Monitoring vegetation recovery after China’s May 2008 Wenchuan earthquake using Landsat TM time-series data: a case study in Mao County

The Wenchuan earthquake (Richter scale 8) on 12 May 2008 in southwestern China caused widespread ecosystem damage in the Longmenshan area. It is important to evaluate natural vegetation recovery processes and provide basic information on ecological aspects of the recovering environment after the earthquake. To circumvent the weather limits of remote sensing in the Wenchuan earthquake-hit areas, and to meet the need for regional observation analyses, three Landsat TM images pre- and post-earthquake in Mao County were used for analysis. Post-earthquake normalized difference vegetation index (NDVI) values were compared to pre-earthquake values with an NDVI-based index differencing method to determine the extent to which the vegetation was damaged in relation to the pre-earthquake pattern, and the rate of recovery was evaluated. The spatial characteristics of vegetation loss and natural recovery patterns were analyzed in relation to elevation, slope and aspect. The results indicated that severely damaged sites occurred mainly in river valleys, within a range of 1,500?C2,500?m elevation and on slopes of 25?C55°. The distance from rivers, rather than the distance from active faults, controls the damage patterns. After 1?year of natural regeneration, 36?% of the destroyed areas showed a decrease in NDVI value, 28.8?% showed very little change, 19.1?% showed an increase, and 16.1?% also increased with a recovery rate greater than 100?%. Moreover, there is a good correlation between recovery rate and both slope and elevation, but recovery patterns in the damaged area are complicated. Our results indicate that natural recovery in this arid valley is a slow process.     

LINC00667 promotes Wilms’ tumor metastasis and stemness by sponging miR‐200b/c/429 family to regulate IKK‐β

Wilms' tumor, also known as nephroblastoma, is a kind of pediatric renal cancer. Previous studies have indicated that microRNAs (miRNAs) regulate various cancers progression. However, whether miR‐200 family regulated Wilms' tumor progression remains to be elucidated. In our study, miR‐200b/c/429 expression was downregulated in Wilms' tumor tissue samples from 25 patients. And data from three independent analyses of quantitative real‐time polymerase chain reaction revealed that the expression of miR‐200b/c/429 was downregulated in Wilms' tumor cell lines. Functionally, Cell counting kit‐8 assay revealed that cell viability was reduced by overexpressing miR‐200b/c/429. Transwell assay manifested that cell migration and invasion was hindered by miR‐200b/c/429 overexpression. Sphere‐forming and western blot assays demonstrated that miR‐200b/c/429 overexpression suppressed the sphere formation ability. Mechanically, nuclear factor‐κB (NF‐κB) pathway was confirmed to be associated with Wilms' tumor progression; miR‐200b/c/429 overexpression inactivated NF‐κB pathway as miR‐200b/c/429 was identified to target IκB kinase β (IKK‐β), an NF‐κB pathway‐related gene. Moreover, miR‐200b/c/429 was sponged by LINC00667 in Wilms' tumor cells. LINC00667 competitively bound with miR‐200b/c/429 to regulate IKK‐β expression and then activated NF‐κB pathway in Wilms' tumor. Subsequently, rescue assays illustrated that silencing of IKK‐β could reverse the effect of miR‐200b/c/429 inhibition on the progression of sh‐LINC00667‐transfected Wilms' tumor cells. In summary, LINC00667 promoted Wilms' tumor progression by sponging miR‐200b/c/429 family to regulate IKK‐β.     

Characterization of the quantitative trait locus OilA1 for oil content in Brassica napus

Increasing seed oil content has become one of the most important breeding criteria in rapeseed (Brassica napus). However, oil content is a complex quantitative trait. QTL mapping in a double haploid population (SG population) emerging from a cross between a German (Sollux) and Chinese (Gaoyou) cultivars revealed one QTL for oil content on linkage group A1 (OilA1), which was mapped to a 17 cM genetic interval. To further validate and characterize the OilA1, we constructed a high-resolution map using B. rapa sequence resources and developed a set of near-isogenic lines (NILs) by employing a DH line SG-DH267 as donor and Chinese parent Gaoyou as recurrent background. The results showed highly conserved synteny order between B. rapa and B. napus within the linkage group A1 and revealed a possible centromere region between two markers ZAASA1-38 and NTP3 (2.5 cM). OilA1 was firstly validated by 250 BC₅F₂ plants and was confirmed in a 10.6 cM interval between the markers ZAASA1-47 and ZAASA1-77. Further substitution mapping was conducted by using two generations of QTL-NILs, 283 lines from eight BC₅F_3:4 families and 428 plants from six BC₅F₄ sub-NILs and thus narrowed the OilA1 interval to 6.9 cM and 4.3 cM (1.4 Mb), respectively. Field investigations with two replications using homozygous BC₅F_3:4 sister sub-NILs indicated that NILs, which carry a Sollux chromosome segment across the target region showed significant higher oil content (1.26 %, p < 0.001) than their sister NILs containing Gaoyou chromosome. The OilA1 locus is of particular interest for breeding purpose in China because 80 % of Chinese cultivars do not carry this desirable allele.     

