Micro/nanoplastics (MNPs), recognized as emerging environmental pollutants, are widely distributed in natural environments. Due to their small particle size and significant migratory capacity, MNPs can infiltrate diverse environmental matrices, then invade and accumulate in the organism via the skin, respiration, and digestion. Recently, concerns have grown over the detrimental effects and potential toxicity of MNPs on reproductive health. This review summarized published epidemiological and toxicological studies related to MNPs exposure and their effects on reproductive health. Firstly, this review critically examined the current landscape of epidemiological evidence and found that MNPs (e.g., polystyrene, polypropylene, polyvinyl chloride, polyethylene, etc.) are present in various biological specimens from both males and females, and their presence may be associated with an increased risk of reproductive disorders. Secondly, extensive toxicological studies revealed that MNPs exposure induces reproductive health damage through mechanisms such as disrupting the microstructure of reproductive organs and altering molecular-level expressions. Oxidative stress, inflammatory responses, and apoptosis are identified as potential links between MNPs exposure and reproductive damage. Finally, this review addressed the prevalent shortcomings in existing studies and proposed future directions to tackle the challenges posed by MNPs-induced reproductive harm. These insights aim to inform strategies for safeguarding public reproductive health and ecological security, providing a scientific foundation for mitigating risks associated with MNPs pollution.

[Objective] To establish a cryopreservation protocol for small-volume (≤1 mL) red blood cells (RBCs) and to evaluate the reactivity and stability of blood group antigens after cryopreservation, so as to explore its potential application in immunohematology reference laboratories. [Methods] Small-volume RBCs were cryopreserved for 120 days, followed by thawing and deglycerolization to restore the RBC components. The quality of the RBCs was assessed. Serum antibodies were serially diluted and reacted with RBCs before and after cryopreservation, and agglutination scores were recorded to quantitatively evaluate the reactivity and stability of blood group antigens such as Rh, Duffy, Lewis, Kidd, M, and H. Flow cytometry was used to analyze the percentage and mean fluorescence intensity of ABO antigen expression on RBCs before and after cryopreservation to assess the usability of cryopreserved RBCs in flow immunophenotyping and blood group subtype studies. [Results] The hemolysis rate of thawed and deglycerolized RBCs was (0.27±0.10)%, with a supernatant free hemoglobin level of (0.52±0.14) g/L, and the RBC recovery rate was (69.12±7.91)%. The direct antiglobulin test (DAT) was negative for all thawed RBCs. There was no difference in the reactivity of blood group antigens before and after cryopreservation, and no difference in the percentage and mean fluorescence intensity of A and B antigen expression on RBCs before and after cryopreservation. [Conclusion] The small-volume RBC cryopreservation protocol can be applied to immunohematology analysis in reference laboratories and is expected to be widely used in blood group identification, antibody screening, identification, and blood group-related research.

Ketone body metabolism plays a significant role in the development and progression of diabetic retinopathy(DR), which closely related to the system and local metabolic disorders as a major microvascular complication of diabetes mellitus. Previous research has established a close relationship between dyslipidemia and DR progression. Ketone bodies, comprising β-hydroxybutyrate, acetoacetate, and acetone, are metabolic products generated from fat breakdown when glucose metabolism is impaired. Studies have revealed that ketone body metabolism is intricately linked to multiple pathophysiological processes in DR, including oxidative stress, inflammatory responses, and neurodegeneration within retinal cells. This article provides a review exploring the impact of ketone body metabolism on the pathogenesis of DR, and systematically reviews the latest research progress on the impact of ketone bodies on the core pathological links such as retinal vascular barrier destruction, glial cell activation and angiogenesis through metabolic reprogramming, epigenetic modification and cell signal transduction, so as to provide a theoretical basis for in-depth understanding of the metabolic driving mechanism of DR.

