Percutaneous radiologic gastrostomy via nasopharyngeal intubation for the treatment of patients with complete malignant pharyngoesophageal obstruction.

BACKGROUND/AIMS: For patients with complete malignant pharyngoesophageal obstruction (CMPO), percutaneous radiologic gastrostomy (PRG) under ultrasound/CT guidance can complicate it to cause failure due to unsatisfied stomach filling. In this study, we retrospectively investigated whether PRG via nasopharyngeal intubation is feasible and effective for these patients. METHODOLOGY: PRG via nasopharyngeal intubation was attempted in 21 patients with CMPO (mean 70.8 ± 8.23 years). The technique comprised a dilation of the stomach via nasopharyngeal intubation using a catheter, followed by fluoroscopically guided puncture and gastrostomy tube placement. Complications including hemorrhage, peritonitis, gastrojejunocolic fistula, infection of puncture site, tube blocking and outleakage was observed during and after the procedure. RESULTS: A 5F catheter was successfully inserted to the stomach under fluoroscopical guidance and subsequent PRG was performed in all 21 patients. Minor complications occurred in 14.3% patients including mild infection of the fistula in 1, tube blocking in 1 and unexpected tube drawing out in 1. Follow-up nutrition indexes revealed obvious improved nutrition compared to before PRG (P < 0.05). CONCLUSION: PRG via nasopharyngeal intubation was simple, feasible and effective for patients with CMPO.

Curcumin protects neurons against oxygen-glucose deprivation/reoxygenation-induced injury through activation of peroxisome proliferator-activated receptor-γ function.

The turmeric derivative curcumin protects against cerebral ischemic injury. We previously demonstrated that curcumin activates peroxisome proliferator-activated receptor-γ (PPARγ), a ligand-activated transcription factor involved in both neuroprotective and anti-inflammatory signaling pathways. This study tested whether the neuroprotective effects of curcumin against oxygen-glucose deprivation/reoxygenation (OGD/R)-induced injury of rat cortical neurons are mediated (at least in part) by PPARγ. Curcumin (10 µM) potently enhanced PPARγ expression and transcriptional activity following OGD/R. In addition, curcumin markedly increased neuronal viability, as evidenced by decreased lactate dehydrogenase release and reduced nitric oxide production, caspase-3 activity, and apoptosis. These protective effects were suppressed by coadministration of the PPARγ antagonist 2-chloro-5-nitrobenzanilide (GW9662) and by prior transfection of a small-interfering RNA (siRNA) targeting PPARγ, treatments that had no toxic effects on healthy neurons. Curcumin reduced OGD/R-induced accumulation of reactive oxygen species and inhibited the mitochondrial apoptosis pathway, as indicated by reduced release of cytochrome c and apoptosis-inducing factor and maintenance of both the mitochondrial membrane potential and the Bax/Bcl-2 ratio. Again, GW9662 or PPARγ siRNA transfection mitigated the protective effects of curcumin on mitochondrial function. Curcumin suppressed IκB kinase phosphorylation and IκB degradation, thereby inhibiting nuclear factor-κ B (NF-κB) nuclear translocation, effects also blocked by GW9662 or PPARγ siRNA. Immunoprecipitation experiments revealed that PPARγ interacted with NF-κB p65 and inhibited NF-κB activation. The present study provides strong evidence that at least some of the neuroprotective effects of curcumin against OGD/R are mediated by PPARγ activation.

Dabigatran etexilate tetra-hydrate.

In the title compound, C34H41N7O5·4H2O (systematic name: ethyl 3-{[2-({4-[(Z)-amino-(hexyl-oxycarbonyl-imino)-meth-yl]anilino}meth-yl)-1-meth-yl-benzimidazole-5-carbon-yl]pyridin-2-yl-amino}-propano-ate tetra-hydrate), the benzene and pyridine rings form dihedral angles of 5.4 (1) and 43.8 (1)°, respectively, with the benzimidazole mean plane. The terminal butyl group is disordered over two conformations in a 0.756 (10):0.244 (10) ratio. There is an intramolecular N-H⋯O hydrogen bond present. In the crystal, the water mol-ecules are involved in the formation of O-H⋯O, O-H⋯N and N-H⋯O hydrogen bonds, which link the components into layers parallel to the ab plane.

microRNA-145-5p attenuates acute lung injury via targeting ETS2.

