Indirect Impact of Eutrophication on Occurrence, Air-Water Exchange, and Vertical Sinking Fluxes of Antibiotics in a Subtropical River.

A significant challenge that warrants attention is the influence of eutrophication on the biogeochemical cycle of emerging contaminants (ECs) in aquatic environments. Antibiotics pollution in the eutrophic Pearl River in South China was examined to offer new insights into the effects of eutrophication on the occurrence, air-water exchange fluxes (Fair-water), and vertical sinking fluxes (Fsinking) of antibiotics. Antibiotics transferred to the atmosphere primarily through aerosolization controlled by phytoplankton biomass and significant spatiotemporal variations were observed in the Fair-water of individual antibiotics throughout all sites and seasons. The Fsinking of ∑AB14 (defined as a summary of 14 antibiotics) was 750.46 ± 283.19, 242.71 ± 122.87, and 346.74 ± 249.52 ng of m-2 d-1 in spring, summer, and winter seasons. Eutrophication indirectly led to an elevated pH, which reduced seasonal Fair-water of antibiotics, sediment aromaticity, and phytoplankton hydrophobicity, thereby decreasing antibiotic accumulation in sediments and phytoplankton. Negative correlations were further found between Fsinking and the water column daily loss of antibiotics with phytoplankton biomass. The novelty of this study is to provide new complementary knowledge for the regulation mechanisms of antibiotics by phytoplankton biological pump, offering novel perspectives and approaches to understanding the coupling between eutrophication and migration and fate of antibiotics in a subtropical eutrophic river.

Exploring the diagnostic value of CLR and CPR in differentiating Kawasaki disease from other infectious diseases based on clinical predictive modeling.

Background: Kawasaki disease (KD) is an important cause of acquired heart disease in children and adolescents worldwide. KD and infectious diseases can be easily confused when the clinical presentation is inadequate or atypical, leading to misdiagnosis or underdiagnosis of KD. In turn, misdiagnosis or underdiagnosis of KD can lead to delayed use of intravenous immunoglobulin (IVIG), increasing the risk of drug resistance and coronary artery lesions (CAL). Objectives: The purpose of this study was to develop a predictive model for identifying KD and infectious diseases in children in the hope of helping pediatricians develop timely and accurate treatment plans. Methods: The data Patients diagnosed with KD from January 2018 to July 2022 in Shenzhen Longgang District Maternity & Child Healthcare Hospital, and children diagnosed with infectious diseases in the same period will be included in this study as controls. We collected demographic information, clinical presentation, and laboratory data on KD before receiving IVIG treatment. All statistical analyses were performed using R-4.2.1 (https://www.rproject.org/). Logistic regression and Least Absolute Shrinkage with Selection Operator (LASSO) regression analyses were used to build predictive models. Calibration curves and C-index were used to validate the accuracy of the prediction models. Results: A total of 1,377 children were enrolled in this study, 187 patients with KD were included in the KD group and 1,190 children with infectious diseases were included in the infected group. We identified 15 variables as independent risk factors for KD by LASSO analysis. Then by logistic regression we identified 7 variables for the construction of nomogram including white blood cell (WBC), Monocyte (MO), erythrocyte sedimentation rate (ESR), alanine transaminase (ALT), albumin (ALB), C-reactive protein to procalcitonin ratio (CPR) and C-reactive protein to lymphocyte ratio (CLR). The calibration curve and C-index of 0.969 (95% confidence interval: 0.960-0.978) validated the model accuracy. Conclusion: Our predictive model can be used to discriminate KD from infectious diseases. Using this predictive model, it may be possible to provide an early determination of the use of IVIG and the application of antibiotics as soon as possible.

Distribution and potential health risks of perfluoroalkyl substances (PFASs) in water, sediment, and fish in Dongjiang River Basin, Southern China.

Per- and polyfluoroalkyl substances (PFASs) have attracted worldwide attention due to their high stability, refractory degradation, and bioaccumulation. The Dongjiang River is one of the most important water sources in the Pearl River Delta region. It flows from Jiangxi Province to Guangdong Province and finally into the Pearl River, providing domestic water for cities such as Guangzhou, Shenzhen, and Hong Kong. In this study, 17 PFASs in water, sediment, and fish in the Dongjiang River Basin in southern China were investigated using high-performance liquid chromatography-mass spectrometry. Total PFAS concentrations ranged from 20.83 to 372.8 ng/L in water, from 1.050 to 3.050 ng/g in sediments, and from 12.28 to 117.4 ng/g in fish. Among six species of fish, Oreochromis mossambicus (mean: 68.55 ng/g) had the highest concentration of PFASs, while Tilapia zillii (36.90 ng/g) had the lowest concentration. Perfluorooctanoic acid (PFOA) predominates in water and sediments, while perfluorooctanesulfonic acid (PFOS) predominates in fish. Long-chain perfluorocarboxylates (PFCAs) and perfluorosulfonates (PFSAs) showed higher bioaccumulation, and the field-sourced sediment-water partition coefficients (Kd) and bioaccumulation factors (BAFs) of PFASs increased with the length of perfluorocarbon chains. PFAS concentration in the lower reaches (urban area) of the Dongjiang River is higher than that in the upper and middle reaches (rural area). The calculated hazard ratio (HR) of PFOS and PFOA levels in fish in the Dongjiang River Basin was far less than 1; hence, the potential risk to human health was limited.