Chronic intermittent hypoxia (CIH) can lead to vascular dysfunction and increase the risk of cardiovascular diseases, cerebrovascular diseases, and arterial diseases. Nevertheless, mechanisms underlying CIH-induced vascular dysfunction remain unclear. Herein, this study analyzed the role of aortic smooth muscle calciumactivated potassium (BK) channels in CIH-induced vascular dysfunction. CIH models were established in rats and rat aortic smooth muscle cells (RASMCs). Hemodynamic parameters such as mean blood pressure (MBP), diastolic blood pressure (DBP), and systolic blood pressure (SBP) were measured in rats, along with an assessment of vascular tone. NO and ET-1 levels were detected in rat serum, and the levels of ET-1, NO, eNOS, p-eNOS, oxidative stress markers (ROS and MDA), and inflammatory factors (IL-6 and TNF-α) were tested in aortic tissues. The Ca2+ concentration in RASMCs was investigated. The activity of BK channels (BKα and BKβ) was evaluated in aortic tissues and RASMCs. SBP, DBP, and MBP were elevated in CIH-treated rats, along with endothelial dysfunction, cellular edema and partial detachment of endothelial cells. BK channel activity was decreased in CIH-treated rats and RASMCs. BK channel activation increased eNOS, p-eNOS, and NO levels while lowering ET-1, ROS, MDA, IL-6, and TNF-α levels in CIH-treated rats. Ca2+ concentration increased in RASMCs following CIH modeling, which was reversed by BK channel activation. BK channel inhibitor (Iberiotoxin) exacerbated CIH-induced vascular disorders and endothelial dysfunction. BK channel activation promoted vasorelaxation while suppressing vascular endothelial dysfunction, inflammation, and oxidative stress, thereby indirectly improving CIH-induced vascular dysfunction.

Objective:To discuss the perioperative management strategy of the HeartCon left ventricular assist device in the treatment of adult patients with end-stage heart failure and evaluate the effectiveness of blood pump.Methods:Ten consecutive patients with end-stage heart failure treated with the LVAD HeartCon at the Department of Cardiovascular Surgery, Jiangsu Province Hospital from July 2021 to July 2023 were enrolled in this study. The clinical data and follow-up results were retrospectively analyzed. Blood pump parameter, cardiac function classification, liver and kidney function, coagulation, myocardial markers, N-terminal pro-B-type natriuretic peptide, von Willebrand factor antigen, echocardiography, cardiothoracic ratio, and 6-minute walking distance test (6MWT) were evaluated before and after implantation of LVAD in 30, 60, 90, 180, 360, 540, and 720 days. EQ-5D-5L questionnaire was used to evaluate the quality of life.Results:There were 9 males and 1 female with a mean age of (53.7±9.7) years. All patients survived. Renal insufficiency occurred in 1 patient and recurrent aseptic granuloma occurred in 1 patient. There were no significant differences in aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), serum creatinine (Scr), blood urea nitrogen (BUN), right ventricular fractional area change (FAC) and tricuspid annular plane systolic excursion (TAPSE) between pre-operation and 30, 60 and 90 days post-operation( P>0.05). The levels of N-terminal pro-B-type natriuretic peptide (NT-proBNP), von Willbrand factor (vWF) antigen, left ventricular end-diastolic diameter (LVDd) and cardiothoracic ratio decreased significantly on the 30th, 60th and 90th day after operation ( P<0.05). The left ventricular ejection fraction (LVEF), 6MWT and EQ-5D-5L scores were significantly increased at 30, 60 and 90 days after operation compared with those before operation ( P<0.05). Conclusion:With the left ventricular assist device HeartCon, the cardiac function and quality of life of patients were significantly improved within 3 months after operation, and no serious complications were observed, proving that the device is safe and effective.

