How much organic carbon could the soil store? The carbon sequestration potential of Australian soil.

Soil is a huge carbon (C) reservoir, but where and how much extra C can be stored is unknown. Current methods to estimate the maximum amount of mineral-associated organic carbon (MAOC) stabilized in the fine fraction (clay + silt, < 20 µm $$ <20\;\upmu \mathrm{m} $$ ) fit through the MAOC versus clay + silt relationship, not their maxima, making their estimates more uncertain and unreliable. We need a function that 'envelopes' that relationship. Here, using 5089 observations, we estimated that the uppermost 30 cm of Australian soil holds 13 Gt (10-18 Gt) of MAOC. We then fitted frontier lines, by soil type, to the relationship between MAOC and the percentage of clay + silt to estimate the maximum amounts of MAOC that Australian soils could store in their current environments, and calculated the MAOC deficit, or C sequestration potential. We propagated the uncertainties from the frontier line fitting and mapped the estimates of these values over Australia using machine learning and kriging with external drift. The maps show regions where the soil is more in MAOC deficit and has greater sequestration potential. The modelling shows that the variation over the whole continent is determined mainly by climate, linked to vegetation and soil mineralogy. We find that the MAOC deficit in Australian soil is 40 Gt (25-60 Gt). The deficit in the vast rangelands is 20.84 Gt (13.97-29.70 Gt) and the deficit in cropping soil is 1.63 Gt (1.12-2.32 Gt). Management could increase C sequestration in these regions if the climate allowed it. Our findings provide new information on the C sequestration potential of Australian soils and highlight priority regions for soil management. Australia could benefit environmentally, socially and economically by unlocking even a tiny portion of its soil's C sequestration potential.

Can serum IgE or blood eosinophil count predict postoperative oral corticosteroid response in chronic rhinosinusitis with nasal polyps?

BACKGROUND: Chronic rhinosinusitis with nasal polyps (CRSwNP) is characterised by inflammatory mucosa and polyp formation in the paranasal sinuses. The study's primary objective was to evaluate the outcomes of postoperative oral corticosteroid (OCS) in treating patients with bilateral CRSwNP. The secondary objective was to determine whether preoperative serum IgE levels (sIgE)and/or blood eosinophil count (BEC) correlate with postoperative outcomes following OCS use. METHODS: Patients with bilateral CRSwNP (n=236) who underwent endoscopic sinus surgery (ESS) were randomly assigned to receive 15 mg OCS twice daily or a placebo for 2 weeks. We investigated the treatment effects based on the subjective visual analogue scale (VAS), Sino-Nasal Outcome Test 22 (SNOT-22), and objective Lund-Kennedy Endoscopy Score (LKES) over 6 months; subgroups were stratified preoperatively as follows: sIgE <150 IU/mL, sIgE>=150 IU/mL, BEC <0.39x10(9) cells/L, and BEC>=0.39x10(9) cells/L. RESULTS: A total of 193 participants completed the study up to the 6-month follow-up; no apparent linear relationship was noted between sIgE and BEC. No significant differences in scores were noted upon assessment of the VAS, SNOT-22, and LKES among the follow-up timepoints in the primary analysis. However, in the primary or subgroup analyses with sIgE or BEC, significant differences in the longitudinal scores of sleep dysfunction were observed at the 1-month follow-up. CONCLUSION: Postoperative OCS did not significantly affect bilateral CRSwNP outcomes. sIgE levels and BEC may not be surrogate predictive biomarkers to assess the role of postoperative OCS use. OCS may increase the risk of transient sleep disturbance.

The role of lymphocyte count in the early diagnosis of surgical site infection following posterior lumbar fusion.

