COVID-19 transmission and control in land public transport: A literature review.

Land public transport is an important link within and between cities, and how to control the transmission of COVID-19 in land public transport is a critical issue in our daily lives. However, there are still many inconsistent opinions and views about the spread of SARS-CoV-2 in land public transport, which limits our ability to implement effective interventions. The purpose of this review is to overview the literature on transmission characteristics and routes of the epidemic in land public transport, as well as to investigate factors affecting its spread and provide feasible measures to mitigate the infection risk of passengers. We obtained 898 papers by searching the Web of Science, Pubmed, and WHO global COVID database by keywords, and finally selected 45 papers that can address the purpose of this review. Land public transport is a high outbreak area for COVID-19 due to characteristics like crowding, inadequate ventilation, long exposure time, and environmental closure. Different from surface touch transmission and drop spray transmission, aerosol inhalation transmission can occur not only in short distances but also in long distances. Insufficient ventilation is the most important factor influencing long-distance aerosol transmission. Other transmission factors (e.g., interpersonal distance, relative orientation, and ambient conditions) should be noticed as well, which have been summarized in this paper. To address various influencing factors, it is essential to suggest practical and efficient preventive measures. Among these, increased ventilation, particularly the fresh air (i.e., natural ventilation), has proven to effectively reduce indoor infection risk. Many preventive measures are also effective, such as enlarging social distance, avoiding face-to-face orientation, setting up physical partitions, disinfection, avoiding talking, and so on. As research on the epidemic has intensified, people have broken down many perceived barriers, but more comprehensive studies on monitoring systems and prevention measures in land public transport are still needed.

The targeting of DAPK1 with miR-190a-3p promotes autophagy in trophoblast cells.

Pre-eclampsia (PE) is a dangerous pathological status that occurs during pregnancy and is a leading reason for both maternal and fetal death. Autophagy is necessary for cellular survival in the face of environmental stress as well as cellular homeostasis and energy management. Aberrant microRNA (miRNA) expression is crucial in the pathophysiology of PE. Although studies have shown that miRNA (miR)-190a-3p function is tissue-specific, the precise involvement of miR-190a-3p in PE has yet to be determined. We discovered that miR-190a-3p was significantly lower and death-associated protein kinase 1 (DAPK1) was significantly higher in PE placental tissues compared to normal tissues, which is consistent with the results in cells. The luciferase analyses demonstrated the target-regulatory relationship between miR-190a-3p and DAPK1. The inhibitory effect of miR-190a-3p on autophagy was reversed by co-transfection of si-DAPK1 and miR-190a-3p inhibitors. Thus, our data indicate that the hypoxia-dependent miR-190a-3p/DAPK1 regulatory pathway is implicated in the development and progression of PE by promoting autophagy in trophoblast cells.

Identification and validation of feature genes associated with M1 macrophages in preeclampsia.

Preeclampsia (PE) is a pregnancy-specific cardiovascular complication that is the leading cause of maternal and neonatal morbidity and mortality. Previous studies have indicated the importance of immune cells, such as M1 and M2 macrophages, in the pathogenesis of PE. However, the mechanisms leading to immune dysregulation are unclear. Data-independent acquisition proteomic analysis was performed on placental tissues collected from patients with PE and healthy controls. Transcriptome data for placenta samples from patients with PE and their corresponding controls were obtained from the Gene Expression Omnibus database. Differential analysis of transcriptome and proteome data between PE and control groups was performed using R software. Immunocytic infiltration scoring was performed using the quantiseq algorithm. Weighted gene co-expression network analysis (WGCNA) screened for feature genes associated with M1 cell infiltration. Protein-protein interaction (PPI) analysis identified hub genes. We confirm that the infiltration score of M1 macrophages was significantly increased in the placental tissues of patients with PE. Differential analysis, WGCNA, and PPI analysis identified four hub molecules associated with M1 cell infiltration (HTRA4, POGK, MFAP5, and INHBA). The hub molecules displayed dysregulated expression in PE tissues. The qPCR, Western blots, and immunohistochemistry analyses confirmed that Inhibin, beta A (INHBA) was highly expressed in placental tissues of patients with PE. Immunofluorescence revealed the extensive infiltration of M1 macrophages in the placental tissues of patients with PE and their co-localization with INHBA. The collective results identified hub genes associated with M1 macrophage infiltration, providing potential targets for the pathogenesis and treatment of PE.

