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This study aimed to assess the prevalence of anti-hepatitis E virus (HEV) immunoglobulin (Ig) M and elevated serum alanine aminotransferase (ALT) levels among employees in catering and public place industries. Blood samples were collected between January and December 2020 from 26,790 employees working in the Qinhuai district of Nanjing, China. Anti-HEV IgM in the serum samples was tested by the capture ELISA method and ALT was tested by the IFCC method. Samples positive for anti-HEV IgM or with ALT levels over 200 U/L were subjected to PCR screening of HEV RNA. The overall seroprevalence of anti-HEV IgM was 0.41%, and the seroprevalence was slightly higher in males (0.47%) than in females (0.37%); however, the difference was not substantial (p = 0.177). Seroprevalence of anti-HEV IgM increased with age, reaching its peak level after 48 years of age. The prevalence of elevated ALT levels was 4.24%, and males exhibited a higher prevalence than females (6.78% vs 2.65%, p < 0.001). Prevalence of elevated ALT levels differed in age groups and the 26-36-year-old group had the highest rate of elevated ALT levels. Employees with elevated ALT levels had a higher prevalence of positive anti-HEV IgM than those with normal ALT (0.57% vs 0.31%, p < 0.001). Positive HEV RNA was detected in one anti-HEV IgM-negative employee with ALT higher than 200 U/L. In our study, all the HEV RNA-positive and IgM-positive individuals are asymptomatic, and a combination of ALT tests, serological methods, and molecular methods is recommended to screen asymptomatic HEV carriers and reduce the risk of transmission.

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BACKGROUND: Clinically, the pulse oxygen saturation of patients with chronic heart failure does not decrease significantly, and the clinical manifestations of labor-related dyspnea are not typical. As such, it is difficult to make a rapid diagnosis. OBJECTIVE: To investigate changes in pulse oxygen saturation in patients with chronic heart failure and examine the relationship between B-type natriuretic peptide (BNP) and normal pulse oxygen saturation. METHODS: A total of 80 hospitalized patients with chronic heart failure and increased BNP were randomly selected as the study group; the family members of 60 patients without dyspnea were randomly selected as the control group. The researchers measured the value of pulse oxygen saturation before and after upper arm compression, calculating the difference and analyzing the correlation between this difference and BNP values. The data were statistically analyzed using the SPSS Statistics 17.0 program. RESULTS: The decrease in pulse oxygen saturation in the study group was greater than in the control group; the decrease in pulse oxygen saturation of patients with chronic heart failure positively correlated with BNP. CONCLUSION: The value of pulse oxygen saturation in patients with chronic heart failure decreased more than in the control group, and this difference positively correlated with BNP. The measurement of pulse oxygen saturation before and after upper arm compression is a simple and effective method for diagnosing and evaluating chronic heart failure.

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Pregnancy complications affect millions of women each year. Some of these diseases have high morbidity and mortality such as preeclampsia. At present, there is no safe and effective treatment for pregnancy complications, so it is still a difficult clinical problem. As many pregnancy complications are closely related to placental dysplasia, placenta-specific therapy, as an important method, is expected to be a safe, effective, and specific therapeutic strategy. This review explains in detail the placenta physiological structure, characteristics, and action mechanism of some biomolecules and signaling pathways that play roles in normal development and disorders of the development of the placenta, and how to use these biomolecules as therapeutic targets when the placenta disorder causes disease, combining the latest progress in the field of nanodelivery systems, so as to lay a foundation for the development of placenta-specific therapy of pregnancy complications.

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In view of the serious clinical harm of preeclampsia and the lack of effective treatment methods, a PEG-modified lipid hybrid micelle was designed with a folic acid molecule on the surface, containing siRNA, targeted delivery to the placenta, interfering with the expression of sFlt-1 and treating preeclampsia. In this paper, the preparation and characterisation of lipid hybrid micelles were investigated in detail, the cytology in vitro and in vivo distribution, pharmacodynamics, safety and action mechanism of the preparation were studied, which laid a foundation for gene therapy of preeclampsia.

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Due to special cavity structure, cyclodextrin can form inclusion complex with a large number of compounds, which can be widely used in food industry, such as enhancing antibacterial activity, extending the storage period of food, increasing the solubility of food ingredients, removing cholesterol in food and so on. In this paper, the formation mechanism, classification and properties of cyclodextrin inclusion complex were reviewed, and the applications of cyclodextrin and its derivatives in food industry were discussed.

