods:The data from 3 422 patients with invasive breast cancer which archived in Peking Union Medical College Hospital between April 2019 and July 2022 were retrospectively reviewed. Among them, 136 patients were treated with neoadjuvant chemotherapy. The tumor size, histological type, tumor differentiation, lymph node metastasis, Ki-67 index, the status of estrogen receptor, progesterone receptor and HER2 as well as pathological complete response (pCR) rate were collected.Results:The HER2 status of 3 286 patients without neoadjuvant therapy, 616 (616/3 286, 18.7%) score 0, 1 047 (1 047/3 286, 31.9%) score 1+, 1 099 (1 099/3 286,33.4%) score 2+ and 524 (524/3 286,15.9%) score 3+ by immunohistochemistry (IHC). Among the 1 070 IHC 2+ cases, 161 were classified as HER2 positive by reflex fluorescence in situ hybridization (FISH) assay. In our cohort, 1 956 cases of HER2-low (IHC 1+ and IHC 2+/FISH-) breast cancer were identified. Compared to the HER2 IHC 0 group, HER2-low tumors more frequently occurred in patients with hormone receptor (HR) positive ( P<0.001), Ki-67 index below 35% ( P<0.001), well or moderate differentiation ( P<0.001) and over the age of 50 ( P=0.008). However, there were no significant differences in histological type, tumor size, and lymph node metastasis between HER2-low and HER2 IHC 0 group. For patients who had neoadjuvant therapy, the pCR rate in the patients with HER2-low was lower than those with HER2 IHC 0 (13.3%, 23.9%), but there was no significant difference. Although HER2-low breast cancers showed a slightly lower pCR rate than HER2 IHC 0 tumors, no remarkable difference was observed between tumors with HER2-low and HER2 IHC 0 regardless of hormone receptor status. Conclusions:The clinicopathological features of HER2-low breast cancers are different from those with HER2 IHC 0. It is necessary to accurately distinguish HER2-low breast cancer from HER2 IHC 0 and to reveal whether HER2-low tumor is a distinct biological entity.

Objective Improving the limb management strategy for patients undergoing coronary intervention through radial artery puncture and observe the application effect,and to provide scientific basis for the prevention of limb complications.Methods From March 2023 to February 2024,patients who underwent coronary intervention in the Cardiovascular Department of a Tertiary A hospital in Wenzhou City were selected.They were randomly di-vided into an experimental group of 241 cases and a control group of 236 cases using a random number table method.After surgery,they were all treated with a rotary hemostatic device for compression hemostasis.The experi-mental group implement improvement strategies for surgical limb management,specifically underwent a reverse Bar-beau test upon returning to the ward after surgery to achieve non-occlusive compression,followed by decompression every hour.The compression intensity of the control group was guided by palpating the distal radial artery pulsa-tion,and the first decompression was performed 1 hour after surgery,followed by decompression at intervals of every 2 hours.The main evaluation indicators are the incidence of surgical limb complications and simplified Chinese version of General Comfort Questionnaire(GCQ)scores in 2 groups of patients,while the secondary evaluation indi-cators are the duration of compression and the number of decompression times in both groups.Results The inci-dence of postoperative complications in the experimental group was 14.11%,which was statistically significant com-pared to 44.49%in the control group(χ2=53.308,P<0.001).The GCQ score of the experimental group was(77.71±5.43)points,which was higher than(74.66±5.83)points in the control group,and the difference was statistically signif-icant(t=-3.354,P=0.001).The compression duration of(172±52)minutes and decompression frequency of 2(2,3)in the experimental group were lower than(289±60)minutes and 4(3,4)in the control group,and the differences were statistically significant(P<0.001).Conclusion The non-occlusive compression method of the radial artery based on the reverse Barbeau test can significantly reduce limb complications in patients undergoing coronary inter-vention,shorten the duration of hemostatic compression,reduce the number of depressions,and improve patient com-fort.It provides objective basis for nursing staff to evaluate the intensity of hemostatic compression and the timing of decompression.