Long Noncoding RNA AC078850.1 Induces NLRP3 Inflammasome-Mediated Pyroptosis in Atherosclerosis by Upregulating ITGB2 Transcription via Transcription Factor HIF-1α.

As a chronic progressive inflammatory disease, atherosclerosis constitutes a leading cause of cardiovascular disease, with high mortality and morbidity worldwide. The effect of lncRNA AC078850.1 in atherosclerosis is unknown; this study aims to explore the regulatory mechanism of the lncRNA AC078850.1/HIF-1α complex in atherosclerosis. Initially, we identified the lncRNA AC078850.1 associated with atherosclerosis using multiple bioinformatic methods, finding that the level of lncRNA AC078850.1 in peripheral blood mononuclear cells was positively related to the severity of carotid atherosclerosis. LncRNA AC078850.1 was upregulated, and found to be predominately localized in the nucleus of THP-1 macrophage-derived foam cells. Both the knockdown of lncRNA AC078850.1 and the transcription factor HIF-1α can each markedly suppress ITGB2 gene transcription, ROS production, NLRP3 inflammasome, IL-1ß/18 release, lipid accumulation, and pyroptotic cell death in ox-LDL-stimulated THP-1-derived macrophages. Additionally, the downregulation of HIF-1α attenuated the positive effects of lncRNA AC078850.1 on pyroptosis and foam cell formation. In addition, the knockdown of lncRNA AC078850.1 suppressed HIF-1α-aggravated macrophages pyroptosis and foam cell formation. Meanwhile, inhibition of ITGB2 gene expression ameliorated HIF-1α-aggravated ROS generation in THP-1-derived macrophages. Taken together, our study demonstrated that lncRNA AC078850.1 was involved in the regulation of ITGB2 gene transcription by binding to the HIF-1α and lncRNA AC078850.1/HIF-1α complex, promoting both NLRP3 inflammasome-mediated pyroptosis and foam cell formation through the ROS-dependent pathway in cases of atherosclerosis.

Influence of natural ventilation design on the dispersion of pathogen-laden droplets in a coach bus.

Natural ventilation is an energy-efficient design approach to reduce infection risk (IR), but its optimized design in a coach bus environment is less studied. Based on a COVID-19 outbreak in a bus in Hunan, China, the indoor-outdoor coupled CFD modeling approach is adopted to comprehensively explore how optimized bus natural ventilation (e.g., opening/closing status of front/middle/rear windows (FW/MW/RW)) and ceiling wind catcher (WCH) affect the dispersion of pathogen-laden droplets (tracer gas, 5 µm, 50 µm) and IR. Other key influential factors including bus speed, infector's location, and ambient temperature (Tref) are also considered. Buses have unique natural ventilation airflow patterns: from bus rear to front, and air change rate per hour (ACH) increases linearly with bus speed. When driving at 60 km/h, ACH is only 6.14 h-1 and intake fractions of tracer gas (IFg) and 5 µm droplets (IFd) are up to 3372 ppm and 1394 ppm with ventilation through leakages on skylights and no windows open. When FW and RW are both open, ACH increases by 43.5 times to 267.50 h-1, and IFg and IFd drop rapidly by 1-2 orders of magnitude compared to when no windows are open. Utilizing a wind catcher and opening front windows significantly increases ACH (up to 8.8 times) and reduces IF (5-30 times) compared to only opening front windows. When the infector locates at the bus front with FW open, IFg and IFd of all passengers are <10 ppm. More droplets suspend and further spread in a higher Tref environment. It is recommended to open two pairs of windows or open front windows and utilize the wind catcher to reduce IR in coach buses.

MiR-141-3p promotes hypoxia-induced autophagy in human placental trophoblast cells.