The protective effect of microRNA (miR)-145-5p in acute lung injury (ALI) has been discovered previously. Thus, in this study, we attempted to further investigate the mechanism of miR-145-5p in ALI through the downstream E26 transformation-specific proto-oncogene 2 (ETS2)/transforming growth factor ß1 (TGF-ß1)/Smad pathway. A lipopolysaccharide (LPS)-induced ALI rat model was established. The expression of miR-145-5p in ALI rat lung tissues was up-regulated. Afterward, pathological damage in the lung tissue, the wet/dry (W/D) ratio, apoptosis, and serum inflammatory factor contents were observed. miR-145-5p, ETS2, TGF-ß1, Smad2/3, and phosphorylated Smad2/3 levels were measured in rats. miR-145-5p expression was down-regulated, ETS2 expression was up-regulated, and the TGF-ß1/Smad pathway was activated in LPS-exposed rats. Overexpression of miR-145-5p inactivated the TGF-ß1/Smad pathway and attenuated ALI, as reflected by relieved pathological damage, a decreased W/D ratio, reduced apoptosis, and suppressed inflammatory response. In contrast, loss of miR-145-5p or elevated ETS2 levels worsened ALI and activated the TGF-ß1/Smad pathway. Moreover, elevation of ETS2 diminished miR-145-5p-mediated protection against ALI. Evidently, miR-145-5p negatively regulates ETS2 expression and inactivates the TGF-ß1/Smad pathway to ameliorate ALI in rats.

Responses of leaf carbon, nitrogen, and phosphorus stoichiometry of Carex muliensis to water table drawdown in an alpine marsh on the Ruoergai Plateau, China.

Based on a field water table drawdown manipulation platform of Naleqiao marsh on the Rueorgai Plateau, we lifted in situ soil block of 1 m×1 m by 20 cm for simulating water table decline, and analyzed the response of carbon, nitrogen, and phosphorus stoichiometry in the wetland species Carex muliensis from June to September 2020. The results showed that there was no significant difference in leaf C content during the whole growing season, while N and P content gra-dually decreased along the growing season. After the drawdown of water table, the C content in leaves during the growing season was not consistent. Water table drawdown increased leaf C content in the early and middle growth stages, but changed little in the peak growth stage. Water table drawdown significantly increased leaf N content, while significantly decreased leaf P content. C:N, C:P, and N:P for leaves all increased along the whole growing period. The relative growth rate of C. muliensis was positively correlated with leaf C:N, but negatively correlated with leaf C:P and N:P. Water table drawdown significantly decreased leaf C:N, while significantly increased leaf C:P and N:P, which significantly reduced the relative growth rate of C. muliensis. The decrease of foliar P content induced by water table drawdown was the main regulating factor for the decrease of single leaf weight and specific leaf weight.

Safety evaluation and ibuprofen removal via an Alternanthera philoxeroides-based biochar.

Pharmaceutical and personal care products (PPCPs) are a representative class of emerging contaminants. This study aimed to investigate the PPCP removal performance and application safety of a biochar fabricated using the invasive plant Alternanthera philoxeroides (APBC). According to scanning electron microscopy and pore size analyses, APBC exhibited a porous structure with a specific surface area of 857.5 m2/g. A Fourier transform infrared spectroscopy analysis indicated the presence of surface functional groups, including phosphorus-containing groups, C=O, C=C, and -OH. The adsorption experiment showed that the maximum removal efficiency of ibuprofen was 97% at an initial concentration of 10 mg/L and APBC dosage of 0.8 g/L. The adsorption kinetics were fitted by the pseudo-second-order model with the highest correlation coefficient (R2 = 0.9999). The adsorption isotherms were well described by the Freundlich model (R2 = 0.9896), which indicates a dominant multilayer adsorption. The maximum adsorption capacity of APBC was 172 mg/g. A toxicity evaluation, based on Chlorella pyrenoidosa and human epidermal BEAS-2B cells, was carried out using a spectrum analysis, thiazolyl blue tetrazolium bromide assay, and flow cytometry. The results of the above showed the low cytotoxicity of APBC and demonstrated its low toxicity in potential environmental applications.

Serum glycine dehydrogenase is associated with increased risk of lung cancer and promotes malignant transformation by regulating DNA methyltransferases expression.