OBJECTIVE: This study aimed to explore the early diagnostic value of lymphocyte count in the early diagnosis of surgical site infection (SSI) following posterior lumbar fusion. PATIENTS AND METHODS: In this study, we retrospectively analyzed the data from a total of 37 patients with lumbar SSI from Guizhou  Province Orthopaedic Hospital and Nanyang Central Hospital, 2008.1-2018.11, and 104 patients without SSI. We analyzed the C-reactive protein (CRP) level, white blood cell count (WBC) and differential count before instrumented lumbar fusion at 3 and 7 days postoperatively. The significance of the differences was evaluated by one-way ANOVA, followed by Fisher's test. The parameters mentioned above were analyzed on postoperative days 3 and 7 using the receiver operating characteristic curve and the area under the curve (AUC). Furthermore, the analyses were conducted by SPSS 22.0 software. RESULTS: The lymphocyte count in the SSI group on postoperative day 3 was significantly lower than that in the no-SSI group after surgery (p=0.000). According to the ROC curve analysis of related parameters on postoperative day 3, the AUC value of lymphocytes (0.840) was significantly larger than the AUC value of C-reactive protein (0.749). CONCLUSIONS: The lymphocyte count and C-reactive protein level on postoperative day 3 are reliable predictors of infection.

Warming and redistribution of nitrogen inputs drive an increase in terrestrial nitrous oxide emission factor.

Anthropogenic nitrogen inputs cause major negative environmental impacts, including emissions of the important greenhouse gas N2O. Despite their importance, shifts in terrestrial N loss pathways driven by global change are highly uncertain. Here we present a coupled soil-atmosphere isotope model (IsoTONE) to quantify terrestrial N losses and N2O emission factors from 1850-2020. We find that N inputs from atmospheric deposition caused 51% of anthropogenic N2O emissions from soils in 2020. The mean effective global emission factor for N2O was 4.3 ± 0.3% in 2020 (weighted by N inputs), much higher than the surface area-weighted mean (1.1 ± 0.1%). Climate change and spatial redistribution of fertilisation N inputs have driven an increase in global emission factor over the past century, which accounts for 18% of the anthropogenic soil flux in 2020. Predicted increases in fertilisation in emerging economies will accelerate N2O-driven climate warming in coming decades, unless targeted mitigation measures are introduced.

Retraction Note: MicroRNA-132 stimulates the growth and invasiveness of trophoblasts by targeting DAPK-1.

The article "MicroRNA-132 stimulates the growth and invasiveness of trophoblasts by targeting DAPK-1, by Y.-P. Wang, P. Zhao, J.-Y. Liu, S.-M. Liu, Y.-X. Wang, published in Eur Rev Med Pharmacol Sci 2020; 24 (19): 9837-9843-DOI: 10.26355/eurrev_202010_23193-PMID: 33090386" has been retracted by the authors due to some inaccuracies in the miRNA-132 primer sequence. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/23193.

Identification of common key genes associated with Crohn's Disease and IgA nephropathy.

OBJECTIVE: Emerging studies have suggested a strong link between Crohn's disease (CD) and IgA nephropathy (IgAN), but the underlying pathogenesis remains unclear. This led us to explore the common pathogenic genes for the two diseases by originally applying a bioinformatic method. MATERIALS AND METHODS: The CD and IgAN datasets were downloaded from the Gene Expression Omnibus (GEO) database. The common differentially expressed genes (DEGs) of the two diseases were identified. GO and KEGG enrichment analyses for the common DEGs were further performed. Then, PPI networks were constructed to identify the hub genes. Afterwards, the receiver operating characteristic (ROC) curves were constructed to assess the diagnostic value of the hub genes. Finally, the immune infiltrations in the samples were analyzed and the correlation of the hub genes with the immune infiltration was studied. RESULTS: 47 common DEGs were identified between CD and IgAN with the threshold of p-value < 0.05 and |log2FC| > 1. The top 5 GO terms and 5 KEGG pathways were displayed, and the top 10 hub genes were selected. The diagnostic value of these hub genes was evaluated by calculating the area under the ROC curves. Among the hub genes, CXCL2 was not only identified as the common hub gene, but also with the highest diagnostic value. Finally, CXCL2 was verified to be crucially correlated with the immune infiltration in the samples of CD and IgAN. CONCLUSIONS: Our study identified critical pathogenic genes commonly responsible for the pathogenesis of CD and IgAN, which provided novel biomarkers and promising therapeutic targets for the two diseases. Further experimental and clinical research are needed to verify our results.

Molecular signalling involved in upper airway remodelling is enhanced in patients with obstructive sleep apnoea.

