KIAA1429 Promotes Nasopharyngeal Carcinoma Progression by Mediating m6A Modification of PTGS2.

Emerging evidence suggests that dysregulation of a N6-methyladenosine (m6A) methyltransferase KIAA1429 participates in the pathogenesis of multiple cancers except for nasopharyngeal carcinoma (NPC). This study is aimed to explore the function of KIAA1429 in NPC progression. The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) datasets were used to confirm the mRNA expression in NPC by bioinformatic analysis. The levels of KIAA1429 and PTGS2 was detected by quantitative reverse transcription polymerase chain reaction and Western blotting. To investigate the effects of KIAA1429/PTGS2 knockdown or overexpression vectors on NPC cell malignancy, cell and animal experiments were performed. Finally, MeRIP and mRNA stability assays were used to verify the m6A modification and mRNA stability, respectively. KIAA1429 was upregulated in NPC tissues and cells. After transfecting KIAA1429 knockdown or overexpression vectors in NPC cells, we proved that KIAA1429 overexpression promoted proliferation, migration, invasion, and tumor growth, whereas KIAA1429 knockdown showed the opposite effect. Our results also indicated that KIAA1429 mediated m6A modification of PTGS2, enhancing PTGS2 mRNA stability in NPC cells. In addition, PTGS2 could also regulate the effects of KIAA1429 on NPC cell malignancy. This study confirmed the oncogenic function of KIAA1429 in NPC through m6A-modification of PTGS2, suggesting that targeting KIAA1429-mediated m6A modification of PTGS2 might provide a new therapeutic strategy for NPC.

Methyltransferase-like 3-mediated m6A modification of miR-1908-5p contributes to nasopharyngeal carcinoma progression by targeting homeodomain-only protein homeobox.

BACKGROUND: N6-methyladenosine (m6A) modification interacting microRNAs (miRNAs) have been confirmed to participate in nasopharyngeal carcinoma (NPC) progression. This research investigated miR-1908-5p's function and regulatory mechanism in the tumorigenesis of NPC via m6A modification and targeting a key gene. METHODS: The levels of miR-1908-5p, homeodomain-only protein homeobox (HOPX), and methyltransferase-like 3 (METTL3) expressions were detected via RT-qPCR. The correlation between miR-1908-5p and the HOPX/METTL3 axis, as well as their regulatory mechanism, was investigated by dual luciferase reporter, western blotting, and MeRIP assays. Moreover, the bio-functions of miR-1908-5p, HOPX, and METTL3 in NPC were explored through CCK8, transwell, caspase-3 activity, and xenograft tumor assays. RESULTS: RT-qPCR results indicated a miR-1908-5p upregulation in NPC. Knocking down miR-1908-5p diminished the NPC cell viability and migration in vitro. In vivo, downregulating miR-1908-5p repressed NPC cell tumor growth. Moreover, HOPX was specifically targeted by miR-1908-5p, and HOPX downregulation led to reversal of the anti-tumor impact of the miR-1908-5p inhibitor against NPC cell malignancy. Also, METTL3 could mediate the m6A modification of miR-1908-5p to regulate its influence on NPC cells. CONCLUSION: This study demonstrated that the METTL3-mediated m6A modification of miR-1908-5p enhanced the tumorigenesis of NPC by targeting HOPX. These findings propose new insights for NPC diagnosis and therapy.

Effect of laparoscopic-assisted transvaginal hysterectomy on wound complications in patients with early stage cervical cancer: A meta-analysis.

Laparoscopic-assisted vaginal radical hysterectomy (LARVH) and abdominal radical hysterectomy (ARH) have been widely applied to treat cervical carcinoma. But LARVH and ARH have not been fully investigated in treating cervical carcinoma after injury associated with injury. This research is intended to provide an up-to-date basis for comparing LARVH with ARH in early stage cervical carcinoma. Comparison between LARVH and ARH in cervical carcinoma was carried out through a combination of related research. Eligible articles from databases such as PubMed and Embase were screened using an established search strategy. This report covered the results of LARVH versus ARH in cervical carcinoma. The average difference and the 95% confidence interval (CI) were used for the combination of consecutive variables. The combination of categorical variables was performed with the odds ratio (OR) 95% confidence interval. Through the identification of 1137 publications, eight of them were chosen to be analysed. Among them, 363 were treated with LARVH and 326 were treated with ARH. Eight trials showed that LARVH was associated with a reduced risk of postoperative wound infection than ARH (OR, 0.23; 95% CI, 0.1-0.55, p = 0.0009). Five trials showed that there was no difference in the risk of postoperative bleeding after surgery (OR, 1.17; 95% CI, 0.42-3.29, p = 0.76). We also did not differ significantly in the duration of the surgery (OR, 1.79; 95% CI, -6.58 to 10.15, p = 0.68). So, the two surgical methods differ significantly only in the risk of postoperative wound infection.