Preeclampsia (PE) is a pregnancy-specific disorder and a significant contributor to maternal, fetal and neonatal morbidity and mortality worldwide. Its pathogenesis is generally accepted as insufficient trophoblast invasion of the maternal endometrium and inadequate remodeling of the maternal spiral arteries. These impairments lead to elevated levels of hypoxia and oxidative stress. Autophagy has become a highly researched field in obstetrics, and this process may be essential for preimplantation development beyond the four- and eight-cell stages, and for blastocyst survival, extra-villous trophoblast functions, invasion and vascular remodeling. Several studies have shown that autophagy activation, shown by an increase in autophagy vacuoles or microtubule-associated protein 1 A/1B-light chain 3 (LC3) dots, was more common in PE than in normal pregnancy. Thus, changes in autophagic status are seen in preeclamptic placentas. MicroRNA-141-3p (miR-141-3p), a multifunctional miRNA, is involved in a variety of physiological and pathological processes, including PE and autophagy. However, the influence of miR-141-3p on autophagy regulation in trophoblast cells has yet to be described. Therefore, the objective of our study was to investigate the role of miR-141-3p in autophagy induced by hypoxia in human placental trophoblast cells. Our results found that hypoxia induced autophagy in trophoblast cells and dramatically elevated the expression of miR-141-3p. Overexpression of miR-141-3p improved autophagic activity, whereas low expression of miR-141-3p inhibited autophagic activity. Therefore, our data demonstrated that miR-141-3p promoted hypoxia-induced autophagy in placental trophoblast cells, which may be related to the development of preeclampsia.

Blood eosinophil count in the diagnosis of allergic-like rhinitis with chronic rhinosinusitis.

BACKGROUND: Allergic rhinitis (AR) and nonallergic rhinitis (NAR) often are comorbid with chronic rhinosinusitis (CRS). Finding a convenient test that distinguishes these complex conditions is helpful for effective treatment. We aimed to analyse blood parameter differences between AR and NAR patients with/without CRS. METHODS: Eight hundred thirteen patients, including AR and NAR with different conditions [CRS with nasal polyps (CRSwNP) and CRS without nasal polyps (CRSsNP)] were analysed in this retrospective study. Patients with a nasal deviation alone were included as healthy controls (HC). Receiver operating characteristic analysis was used to assess the value of blood parameters for diagnosing AR or NAR with/without CRS. RESULTS: Compared to nonallergic-like rhinitis (HC, CRSwNP and CRSsNP), the blood eosinophil count was significantly increased in the allergic-like rhinitis groups, except for NAR-CRSsNP (AR, AR-CRSwNP, AR-CRSsNP, NAR and NAR-CRSwNP). The NAR-CRSsNP group had a higher level of eosinophils than the HC and CRSsNP groups. Among allergic-like rhinitis patients, eosinophils were higher in allergic-like rhinitis patients with CRSwNP (AR-CRSwNP and NAR-CRSwNP) than in allergic-like rhinitis patients without CRSwNP (AR, AR-CRSsNP, NAR and NAR-CRSsNP). However, no difference in blood eosinophils was observed between AR and NAR. There was also no difference among nonallergic-like rhinitis patients. Similar findings were found for the blood eosinophil proportion. Furthermore, the blood eosinophil count was a good predictor of allergic-like rhinitis, especially allergic-like rhinitis with CRSwNP. CONCLUSION: The blood eosinophil count and proportion may be good diagnostic predictors of allergic-like rhinitis but cannot differentiate between AR and NAR. This indicator may be much better in predicting allergic-like rhinitis with CRSwNP.

Identification of diagnostic signatures associated with immune infiltration in Alzheimer's disease by integrating bioinformatic analysis and machine-learning strategies.

