Compound erosion effect of snowmelt, wind, and rainfall on sloping farmlands of Chinese typical Mollisol region.

Research on the processes and mechanisms of compound soil erosion by multiple forces can provide scientific guidance for precisely controlling cropland soil erosion. Based on the seasonal alternation of freezing-thawing, snowmelt, wind, and rainfall erosion forces on sloping farmlands under natural conditions from November to next October of each year, we used a set of indoor simulation experiments of multi-force superimpositions to analyze the compound soil erosion processes of snowmelt (1 and 2 L·min-1), wind (12 m·s-1), and rainfall (100 mm·h-1). We further discussed the erosion effects of multi-force superimpositions. The results showed that, under single snowmelt erosion, an increase in snowmelt flow had a greater effect on sloping snowmelt erosion intensity than that of sloping runoff rate. When sloping snowmelt flow increased from 1 L·min-1 to 2 L·min-1, sloping runoff rate and erosion intensity increased by 2.7 and 4.0 times, respectively. Under snowmelt-wind superimposition erosion, previous sloping snowmelt erosion inhibited late wind erosion occurrence. As sloping snowmelt flow increased from 1 L·min-1 to 2 L·min-1, the inhibiting action subsequently increased and wind erosion intensity caused by previous snowmelt reduced by more than 50%. Both wind erosion and snowmelt-wind superimposed erosion intensified late rainfall erosion. The early wind erosion increased rainfall erosion by 24.5%. The snowmelt-wind superimposed effect increased the later slope rainfall erosion by 132.8% and 465.4% under 1 and 2 L·min-1 snowmelt runoff rates, respectively. The compound soil erosion amount driven by multiple force superimposition was not the sum of the corresponding erosion amount caused by single erosion force, with promoting or inhibiting effects of erosion force superimposition. The erosion effect of snowmelt-wind superposition was negative, but that of wind-rainfall superposition and snowmelt-wind-rainfall superpositions were positive.

Diffusion-relaxation correlation spectrum imaging for predicting tumor consistency and gross total resection in patients with pituitary adenomas: a preliminary study.

OBJECTIVE: To evaluate the ability of diffusion-relaxation correlation spectrum imaging (DR-CSI) to predict the consistency and extent of resection (EOR) of pituitary adenomas (PAs). METHODS: Forty-four patients with PAs were prospectively enrolled. Tumor consistency was evaluated at surgery as either soft or hard, followed by histological assessment. In vivo DR-CSI was performed and spectra were segmented following to a peak-based strategy into four compartments, designated A (low ADC), B (mediate ADC, short T2), C (mediate ADC, long T2), and D (high ADC). The corresponding volume fractions ([Formula: see text], [Formula: see text], [Formula: see text], [Formula: see text]) along with the ADC and T2 values were calculated and assessed using univariable analysis for discrimination between hard and soft PAs. Predictors of EOR > 95% were analyzed using logistic regression model and receiver-operating-characteristic analysis. RESULTS: Tumor consistency was classified as soft (n = 28) or hard (n = 16). Hard PAs presented higher [Formula: see text] (p = 0.001) and lower [Formula: see text] (p = 0.013) than soft PAs, while no significant difference was found in other parameters. [Formula: see text] significantly correlated with the level of collagen content (r = 0.448, p = 0.002). Knosp grade (odds ratio [OR], 0.299; 95% confidence interval [CI], 0.124-0.716; p = 0.007) and [Formula: see text] (OR, 0.834, per 1% increase; 95% CI, 0.731-0.951; p = 0.007) were independently associated with EOR > 95%. A prediction model based on these variables yielded an AUC of 0.934 (sensitivity, 90.9%; specificity, 90.9%), outperforming the Knosp grade alone (AUC, 0.785; p < 0.05). CONCLUSION: DR-CSI may serve as a promising tool to predict the consistency and EOR of PAs. CLINICAL RELEVANCE STATEMENT: DR-CSI provides an imaging dimension for characterizing tissue microstructure of PAs and may serve as a promising tool to predict the tumor consistency and extent of resection in patients with PAs. KEY POINTS: • DR-CSI provides an imaging dimension for characterizing tissue microstructure of PAs by visualizing the volume fraction and corresponding spatial distribution of four compartments ([Formula: see text], [Formula: see text], [Formula: see text], [Formula: see text]). • [Formula: see text] correlated with the level of collagen content and may be the best DR-CSI parameter for discrimination between hard and soft PAs. • The combination of Knosp grade and [Formula: see text] achieved an AUC of 0.934 for predicting the total or near-total resection, outperforming the Knosp grade alone (AUC, 0.785).