In this study, the pharmacodynamic substance basis of the therapeutic activity of different origin sources of the Tibetan medicinal herb Zha xun was evaluated, and the protective effect of the Zha xun, from Habahe county of Altay region, Xinjiang Uygur Autonomous Region; Gilgit region, Pakistan; Lhozhag county of Lhozhag city, Tibet Autonomous Region; Lhorong county of Chamdo city, Tibet Autonomous Region; and Jiulong county of Ganzi Tibetan Autonomous Prefecture, Sichuan Province, on 0.2% carbon tetrachloride (CCl₄)-induced acute liver injury in ICR mice was evaluated. The results showed that different sources of Zha xun significantly reduced serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH) in the CCl₄-induced acute oxidative liver injury model, improved liver histopathological damage. Among them, Zha xun from Habahe County, Altay Region, Xinjiang Uygur Autonomous Region; Gilgit Region, Pakistan; and Lhorong County, Chamdo City, Tibet Autonomous Region significantly reduced the malondialdehyde (MDA) content in liver tissues (P < 0.05), increased the glutathione (GSH) content (P < 0.01), improved the oxidative stress in liver tissues. The preliminary evaluation of the hepatoprotective activity of Zha xun from different origins was carried out using the model of HepG2 cell injury induced by acetaminophen (APAP). The results showed that Zha xun from different origins could significantly inhibit APAP-induced hepatocellular injury and improve the survival rate of hepatocytes. The present study demonstrated that the different origins of Zha xun had definite hepatoprotective activities in vivo and ex vivo, among which, Zha xun from Lhorong County, Chamdo City, Tibet Autonomous Region, had stronger hepatoprotective activities. The animals used in this experiment and the related dispositions were in accordance with the requirements of animal welfare, and the experiment was approved by the Committee of Laboratory Animal Management and Use of the Institute of Pharmaceutical Sciences of the Chinese Academy of Medical Sciences (approval No. 00004024) before the experiment was carried out.

Objective To explore the effect of pristimerin combined with cisplatin on proliferation and apoptosis of nasopharyngeal carcinoma cells.Methods CCK-8 assay was used to examine the survival rate of HNE-1 and CNE-2Z cells following treatment for 24 h with different concentrations of pristimerin,cisplatin or their combination.The changes in colony formation ability,apoptosis,and intracellular reactive oxygen species(ROS)levels of the treated cells were analyzed using colony formation assay and flow cytometry.Western blotting was performed to detect the changes in protein expressions in the cells.The effects of pre-treatment with NAC on proliferation,apoptosis,and PI3K/AKT signaling pathway were observed in pristimerin-and/or cisplatin-treated cells.Results Both pristimerin and cisplatin significantly lowered the survival rate of HNE-1 and CNE-2Z cells(P<0.05).Compared with pristimerin or cisplatin alone,their combination more strongly inhibited survival and colony formation ability of the cells,increased cell apoptosis rate and intracellular ROS levels,upregulated the protein expressions of Bax,cleaved caspase-3,and cleaved PARP,and downregulated the protein expressions of Bcl-2,Mcl-1,PARP and p-PI3K and p-AKT(P<0.05).NAC pretreatment significantly attenuated proliferation inhibition and apoptosis-promoting effects of pristimerin combined with cisplatin,and partially restored the downregulated protein expressions of p-PI3K and p-AKT in HNE-1 and CNE-2Z cells with the combined treatment(P<0.05).Conclusion Pristimerin can enhance cisplatin-induced proliferation inhibition and apoptosis in nasopharyngeal carcinoma cells,the mechanism of which may involve ROS-mediated deactivation of the PI3K/AKT signaling pathway.

Objective To investigate the effect of dihydroartemisinin(DHA)for enhancing the inhibitory effect of cisplatin(DDP)on DDP-resistant nasopharyngeal carcinoma cell line HNE1/DDP and explore the mechanism.Methods CCK-8 method was used to assess the survival rate of HNE1/DDP cells treated with DHA(0,5,10,20,40,80,and 160 μmol/L)and DDP(0,4,8,16,32,64,128 μmol/L)for 24 or 48 h,and the combination index of DHA and DDP was calculated using Compusyn software.HNE1/DDP cells treated with DHA,DDP,or their combination for 24 h were examined for cell viability,proliferation and colony formation ability using CCK-8,EdU and colony-forming assays.Flow cytometry was used to detect cell apoptosis and intracellular reactive oxygen species(ROS).The expression levels of apoptosis-related proteins cleaved PARP,cleaved caspase-9 and cleaved caspase-3 were detected by Western blotting.The effects of N-acetyl-cysteine(a ROS inhibitor)on proliferation and apoptosis of HNE1/DDP cells with combined treatment with DHA and DDP were analyzed.Results Different concentrations of DHA and DDP alone both significantly inhibited the viability of HNE1/DDP cells.The combination index of DHA(5 μmol/L)combined with DDP(8,16,32,64,128 μmol/L)were all below 1.Compared with DHA or DDP alone,their combined treatment more potently decreased the cell viability,colony-forming ability and the number of EdU-positive cells,and significantly increased the apoptotic rate,intracellular ROS level,and the expression levels of cleaved PARP,cleaved caspase-9 and cleaved caspase-3 in HNE1/DDP cells.N-acetyl-cysteine pretreatment obviously attenuated the inhibitory effect on proliferation and apoptosis-inducing effect of DHA combined with DDP in HNE1/DDP cells(P<0.01).Conclusion DHA enhances the growth-inhibitory and apoptosis-inducing effect of DDP on HNE1/DDP cells possibly by promoting accumulation of intracellular ROS.