Objective: As a chronic neurodegenerative disorder, Alzheimer's disease (AD) is the most common form of progressive dementia. The purpose of this study was to identify diagnostic signatures of AD and the effect of immune cell infiltration in this pathology. Methods: The expression profiles of GSE109887, GSE122063, GSE28146, and GSE1297 were downloaded from the Gene Expression Omnibus (GEO) database to obtain differentially expressed genes (DEGs) between AD and control brain samples. Functional enrichment analysis was performed to reveal AD-associated biological functions and key pathways. Besides, we applied the Least Absolute Shrinkage Selection Operator (LASSO) and support vector machine-recursive feature elimination (SVM-RFE) analysis to screen potential diagnostic feature genes in AD, which were further tested in AD brains of the validation cohort (GSE5281). The discriminatory ability was then assessed by the area under the receiver operating characteristic curves (AUC). Finally, the CIBERSORT algorithm and immune cell infiltration analysis were employed to assess the inflammatory state of AD. Results: A total of 49 DEGs were identified. The functional enrichment analysis revealed that leukocyte transendothelial migration, cytokine receptor interaction, and JAK-STAT signaling pathway were enriched in the AD group. MAF basic leucine zipper transcription factor F (MAFF), ADCYAP1, and ZFP36L1 were identified as the diagnostic biomarkers of AD with high discriminatory ability (AUC = 0.850) and validated in AD brains (AUC = 0.935). As indicated from the immune cell infiltration analysis, naive B cells, plasma cells, activated/resting NK cells, M0 macrophages, M1 macrophages, resting CD4+ T memory cells, resting mast cells, memory B cells, and resting/activated dendritic cells may participate in the development of AD. Additionally, all diagnostic signatures presented different degrees of correlation with different infiltrating immune cells. Conclusion: MAFF, ADCYAP1, and ZFP36L1 may become new candidate biomarkers of AD, which were closely related to the pathogenesis of AD. Moreover, the immune cells mentioned above may play crucial roles in disease occurrence and progression.

Soil moisture-atmosphere feedback dominates land N2 O nitrification emissions and denitrification reduction.

Soil moisture (SM) is essential to microbial nitrogen (N)-cycling networks in terrestrial ecosystems. Studies have found that SM-atmosphere feedbacks dominate the changes in land carbon fluxes. However, the influence of SM-atmosphere feedbacks on the N fluxes changes, and the underlying mechanisms remain highly unsure, leading to uncertainties in climate projections. To fill this gap, we used in situ observation coupled with gridded and remote sensing data to analyze N2 O fluxes emissions globally. Here, we investigated the synergistic effects of temperature, hydroclimate on global N2 O fluxes, as the result of SM-atmosphere feedback impact on N fluxes. We found that SM-temperature feedback dominates land N2 O emissions by controlling the balance between nitrifier and denitrifier genes. The mechanism is that atmospheric water demand increases with temperature and thereby reduces SM, which increases the dominant N2 O production nitrifier (containing amoA AOB gene) and decreases the N2 O consumption denitrifier (containing the nosZ gene), consequently will potential increasing N2 O emissions. However, we find that the spatial variations of soil-water availability as a result of the nonlinear response of SM to vapor pressure deficit caused by temperature are some of the greatest challenges in predicting future N2 O emissions. Our data-driven assessment deepens the understanding of the impact of SM-atmosphere interactions on the soil N cycle, which remains uncertain in earth system models. We suggest that the model needs to account for feedback between SM and atmospheric temperature when estimating the response of the N2 O emissions to climatic change globally, as well as when conducting field-scale investigations of the response of the ecosystem to warming.

Functional mechanism and clinical implications of miR-141 in human cancers.

Cancer is caused by the abnormal proliferation of local tissue cells under the control of many oncogenic factors. MicroRNAs (miRNAs) are a class of evolutionarily conserved, approximately 22-nucleotide noncoding small RNAs that influence transcriptional regulationby binding to the 3'-untranslated region of target messenger RNA. As a member of the miRNA family, miR-141 acts as a suppressor or an oncomiR in various cancers and regulates cancer cell proliferation, apoptosis, invasion, and metastasis through a variety of signaling pathways, such as phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT) and constitutive activation of nuclear factor-κB (NF-κB). Target gene validation and pathway analysis have provided mechanistic insight into the role of this miRNA in different tissues. This review also outlines novel findings that suggest miR-141 may be useful as a noninvasive biomarker and as a therapeutic target in several cancers.

Role of pathogen-laden expiratory droplet dispersion and natural ventilation explaining a COVID-19 outbreak in a coach bus.

