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The decline in biodiversity poses a serious threat to natural ecosystems and has become one of the most pressing global environmental issues. Establishing conservation priorities for protected areas (PAs) is one of the most direct and effective biodiversity conservation measures. However, conservation gaps arise as a result of existing problems in spatial layout of PAs, including overlapping protection scopes, artificial fragmentation of natural ecological regions, as well as "over-protection" and "over-exploitation." To optimize the spatial layout of PAs and improve the efficiency of biodiversity conservation, we employed the Habitat Quality module of the Integrated Assessment of Ecosystem Services and Tradeoffs (InVEST) model and the Maximum Entropy (MaxEnt) model to assess the PAs in the Songnen Plain, China. The combined model (MaxEnt-InVEST) revealed that the conservation priorities for PAs in the Songnen Plain occupied a total area of 14,764.14 km 2 (10.24% of the total area of the Songnen Plain). The conservation priorities outside PAs occupied a total area of 7858.45 km 2 (5.45% of the total area of the Songnen Plain) and were primarily distributed in the northeastern, central, and southwestern regions of the Songnen Plain. This indicated that existing PAs did not offer adequate protection for local biodiversity. The consistency of our combined modeling framework was 72.11%, which enabled a more accurate assessment of biodiversity hotspots and respects the land uses of the Songnen Plain. In addition, the modeling framework successfully created maps of conservation gaps of biodiversity hotspots based on actual species distribution data and considers current land uses. Our study was aimed at optimizing the spatial conservation efficiency of the Songnen Plain by assessing the conservation gaps in the Songnen Plain. It could provide a reference for the future development of a PA system centering on national parks., Competing Interests: The authors declare no conflicts of interest., (© 2024 The Author(s). Ecology and Evolution published by John Wiley & Sons Ltd.)

MicroRNAs (miRNAs) may serve important roles in the regulation of human non-small cell lung cancer (NSCLC) cell growth and apoptosis. To the best of our knowledge, the present study was the first to explore the role of miRNA-133a/epidermal growth factor receptor (EGFR) in regulating NSCLC cell growth and apoptosis via the AKT/extracellular signal-regulated kinase (ERK) signaling pathway. It was determined that miRNA-133a expression was lower in NSCLC tissue than in the adjacent mucosae. Additionally, EGFR expression in the NSCLC tissue was higher compared with in the adjacent mucosae. Furthermore, the upregulation of miRNA-133a in NSCLC cells suppressed cell growth and induced apoptosis. Upregulating miRNA-133a also increased caspase-3 protein expression, while suppressing that of EGFR, phosphorylated (p)-AKT and p-ERK in NSCLC cells. Therefore, the results of the current study demonstrated that miRNA-133a downregulates EGFR expression in NSCLC via the AKT/ERK signaling pathway. These findings provide insights into the function of miRNA-133a in NSCLC, as well as into the molecular mechanisms underlying the miRNA-133a-mediated downregulation of the EGFR/AKT/ERK signaling pathway in NSCLC.

Objective: To investigate the effects of electroacupuncture (EA) on mRNA and protein expression of agrin, acetylcholine receptor (AChR)-ε and AChR-γ in a rat model of tibialis anterior muscle atrophy induced by sciatic nerve injection injury, and to examine the underlying mechanism of action., Methods: Fifty-four adult Sprague-Dawley rats were divided into four groups: healthy control group (CON, n=6); sciatic nerve injury group (SNI, n=24), comprising rats euthanased at 1, 2, 4 and 6 weeks, respectively, after penicillin injection-induced SNI (n=6 each); CON+EA group (n=12), comprising healthy rats euthanased at 4 and 6 weeks (after 2 and 4 weeks, respectively, of EA at GB30 and ST36); and SNI+EA group, comprising rats euthanased at 4 and 6 weeks (after 2 and 4 weeks, respectively, of EA). The sciatic nerve functional index (SFI), tibialis anterior muscle weight, muscle fibre cross-sectional area (CSA), and changes in agrin, AChR-ε, and AChR-γ expression levels were analysed., Results: Compared with the control group (CON), SNI rats showed decreased SFI. The weight of the tibialis anterior muscle and muscle fibre CSA decreased initially and recovered slightly over time. mRNA/protein expression of agrin and AChR-ε were downregulated and AChR-γ expression was detectable (vs zero expression in the CON/CON+EA groups). There were no significant differences in CON+EA versus CON groups. However, the SNI+EA group exhibited significant improvements compared with the untreated SNI group (p<0.05)., Conclusions: EA may alleviate tibialis anterior muscle atrophy induced by sciatic nerve injection injury by upregulating agrin and AChR-ε and downregulating AChR-γ., Competing Interests: Competing interests: None declared., (Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/.)