Identification of novel risk factors that are critical to the initiation of lung cancer will be key for its prevention. Recently, it has been reported that glycine dehydrogenase (GLDC) can drive the formation of lung cancer initiating cells. However, there have been no perspective studies on the association between circulating GLDC and lung cancer until now. To identify whether serum GLDC is a risk factor for lung cancer, the present study conducted a nested case­control study within a Chinese cohort. Using ELISAs, serum GLDC was measured in 300 case subjects, who were subsequently diagnosed with lung cancer during follow­up, and in 600 matched healthy controls. The results revealed that serum GLDC was associated with increased lung cancer risk [odds ratio=1.48; 95% confidence intervals (1.01­2.04)]. Spearman correlation was employed to analyze the associations between age, body mass index, years of smoking and the serum concentration of GLDC. It was demonstrated that years of smoking was associated with serum GLDC (spearman's correlation, ρ=0.81) in patients with lung cancer. However, the association was attenuated in the serum of matched controls (ρ=0.48). In addition, overexpression of GLDC protein contributed to malignant transformation and inhibited microRNA (miR)­29 family expression in normal human bronchial epithelial (NHBE) cells. Aberrant methylation of tumor suppressive gene (TSG) is an early event in the development of lung cancer, which is controlled by DNA methyltransferases (DNMTs). The present study demonstrated that GLDC promoted the expression of DNMT proteins; however, the miR­29 family inhibited their expression in NHBE cells. Thus, it was concluded that elevated serum GLDC may increase lung cancer risk, and that smoking, GLDC, the miR­29 family and DNMT signaling pathways may serve an important role in early malignant transformation during the development of lung cancer.

MicroRNA 192 regulates chemo-resistance of lung adenocarcinoma for gemcitabine and cisplatin combined therapy by targeting Bcl-2.

Lung cancer is the most leading cause of cancer-related death worldwide, with non-small-cell lung cancer (NSCLC) accounting for over 80% of all lung cancer cases. Patients with NSCLC are mostly treated with platinum-based chemotherapy. Chemoresistance is a leading cause of chemo-therapy failure in NSCLC treatment. Recent studies have shown that dysregulation of microRNAs might modulate the resistance of cancer cells to anti-cancer drugs, yet the modulation mechanism is not fully understood. In this paper, we try to test whether miR-192 regulates chemo-resistance in human carcinoma A549 mice model by targeting Bcl-2. Mice model of human lung adenocarcinoma was built up, and was used for gemcitabine and cisplatin combined chemotherapy. MTT assay, real-time RT-PCR, western blotting assay were used to investigate miR-192 expression levels, cell viability ratio and Bcl-2 protein expression levels. MiR-192 expression level in A549 cells is significantly higher than in normal human bronchial epithelial cells. MiR-192 inhibitor treated tumor exhibits sensitivity to cisplatin and gemcitabine therapy. Bcl-2 mRNA and protein expression levels up-regulated in miR-192 inhibitor treated tumor. Bcl-2 is a key regulator for miR-192 related chemotherapy resistance. In this study, we demonstrate that miR-192 regulates chemoresistance for gemcitabine and cisplatin combined chemotherapy in human adenocarcinoma lung cancer A549 cells, and Bcl-2 is the target of miR-192.

Influence of two common polymorphisms in the EPHX1 gene on warfarin maintenance dosage: a meta-analysis.

We conducted a meta-analysis to investigate the influence of two common single nucleotide polymorphisms (SNPs) (rs2292566 G>A and rs4653436 A>G) in the EPHX1 gene on warfarin maintenance dosages. Relevant literatures were searched using the PubMed, Embase, Web of Science, Cochrane Library, CISCOM, CINAHL, Google Scholar, CBM, and CNKI databases without any language restrictions. STATA Version 12.0 software (Stata Corporation, College Station, TX, USA) was used for this meta-analysis. Standard mean difference and its corresponding 95% confidence interval (95% CI) were calculated. Seven studies met the inclusion criteria, including 2,063 warfarin-treated patients. Meta-analysis results illustrated that EPHX1 rs2292566 G>A polymorphism might be strongly correlated with a higher maintenance dose of warfarin. However, no interaction of EPHX1 rs4653436 A>G polymorphism with warfarin maintenance dosage was detected. A further subgroup analysis based on stratification by ethnicity indicated that EPHX1 rs2292566 G>A polymorphism was positively correlated with warfarin maintenance dosage among Caucasians, but not Asians. No associations were observed between EPHX1 rs4653436 A>G polymorphism warfarin maintenance dosage among both Caucasians and Asians. Our meta-analysis provides robust and unambiguous evidence that EPHX1 rs2292566 polymorphism may affect the maintenance dose of warfarin in Caucasians.