OBJECTIVE: This study aimed to elucidate whether molecular signalling involved in upper airway remodelling is enhanced in patients with obstructive sleep apnoea. METHOD: Twenty patients with mild obstructive sleep apnoea (control group) and 40 patients with moderate to severe obstructive sleep apnoea (obstructive sleep apnoea group) who desired uvulopalatopharyngoplasty were recruited for the study. After uvulopalatopharyngoplasty, surgical specimens of the uvula were subjected to haematoxylin and eosin, Masson's trichrome and immunohistochemical staining. Western blot and reverse transcriptase-polymerase chain reaction were used to evaluate the protein and messenger RNA expressions. RESULTS: The obstructive sleep apnoea group showed more severe inflammation, increased collagen deposition and higher immunohistochemical staining intensity for TGF-ß and MMP-9 as well as higher protein and messenger RNA expression of MMP-9, VEGF, TGF-ß, p38 MAPK, SMAD 2/3, AKT and JNK in the uvula than control group. CONCLUSION: Patients with obstructive sleep apnoea demonstrated more severe inflammation, increased airway remodelling, and increased protein and messenger RNA expression of pro-inflammatory and pro-fibrotic cytokines in the uvula than control participants.

The treatment of menopausal symptoms by traditional Chinese medicine in Asian countries.

Menopausal symptoms (or climacteric syndrome) refer to a series of symptoms that occur during the perimenopausal and early postmenopausal period. About 80% of women will have various degrees of menopausal symptoms, and most of them need associated treatment. Asian women are more inclined to choose traditional Chinese medicine (TCM) in terms of therapeutic method, and menopausal hormone therapy has low acceptance because the women have been misinformed about the side effects of hormones. Therefore, TCM is used for menopausal symptoms in women in most Asian countries, including China, Japan, Vietnam, and South Korea. In the basic theory of TCM, the menopause is classified as the Kidney deficiency and imbalance of Yin and Yang; therefore, the treatment methods in either Chinese patent medicine or Chinese herbal medicine are aimed at supplementing the Kidney function and rebalancing Yin and Yang. It is believed that TCM treatment is suitable for patients with mild or moderate menopausal symptoms. The incidence rate of adverse reactions in terms of breast tenderness and irregular vaginal bleeding is lower than that of hormone therapy. However, there are few randomized, double-blind, placebo-controlled studies on TCM treatment of menopausal syndrome. Future studies should be undertaken to confirm its merits.

Add-on effect of clarithromycin to oral steroids as post- operative therapy for chronic rhinosinusitis with nasal polyps: a randomised controlled trial.

BACKGROUND: Evidence is lacking regarding the efficacy of macrolides and oral corticosteroids in chronic rhinosinusitis with nasal polyps (CRSwNP) after endoscopic sinus surgery (ESS). Therefore, we examined the benefits of adding clarithromycin to oral pred- nisolone as post-ESS medical therapy in patients with CRSwNP. METHODS: In this randomised, double-blind, placebo-controlled trial, patients were enrolled and allocated to three study groups receiving different post-ESS medical therapies: group A (placebo for 14 weeks), group B (oral prednisolone [15 mg twice daily] for 2 weeks, followed by placebo for 12 weeks), and group C (oral prednisolone [15 mg twice daily] for 2 weeks, followed by clari- thromycin [500 mg daily] for 12 weeks). All enrolled patients received the perioperative care following a routine protocol, which included oral amoxicillin/clavulanate, and intranasal corticosteroid spray. The baseline and post-operative visual analogue scale (VAS) scores, Sino-nasal Outcome Test (SNOT-22) scores, and Lund-Kennedy endoscopy scores (LKES) were determined as the primary outcomes. RESULTS: One hundred twenty-six patients who received ESS for bilateral CRSwNP were randomised into group A (n=43), B (n=42), or C (n=41). Compared to groups A and B, group C showed greater VAS and SNOT-22 score improvement at 12 weeks after ESS. Group C showed significantly better LKES than did groups A and B at 8, 12, and 24 weeks after ESS. On stratifying the LKES results according to the presence/absence of tissue eosinophilia, greater add-on effects of clarithromycin were observed in the patient subgroup without tissue eosinophilia. CONCLUSIONS: Adding low-dose clarithromycin to oral corticosteroids as post-ESS therapy was well tolerated and showed benefi- cial subjective and objective outcomes in patients with CRSwNP, especially those without tissue eosinophilia.

