Combination of Aspergillus niger MJ1 with Pseudomonas stutzeri DSM4166 or mutant Pseudomonas fluorescens CHA0-nif improved crop quality, soil properties, and microbial communities in barrier soil.

Soil salinization and acidification seriously damage soil health and restricts the sustainable development of planting. Excessive application of chemical fertilizer and other reasons will lead to soil acidification and salinization. This study focus on acid and salinized soil, investigated the effect of phosphate-solubilizing bacteria, Aspergillus niger MJ1 combined with nitrogen-fixing bacteria Pseudomonas stutzeri DSM4166 or mutant Pseudomonas fluorescens CHA0-nif on crop quality, soil physicochemical properties, and microbial communities. A total of 5 treatments were set: regular fertilization (T1), regular fertilization with MJ1 and DSM4166 (T2), regular fertilization with MJ1 and CHA0-nif (T3), 30%-reducing fertilization with MJ1 and DSM4166 (T4), and 30%-reducing fertilization with MJ1 and CHA0-nif (T5). It was found that the soil properties (OM, HN, TN, AP, AK, and SS) and crop quality of cucumber (yield production, protein, and vitamin C) and lettuce (yield production, vitamin C, nitrate, soluble protein, and crude fiber) showed a significant response to the inoculated strains. The combination of MJ1 with DSM4166 or CHA0-nif influenced the diversity and richness of bacterial community in the lettuce-grown soil. The organismal system-, cellular process-, and metabolism-correlated bacteria and saprophytic fungi were enriched, which were speculated to mediate the response to inoculated strains. pH, OM, HN, and TN were identified to be the major factors correlated with the soil microbial community. The inoculation of MJ1 with DSM4166 and CHA0-nif could meet the requirement of lettuce and cucumber growth after reducing fertilization in acid and salinized soil, which provides a novel candidate for the eco-friendly technique to meet the carbon-neutral topic.

Exogenous Orexin-A Microinjected Into Central Nucleus of the Amygdala Modulates Feeding and Gastric Motility in Rats.

Orexin-A is a circulating neuropeptide and neurotransmitter that regulates food intake and gastric motility. The central nucleus of the amygdala (CeA), which regulates feeding behavior and gastric function, expresses the orexin-1 receptor. The aim of this study was to evaluate the effects of microinjection of exogenous orexin-A into the CeA, on food intake and gastric motility, and to explore the mechanisms of these effects. Normal chow and high fat food (HFF) intake were measured, gastric motility and gastric emptying were evaluated, extracellular single unit firing was recorded, and c-fos expression was determined. The results showed that microinjection of orexin-A into the CeA resulted in increased HFF intake but did not affect normal chow intake. This effect was blocked by an orexin-1 receptor antagonist-SB-334867 and was partially blocked by a dopamine D1 receptor antagonist-SCH-23390. Gastric motility and gastric emptying were enhanced by orexin-A, and the former effect was abolished by subdiaphragmatic vagotomy. The firing frequency of gastric distention-related neurons was regulated by orexin-A via the orexin-1 receptor. Furthermore, c-fos expression was increased in the ventral tegmental area (VTA) and the nucleus accumbens (NAc), the lateral hypothalamus (LHA), and the dorsal motor nucleus of the vagus (DMV) in response to microinjection of orexin-A into the CeA. These findings showed that orexin-A regulated palatable food intake and gastric motility via the CeA. The LHA, the VTA, and the NAc may participate in palatable food intake and the CeA-DMV-vagus-stomach pathway may be involved in regulating gastric motility through the regulation of neuronal activity in the CeA.

Grandinin down-regulates phosphorylation of epidermal growth factor receptor.

AIMS: Grandinin (C(46)H(34)O(30)) is a compound found in Melaleuca quinquenervia leaves and in oaks. This study is to determine effects of grandinin on malignant lung cells and the related molecular mechanisms. METHODS: Malignant cells were treated with grandinin with various concentrations. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrozolium bromide (MTT) assays and apoptosis assays were performed to determine effects of grandinin on cell viability and apoptosis. Western blotting and real time-PCR were used to determine if grandinin affects levels of phosphorylated EGFR (p-EGFR) and phosphorylated AKT (p-AKT), as well as their mRNA transcript levels. RESULTS: It was found that grandinin treatments reduce viability of malignant lung cells and induces apoptosis. When treated with grandinin (16 µM), the apoptosis of the three lung cancer cell lines MS-1, A549, and LK-2 were increased by 8-9 folds, in comparison with the cells treated with DMSO only (the control condition). Furthermore, grandinin treatments lead to down-regulation of levels of p-EGFR and p-AKT in three malignant lung cell lines. However, grandinin does not affect mRNA levels of EGFR and AKT. CONCLUSIONS: These experimental results indicated grandinin significantly reduce malignant cell viability and effectively induces apoptosis of malignant lung cells by mediating phosphorylation down-regulation of cellular signaling proteins EGFR and AKT. It is suggested that grandinin treatments might be an effective therapeutic strategy of lung malignancies upon further studies in the future.

PU-H71 effectively induces degradation of IκB kinase ß in the presence of TNF-α.

