Puccinellia tenuiflora is a typical salt-excluding halophytic grass with excellent salt tolerance. Plasma membrane Na+/H+ transporter SOS1, HKT-type protein and tonoplast Na+/H+ antiporter NHX1 are key Na+ transporters involved in plant salt tolerance. Based on our previous research, we had proposed a function model for these transporters in Na+ homeostasis according to the expression of PtSOS1 and Na+, K+ levels in P. tenuiflora responding to salt stress. Here, we analyzed the expression patterns of PtSOS1, PtHKT1;5, and PtNHX1 in P. tenuiflora under 25 and 150 mM NaCl to further validate this model by combining previous physiological characteristics. Results showed that the expressions of PtSOS1 and PtHKT1;5 in roots were significantly induced and peaked at 6 h under both 25 and 150 mM NaCl. Compared to the control, the expression of PtSOS1 significantly increased by 5.8-folds, while that of PtHKT1;5 increased only by 1.2-folds in roots under 25 mM NaCl; on the contrary, the expression of PtSOS1 increased by 1.4-folds, whereas that of PtHKT1;5 increased by 2.2-folds in roots under 150 mM NaCl. In addition, PtNHX1 was induced instantaneously under 25 mM NaCl, while its expression was much higher and more persistent in shoots under 150 mM NaCl. These results provide stronger evidences for the previous hypothesis and extend the model which highlights that SOS1, HKT1;5, and NHX1 synergistically regulate Na+ homeostasis by controlling Na+ transport systems at the whole-plant level under both lower and higher salt conditions. Under mild salinity, PtNHX1 in shoots compartmentalized Na+ into vacuole slowly, and vacuole potential capacity for sequestering Na+ would enhance Na+ loading into the xylem of roots by PtSOS1 through feedback regulation; and consequently, Na+ could be transported from roots to shoots by transpiration stream for osmotic adjustment. While under severe salinity, Na+ was rapidly sequestrated into vacuoles of mesophyll cells by PtNHX1 and the vacuole capacity became saturated for sequestering more Na+, which in turn regulated long-distance Na+ transport from roots to shoots. As a result, the expression of PtHKT1;5 was strongly induced so that the excessive Na+ was unloaded from xylem into xylem parenchyma cells by PtHKT1;5.

Chemotherapy resistance, the molecular mechanism of which is complex and has not been fully understood, poses a major challenge in the treatment of patients with non‑small cell lung cancer (NSCLC). The dysregulation of microRNAs (miRs) has been reported to serve a pivotal role in the development of cancer and drug resistance. In the present study, reverse transcription‑quantitative polymerase chain reaction analysis revealed a significant increase in miR‑328 and a significant decrease in phosphatase and tensin homolog (PTEN) mRNA expression levels within tumor tissues from patients with cisplatin‑resistant NSCLC compared with those of cisplatin‑sensitive NSCLC patients. In addition, there was a negative correlation between PTEN mRNA and the miR‑328 expression levels. In addition, higher miR‑328 expression levels, and lower PTEN mRNA and protein expression levels, were detected in cisplatin‑resistant A549 (A549rCDDP) cells when compared with in their parental cells. A549rCDDP cells demonstrated significantly higher cell viability compared with A549 cells following treatment with all concentrations of cisplatin tested (2, 4, 6 and 8 µM). Additionally, transfection of miR‑328 inhibitor significantly increased PTEN mRNA and protein expression levels. Furthermore, the present study predicted and confirmed PTEN, a well‑known tumor suppressor, as a direct target of miR‑328 in NSCLC cells via the online tool MiRanda and a dual luciferase assay, respectively. Cell viability assay and flow cytometry analysis demonstrated that inhibition of miR‑328 also induced cellular apoptosis and decreased cell proliferation in A549rCDDP cells treated with cisplatin. In conclusion, these results suggested that abnormal expression of miR‑328 may contribute to cisplatin resistance in NSCLC, and may be considered to be a novel therapeutic target and indicator for the treatment and prognosis of patients with NSCLC treated with cisplatin‑based chemotherapy.

The risk factors and coping strategies of severe community-acquired pneumonia (SCAP) in chemotherapy induction period of acute leukemia were investigated. Eighty-six patients with CAP in chemotherapy induction period of acute leukemia in Dezhou Hospital from March 2014 to February 2017 were selected and divided into observation group (SCAP group, n=45) and control group (non-SCAP group, n=41) according to the acute physiology and chronic health evolution II (APACHE II) score. The blood, sputum, nasopharyngeal secretion and pleural effusion samples were collected from patients in both groups, and the samples were detected for pathogens, followed by the analysis of relevant factors. The dynamic changes in the sequential organ failure assessment (SOFA) score, procalcitonin (PCT), D-dimer (D-D) and C-reactive protein (CRP) levels in patients were observed before and after the corresponding treatment strategies were taken. The total distribution ratio of pathogens from high to low in the two groups was as follows: bacterium, virus, fungus, mycoplasma and chlamydia trachomatis; there was no significant difference between the two groups (P>0.05). Logistic regression analysis showed that the repeated infection (OR=3.315, P=0.005), multi-resistant bacterial infection (OR=1.915, P=0.008) and D-D (OR=1.936, P=0.009) were independent risk factors for SCAP (P<0.05). After different coping strategies were taken, the SOFA score, PCT, D-D and CRP levels in the two groups were significantly decreased, and they were obviously higher in observation group than those in control group (P<0.05). Repeated infection, D-D level and multi-resistant bacterial infection are the risk factors affecting the SCAP in chemotherapy induction period of acute leukemia. The coping strategies can effectively relieve the patient's condition, reduce the severity of disease and improve the survival rate of patients.

Puccinellia tenuiflora is a typical salt-excluding halophytic grass with strong salt-tolerance, which enhances tolerance by restricting Na + influx as well as having a strong selectivity for K + over Na + . The HAK5 K + transporters generally modulate effective K + acquisition in plants, especially under low K + condition. In this study, PtHAK5 from P. tenuiflora was isolated by RT-PCR and characterized using yeast complementation. The results showed PtHAK5 consisted of 784 amino acids and shared over 80% homology with the identified high-affinity K + transporter HAK5 from other higher plants. The expression of PtHAK5 rescued the K + -uptake-defective phenotype of yeast strain CY162. In conclusion, PtHAK5 is a candidate for mediating high-affinity K + uptake under low K + conditions.

In the current study, nanofibrous polymeric tubes were fabricated to develop a drug-delivering artificial urethra. Scaffolds were produced via electrospinning of collagen and polycaprolacton solution loaded with trimethoprim and curcumin and then rolled up to produce urethra-resembling tubes. Various In Vitro experiments such as scanning electron microscopy imaging, cell attachment studies, cytocompatiblity test, cell protection assay, antibacterial tests, biodegradation analysis, antiinflammatory assay, and gene expression analysis were utilized for the characterization of the scaffolds. In Vitro experiments showed that the electrospun tubes were biocompatible with human urothelial cells and promoted their adhesion and proliferation. Antibacterial assay showed that drug-delivering scaffolds showed a strong antibacterial activity against Escherichia coli Staphylococcus aureus bacteria. Meantime, the developed scaffolds downregulated fibrosis-associated genes. This study suggests potential applicability of polycaprolacton/collagen/curcumin/ trimethoprim tubes for urethra reconstruction surgeries and prevention of its bacterial infection.