MicroRNA-132 stimulates the growth and invasiveness of trophoblasts by targeting DAPK-1.

OBJECTIVE: The purpose of this study was to elucidate the regulatory effects of microRNA-132 on the growth and invasiveness of trophoblasts, thus influencing the development of preeclampsia (PE). PATIENTS AND METHODS: Placenta tissues from 24 PE pregnancies and 24 healthy pregnancies were collected. Expression levels of microRNA-132 and DAPK-1 in collected placenta tissues were detected. Then, the regulatory effects of microRNA-132 and DAPK-1 on expression levels of apoptosis-associated genes, viability, and invasiveness in trophoblasts were assessed. Finally, through Dual-Luciferase reporter assay, the binding relationship between microRNA-132 and DAPK-1 was determined. RESULTS: The results showed that microRNA-132 was downregulated in placenta of PE pregnancies, while DAPK-1 was upregulated. Overexpression of microRNA-132 stimulated viability and invasiveness, but inhibited apoptosis in trophoblasts. Besides, it was found that DAPK-1 was the target gene binding microRNA-132, and a negative correlation was identified between their expression levels. Notably, the overexpression of DAPK-1 inhibited viability and invasiveness, but stimulated apoptosis in trophoblasts. CONCLUSIONS: MicroRNA-132 stimulates proliferative and invasive capacities and inhibits apoptosis in trophoblasts by targeting DAPK-1.

MiR-532-5p acts as a tumor suppressor and inhibits glioma cell proliferation by targeting CSF1.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "MiR-532-5p acts as a tumor suppressor and inhibits glioma cell proliferation by targeting CSF1, by Y.-P. Wang, J. Liu, D. Liu, X.-D. Wang, A.-M. Bian, D.-Z. Fang, X.-B. Hui, published in Eur Rev Med Pharmacol Sci 2019; 23 (20): 8964-8970-DOI: 10.26355/eurrev_201910_19295-PMID: 31696484" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/19295.

Overexpression of XIST facilitates cell proliferation, invasion and suppresses cell apoptosis by reducing radio-sensitivity of glioma cells via miR-329-3p/CREB1 axis.

OBJECTIVE: Glioma is a malignant brain cancer capable of spreading to the microenvironment. Long non-coding RNA (lncRNA) X inactive specific transcript (XIST) was recognized as a significant regulator in many cancers. However, the molecular mechanism of XIST in glioma cell radio-sensitivity requires further exploration. PATIENTS AND METHODS: The expression of XIST, microRNA (miR)-329-3p and cyclic AMP response element-binding protein 1 (CREB1) was evaluated by quantitative Real-time polymerase chain reaction (qRT-PCR). Cell viability and apoptosis were examined by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) and flow cytometry, respectively. Transwell assay was performed to detect cell invasion. Protein expression of gamma-H2AX (γ-H2AX) and CREB1 was determined by Western blot. The correlation between miR-329-3p and XIST or CREB1 was determined by dual-luciferase reporter assay. Animal models were established by subcutaneously injecting U251 cells transfected with sh-XIST and sh-NC. RESULTS: XIST and CREB1 were overexpressed whereas miR-329-3p was low-expressed in glioma tumors and cells compared with the normal counterparts. XIST knockdown inhibited cell proliferation, invasion and induced cell apoptosis by enhancing cell sensitivity to X-ray radiation in glioma. Then, we discovered that miR-329-3p directly interacted with XIST or CREB1 in glioma. In addition, miR-329-3p inhibitor abolished XIST silencing-induced regulatory effects on cell proliferation, apoptosis, invasion, and radio-sensitivity. Meanwhile, miR-329-3p inhibitor counteracted CREB1 silencing-induced inhibition on cell progression and facilitation on radio-sensitivity in glioma. Moreover, we found that XIST could increase CREB1 expression by sponging miR-329-3p. Animal experiments revealed that XIST silencing restrained tumor growth in vivo. CONCLUSIONS: XIST accelerates cell proliferation, invasion and inhibits cell apoptosis by repressing radio-sensitivity of glioma via enhancing CREB1 expression through sponging miR-329-3p, representing prospective methods for glioma treatment.