Mfn2 inhibits proliferation and cell-cycle in Hela cells via Ras-NF-κB signal pathway.

BACKGROUND: Mitofusin 2 (Mfn2) is outer membrane protein, as the inhibitor of Ras protein. This study aimed to investigate the effect of Mfn2 on cell proliferation, and cell-cycle in Hela cervical carcinoma cell lines. METHODS: After treated with Adv-mfn2 or Adv-control for 48 h and 60 h, the RNA and protein of Mfn2 in Hela cells were detected by qRT-PCR and western blot. The immunofluorescence assay was performed to observe the expression and sub-location of Mfn2 in Hela cells. The flow cytometry was performed to detect the cell cycle of Hela cells, while western blots were performed to observe the Ras-NF-κB signal pathway. Then, the xenografted cervix carcinoma mouse model was used to confirm the effect of Mfn2 in Hela cells in vivo and the expression of Ras-NF-κB signaling pathway in vivo. RESULTS: In immunofluorescence detection, Mfn2 was located in cytoplasmic, not in the nucleus. In addition, Mfn2 inhibited cell proliferation of Hela cells through reducing PCNA protein expression. Mfn2 induced arrest in G0/G1 phase of the cell cycle in Hela cells. Meanwhile, Mfn2 reduced Cyclin D1 protein expression. Moreover, Mfn2 decreased the Ras signal pathway proteins such as Myc, NF-κB p65, STAT3 in a dose-dependent manner. Then, the in vivo experiment also confirmed that Mfn2 could inhibit the tumor growth, and depress the Cyclin D1, Ras, Myc, NF-κB p65, Erk1/2 and mTOR protein expression. CONCLUSIONS: Mfn2 could significantly inhibit cell proliferation in Hela cells. It might be acted as an potential anti-cancer target through inducing cell cycle arrest in human cervical carcinoma cells.

Antivirals for Respiratory Viral Infections: Problems and Prospects.

In the past two decades, several newly emerging and reemerging viral respiratory pathogens including several influenza viruses (avian influenza and pandemic influenza), severe acute respiratory syndrome coronavirus (SARS-CoV), and Middle East respiratory syndrome coronavirus (MERS-CoV), have continued to challenge medical and public health systems. Thereafter, the development of cost-effective, broad-spectrum antiviral agents is the urgent mission of both virologists and pharmacologists. Current antiviral developments have focused targets on viral entry, replication, release, and intercellular pathways essential for viral life cycle. Here, we review the current literature on challenges and prospects in the development of these antivirals.

IL-6 cooperates with G-CSF to induce protumor function of neutrophils in bone marrow by enhancing STAT3 activation.

Neutrophils are known to have antitumor potential. However, in recent years the tumor-promoting effect of neutrophils has been well demonstrated. So far, it remains unclear what causes the conversion of neutrophil function from tumor suppressive to tumor promoting. In this article, we report that the conversion of murine neutrophil function occurs in bone marrow, and that IL-6 cooperation with G-CSF is required for this conversion. IL-6 cooperated with G-CSF to modulate neutrophils in bone marrow, altering the activation potential of signaling pathways in neutrophils, especially that of STAT3. Costimulation with G-CSF and IL-6 induced a higher level of phospho-STAT3 in neutrophils, which was further increased by upregulation of STAT3 expression in neutrophils owing to downregulation of IFN-ß expression in bone marrow macrophages by IL-6. Augmented STAT3 activation was crucial for upregulating the expression of Mmp9 and Bv8 genes and downregulating the expression of Trail and Rab27a genes in neutrophils. Moreover, G-CSF/IL-6-modulated neutrophils could not efficiently release azurophilic granules because of downregulation of Rab27a and inefficient activation of PI3K and p38 MAPK pathways. Because of premodulation by G-CSF and IL-6, neutrophils in response to complex stimuli in tumor released much less myeloperoxidase, neutrophil elastase, and TRAIL, but showed much higher expression of Mmp9 and Bv8 genes. Taken together, these results demonstrate that G-CSF and IL-6, despite their well-known physiological functions, could modulate the activation potential of signaling pathways in neutrophils, resulting in the production or release of the above-mentioned factors in a way that favors tumor angiogenesis and tumor growth.