Objective:To identify the key genes in the process inhibiting inflammation by overexpression adenovirus-mediated pigment epithelium-derived factor ( PEDF) gene in human monocytic leukemia cells THP1. Methods:Proteomic analysis of THP1 overexpressing adenovirus-mediated PEDF gene was performed.The THP1 cells were divided into GFP and PEDF groups, transfected with GFP and PEDF adenovirus, respectively.The THP1 cells were divided into mannitol group, high glucose group, high glucose+ GFP group, and high glucose+ PEDF group, which were cultured with mannitol for 4 days, anhydrous glucose for 4 days, GFP adenovirus for 3 days, and PEDF adenovirus for 3 days, respectively.The Pedf-/- mice were divided into Pedf-/- group and Pedf-/- diabetes group according to the random table method, with 12 mice in each group.Another 10 C57BL/6 mice were taken as the control group.Mouse retinas were collected for experiments.The mRNA expression levels of differentially expressed genes (DEGs) in retina and THP1 cells were verified by real-time fluorescence quantitative PCR.The DEGs were intersected with the GSE5504 dataset, and the protein-protein interaction (PPI) network was built using the String database.Modules of the PPI were extracted using the Cytoscape software and the MCODE application.Intersections were taken with the Set1 dataset and key genes were found.The expression levels of key genes in THP1 cells and Pedf-/- mice were verified by Western blot.The feeding and operation of experimental animals were in accordance with the regulations of the State Science and Technology Commission on the management of experimental animals and approved by the Animal Management and Use Committee of Tianjin Medical University (No.TTYY2023120217). Results:Through proteomics and bioinformatics analysis, 105 DEGs in the Set1 dataset were screened.The results of real-time PCR showed that the relative expression levels of ARF5, TCF25 and KCTD9 mRNA were significantly higher and the relative expression levels of RNPS1, CSF1R, OGA, IBA57 and MGST2 mRNA were significantly lower in PEDF group than in GFP group, showing statistically significant differences (all at P<0.001).There were significant overall differences in the relative expression levels of down-regulated TCF25, KCTD9 and ARF5 mRNA and up-regulated CSF1R, RNPS1 and IBA57 mRNA among control group, Pedf-/- group and Pedf-/- diabetes group ( F=64.057, 27.561, 37.179, 65.757, 44.024, 34.248; all at P<0.001).Compared with control group, the relative expression levels of TCF25, KCTD9 and ARF5 mRNA were decreased and the relative expression levels of CSF1R and RNPS1 mRNA were increased in Pedf-/- group, showing statistically significant differences (all at P<0.05).Compared with control group, the relative expression levels of TCF25, KCTD9 and ARF5 mRNA were decreased and the relative expression levels of CSF1R, RNPS1 and IBA57 mRNA were increased in Pedf-/- diabetes group, showing statistically significant differences (all at P<0.05).Compared with Pedf-/- group, the relative expression level of TCF25 mRNA was decreased and the relative expression levels of CSF1R, RNPS1 and IBA57 mRNA were increased in Pedf-/- diabetes group, showing statistically significant differences (all at P<0.05).After intersection with the GSE5504 dataset, 20 differential proteins were obtained, which were mainly enriched in positive regulation of gene expression, positive regulation of ERK1 and ERK2 cascade, positive regulation of insulin secretion involved in cell response to glucose stimulation and antigen processing and presentation pathways.The key gene CSF1R was screened by constructing PPI network and MCODE plugin in Cytoscape software.Western blot results showed that the expression levels of CSF1R in high glucose group and high glucose+ GFP group were 1.961±0.085 and 1.000±0.069, which were higher than 1.000±0.072 in mannitol group and 0.469±0.079 in high glucose+ PEDF group, respectively, and the differences were statistically significant ( t=14.940, 8.765; both at P < 0.01).The expression of CSF1R in the retina of Pedf-/- diabetes group was 1.633±0.192, which was higher than 1.000±0.050 in Pedf-/- group, and the difference was statistically significant ( t=5.537, P<0.01). Conclusions:CSF1R may be a key gene and therapeutic target for the inhibition of inflammation by overexpression of adenovirus-mediated PEDF gene in THP1 cell.

Chronic intermittent hypoxia (CIH) can lead to vascular dysfunction and increase the risk of cardiovascular diseases, cerebrovascular diseases, and arterial diseases. Nevertheless, mechanisms underlying CIH-induced vascular dysfunction remain unclear. Herein, this study analyzed the role of aortic smooth muscle calciumactivated potassium (BK) channels in CIH-induced vascular dysfunction. CIH models were established in rats and rat aortic smooth muscle cells (RASMCs). Hemodynamic parameters such as mean blood pressure (MBP), diastolic blood pressure (DBP), and systolic blood pressure (SBP) were measured in rats, along with an assessment of vascular tone. NO and ET-1 levels were detected in rat serum, and the levels of ET-1, NO, eNOS, p-eNOS, oxidative stress markers (ROS and MDA), and inflammatory factors (IL-6 and TNF-α) were tested in aortic tissues. The Ca2+ concentration in RASMCs was investigated. The activity of BK channels (BKα and BKβ) was evaluated in aortic tissues and RASMCs. SBP, DBP, and MBP were elevated in CIH-treated rats, along with endothelial dysfunction, cellular edema and partial detachment of endothelial cells. BK channel activity was decreased in CIH-treated rats and RASMCs. BK channel activation increased eNOS, p-eNOS, and NO levels while lowering ET-1, ROS, MDA, IL-6, and TNF-α levels in CIH-treated rats. Ca2+ concentration increased in RASMCs following CIH modeling, which was reversed by BK channel activation. BK channel inhibitor (Iberiotoxin) exacerbated CIH-induced vascular disorders and endothelial dysfunction. BK channel activation promoted vasorelaxation while suppressing vascular endothelial dysfunction, inflammation, and oxidative stress, thereby indirectly improving CIH-induced vascular dysfunction.

