Coastal wetlands such as saltmarshes are valued as prominent buffering ecosystems to global climate change and sea level rise (SLR), yet their long‐term persistence may also be threatened by these global change stressors. While saltmarshes are increasingly thought to be resilient to SLR owing to high vertical marsh adaptability, their long‐term stability remains uncertain due to our poor understanding of marsh resilience at the marsh‐tidal flat interface, where wave disturbance can progressively shift vegetated marsh toward a bare tidal flat state. Here, we explore how SLR affects vegetation recoverability on tidal flats using cordgrass, a globally common saltmarsh foundation species, as a model plant. Combined field and model results demonstrate that small increases in wave forcing due to raised water depth over tidal flats can dramatically weaken or even block vegetation recovery from eroding marsh edges, through hampering seed persistence. Vegetation recovery on tidal flats next to the marsh edge thus represents an unrecognized Achilles' heel of marsh resilience to SLR, which if ignored may cause underestimation of marsh vulnerability. These findings are highly relevant for a more comprehensive assessment of marsh susceptibility to SLR in systems where seeds play an essential role in revegetation of tidal flats, and highlight the importance of maintaining either a wave‐protected or well‐elevated tidal flat near the marsh edge that allows for quick vegetation recovery for supporting resilient marshes.
BackgroundMatrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS) has been rapidly developed and widely used as an analytical technique in clinical laboratories with high accuracy in microorganism identification.ObjectiveTo validate the efficacy of MALDI-TOF MS in identification of clinical pathogenic anaerobes.MethodsTwenty-eight studies covering 6685 strains of anaerobic bacteria were included in this meta-analysis. Fixed-effects models based on the P-value and the I-squared were used for meta-analysis to consider the possibility of heterogeneity between studies. Statistical analyses were performed by using STATA 12.0.ResultsThe identification accuracy of MALDI-TOF MS was 84% for species (I2 = 98.0%, P < 0.1), and 92% for genus (I2 = 96.6%, P < 0.1). Thereinto, the identification accuracy of Bacteroides was the highest at 96% with a 95% CI of 95–97%, followed by Lactobacillus spp., Parabacteroides spp., Clostridium spp., Propionibacterium spp., Prevotella spp., Veillonella spp. and Peptostreptococcus spp., and their correct identification rates were all above 90%, while the accuracy of rare anaerobic bacteria was relatively low. Meanwhile, the overall capabilities of two MALDI-TOF MS systems were different. The identification accuracy rate was 90% for VITEK MS vs. 86% for MALDI biotyper system.ConclusionsOur research showed that MALDI-TOF-MS was satisfactory in genus identification of clinical pathogenic anaerobic bacteria. However, this method still suffers from different drawbacks in precise identification of rare anaerobe and species levels of common anaerobic bacteria.
The purpose of this study was to investigate the pathophysiologic change of ghrelin in gastric and colorectal cancer patients, especially in those with cachexia. Fifty-eight gastric cancer patients, 20 colorectal cancer patients, and 24 healthy control individuals were included in this study. Thirty-one patients were defined as cachectic, based on the percentage of weight loss versus the previous normal weight. The remaining 47 patients were defined as noncachectic. Peripheral hormones, including ghrelin, insulin, leptin, growth hormone, glucagon, and cortisol, and body composition parameters were measured. Plasma ghrelin levels did not increase significantly in cachectic gastric (p = 0.352) or colorectal (p = 0.871) cancer patients as compared with controls and were not correlated with nutrition status and other hormones. The location of gastric cancer (proximal vs. distal) had no influence on ghrelin levels (p = 0.966). These findings suggest that gastric and colorectal cancers may have their special effects on the production of ghrelin. Gastric or colorectal cancer cachexia may be partly due to the lack of increase in ghrelin, which makes exogenous ghrelin therapy feasible in this setting.
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