SNAI2 enhances HPV­negative cervical cancer cell dormancy by modulating u­PAR expression and the activity of the ERK/p38 signaling pathway in vitro.

The prognosis of patients with human papillomavirus (HPV)­negative cervical cancer is significantly worse than that of patients with HPV­positive cervical cancer. Understanding the mechanisms of this is crucial for preventing disease evolution. In the present study, the GV367­snail family transcriptional repressor 2 (SNAI2) lentiviral vector was constructed and transduced into C­33A cells. Subsequently, the proliferation of tumor cells was detected using the Cell Counting Kit (CCK)­8 method. Flow cytometry was used to analyze the cell cycle progression of tumor cells. The glucose consumption of tumor cells was detected using an oxidase assay, and the senescence of tumor cells was detected using beta­galactosidase staining. The gene expression and the activity of p38 and ERK1/2 were detected using reverse transcription­quantitative PCR and western blotting, respectively. The C­33A­SNAI2 cell line was successfully established. Compared with HeLa and C­33A­Wild cells, the proliferation and percentage of G0/G1­phase cells in the C­33A­SNAI2 group were decreased, as detected by the CCK­8 assay (100±0 vs. 239.1±58.3 vs. 39.7±20.1, P<0.01) and flow cytometry (34.0±7.1% vs. 46.2±10.6% vs. 61.3±5.3%, P<0.05). Compared with the HeLa group, the glucose consumption of the C­33A­Wild and C­33A­SNAI2 groups was significantly decreased (P<0.01). The results of beta­galactosidase staining showed that the proportion of beta­galactosidase­positive cells in the C­33A­SNAI2 group was significantly decreased compared with the C­33A­Wild group (P<0.01). Upregulation of SNAI2 enhanced the increase in p21 expression, and the decrease in CDK1, urokinase plasminogen activator receptor (u­PAR) and cyclin D1 expression in C­33A cells compared with C­33A­Wild cells (P<0.05). In addition, the activities of p38, ERK1/2 and the phosphorylated (p)­ERK1/2/p­p38 ratio were decreased in the C­33A­SNAI2 group compared with the C­33A­Wild and HeLa groups (P<0.05). In conclusion, SNAI2 enhanced HPV­negative cervical cancer C­33A cell dormancy, which was characterized by G0/G1 arrest, by the downregulation of u­PAR expression, and a decrease in the activity of the p­ERK1/2 and p­p38MAPK signaling pathways in vitro. Cancer recurrence and metastases are responsible for most cancer­related deaths. Given that SNAI2 is required for enhancing HPV­negative cervical cancer cell dormancy, regulating this process may promote cervical tumor cells to enter a continuous dormant state, which could be a potential approach for tumor therapy.

Astragaloside IV inhibits inflammation caused by influenza virus via reactive oxygen species/NOD-like receptor thermal protein domain associated protein 3/Caspase-1 signaling pathway.

BACKGROUND: Astragaloside IV (AS-IV) is the most active monomer in the traditional Chinese herbal medicine Radix Astragali, which has a wide range of antiviral, anti-inflammatory, and antifibrosis pharmacological effects, and shows protective effects in acute lung injury. METHODS: This study utilized the immunofluorescence, flow cytometry, enzyme-linked immunosorbent assay, quantitative reverse transcription-polymerase chain reaction, western blot, and hematoxylin and eosin staining methods to investigate the mechanism of AS-IV in reducing viral pneumonia caused by influenza A virus in A549 cells and BALB/c mice. RESULTS: The results showed that AS-IV suppressed reactive oxygen species production in influenza virus-infected A549 cells in a dose-dependent manner, and subsequently inhibited the activation of nucleotide-binding oligomerization domain-like receptor thermal protein domain associated protein 3 inflammasome and Caspase-1, decreased interleukin (IL) -1ß and IL-18 secretion. In BALB/c mice infected with Poly (I:C), oral administration of AS-IV can significantly reduce Poly (I:C)-induced acute pneumonia and lung pathological injury. CONCLUSIONS: AS-IV alleviates the inflammatory response induced by influenza virus in vitro and lung flammation and structural damage caused by poly (I:C) in vivo.