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With the deepening of tumor targeting research, the application of intelligent responsive drug carriers in the field of controlled drug release has become more and more extensive, and multiple responsive nano drug carriers have attracted greater attention. In this paper, nanoparticles with gold nanorods (GNR) as the core, mesoporous silica (mSiO2) doped with hydroxyapatite (HAP) as the inorganic hybrid shell and physically loaded with doxorubicin hydrochloride (DOX·HCl) are prepared (DOX/GNR/mSiO2/HAP, DNPs). DNPs nanoparticles have a typical core-shell structure. The gold nanorods as the core have extremely high light-to-heat conversion efficiency. Under the irradiation of near-infrared light, light can be converted into heat. The inorganic hybrid shell is a drug reservoir. The excellent photothermal response of gold nanorods combined with the excellent pH response of hydroxyapatite can obtain slow and sustained release of chemotherapeutic drugs. In vivo and in vitro anti-tumor cell activity study show that the DNPs in the laser showed stronger cytotoxicity than the other groups. Compared to chemotherapy and phototherapy alone, DNPs selectively accumulate in the tumor through the enhanced penetration and retention (EPR) effects. and have the unified function of hyperthermia and chemotherapy, and have significant inhibitory effect on tumor growth. Therefore, this study provides a new idea for the study of the combination of multiple therapeutic methods in the treatment of cancer.

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Bifenthrin (BF) is an important synthetic pyrethroid. Previous studies have demonstrated that cis-BF exhibits toxic effects on development, the neurological, reproductive and endocrine system. In this study, we evaluated the immunotoxicity caused by cis-BF in adolescent male C57BL/6 mice. Mice were exposed orally to 0, 5, 10, and 20 mg/kg/d for 3 weeks. The results showed that body weight, spleen weight, and splenic cellularity decreased in mice exposed to 20 mg/kg/d cis-BF. Additionally, we found that the mRNA levels of the pro-inflammatory factors IL-1ß, IL-6, CXCL-1, and TNF-α, in peritoneal macrophages, the spleen, and the thymus were inhibited in the cis-BF-treated groups. Moreover, MTT assays demonstrated that cis-BF inhibited splenocyte proliferation stimulated by LPS or Con A, as well as the secretion of IFN-γ on Con A stimulation. Collectively, the results of this study suggest that exposure to cis-BF has the potential to induce immunotoxicity in adolescent male C57BL/6 mice.

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Synthetic pyrethroids (SPs) are commonly used insecticides that have been detected in mammals, including humans, indicating a potential threat to human health. Bifenthrin (BF), as well as other pyrethroids, has been shown to possess neurotoxic, reproductive, hepatotoxic and nephrotoxic potential in mammals. However, studies regarding the immunotoxicity of BF and its mechanism are limited. In this study, we aim to exam the immunotoxicity of cis-BF on the murine macrophage cell line, RAW 264.7. MTT assay results demonstrated that cis-BF exposure induced apoptosis in RAW 264.7 cells in a concentration-dependent manner. We found that the expression of p53 and caspase-3 was up-regulated, while the expression of Bcl-2 was down-regulated during cis-BF-induced apoptosis. In addition, we also found that cis-BF exposure caused oxidative stress in RAW 264.7 cells in a dose-dependent manner. Interestingly, cis-BF exposure was found to inhibit the increase in transcription levels of IL-1ß, IL-6 and TNF-α responding to LPS stimulation. We also found that the induced increase in IFN-ß mRNA levels upon Sendai virus infection was blocked with cis-BF exposure. Finally, we found that cis-BF exposure increased ROS levels and dysregulated mRNA levels of oxidative stress-related genes in RAW 264.7 cells. The present study elucidates the immunotoxicity effect of cis-BF on macrophages and its possible underlying mechanism. The results from this study support the necessity to evaluate immune dysfunction in the risk assessment of cis-BF exposure.

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BACKGROUND: Interleukin (IL)-17A, a newly identified cytokine, may participate in the transition of a stable plaque into an unstable plaque. Macrophages play a critical role in the destabilization of atherosclerotic plaque. METHODS: RAW 264.7 cells were stimulated with IL-17A. The mRNA expression of inflammatory cytokines was determined by RT-PCR. The cytokines production in the supernatants was measured by ELISA. Small interfering RNA (siRNA) was used to confirm that IL-17A-induced pro-inflammatory cytokines production via IL-17RA signaling. The western blot assay was used to detect the phosphorylation of MAPKinases including p38 and ERK1/2. The DNA binding activity of nuclear factor NF-κB and AP-1 were detected by EMSA. RESULTS: IL-17A induced the production of pro-inflammatory cytokines in macrophages in a time- and dose-dependent manner, such as tumor necrosis factor (TNF)-α, IL-1ß, and IL-6. Meanwhile, IL-17A resulted in the phosphorylation of p38 and ERK1/2 and increased DNA-binding activity of NF-κB and AP-1. Pharmacological inhibitors of p38 and ERK1/2 partly attenuated IL-17A-induced TNF-α, IL-1ß, and IL-6 production. Either NF-κB inhibitor or AP-1 inhibitor also partly decreased the IL-17A-induced cytokine production. CONCLUSIONS: IL-17A induces pro-inflammatory cytokines production in macrophages via MAPKinases, NF-κB and AP-1 pathway.