The influencing mechanism of droplet transmissions inside crowded and poorly ventilated buses on infection risks of respiratory diseases is still unclear. Based on experiments of one-infecting-seven COVID-19 outbreak with an index patient at bus rear, we conducted CFD simulations to investigate integrated effects of initial droplet diameters(tracer gas, 5 µm, 50 µm and 100 µm), natural air change rates per hour(ACH = 0.62, 2.27 and 5.66 h-1 related to bus speeds) and relative humidity(RH = 35% and 95%) on pathogen-laden droplet dispersion and infection risks. Outdoor pressure difference around bus surfaces introduces natural ventilation airflow entering from bus-rear skylight and leaving from the front one. When ACH = 0.62 h-1(idling state), the 30-min-exposure infection risk(TIR) of tracer gas is 15.3%(bus rear) - 11.1%(bus front), and decreases to 3.1%(bus rear)-1.3%(bus front) under ACH = 5.66 h-1(high bus speed).The TIR of large droplets(i.e., 100 µm/50 µm) is almost independent of ACH, with a peak value(∼3.1%) near the index patient, because over 99.5%/97.0% of droplets deposit locally due to gravity. Moreover, 5 µm droplets can disperse further with the increasing ventilation. However, TIR for 5 µm droplets at ACH = 5.66 h-1 stays relatively small for rear passengers(maximum 0.4%), and is even smaller in the bus middle and front(<0.1%). This study verifies that differing from general rooms, most 5 µm droplets deposit on the route through the long-and-narrow bus space with large-area surfaces(L∼11.4 m). Therefore, tracer gas can only simulate fine droplet with little deposition but cannot replace 5-100 µm droplet dispersion in coach buses.

Iron catalyzed C-C dehydrogenative coupling reaction: synthesis of arylquinones from quinones/hydroquinones.

An atom-economical approach for the synthesis of arylquinones was achieved successfully via direct oxidative C-C dehydrogenative coupling reaction of quinones/hydroquinones with electron-rich arenes using an inexpensive Fe-I2-(NH4)2S2O8 system. The efficiency of this catalytic approach was established with a broad scope of substrates involving quinones and hydroquinones to give high yields (60-89%) of several arylated quinones. The present protocol is simple, practical, and shows good functional group tolerance.

Thermally induced isomerization of linoleic acid and α-linolenic acid in Rosa roxburghii Tratt seed oil.

Rosa roxburghii seed oil is obtained from the seeds left following pressing of the juice from R. roxburghii fruit. The total oil content of R. roxburghii seed was around 9.30%. The fatty acid profile of the oil was determined by gas chromatography (GC). Among the 11 fatty acids identified in the oil, seven were unsaturated fatty acids (UFAs) (92.6%); four were saturated fatty acids (SFAs) (7.17%). Then, the kinetics of formation of trans-fatty acids was studied by GC. Heat treatment of R. roxburghii seed oil showed an increase in the relative percentage of linoleic acid and α-linolenic acid isomers with increasing temperature and time. The formation of linoleic acid and α-linolenic acid isomers followed a zero-order reaction. The presence of O2 enhanced the isomerization of these UFAs. In addition, the rate constants and activation energies for the geometrical isomerization of UFAs in R. roxburghii seed oil were presented. Overall, R. roxburghii seed oil contains high UFA contents. Heating temperature and duration and the presence of O2 should be considered to reduce the formation of trans-fatty acids during thermal treatment of R. roxburghii seed oil.

t-BuOK mediated oxidative coupling amination of 1,4-naphthoquinone and related 3-indolylnaphthoquinones with amines.

The transition-metal free amination of 1,4-naphthoquinone and related 3-indolylnaphthoquinones with amines, such as various (hetero)aromatic amine and aliphatic amine via t-BuOK-mediated oxidative coupling at room temperature has been developed. This reaction provides efficient access to the biologically important and synthetically useful 2-amino-1,4-naphthoquinones and 2-amino-3-indolylnaphthoquinones with good yields under mild conditions. The present protocol is simple, practical and shows good functional group tolerance. In addition, the obtained 2-amino-3-indolylnaphthoquinones were further transformed to synthesize polycyclic N-heterocycles.