Isocitrate dehydrogenase 2 regulates the proliferation of triple-negative breast cancer through the ferroptosis pathway.

Triple-negative breast cancer (TNBC) is currently the type of breast cancer with the worst prognosis; it lacks specific treatments, such as ER/PR antagonistic endocrine and anti-HER2 targeted therapies. Although immunotherapy with immune checkpoints has shown some efficacy in many solid tumors, clinical data in TNBC suggest significant limitations. The essence of ferroptosis is the impaired metabolism of intracellular lipid oxides, which in turn causes the activation and abnormalities of the immune system, including ROS, and not only plays an important role in liver injury and organ aging but also a large amount of data points to the close correlation between the ferroptosis process and tumor development. In this study, through the analysis of large-throughput biological data of breast tumors, combined with the characteristics of the biological process of ferroptosis, the specific gene IDH2 was found to be significantly highly expressed in TNBC and functionally correlated with ferroptosis. Through clinical specimens validated at the gene and protein levels, in vitro tumor cell line validation, and in vivo mouse models, we found that the high expression of IDH2 in TNBC has a role in inhibiting the ferroptosis process in TNBC, thus promoting the proliferation of TNBC cells and other malignant features.

Machine learning based peri-surgical risk calculator for abdominal related emergency general surgery: a multicenter retrospective study.

BACKGROUND: Currently, there is a lack of ideal risk prediction tools in the field of emergency general surgery (EGS). The American Association for the Surgery of Trauma recommends developing risk assessment tools specifically for EGS-related diseases. In this study, we sought to utilize machine learning (ML) algorithms to explore and develop a web-based calculator for predicting five perioperative risk events of eight common operations in EGS. METHOD: This study focused on patients with EGS and utilized electronic medical record systems to obtain data retrospectively from five centers in China. Five ML algorithms, including Random Forest (RF), Support Vector Machine, Naive Bayes, XGBoost, and Logistic Regression, were employed to construct predictive models for postoperative mortality, pneumonia, surgical site infection, thrombosis, and mechanical ventilation >48 h. The optimal models for each outcome event were determined based on metrics, including the value of the Area Under the Curve, F1 score, and sensitivity. A comparative analysis was conducted between the optimal models and Emergency Surgery Score (ESS), Acute Physiology and Chronic Health Evaluation II (APACHE II) score, and American Society of Anesthesiologists (ASA) classification. A web-based calculator was developed to determine corresponding risk probabilities. RESULT: Based on 10 993 patients with EGS, we determined the optimal RF model. The RF model also exhibited strong predictive performance compared with the ESS, APACHE II score, and ASA classification. Using this optimal model, the authors developed an online calculator with a questionnaire-guided interactive interface, catering to both the preoperative and postoperative application scenarios. CONCLUSIONS: The authors successfully developed an ML-based calculator for predicting the risk of postoperative adverse events in patients with EGS. This calculator accurately predicted the occurrence risk of five outcome events, providing quantified risk probabilities for clinical diagnosis and treatment.

LncRNA BBOX1-AS1 Contributes to the Development of Nasopharyngeal Carcinoma via miR-204-5p/MUC4 Axis.

OBJECTIVE: Dysregulation of long non-coding RNAs (lncRNAs) is common in nasopharyngeal carcinoma (NPC) progression, and it is important to have an in-depth understanding of their functions in NPC. This study is the first to explore the role of the lncRNA BBOX1-AS1 in NPC development. METHODS: The expression of lncRNA BBOX1-AS1, MUC4, or miR-204-5p was measured in NPC cell lines or tissues via RT-qPCR and western blotting. Wound healing assays and CCK-8 were used to identify cell migration and cell viability, respectively. The protein expression of Bax and Bcl-2 was measured by western blotting. The tumorigenic effect of NPC cells in vivo was verified using xenograft tumors in nude mice. Luciferase reporter and RIP assays were conducted to clarify the association between miR-204-5p and lncRNA BBOX1-AS1 or MUC4. RESULTS: lncRNA BBOX1-AS1 upregulation was observed in NPC cells and tissues. Silencing lncRNA BBOX1-AS1 suppressed the migration and viability of C666-1 and TW03 cells while promoting cell apoptosis. Knockdown of the lncRNA BBOX1-AS1 repressed tumor growth in vivo. Moreover, the tumor suppression effect of silenced lncRNA BBOX1-AS1 might be reversed with the help of the miR-204-5p inhibitor. lncRNA BBOX1-AS1 targets miR-204-5p and regulates MUC4 expression in NPC. MUC4 is a miR-204-5p target and exerts a function similar to that of lncRNA BBOX1-AS1. CONCLUSION: These observations highlight that lncRNA BBOX1-AS1 is an essential NPC progression promoter and suggest that the lncRNA BBOX1-AS1/miR-204-5p/MUC4 axis is a potential therapeutic target in NPC.