Arbuscular mycorrhiza mitigates zinc stress on Eucalyptus grandis through regulating metal tolerance protein gene expression and ionome uptake.

Arbuscular mycorrhizal (AM) fungi are symbionts of most terrestrial plants and enhance their adaptability in metal-contaminated soils. In this study, mycorrhized and non-mycorrhized Eucalyptus grandis were grown under different Zn treatments. After 6 weeks of treatment, the growing status and ionome content of plants as well as the expression patterns of metal tolerance proteins and auxin biosynthesis-related genes were measured. In this study, mycorrhized E. grandis showed higher biomass and height at a high level of Zn compared with non-mycorrhized plants. In addition, AM plants accumulated P, Mg, and Mn in roots and P, Fe, and Cu in shoots, which indicate that AM fungi facilitate the uptake of ionome nutrients to promote plant growth. In addition, mycorrhiza upregulated the expression of EgMTP1 and EgMTP7, whose encoding proteins were predicted to be located at the vacuolar membrane. Meanwhile, Golgi membrane transporter EgMTP5 was also induced in AM shoot. Our results suggest that AM likely mitigates Zn toxicity through sequestrating excess Zn into vacuolar and Golgi. Furthermore, the expression of auxin biosynthesis-related genes was facilitated by AM, and this is probably another approach for Zn tolerance.

[Transcutaneous neuromuscular electrical stimulation for the treatment of erectile dysfunction: A clinical observation].

OBJECTIVE: To observe the clinical efficacy of transcutaneous neuromuscular electrical stimulation (TNES) in the treatment of ED. METHODS: According to the inclusion and exclusion criteria, we included and studied 25 cases of ED treated by TNES in Northern Jiangsu People's Hospital from June 2021 to February 2022 using the self-matched pre- and post-control method. Before and after treatment, we conducted RigiScan penile hardness test under audiovisual sexual stimulation (AVSS) for all the patients and obtained their scores on the Erectile Hardness Scale (EHS), IIEF-5, Premature Ejaculation Diagnostic Tool (PEDT), Patient Health Questionnaire 9 (PHQ-9) and Generalized Anxiety Disorder Questionnaire 7 (GAD-7). RESULTS: No adverse reactions such as pain, allergy, skin burn, and subcutaneous congestion were observed in any of the patients. There were statistically significant differences after treatment in erection time, average and maximum hardness of the penile tip, mean hardness of the penile root, and circumference of the penile tip (P < 0.05), but not in the circumference and maximum hardness of the penile root during erection compared with the baseline (P > 0.05). Significant improvement was observed after treatment in the IIEF-5 score (P < 0.05), with a total effectiveness rate of 68%, as well as in the PEDT score (P < 0.05) GAD-7 anxiety score (P < 0.05), but not in the PHQ-9 depression score (P > 0.05). CONCLUSION: TNES, as a safe and non-invasive therapy, can improve penile hardness under AVSS and the erectile function and anxiety symptoms of ED patients, and can be used as a new option for the treatment of ED.

1α,25(OH)2D3 Radiosensitizes Cancer Cells by Activating the NADPH/ROS Pathway.