Radiotherapy for primary thyroid adenoid cystic carcinoma.

Primary thyroid adenoid cystic carcinoma (PTACC) is an extremely rare type of mucin-secreting adenocarcinoma. Currently, it is difficult to diagnose, and it lacks standard treatment protocols. We report the case of a 53-year-old female patient with PTACC who underwent additional intensity-modulated radiotherapy 1 month after surgical treatment with an uneventful course. No invasion or distant metastasis was detected at the 7-month follow-up after radiotherapy, and the prognosis was favorable. In this case, herein, we have summarized the diagnostic features of the disease and proposed that postoperative adjuvant radiotherapy can significantly improve the patient's prognosis. Finally, we further confirmed the important role of radiotherapy in PTACC by reviewing relevant literature, which may provide clinicians with valuable treatment experience.

Diagnostic accuracy of ultrasonography for the confirmation of endotracheal tube intubation: a systematic review and meta-analysis.

AIM: Despite several studies and reviews reporting data accuracy of ultrasonography for confirmation of endotracheal intubation, there has been limited pooled evidence summarizing the diagnostic accuracy of this imaging modality, especially based on recent evidence. Hence, the current study reviews the recent literature and conducts a meta-analysis to compare the accuracy of ultrasonography for the confirmation of endotracheal tube placement. MATERIAL AND METHODS: We conducted a systematic search for all studies reporting the diagnostic accuracy of ultrasonography in the databases of Medline, EMBASE,PubMed Central, ScienceDirect, Google Scholar & Cochrane library from inception till December 2021. Meta-analysis was performed using STATA software "midas" package. RESULTS: Thirty-eight studies with 3,268 participants were included. Thepooled sensitivity was 98% (95% CI, 97%-99%) and specificity was 95% (95% CI, 90%-98%), respectively. The AUC was 0.98 (95%CI: 0.96-1.00). The pooled DOR was 1090 (95% CI, 408-2910). Pooled LRP was 19 (95% CI, 9-39) and pooled LRN was 0.02 (0.01-0.03). There was significant heterogeneity found in the outcome with significant chi-square tests and I2 statistics > 75%. CONCLUSION: Findings from our review demonstrate promise in the applicability of ultrasonography as a major diagnostic tool for confirming the endotracheal tube intubation.

Investigation of pilots' mental health and analysis of influencing factors in China: based on structural equation model.

BACKGROUND: Pilots' physical and mental health might be significant contributing factors to flight safety. Exploring pilots' health-related quality of life (HRQoL) is crucial for aviation security, health management, and psychological security. This study aimed to explore HRQoL and mental health of pilots and analyze the health characteristics and influencing factors, such as demographic data, personality traits, social support, and resilience. It may provide data for a theoretical basis for aviation security work and health management strategy. METHODS: This is a cross-sectional study using quantitative approaches. Two hundred twenty male pilots with an average age of 33.31 years participated. They answered a social demographic questionnaire, Symptom Checklist-90, Short Form 36 Health Survey Questionnaire, Perceived social support scale, Connor-Davidson resilience scale, and Big Five Personality Inventories, whose data were analyzed using descriptive and inferential statistics. RESULTS: The mediating effect of personality factors between resilience and the HRQoL of pilots was observed. Personality factors also mediated the relationship between social support and the mental health of pilots. CONCLUSION: Pilots' mental health and quality of life need to be taken seriously. Social support, resilience, and personality factors affect pilots' mental health and quality of life.

Small molecule QF84139 ameliorates cardiac hypertrophy via activating the AMPK signaling pathway.