Oxidized Low Density Lipoprotein Induced Caspase-1 Mediated Pyroptotic Cell Death in Macrophages: Implication in Lesion Instability?

Background

Macrophage death in advanced lesion has been confirmed to play an important role in plaque instability. However, the mechanism underlying lesion macrophage death still remains largely unknown.

Methods and Results

Immunohistochemistry showed that caspase-1 activated in advanced lesion and co-located with macrophages and TUNEL positive reaction. In in-vitro experiments showed that ox-LDL induced caspase-1 activation and this activation was required for ox-LDL induced macrophages lysis, IL-1β and IL-18 production as well as DNA fragmentation. Mechanism experiments showed that CD36 and NLRP3/caspase-1/pathway involved in ox-LDL induced macrophage pyroptosis.

Conclusion

Our study here identified a novel cell death, pyroptosis in ox-LDL induced human macrophage, which may be implicated in lesion macrophages death and play an important role in lesion instability.     

Structural effect of a recombinant monoclonal antibody on hinge region peptide bond hydrolysis

IgG hinge region peptide bonds are susceptible to degradation by hydrolysis. To study the effect of Fab and Fc on hinge region peptide bond hydrolysis, a recombinant humanized monoclonal IgG1 antibody, its F(ab')2 fragment, and a model peptide with amino acid sequence corresponding to the hinge region were incubated at 40 degrees C in formulation buffer including complete protease inhibitor and EDTA for 0, 2, 4, 6 and 8 weeks. Two major cleavage sites were identified in the hinge region of the intact recombinant humanized monoclonal antibody and its F(ab')2 fragment, but only one major cleavage site of the model peptide was identified. Hinge region peptide bond hydrolysis of the intact antibody and its F(ab')2 fragment degraded at comparable rates, while the model peptide degraded much faster. It was concluded that Fab region of the IgG, but not Fc portion had significant effect on preventing peptide bond cleavage by direct hydrolysis. Hydrolysis of hinge region peptide bonds was accelerated under both acidic and basic conditions.     

Kinetic differences between the isoforms of glutamate decarboxylase: implications for the regulation of GABA synthesis

Glutamate decarboxylase (GAD) exists as two isoforms, GAD65 and GAD67. GAD activity is regulated by a cycle of activation and inactivation determined by the binding and release of its co-factor, pyridoxal 5'-phosphate. Holoenzyme (GAD with bound co-factor) decarboxylates glutamate to form GABA, but it also catalyzes a slower transamination reaction that produces inactive apoGAD (without bound co-factor). Apoenzyme can reassociate with pyridoxal phosphate to form holoGAD, thus completing the cycle. Within cells, GAD65 is largely apoenzyme (approximately 93%) while GAD67 is mainly holoenzyme (approximately 72%). We found striking kinetic differences between the GAD isoforms that appear to account for this difference in co-factor saturation. The glutamate dependent conversion of holoGAD65 to apoGAD was about 15 times faster than that of holoGAD67 at saturating glutamate. Aspartate and GABA also converted holoGAD65 to apoGAD at higher rates than they did holoGAD67. Nucleoside triphosphates (such as ATP) are known to affect the activation reactions of the cycle. ATP slowed the activation of GAD65 and markedly reduced its steady-state activity, but had little affect on the activation of GAD67 or its steady-state activity. Inorganic phosphate opposed the effect of ATP; it increased the rate of apoGAD65 activation but had little effect on apoGAD67 activation. We conclude that the apo-/holoenzyme cycle of inactivation and reactivation is more important in regulating the activity of GAD65 than of GAD67.