The radioresistance of tumors affect the outcome of radiotherapy. Accumulating data suggest that 1α,25(OH)2D3 is a potential anti-oncogenic molecule in various cancers. In the present study, we investigated the radiosensitive effects and underlying mechanisms of 1α,25(OH)2D3 in vitro and in vivo. We found that 1α,25(OH)2D3 enhanced the radiosensitivity of lung cancer and ovarian cancer cells by promoting the NADPH oxidase-ROS-apoptosis axis. Compared to the group that only received radiation, the survival fraction and self-renewal capacity of cancer cells treated with a combination of 1α,25(OH)2D3 and radiation were decreased. Both apoptosis and ROS were significantly increased in the combination group compared with the radiation only group. Moreover, N-acetyl-L-cysteine, a scavenger of intracellular ROS, reversed the apoptosis and ROS induced by 1α,25(OH)2D3, indicating that 1α,25(OH)2D3 enhanced the radiosensitivity of cancer cells in vitro by promoting ROS-induced apoptosis. Moreover, our results demonstrated that 1α,25(OH)2D3 promoted the ROS level via activating NADPH oxidase complexes, NOX4, p22phox, and p47phox. In addition, knockdown of the vitamin D receptor (VDR) abolished the radiosensitization of 1α,25(OH)2D3, which confirmed that 1α,25(OH)2D3 radiosensitized tumor cells that depend on VDR. Similarly, our study also evidenced that vitamin D3 enhanced the radiosensitivity of cancer cells in vivo and extended the overall survival of mice with tumors. In summary, these results demonstrate that 1α,25(OH)2D3 enhances the radiosensitivity depending on VDR and activates the NADPH oxidase-ROS-apoptosis axis. Our findings suggest that 1α,25(OH)2D3 in combination with radiation enhances lung and ovarian cell radiosensitivity, potentially providing a novel combination therapeutic strategy.

Dopaminergic neuron injury in Parkinson's disease is mitigated by interfering lncRNA SNHG14 expression to regulate the miR-133b/ α-synuclein pathway.

This study explored the influence of long non-coding RNA (lncRNA) SNHG14 on α-synuclein (α-syn) expression and Parkinson's disease (PD) pathogenesis. Firstly, we found that the expression level of SNHG14 was elevated in brain tissues of PD mice. In MN9D cells, the rotenone treatment (1µmol/L) enhanced the binding between transcriptional factor SP-1 and SNHG14 promoter, thus promoting SNHG14 expression. Interference of SNHG14 ameliorated the DA neuron injury induced by rotenone. Next, we found an interaction between SNHG14 and miR-133b. Further study showed that miR-133b down-regulated α-syn expression by targeting its 3'-UTR of mRNA and SNHG14 could reverse the negative effect of miR-133b on α-syn expression. Interference of SNHG14 reduced rotenone-induced DA neuron damage through miR-133b in MN9D cells and α-syn was responsible for the protective effect of miR-133b. Similarly, interference of SNHG14 mitigated neuron injury in PD mouse model. All in all, silence of SNHG14 mitigates dopaminergic neuron injury by down-regulating α-syn via targeting miR-133b, which contributes to improving PD.

Successful Rescue of the Victim Exposed to a Super High Dose of Iridium-192 during the Nanjing Radiological Accident in 2014.

Here we report on the interventions taken to treat a patient exposed to high-dose radiation and provide a protocol for treating such patients in the future. The patient, Mr. Wang, was a 58-year-old male janitor who was accidentally exposed to a 192Ir source with an activity of 966.4 GBq or 26.1 Ci. The dose estimated to the lower right limb was 4,100 Gy, whereas the whole-body effective dose was 1.51 Gy. The diagnosis was made according to the results of the patient dose estimation and clinical manifestations. Systemic treatment included stimulating bone marrow hematopoietic cells, enhancing immunity, anti-infection and vitamin supplements. The treatment of radiation-induced skin lesions consisted of several debridements, two skin-flap transplantations and application of mesenchymal stem cells (MSCs). Skin-flap transplantations and MSCs play important roles in the recovery of skin wound. A combination of antibiotics and antimycotic was useful in reducing inflammation. The application of vacuum sealing drainage was effective in removing necrotic tissue and bacteria, ameliorating ischemia and hypoxia of wound tissue, providing a fresh wound bed for wound healing and improving skin or flap graft survival rates. The victim survived the accident without amputation, and function of his highly exposed right leg was partially recovered. These results demonstrate the importance of collaboration among members of a multidisciplinary team in the treatment of this patient.

Celecoxib enhances the radiosensitivity of HCT116 cells in a COX-2 independent manner by up-regulating BCCIP.