Influence of exposure history on the particle retention capacity and physiological responses of Euonymus japonicus Thunb. var. aurea-marginatus Hort.

Green plants in urban environments experience cyclical particulate matter stress. And this history of exhaust exposure may generate stress memory in plants, which may alter their subsequent response. Studies combining urban pollution characteristics and stress memory are limited. Therefore, we selected E. japonicus var. aurea-marginatus, a common urban greening tree species in the Yangtze River Delta, and conducted an experiment in three periods: the initial pollution period (S1: 28 days), the recovery period (R: 14 days) and the secondary pollution period (S2: 28 days). The experimental design consisted of an elevated pollution treatment (173 µg•cm-3) and an ambient control (34 µg•cm-3) with three replicates. In S2, the net total particle retention and saturated particle retention decreased by 11.5% and 19.3%, respectively, while PM10 and PM2.5 did not change significantly. E. japonicus var. aurea-marginatus exhibited recovery of chlorophyll levels, slower degradation of carotenoid, faster accumulation of ASA, lower accumulation of MDA, reduced activity of SOD under the second pollution period, and the period had a significant effect on the physiological indicators. Collectively, the effect of autoexhaust exposure history on the particle retention capacity of selected plant varied across particle sizes, and stress memory may confer plant resistance to recurrent exhaust pollution via combined regulations of physiological responses. Fine particles which pose a great risk to human health arise predominantly from vehicular traffic and energy production. So, E. japonicus tends to play a stabilising role in particle retention in industrial, traffic and residential areas.

Ru(II) Complex Grafted Ti3C2Tx MXene Nano Sheet with Photothermal/Photodynamic Synergistic Antibacterial Activity.

For a long time, the emergence of microbial drug resistance due to the abuse of antibiotics has greatly reduced the therapeutic effect of many existing antibiotics. This makes the development of new antimicrobial materials urgent. Light-assisted antimicrobial therapy is an alternative to antibiotic therapy due to its high antimicrobial efficiency and non-resistance. Here, we develop a nanocomposite material (Ru@MXene) which is based on Ru(bpy)(dcb)2+ connected to MXene nanosheets by ester bonding as a photothermal/photodynamic synergistic antibacterial material. The obtained Ru@MXene nanocomposites exhibit a strengthened antimicrobial capacity compared to Ru or MXene alone, which can be attributed to the higher reactive oxygen species (ROS) yield and the thermal effect. Once exposed to a xenon lamp, Ru@MXene promptly achieved almost 100% bactericidal activity against Escherichia coli (200 µg/mL) and Staphylococcus aureus (100 µg/mL). This is ascribed to its synergistic photothermal therapy (PTT) and photodynamic therapy (PDT) capabilities. Consequently, the innovative Ru@MXene can be a prospective non-drug antimicrobial therapy that avoids antibiotic resistance in practice. Notably, this high-efficiency PTT/PDT synergistic antimicrobial material by bonding Ru complexes to MXene is the first such reported model. However, the toxic effects of Ru@MXene materials need to be studied to evaluate them for further medical applications.

Targeting nuclear factor-κB suppresses the negative effect of toll-like receptor 4 signaling on antimetastasis therapy based on targeting αvß3.