Cardiac hypertrophy is a common adaptive response to a variety of stimuli, but prolonged hypertrophy leads to heart failure. Hence, discovery of agents treating cardiac hypertrophy is urgently needed. In the present study, we investigated the effects of QF84139, a newly synthesized pyrazine derivative, on cardiac hypertrophy and the underlying mechanisms. In neonatal rat cardiomyocytes (NRCMs), pretreatment with QF84139 (1-10 µM) concentration-dependently inhibited phenylephrine-induced hypertrophic responses characterized by fetal genes reactivation, increased ANP protein level and enlarged cardiomyocytes. In adult male mice, administration of QF84139 (5-90 mg·kg-1·d-1, i.p., for 2 weeks) dose-dependently reversed transverse aortic constriction (TAC)-induced cardiac hypertrophy displayed by cardiomyocyte size, left ventricular mass, heart weights, and reactivation of fetal genes. We further revealed that QF84139 selectively activated the AMPK signaling pathway without affecting the phosphorylation of CaMKIIδ, ERK1/2, AKT, PKCε, and P38 kinases in phenylephrine-treated NRCMs and in the hearts of TAC-treated mice. In NRCMs, QF84139 did not show additive effects with metformin on the AMPK activation, whereas the anti-hypertrophic effect of QF84139 was abolished by an AMPK inhibitor Compound C or knockdown of AMPKα2. In AMPKα2-deficient mice, the anti-hypertrophic effect of QF84139 was also vanished. These results demonstrate that QF84139 attenuates the PE- and TAC-induced cardiac hypertrophy via activating the AMPK signaling. This structurally novel compound would be a promising lead compound for developing effective agents for the treatment of cardiac hypertrophy.

Ginsenoside Rg3 treats acute radiation proctitis through the TLR4/MyD88/NF-κB pathway and regulation of intestinal flora.

Objectives: This study aimed to investigate the protective effect of ginsenoside Rg3 (GRg3) against acute radiation proctitis (ARP) in rats. Methods: Wistar rats were randomly divided into control, model, dexamethasone-positive, GRg3 low-dose, GRg3 medium-dose, and GRg3 high-dose groups. The ARP rat model was established by a single 22-Gy irradiation of 6 MV) X-rays. The distribution and function of intestinal flora were detected using 16S rRNA high-throughput sequencing, rectal tissue was observed by hematoxylin and eosin (H&E) staining, the expression of interleukin 1ß (IL-1ß) and IL-10 inflammatory factors was detected by ELISA, and mRNA and protein expression of toll-like receptor 4 (TLR4), myeloid differentiation primary response 88 (MyD88), and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) were detected by RT-qPCR and Western blotting, respectively. Results: GRg3 improved the symptoms of ARP in rats in a dose-dependent manner. The species distribution of intestinal flora in GRg3 rats was significantly different from that in ARP rats. These differences were more significant in the high-dose group, where the numbers of Ruminococcus, Lactobacillus, and other beneficial bacteria were significantly increased, whereas those of Escherichia, Alloprevotella, and other harmful bacteria were decreased. In addition, GRg3 was closely related to amino acid metabolism. After GRg3 treatment, the mRNA and protein expression of TLR4, MyD88, and NF-κB in rectal tissue was significantly down-regulated, and the level of downstream inflammatory factor IL-1ß decreased, whereas that of IL-10 increased. Conclusion: Our study indicated GRg3 as a new compound for the treatment of ARP by inhibiting the TLR4/MyD88/NF-κB pathway, down-regulating the expression of proinflammatory factors, thus effectively regulating intestinal flora and reducing inflammatory reactions.

Downregulation of LAPTM4B Contributes to the Impairment of the Autophagic Flux via Unopposed Activation of mTORC1 Signaling During Myocardial Ischemia/Reperfusion Injury.