Background: The optimal chemotherapy route for non-small cell lung cancers involving the phrenic nerve and diaphragm is unclear. The pharmacokinetic properties of paclitaxel following intravenous (IV) or intrapleural (IP) administration were analyzed in the plasma, lung, and diaphragm in a rat model. The purpose of this study was to determine whether IP injection increased paclitaxel concentration in the diaphragm., Methods: Paclitaxel was administered by IV or IP to male Sprague-Dawley rats. The concentration of drug in the plasma, lung, and diaphragm was determined using liquid chromatography-tandem mass spectrometry (LC-MS/MS). The pharmacokinetic parameters area under the curve (AUC), mean residence time (MRT), peak plasma concentration (Cmax), and half-life (t1/2) were analyzed., Results: Paclitaxel concentration in the plasma, lung, and diaphragm decreased quickly following IV administration. However, after IP injection, paclitaxel reached a high concentration in the plasma, lung, and diaphragm that declined gradually. Significant differences in all parameters, except Cmax in the lung, were observed between the two routes of administration (all P < 0.05). Plasma exposure to paclitaxel IP was 41.1% of that observed after IV in the first 24 hours (P < 0.05). IP also significantly increased exposure of paclitaxel in comparison with IV administration to 267.3% and 905.7% of IV administration in the lung and diaphragm, respectively (P < 0.05)., Conclusion: These results suggest that IP administration may reduce systemic distribution of paclitaxel and increase the concentration in the lung and diaphragm. This could increase therapeutic efficacy by increasing the available drug and reduce systemic toxicity.

Objective: To investigate the differential expressions of multidrug resistance protein 1 (MDR-1), ribonucleotide reductase M1(RRM-1), epidermal growth factor receptor(EGFR), excision repair cross-complementation group 1 (ERCC-1) in primary tumors and metastatic lymph nodes of patients with non-small cell lung cancer (NSCLC), and analyze the relationship between the differential expressions and pathological types of NSCLC. Methods The expressions of MDR-1, RRM-1, EGFR and ERCC-1 were detected by immunohistochemistry in primary tumors and metastatic lymph nodes of 46 cases NSCLC patients. Wilcoxon signed ranks test was used to compare the differences in the expressions of these four molecular markers in primary lesions and metastatic lymph nodes. Fisher's exact test was used to analyze the relationship between differential expressions and pathological types of NSCLC., Results: The expressions of MDR-1, RRM-1, EGFR, ERCC-1 were observed in a variety of pathological types of NSCLC. The expression of ERCC-1 was significantly different between primary tumors and metastatic lymph nodes for lung adenocarcinoma (P=0.026). But the expressions of MDR-1, RRM-1, EGFR were not significantly different between primary tumors and metastatic lymph nodes for all pathological types of NSCLC (P>0.05). Conclusion The expression of MDR-1, RRM-1, EGFR, ERCC-1 of primary tumors and metastatic lymph nodes is found in all NSCLC. The expression of ERCC-1 is significantly different in primary tumors from in metastatic lymph nodes of lung adenocarcinoma.

Non-small cell lung cancer (NSCLC) has a high mortality rate and poor prognosis. The aim of the present study was to silence EZH2 and explore the antitumor effect of small interfering RNA (siRNA)-EZH2 in combination with radiotherapy, which is a main treatment for NSCLC. The results showed that irradiation in the presence of siRNA-EZH2 arrested A549 cells in the G(0) and G(1) phases, delayed cell cycle progression and effectively inhibited cell proliferation, compared with cells that received radiotherapy alone. The combined therapy enhanced the percentage of apoptotic A549 cells in vitro and reduced the tumor size, in addition to increasing the survival rate in tumor xenograft experiments. This study demonstrates the antitumor activity of ionizing radiation therapy in combination with siRNA-EZH2 in NSCLC, both in vitro and in vivo, as well as providing a scientific rationale for targeting EZH2 to enhance the sensitivity of cancer to radiotherapy in NSCLC patients.

Objective: To assess the effects of tumor necrosis factor-α (TNF-α) in enhancing the radiosensitivity of lung cancer cells in vitro., Methods: A549 cells were exposed to γ-ray with or without TNF-α treatment. MTT assay was used to evaluate the cell viability, and flow cytometry was performed to assess the cell apoptosis. Western blotting was used to observe the expression of caspase-3 protein in the exposed cells., Results: Compared with the exposed cells without TNF-α treatment, the cells treated with TNF-α showed significantly suppressed cell proliferation, increased the cell apoptosis, altered cell cycle, and increased caspase-3 protein expression after γ-ray exposure., Conclusion: TNF-α can enhance the radiosensitivity of A549 cells to increase the efficiency of radiotherapy with γ-ray irradiation.