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Excessive tumor necrosis factor-α (TNF-α) expression is increasingly thought to be detrimental to cardiomyocytes in acute myocardial infarction. During myocardial ischemia, TNF-α is mainly released from macrophages, but with persistent ischemia, it can originate from cardiomyocytes and contribute to cardiac remodeling. The initiating factor and exact molecular mechanism of TNF-α release from cardiomyocytes is presently unclear. In this study, we investigated direct effects of hypoxia on TNF-α expression of cardiomyocytes, the role of hypoxia inducible factor-1α (HIF-1α) in TNF-α regulation and potential secretory pathway of TNF-α. Elevated TNF-α expression and HIF-1α activation in primary cultured cardiomyocytes under hypoxia were detected by real-time PCR, Western blotting and immunofluorescence. TNF-α mRNA elevation and protein secretion were obviously inhibited by nucleofection of HIF-1α small interfering RNA (siRNA) and treatment with 2-methoxyestradiol (inhibitor of HIF-1α protein). Similar results were observed in HEK293 and HepG2 cells. Putative hypoxia response elements were identified in the human TNF-α gene promoter. Deletion analysis and site-directed mutagenesis demonstrated that HIF consensus binding sites spanning bp-1295 to bp-1292 relative to the transcription start site were functional for activation of the TNF-α promoter which was confirmed by electrophoretic mobility-shift assay (EMSA) and chromatin immunoprecipitation (ChIP) analysis. Exosomes (vesicles mediating a non-classical route of protein secretion) in supernatants from hypoxic cardiomyocytes were identified by an anti-CD63 antibody in Western blot and observed by electron microscopy. The presence of TNF-α within exosomes precipitated from supernatants of hypoxic cardiomyocytes was verified by immunoelectron microscopy and immunoblotting. Results of this study indicate that under hypoxia, HIF-1α initiates expression of TNF-α, mediated by exosomes in cardiomyocytes.

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OBJECTIVE: To determine the effects of interleukin (IL)-17A inhibition on experimental atherosclerosis. METHODS AND RESULTS: ApoE(-/-) mice were treated with either rat anti-mouse IL-17A, mouse anti-mouse IL-17A or isotype-matched control antibodies for 12 weeks (n=8-10 per group). Ldlr(-/-) mice were transplanted with IL-17A-deficient or wild type bone marrow (n=8 per group). Rat anti-mouse IL-17A treatment obviously reduced plaque size by 43% (p<0.01) without evidence of reduced IL-17A signaling. In contrast, mouse anti-mouse IL-17A treatment and IL-17A deficiency in bone marrow cells did not alter lesion size despite significant reduction of IL-17A production. CONCLUSIONS: Inhibition of IL-17A signaling does not alter lesion development in Th1-biased C57BL/6 ApoE(-/-) and Ldlr(-/-) mice with already low levels of IL-17A production. Alteration of lesion development after repeated injections of rat anti-mouse IL-17A antibody in ApoE(-/-) mice could not be attributed to blockade of IL-17A signaling.

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OBJECTIVE: Atherosclerosis is a chronic inflammatory disease regulated by T lymphocyte subsets. Recently, CD4(+) CD25(+) Foxp3(+) regulatory T (Treg) cells and Th17 cells have been described as two distinct subsets and have the opposite effects on autoimmunity. Clinical observation has revealed that the Th17/Treg imbalance exists in patients with acute coronary syndrome. We investigated whether the Th17/Treg functional imbalance existed during atherogenesis in ApoE(-/-) mice. METHODS AND RESULTS: Th17/Treg functions at different levels including cell frequencies, related cytokine secretion and key transcription factors were investigated comparatively between ApoE(-/-) mice and their age-matched C57BL/6J mice. The results demonstrated that ApoE(-/-) mice revealed significantly increased secretion of Th17 related cytokines (IL-17 and IL-6) and expression of transcription factor (RORgammat) levels and obviously decreased number in Treg cells, secretion of Treg related cytokines (TGF-beta(1)) and expression of transcription factor (Foxp3) levels as compared with age-matched C57BL/6J mice. Th17 related mediators reached their maximum expression values at the early stage (8-16weeks of age) in ApoE(-/-) mice, and then followed by continuous depression of their expression levels. Meanwhile, the expression of Treg related mediators was much lower in ApoE(-/-) mice than in their age-matched wild-type littermates. CONCLUSIONS: Th17/Treg functional imbalance exists during atherogenesis in ApoE(-/-) mice, suggesting a potential role of Th17/Treg imbalance in the formation and progression of atherosclerosis.

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