RATIONALE: Impaired autophagic flux contributes to ischemia/reperfusion (I/R)-induced cardiomyocyte death, but the underlying molecular mechanisms remain largely unexplored. OBJECTIVE: To determine the role of LAPTM4B (lysosomal-associated transmembrane protein 4B) in the regulation of autophagic flux and myocardial I/R injury. METHODS AND RESULTS: LAPTM4B was expressed in murine hearts but downregulated in hearts with I/R (30 minutes/2 hours) injury and neonatal rat cardiomyocytes with hypoxia/reoxygenation (6 hours/2 hours) injury. During myocardial reperfusion, LAPTM4B-knockout (LAPTM4B-/-) mice had a significantly increased infarct size and lactate dehydrogenase release, whereas adenovirus-mediated LAPTM4B-overexpression was cardioprotective. Concomitantly, LAPTM4B-/- mice showed higher accumulation of the autophagy markers LC3-II (microtubule-associated protein 1A/1B-light chain 3), but not P62, in the I/R heart, whereas they did not alter chloroquine-induced further increases of LC3-II and P62 in both sham and I/R hearts. Conversely, LAPTM4B-overexpression had opposite effects. The hypoxia/reoxygenation-reduced viability of neonatal rat cardiomyocytes, ratio of autolysosomes/autophagosomes, and function of lysosomes were further decreased by LAPTM4B-knockdown but reversed by LAPTM4B-overexpression. Moreover, the LAPTM4B-overexpression-mediated benefits were abolished by knockdown of lysosome-associated membrane protein-2 (an autophagosome-lysosome fusion protein) in vivo and by the autophagy inhibitor bafilomycin A1 in vivo. In contrast, rapamycin (Rapa) successfully restored the impaired autophagic flux in LAPTM4B-/- mice and the subsequent myocardial I/R injury. Mechanistically, LAPTM4B regulated the activity of mTORC1 (mammalian target of rapamycin complex 1) via interacting with mTOR through its EC3 (extracelluar) domain. Thus, mTORC1 was overactivated in LAPTM4B-/- mice, leading to the repression of TFEB (transcription factor EB), a master regulator of lysosomal and autophagic genes, during myocardial I/R. The mTORC1 inhibition or TFEB-overexpression rescued the LAPTM4B-/--induced impairment in autophagic flux and I/R injury, whereas TFEB-knockdown abolished the LAPTM4B-overexpression-mediated recovery of autophagic flux and cardioprotection. CONCLUSIONS: The downregulation of LAPTM4B contributes to myocardial I/R-induced impairment of autophagic flux via modulation of the mTORC1/TFEB pathway. Graphic Abstract: A graphic abstract is available for this article.

Impact of environmental tax on green development: A nonlinear dynamical system analysis.

With green development becoming a global movement, environmental tax has been adopted by many governments to promote green development. This study analyzes the impact of environmental tax on green development by using a four-dimension dynamical system. The establishment of the system is based on the complex and dynamic interactions among economic development, pollution emissions, resources consumption, and environmental tax, where roles of environmental tax are reflected by the linear parameters. A theoretic analysis shows the complexity of the behavior of the system. Mainly, the existence of chaos is inferred by Lyapunov exponent spectrum and bifurcation diagram, then verified by the presence of a chaotic attractor. An empirical study of the green development dynamical system in China demonstrates the particular evolution paths of economic growth, pollution intensity, and resource intensity under different environmental tax parameters. Results indicate a robust beneficial role of environmental tax on green development. Furthermore, when an environmental tax is imposed, a firm government control, an active consumer awareness, an advanced technology level can stimulate economic growth, decrease pollution intensity, and control the resource intensity. But the government control has a stronger effect. This study provides a viable and promising approach to analyze the role of imposing an environmental tax on green development and may have potential application in other areas and countries.

Berbamine postconditioning protects the heart from ischemia/reperfusion injury through modulation of autophagy.

Pretreatment of berbamine protects the heart from ischemia/reperfusion (I/R) injury. However it is unknown whether it has cardioprotection when given at the onset of reperfusion (postconditioning (PoC)), a protocol with more clinical impact. Autophagy is upregulated in I/R myocardium and exacerbates cardiomyocyte death during reperfusion. However, it is unknown whether the autophagy during reperfusion is regulated by berbamine. Here we investigated whether berbamine PoC (BMPoC) protects the heart through regulation of autophagy by analyzing the effects of BMPoC on infarct size and/or cell death, functional recovery and autophagy in perfused rat hearts and isolated cardiomyocytes subjected to I/R. Berbamine from 10 to 100 nM given during the first 5 min of reperfusion concentration-dependently improved post-ischemic myocardial function and attenuated cell death. Similar protections were observed in cardiomyocytes subjected to simulated I/R. Meanwhile, BMPoC prevented I/R-induced impairment of autophagosome processing in cardiomyocytes, characterized by increased LC3-II level and GFP-LC3 puncta, and decreased p62 degradation. Besides, lysosomal inhibitor chloroquine did not induce additional increase of LC3-II and P62 abundance after I/R but it reversed the effects of BMPoC in those parameters in cardiomyocytes, suggesting that I/R-impaired autophagic flux is restored by BMPoC. Moreover, I/R injury was accompanied by enhanced expression of Beclin 1, which was significantly inhibited by BMPoC. In vitro and in vivo adenovirus-mediated knockdown of Beclin 1 in myocardium and cardiomyocytes restored I/R-impaired autophagosome processing, associated with an improvement of post-ischemic recovery of myocardial contractile function and a reduction of cell death, but it did not have additive effects to BMPoC. Conversely, overexpression of Beclin 1 abolished the cardioprotection of BMPoC as did by overexpression of an essential autophagy gene Atg5. Furthermore, BMPoC-mediated cardioprotection was abolished by a specific Akt1/2 inhibitor A6730. Our results demonstrate that BMPoC confers cardioprotection by modulating autophagy during reperfusion through the activation of PI3K/Akt signaling pathway.