This study is to determine if PU-H71, a heat shock protein inhibitor, induces killing of malignant breast cells together with treatment of tumor necrosis factor-α (TNF-α). The related molecular mechanisms were also studied. A primary mammary epithelial cell line HMEC2595 cells and the highly metastatic breast cell line MDA-MB-231, the HER2-positive BT-474 cells, and the ER-positive MCF7 cells were treated with PU-H71 in the presence or absence of TNF-α. The effects of PU-H71 and TNF-α treatments on cells viabilities and on intracellular signaling pathway proteins were determined using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, apoptosis assays, immunoblot assays, and luciferase assays. It was found that TNF-α enhances the toxic effects of PU-H71 on tumor cells but not normal cells. PU-H71 treatments lead to degradation of IKKß. Moreover, PU-H71 down-regulates the NF-κB transcriptional activity induced by TNF-α treatment. The experimental results indicated PU-H71 effectively induces cell killing of malignant breast cells in the presence of TNF-α, possibly through a mechanism related to degradation of IKKß. It is suggested that combination of PU-H71 and TNF-α treatments might be an effective therapeutic strategy of breast malignancies.

Effects of ghrelin on gastric distention sensitive neurons in the arcuate nucleus of hypothalamus and gastric motility in diabetic rats.

This study was performed to observe the effects of ghrelin on the activity of gastric distention (GD) sensitive neurons in the arcuate nucleus of hypothalamus (Arc) and on gastric motility in vivo in streptozocin (STZ) induced diabetes mellitus (DM) rats. Electrophysiological results showed that ghrelin could excite GD-excitatory (GD-E) neurons and inhibit GD-inhibitory (GD-I) neurons in the Arc. However, fewer GD-E neurons were excited by ghrelin and the excitatory effect of ghrelin on GD-E neurons was much weaker in DM rats. Gastric motility research in vivo showed that microinjection of ghrelin into the Arc could significantly promote gastric motility and it showed a dose-dependent manner. The effect of ghrelin promoting gastric motility in DM rats was weaker than that in normal rats. The effects induced by ghrelin could be blocked by growth hormone secretagogue receptor (GHSR) antagonist [d-Lys-3]-GHRP-6 or BIM28163. RIA and real-time PCR data showed that the levels of ghrelin in the plasma, stomach and ghrelin mRNA in the Arc increased at first but decreased later and the expression of GHSR-1a mRNA in the Arc maintained a low level in DM rats. The present findings indicate that ghrelin could regulate the activity of GD sensitive neurons and gastric motility via ghrelin receptors in the Arc. The reduced effects of promoting gastric motility induced by ghrelin could be connected with the decreased expression of ghrelin receptors in the Arc in diabetes. Our data provide new experimental evidence for the role of ghrelin in gastric motility disorder in diabetes.

Combined effects of 17-DMAG and TNF on cells through a mechanism related to the NF-kappaB pathway.

OBJECTIVE: The tumor necrosis factor (TNF) and the cellular NF-κB pathway protein IKKß play important roles in various cellular processes such as cell proliferation, survival, differentiation, and apoptosis. A heat shock protein 90 inhibitor, 17-DMAG, can induce apoptosis of some tumor cells. This study is to determine the combined effects of 17-DMAG and TNF on malignant cells and the related mechanisms. METHODS: We have determined effects of 17-DMAG, an Hsp90 inhibitor, and TNF treatments on the small cell lung cancer cell line (MS-1), the adenocarcinoma cell line (A549), the squamous-cell carcinoma cell line (LK-2), and the normal human bronchial epithelium cell line (NuLi-1) by using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrozolium bromide assay. To determine if 17-DMAG inhibit the expression of IKKß in the normal human NuLi-1 cells, and the malignant MS-1, A549, and LK-2 cells, immunoblotting assays and luciferase assays were performed. RESULTS: It was found that the combined treatments resulted in synergistic killing of malignant cells, which was confirmed by the apoptosis determination using a fluorescence microscopic assay following staining of the drug-treated cells with Hoescht 33258. The immunoblotting results indicated that the synergistic killing due to 17-DMAG and TNF treatments may be related to the decreases in IKKß levels in the presence of 17-DMAG. CONCLUSIONS: The results suggest that combination of 17-DMAG and TNF treatments might be useful for treating malignancies upon further study in the further. VIRTUAL SLIDES: The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/2041198513886824.

[Effects of astragalus injection on renal function in patients after cardiac valve replacement with cardiopulmonary bypass].

OBJECTIVE: To observe the effects of Astragalus Injection (AI) on renal function in patients after cardiac valve replacement with cardiopulmonary bypass (CPB). METHODS: Forty patients scheduled to receive cardiac valve replacement with CPB were randomly assigned to 2 groups equally, the control group and the AI group. Patients in the AI group were administered with AI 40 mL before anesthesia by diluting it in 250 mL 5% glucose solution via intravenous dripping, 20 mL by adding it into the priming solution before CPB and 40 mL once a day diluted as before via intravenous dripping at the foremost 5 successive days after operation. For patients in the control group, equal volume of Ringer's Liquid was given instead of AI. Peripheral blood sample and urine were collected at various time points: before anesthesia (T0), the 1st (T1), 3rd (T3), 5th (T5) and 7th day (T7) after operation, for determining blood levels of urea nitrogen (BUN), creatinine (Cr) and beta2-microglobulin (beta2-MG), as well as urinary levels of beta2-MG, microalbumin (m-Alb) and N-acetyl-D-glucosaminidase (NAG). RESULTS: As compared with those at T0, in the control group, BUN, Cr at T1 and T3, serum beta2-MG at T3, urinary beta2-MG m-Alb and NAG at T1-T7 were significantly higher, while in the AI group, urinary m-Alb, NAG at T1-5 n and urinary beta2-MG at T1-7 were higher (P < 0.05). As compared with those in the control group, serum BUN at T1-3., Cr and blood beta2-MG at T3, urinary beta2-MG, m-Alb and NAG at T1-7 were lower (P < 0.05) in the AI group. CONCLUSION: CPB could induce renal failure, and applying AI at the perioperative stage can protect renal function to some certain extent.