Chronic intermittent hypoxia (CIH) can lead to vascular dysfunction and increase the risk of cardiovascular diseases, cerebrovascular diseases, and arterial diseases. Nevertheless, mechanisms underlying CIH-induced vascular dysfunction remain unclear. Herein, this study analyzed the role of aortic smooth muscle calciumactivated potassium (BK) channels in CIH-induced vascular dysfunction. CIH models were established in rats and rat aortic smooth muscle cells (RASMCs). Hemodynamic parameters such as mean blood pressure (MBP), diastolic blood pressure (DBP), and systolic blood pressure (SBP) were measured in rats, along with an assessment of vascular tone. NO and ET-1 levels were detected in rat serum, and the levels of ET-1, NO, eNOS, p-eNOS, oxidative stress markers (ROS and MDA), and inflammatory factors (IL-6 and TNF-α) were tested in aortic tissues. The Ca2+ concentration in RASMCs was investigated. The activity of BK channels (BKα and BKβ) was evaluated in aortic tissues and RASMCs. SBP, DBP, and MBP were elevated in CIH-treated rats, along with endothelial dysfunction, cellular edema and partial detachment of endothelial cells. BK channel activity was decreased in CIH-treated rats and RASMCs. BK channel activation increased eNOS, p-eNOS, and NO levels while lowering ET-1, ROS, MDA, IL-6, and TNF-α levels in CIH-treated rats. Ca2+ concentration increased in RASMCs following CIH modeling, which was reversed by BK channel activation. BK channel inhibitor (Iberiotoxin) exacerbated CIH-induced vascular disorders and endothelial dysfunction. BK channel activation promoted vasorelaxation while suppressing vascular endothelial dysfunction, inflammation, and oxidative stress, thereby indirectly improving CIH-induced vascular dysfunction.

Arsenic is a widely occurring metalloid element in the natural environment and is one of the primary carcinogens identified by the World Health Organization (WHO), but the specific carcinogenic mechanism is currently unclear. In recent years, through toxicological studies on arsenic, it has been found that exposure to arsenic can affect cellular metabolism in the body, which may be closely related to the carcinogenic mechanism of arsenic. Therefore, the authors review the research progress on arsenic exposure-induced effects on glucose metabolism, lipid metabolism, and amino acid metabolism, with a view to providing a theoretical basis for the study of the mechanism of arsenic carcinogenesis.

Objective To observe the risk factors of ischemic mitral regurgitation(IMR)in ischemic cardiomyopathy.Methods Totally 143 patients with ischemic cardiomyopathy were retrospectively enrolled and divided into IMR+group(n=68)or IMR-group(n=75)based on IMR,while 50 healthy volunteers were taken as controls(control group).The general information,conventional ultrasonic parameters of left ventricle,three-dimensional speckle tracking imaging(3D-STI)parameters as well as mitral valve structural and functional parameters were compared among groups,and the risk factors of IMR were screened with logistic regression analysis.Results Significant differences of left ventricular end-diastolic volume(LVEDV),left ventricular end-systolic volume(LVESV),left ventricular global longitudinal strain(LVGLS),the peak systolic twist(Twist),tenting volume(VTent)and total leaflet area(TLA)/annulus area(AA)were found between IMR+group and IMR-group(all P＜0.05).Decreased LVGLS,decreased Twist and increased VTent were all independent risk factors of IMR in ischemic cardiomyopathy(all P＜0.05).Conclusion Decreased LVGLS,decreased Twist and increased VTent were independent risk factors of IMR in ischemic cardiomyopathy.