The targeting of αvß3 is a promising therapeutic strategy for suppressing tumor metastasis. However, it is unclear whether the therapeutic efficacy could be influenced by metastasis-promoting factor(s) in vivo. Here we report that Toll-like receptor 4 (TLR4) ligand released from damaged tumor cells or bacteria had a negative effect on the therapeutic effect of a recombinant CBD-HepII polypeptide of fibronectin (CH50) that suppresses tumor metastasis by targeting αvß3. The TLR4 ligand could antagonize the inhibitory effect of CH50 on tumor cell adhesion and invasion by promoting the expression and activity of αvß3 in tumor cells. The TLR4 ligand also reduced the antimetastasis effect of CH50 by promoting tumor cell survival in circulation. Moreover, TLR4 ligands released by tumor cells in circulation could increase the survival and proliferation capacity of tumor cells after extravasation, resulting in the formation of more metastatic nodules. The effect of TLR4 signaling was mainly mediated by nuclear factor-κB (NF-κB). Inhibiting NF-κB could abrogate the negative effect of TLR4 ligand, and augment the inhibitory effect of CH50 on tumor metastasis. Consistently, the combination of NF-κB inhibitor and CH50 significantly inhibited metastasis of tumor cells in vivo and prolonged the survival of mice. The findings in this study suggest that the combination of NF-κB inhibitor and αvß3 antagonist would be a novel therapeutic option for the prevention of tumor metastasis.

Triggering of Toll-like receptor 4 on metastatic breast cancer cells promotes αvß3-mediated adhesion and invasive migration.

Triggering of Toll-like receptor 4 (TLR4) on tumor cells has been found to promote tumor progression by promoting tumor cell proliferation and survival. So far, however, the effect of TLR4 signaling on tumor metastasis has not been well elucidated. Here, we report that triggering of TLR4 on metastatic breast cancer cells could reciprocally regulate the expression of αvß3 and the expressions of TPM1 and maspin, and promote αvß3-mediated adhesion and invasive migration of the cells. In metastatic breast cancer cells, TLR4 signaling increased the expression of integrin αvß3 by activating NF-κB, resulting in the increased adhesion capacity of tumor cells to the ligand for αvß3, and the increased polymerization of actin and production of MMP-9 in tumor cells in response to ECM. HoxD3 was required for the up-regulation of αv and ß3 expressions by NF-κB. Moreover, TLR4 signaling increased the expression of miR-21 in breast cancer cells by activating NF-κB. Accordingly, the expressions of TPM1 and maspin were decreased at protein level, whereas the transcription activity of these genes was not influenced. Consistent with the promoting effect on αvß3-mediated adhesion and invasive migration, TLR4 signaling promoted the arrest of metastatic breast cancer cells in circulation and following invasion. The effect of TLR4 signaling could be abrogated by inhibiting NF-κB. These findings suggest that metastatic breast cancer cells could acquire higher metastatic potential due to triggering of TLR4 and activation of NF-κB in the cells, and that both TLR4 and NF-κB could be therapeutic targets for preventing metastasis of breast cancer cells.

Season impacts on estimating plant's particulate retention: Field experiments and meta-analysis.

Plants can effectively remove atmospheric particles, which contribute to air pollution. However, few studies have focused on seasonal variability of plant dust retention, an essential factor to estimate annual dust removal from the atmosphere. This study conducted a field experiment to explore the seasonal variability of particulate retention on evergreen leaved urban greening shrub plants. We performed a meta-analysis to synthesize the available literature on the subject to discuss our findings further. Results showed that particulate matter deposited on leaf surfaces (sPM) in autumn and winter was significantly higher than in spring and summer. In comparison, the particulate matter trapped in epicuticular waxes (wPM) in summer was significantly higher than in the other three seasons. The seasonal differences also existed in both sPM and wPM among particle sizes. The total dust retention of Rhododendron × pulchrum Sweet, Osmanthus fragrans Lour, and Photinia × fraseri Dress were estimated as 360.89 t, 586.66 t, and 448.84 t per year, respectively. They were significantly different from model estimates if only one season was chosen as an estimator. Furthermore, the meta-analysis revealed significant differences among seasons, particle sizes, and different leaf habits (evergreen or deciduous). In contrast, no significant differences were observed between life forms or between growth forms. Our findings both from field experiment and met-analysis highlights that seasonal variation can significantly affect the dust retention capacity of plants, which should be taken into account into particle matter retention capacity evaluations.

The legacy effects of PM2.5 depositon on Nerium Oleander L.