Circular RNA hsa_circ_0010882 promotes the progression of gastric cancer via regulation of the PI3K/Akt/mTOR signaling pathway.

OBJECTIVE: Accumulating studies have reported that circular RNAs (circRNAs) can act as novel prognostic biomarkers in multiple malignant tumors. Here, we conducted a study to investigate the potential function and molecular mechanism of action of hsa_circ_0010882 in gastric cancer (GC). PATIENTS AND METHODS: The expression of hsa_circ_0010882 in the plasma of GC patients and in GC cell lines was verified by qRT-PCR. Its association with overall survival of GC patients was then analyzed by statistical analysis. Gain-of-function and loss-of-function assays were used to investigate the physiological function of hsa_circ_0010882 in GC cells in vitro in the context of proliferation, apoptosis, migration, and invasion. Moreover, the molecular mechanism of action of hsa_circ_0010882 was predicted using online databases and a literature review. A Western blot assay was used to detect the levels of proteins in the PI3K/Akt/mTOR signaling pathway. RESULTS: We found that hsa_circ_0010882 expression was significantly upregulated in the plasma of GC patients and GC cell lines. Increased expression of hsa_circ_0010882 was significantly correlated with tumor size and histological grade. In addition, GC patients with higher expression of hsa_circ_0010882 had significantly lower overall survival than patients with lower expression of hsa_circ_0010882. Multivariate analysis showed that hsa_circ_0010882 expression could be an independent prognostic factor for overall survival. The proliferation, migration, and invasiveness of GC cell lines were inhibited following hsa_circ_0010882 knock-down, while GC cellular apoptosis increased. Further, overexpression of hsa_circ_0010882 leads to increased proliferation, migration, and invasiveness of GC cell lines. While apoptosis was higher in the GC cell line group with low expressing hsa_circ_0010882 than the control group, no significant difference in apoptosis was detected between the hsa_circ_0010882 overexpressing and the control group. Finally, a mechanistic analysis demonstrated that the hsa_circ_0010882 was positively associated with PI3K/Akt/mTOR signaling pathway. CONCLUSIONS: Hsa_circ_0010882, as an oncogenic molecule, is highly expressed in the plasma of patients with GC and is associated with poor prognosis. It plays an important role in proliferation, migration, and invasive genotypes of GC cell lines via regulation of the PI3K/Akt/mTOR signaling pathway. Additionally, it might be a potential prognostic biomarker for GC patients.

MiR-497 inhibits cell proliferation and invasion ability by targeting HMGA2 in pancreatic ductal adenocarcinoma.

OBJECTIVE: MicroRNAs have been implicated to play a crucial regulating role in human cancers. The study aims to explore the role and clinical significance of miR-497 in pancreatic ductal adenocarcinoma (PDAC). PATIENTS AND METHODS: The relative expression of miR-497 in human PDAC tissue samples and adjacent normal tissues was measured using the quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Cell Counting Kit (CCK-8) assay, cell migration, and invasion assays were performed to detect cell proliferation and invasion ability. Downstream target gene was confirmed by using luciferase activity assays. QRT-PCR and Western blotting assays also were performed. RESULTS: We found that miR-497 expression was significantly downregulated in PDAC tissues and cells. Lower miR-497 expression associated with lymph node metastasis and predicts a poor prognosis in PDAC patients. In in vitro assay, we demonstrated that miR-497 overexpression inhibited cell proliferation, migration, and invasion of PDAC. Furthermore, we demonstrated that HMGA2 was a direct target of miR-497 in PDAC cells. MiR-497 inhibited cell proliferation and invasion by regulating HMGA2 expression. CONCLUSIONS: Our results indicated that miR-497 may serve as a predictor for PDAC and could be a novel target of PDAC treatment.