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Knowledge of tree biomass allocation is fundamental for estimating forest acclimation and carbon stock for global changes in the future. Optimal partitioning theory (OPT) and allometric partitioning theory (APT) are two major patterns of biomass allocation, and occurrences have been tested on taxonomical, ontogenetic, geographic and environmental scales, showing conflicting results and unclear ecophysiological mechanisms. Here, we examine the biomass allocation patterns of two young poplar (Populus) clones varying greatly in drought resistance under different soil water and nitrogen availabilities and the major physiological processes involved in biomass partitioning. We found that Biyu, a drought-sensitive hybrid poplar clone, had significant relations among biomass of leaf, stem and root, showing allometric partitioning. Xiaoye, a drought-tolerant poplar clone native to semi-arid areas, on the contrary, showed tightly regulated biomass allocation following optimal partitioning theory. Biyu had higher nitrate reductase activity in the fine roots, while Xiaoye had higher nitrate reductase activity in the leaves. Biochemical analyses and measurements of fluorescence and gas exchange showed that Xiaoye maintained more stable chloroplast membranes and photosystem electron flow, showing higher water use efficiency and a higher resistance to drought. A nitrogen addition could improve leaf photosynthesis and growth both in Biyu and Xiaoye seedlings under drought conditions. We concluded that the two poplar clones showed different biomass allocation patterns and suggest that the site of nitrate assimilation may play a role in biomass partitioning under varying water and nitrogen availabilities. [ABSTRACT FROM AUTHOR]

Turmeric is widely used worldwide, and there are many examples of its use in treating hepatobiliary diseases. The gut–liver axis is a bidirectional relationship between gut microorganisms and the liver that is closely related to the pathogenesis of hepatobiliary diseases. This review systematically summarizes the components of turmeric. It links the studies on turmeric affecting gut microorganisms to its effects on liver and biliary diseases to explain the potential mechanism of turmeric's regulation of the gut–liver axis. Besides, ethnopharmacology, phytochemicals, and clinical adverse events associated with turmeric have been researched. Furthermore, turmeric is a safe agent with good clinical efficacy and without apparent toxicity at a certain amount. By summarizing the influence of turmeric on the liver by regulating the gut–liver axis, especially the gut microbiota, it provides a preclinical basis for using turmeric as a safe and effective therapeutic agent for the prevention and treatment of hepatobiliary diseases based on the gut–liver axis. However, more efforts should be made to exploit its clinical application further. [ABSTRACT FROM AUTHOR]

Background/Aims: Ketamine has been reported to exert anti-inflammatory effects on astrocytes stimulated by lipopolysaccharide (LPS) in vitro and in vivo. However, the mechanism has not been elicited clearly. The aim of this study was to investigate the effects of ketamine on TLR4 expression and NF-κB-p65 phosphorylation, as well as the production of proinflammatory cytokines in LPS challenged astrocytes. Methods: Astrocytes were stimulated with LPS (1μg/ ml) in the absence and presence of various concentrations of ketamine (10, 100, 1000μM). The concentrations of IL-1β, IL-6 and TNF-α were measured by ELISA, the expression of glial fibrillary acidic protein (GFAP) in astrocytes was detected by immunofluorescence staining, the level of phosphorylated NF-κB p65 and the expression of TLR4 were detected by western blotting. Results: LPS increased TLR4 expression and the phosphorylation of NF-κB p65 subunit as well as GFAP expression and the production of IL-1β, IL-6 and TNF-α in cultured astrocytes. Ketamine (100 and 1000 μM) reduced the expression of GFAP and the production of these proinflammatory cytokines, inhibited the expression of TLR4 and attenuated the phosphorylation of NF-κB p65 in astrocytes challenged by LPS. Conclusion: The inhibitory effects of ketamine on LPS-induced astrocytes activation and inflammation response may be mediated by suppressing NF-κB activation through reducing the expression of TLR4. Copyright © 2012 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Aim: Fluoroquinolones (FQs) are the cornerstone in treating drug-resistant tuberculosis (TB); the prevalence of TB among the population is diverse in different regions, understanding the relationship between resistance pattern and molecular characteristic of FQs in preextensive drug-resistant (pre-XDR) clinical isolates is limited in China. Methods: A total of 141 pre-XDR clinical isolates from different individuals stored at the National Clinical Centre were collected from the Beijing Chest Hospital, minimal inhibitory concentrations of levofloxacin (Lfx) and moxifloxacin (Mfx) as well as sequences of quinolone-resistant determining regions in gyrA and gyrB genes were examined. Results: One hundred twelve pre-XDR clinical isolates were resistant to both Lfx and Mfx, molecular analyses showed that 87.50%, 0.89%, and 6.25% of the pre-XDR clinical isolates harbored FQ resistance mutations in gyrA, gyrB, and in both. We found five amino acid mutation positions in gyrA and four in gyrB, The mutation position in gyrA included codons 94, 91, 90, 88, and 74, and in gyrB included codons 504, 500, 512, and 501. Codon 94 of gyrA was the most prevalent mutation (83.04%), containing the Asp amino acid substitution with Gly (50.89%), Asn (15.17%), Ala (8.93%), Tyr (6.25%), and His (1.79%). Conclusions: The mutations of gyrA were most common and the frequency of Asp94Gly was the highest in pre-XDR clinical isolates in Beijing, China. The mutations at codon 94 significantly contributed to the resistance to both Lfx and Mfx in pre-XDR clinical isolates and may cause a high resistance level. [ABSTRACT FROM AUTHOR]