Green plants have the capability to retain atmospheric particulate matter (PM) on their leaves, which can effectively reduce PM pollution, especially in the urban settings. Some studies reported that the periodic PM pollution could change plant retaining PM capacity, which, indeed, was the reason of physiological responses. In advancing the previous studies, we selected Nerium oleander L. to measure PM retention on leaf surface in a controlled environment by the following periods: initial pollution period (S1), recovery period (R), and secondary pollution period (S2) for a total of 12 weeks. The experimental design was one elevated pollution treatment (166 µg m-3) and one ambient control (28 µg m-3) with three replications. Results showed that during S2, the total retention decreased by 8.87 µg cm-2, which was about 10.4% significant lower than in S1. During the third week, the ascorbic acid content (ASA) in S1 was 6.71 mg g-1 significantly lower than that in S2 in the treatment. The total chlorophyll (Chl T) of the treatment decreased continuously and significantly by 33.8% in S1, but showed no similar trend in S2. The net photosynthetic rate of the treatment was significantly lower than that of the control, and the plants in the treatment showed a consistently high dark respiration rate than that in the control. The correlations between PM retention and ASA, Chl T and RWC were weaker in S1 than that in S2. In addition, air pollution tolerance index (APTI) showed a significant decline in plant pollution tolerance in the treatment during the third week.

Dynamics of particle retention and physiology in Euonymus japonicus Thunb. var. aurea-marginatus Hort. with severe exhaust exposure under continuous drought.

Frequent drought events and particulate matter pollution from vehicular exhaust seriously affect urban plant growth and provisioning of ecological services. Yet, how plants respond physiologically and morphologically to these two combined stressors remains unknown. Here, we assessed particle retention dynamics and plant morphology and physiology of Euonymus japonicus Thunb. var. aurea-marginatus Hort. under continuous drought with severe exhaust exposure. Our results showed that continuous drought insignificantly lowered particle retention in each of three size fractions by 1.02 µg·cm-2 on average in the first 28 days, but significantly lowered total particle retention by 35.75 µg·cm-2 on the 35th day. We observed evident changes in morphology, leaf mass per area (LMA), pigments, gas exchange in all stressed plants. Compared with single stress, combined drought and pollution caused earlier yellowing and shedding of old leaves, significantly lowered LMA by 1.21 mg·cm-2, caused a greater decline in pigments and net photosynthetic rate (Pn). Large particles may mainly explain pigment reduction, lower weekly LMA increases, and stomatal restriction, while coarse particles may be the main drivers of the decline in Pn. Continuous drought mediated the influence of all three particle sizes on some parameters, such as weakening the impact of total particles on LMA, strengthening the impact of fine particles on photosynthesis. Our findings suggest that drought accelerates the physiological responses of plants to exhaust pollution. Under controlled severe exhaust pollution conditions, the optimal time to maintain high particle retention during continuous drought without decline in physiological conditions for E. japonicus var. aurea-marginatus was 14 days. Some additional interventions after 14 days (it could be postponed appropriately under field conditions) may help ensure healthy growth of plants and retention of particulate matter.

Effect of low-dose aspirin on mortality and viral duration of the hospitalized adults with COVID-19.

ABSTRACT: To clarify the effect of aspirin on mortality and viral duration in adults infected with respiratory syndrome coronavirus 2 (SARS-Cov-2).After propensity score-matched (PSM) case-control analyses 24 pairs of patients were enrolled and followed up for 2 months. Both 30-day and 60-day mortality in the aspirin group were significantly lower than that in the non-aspirin group (P = .021 and P = .030, respectively). The viral duration time between the 2 groups was not significantly different (P = .942).Among adults (with hypertension, cardiovascular diseases) infected with SARS-Cov-2, low-dose aspirin medication (100 mg/day) was associated with lower risk of mortality compared with non-aspirin users.

COVID-19 in two infants in China.

INTRODUCTION: Since December 2019, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has spread rapidly around the world and caused more than 487 000 infections and 22 000 deaths worldwide. METHODS: We report two infant cases with coronavirus disease 2019 (COVID-19) in Yichang, Hubei, China. The younger of the two is only 5-months old. We recorded their clinical manifestations, epidemiological history, laboratory examination, and treatment in detail. In addition, we provide computed tomographic images of their chest, which are the most serious imaging manifestation among the infants recorded so far. RESULTS: Although both of them eventually recovered and were discharged from the hospital, they were complicated with varying degrees of liver and myocardial injury. In addition, one of them was complicated with mycoplasma pneumoniae infection. CONCLUSIONS: Pediatricians should consider the potential risks of developing severe illness of infants infected by SARS-CoV-2 and take them seriously.