It has been reported that celecoxib, a cyclooxygenase-2 (COX-2)-selective nonsteroidal anti-inflammatory drug (NSAID), regulates the radiosensitivity of several cancer cells. BCCIP (BRCA2 and CDKN1A interacting protein) plays a critical role in maintaining the critical functions of p53 in tumor suppression and response to therapy. However, whether the effect of celecoxib on the radiosensitivity of colorectal cancer (CRC) cells is dependent on BCCIP is largely unclear. In this study, we found that celecoxib enhanced the radiosensitivity of HeLa (a human cervical carcinoma cell line), A549 (a human lung carcinoma cell line), and HCT116 cells (a human CRC cells line). Among these cells, COX-2 expression was undetected in HCT116 cells. Treatment with celecoxib significantly increased BCCIP expression in COX-2 negative HCT116 cells. Knockdown of BCCIP obviously abrogated the enhanced radiosensitivity of HCT116 cells induced by celecoxib. A combination of celecoxib and irradiation treatment induced much more γ-H2AX foci formation, higher levels of radiation injury-related proteins phosphorylation, G2/M arrest, apoptosis, and p53 and p21 expression, and lower levels of Cyclin B1 in HCT116 cells than those in cells treated with irradiation alone. However, these changes were undetected in BCCIP-silenced HCT116 cells. Therefore, these data suggest that BCCIP gene may be a radiosensitivity-related gene in CRC. Celecoxib affects the functions of p53 and inhibits the recovery from the irradiation-induced injury by up-regulating the expression of BCCIP, and subsequently regulates the expressions of genes such as p21 and Cyclin B1 to enhance the radiosensitivity of HCT116 cells in a COX-2 independent manner.

Plant toxin ß-ODAP activates integrin ß1 and focal adhesion: A critical pathway to cause neurolathyrism.

Neurolathyrism is a unique neurodegeneration disease caused by ß-N-oxalyl-L-α, ß- diaminopropionic (ß-ODAP) present in grass pea seed (Lathyrus stativus L.) and its pathogenetic mechanism is unclear. This issue has become a critical restriction to take full advantage of drought-tolerant grass pea as an elite germplasm resource under climate change. We found that, in a human glioma cell line, ß-ODAP treatment decreased mitochondrial membrane potential, leading to outside release and overfall of Ca2+ from mitochondria to cellular matrix. Increased Ca2+ in cellular matrix activated the pathway of ECM, and brought about the overexpression of ß1 integrin on cytomembrane surface and the phosphorylation of focal adhesion kinase (FAK). The formation of high concentration of FA units on the cell microfilaments further induced overexpression of paxillin, and then inhibited cytoskeleton polymerization. This phenomenon turned to cause serious cell microfilaments distortion and ultimately cytoskeleton collapse. We also conducted qRT-PCR verification on RNA-sequence data using 8 randomly chosen genes of pathway enrichment, and confirmed that the data was statistically reliable. For the first time, we proposed a relatively complete signal pathway to neurolathyrism. This work would help open a new window to cure neurolathyrism, and fully utilize grass pea germplasm resource under climate change.

Transient folate deprivation in combination with small-molecule compounds facilitates the generation of somatic cell-derived pluripotent stem cells in mice.

Induced pluripotent stem cells (iPSCs) can be propagated indefinitely, while maintaining the capacity to differentiate into all cell types in the body except for the extra-embryonic tissues. This iPSC technology not only represents a new way to use individual-specific stem cells for regenerative medicine but also constitutes a novel method to obtain large numbers of disease-specific cells for biomedical research. However, the low efficiency of reprogramming and genomic integration of oncogenes and viral vectors limit the potential application of iPSCs. Chemical-induced reprogramming offers a novel approach to generating iPSCs. In this study, a new combination of small-molecule compounds (SMs) (sodium butyrate, A-83-01, CHIR99021, Y-27632) under conditions of transient folate deprivation was used to generate iPSC. It was found that transient folate deprivation combined with SMs was sufficient to permit reprogramming from mouse embryonic fibroblasts (MEFs) in the presence of transcription factors, Oct4 and Klf4, within 25 days, replacing Sox2 and c-Myc, and accelerated the generation of mouse iPSCs. The resulting cell lines resembled mouse embryonic stem (ES) cells with respect to proliferation rate, morphology, pluripotency-associated markers and gene expressions. Deprivation of folic acid, combined with treating MEFs with SMs, can improve the inducing efficiency of iPSCs and reduce their carcinogenicity and the use of exogenous reprogramming factors.