Esophageal cancer-related gene 4 (ECRG4) is a tumor suppressor gene associated with the prognosis of esophageal squamous-cell carcinoma (ESCC). Studies have reported that ECRG4 effectively inhibits the proliferation, migration and invasion of ESCC cells. In the current study, ectopic expression of ECRG4 significantly induced ESCC cell apoptosis. To further understand the molecular profile of ECRG4 overexpression in ESCC cells, tandem mass tag (TMT) labeling followed by LC-MS/MS analysis was applied on samples from ECRG4 overexpressed cells and control cells. Among the identified differentially expressed proteins, four up-regulated proteins (PLK1, CDK4, PLOD1 and PLOD2) associated with cell apoptosis, cell cycle and metastasis were chosen for the further investigation. The effects of ECRG4 protein levels on the expression of these four proteins were validated by manipulating the expression of ECRG4 in ESCC cells followed by Western blotting analysis. The immunohistochemical staining results showed a significant decrease in ECRG4 levels and a notable increase in the four proteins in ESCC samples as compared to matched esophageal tissues (n=75). More importantly, the protein levels of ECRG4 had a negative association with those of PLK1, CDK4, PLOD1 and PLOD2. Thus, our data suggested that the tumor-repressor functions of ECRG4 may be associated with PLK1, CDK4, PLOD1 and PLOD2, providing important insights into the molecular mechanisms of esophageal carcinogenesis., Competing Interests: None.

Objective: To evaluate the prognosis and predictive values of preoperative Glasgow prognostic score (GPS) for adenocarcinoma of esophagogastric junction(AEG) patients., Methods: A retrospective study of 322 AEG patients who received operation between January 2007 and March 2010 in Henan Provincial People's Hospital was performed. Clinical data, pathological characteristics, laboratory parameters and survival data were collected. The GPS was calculated based on C-reactive protein(CRP) and serum albumin(ALB) levels. Univariate and multivariate analysis were used to evaluate the prognostic value of GPS., Results: Among 322 patients, 0, 1, 2 of GPS were 192, 104 and 26 patients respectively. The median follow-up was 37 (4-73) months. In Kaplan-Meier analysis, median diseases-free survival (DFS) of GPS 0, 1, 2 was 47.0 (95% CI: 31.6-62.4), 15.0 (95% CI: 11.8-8.2) and 4.7 (95% CI: 3.8-5.6) months (P<0.01), and median overall survival (OS) was out of reach, 20.6 (95% CI: 15.8-25.4) and 7.0 (95% CI: 5.8-8.2) months (P<0.01). Univariate and multivariate analysis revealed that GPS was an independent predictor of DFS (P<0.01) and OS (P<0.01) of AEG., Conclusion: GPS is an effective predictor of survival in AEG.

Background/aims: Ketamine has been reported to exert anti-inflammatory effects on astrocytes stimulated by lipopolysaccharide (LPS) in vitro and in vivo. However, the mechanism has not been elicited clearly. The aim of this study was to investigate the effects of ketamine on TLR4 expression and NF-ĸB-p65 phosphorylation, as well as the production of proinflammatory cytokines in LPS challenged astrocytes., Methods: Astrocytes were stimulated with LPS (1µg/ ml) in the absence and presence of various concentrations of ketamine (10, 100, 1000µM). The concentrations of IL-1β, IL-6 and TNF-α were measured by ELISA, the expression of glial fibrillary acidic protein (GFAP) in astrocytes was detected by immunofluorescence staining, the level of phosphorylated NF-ĸB p65 and the expression of TLR4 were detected by western blotting., Results: LPS increased TLR4 expression and the phosphorylation of NF-ĸB p65 subunit as well as GFAP expression and the production of IL-1β, IL-6 and TNF-α in cultured astrocytes. Ketamine (100 and 1000 µM) reduced the expression of GFAP and the production of these proinflammatory cytokines, inhibited the expression of TLR4 and attenuated the phosphorylation of NF-ĸB p65 in astrocytes challenged by LPS., Conclusion: The inhibitory effects of ketamine on LPS-induced astrocytes activation and inflammation response may be mediated by suppressing NF-ĸB activation through reducing the expression of TLR4., (Copyright © 2012 S. Karger AG, Basel.)