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991.
GATA4 is a dosage-sensitive regulator of cardiac morphogenesis   总被引:15,自引:0,他引:15  
  相似文献   
992.
Based on egg collection records, spontaneous spawning activity of sea bass, Lates calcarifer (Bloch), reared in floating net cages followed a semilunar cycle. The peak of multiple spawnings coincided with declining spring tides of quarter moon periods. Maximum diameter of intra-ovarian, ripe oocytes (0.51–0.55 mm) occurred in synchrony with the quarter moon periods. Smaller oocytes (0.44–0.47 mm) were sampled during the new and full moon periods. Two structural analogues of luteinizing hormone-releasing hormone (LHRHa) (des-Gly10, d -Ala6-LHRH ethylamide and d -Ala6, Pro9-Nethylamide-LHRH), in pelleted or dissolved form, induced mature female sea bass with a mean egg diameter of at least 0.40 mm to spawn at any day during the lunar cycle. The onset of spontaneous and LHRHa-induced spawnings occurred during low tides in the evening until dawn (from 19.00 to 05.00 hours). These results demonstrate that LHRHa can effectively induce mature sea bass to spawn independent of the highly predictable semilunar spawning rhythm. In addition, the occurrence of both spontaneous and hormone-induced spawnings at a precise period of the day suggest a tidal and diurnal cue entraining spawning of mature female sea bass.  相似文献   
993.
Wheat head blight caused mainly by Fusarium graminearum, is an important wheat disease, causing yield and quality losses. The breeding of resistant varieties is the key measure to control this disease, but the conventional breeding method is of low efficiency. The marker-assisted selection (MAS) can significantly improve the breeding efficiency. In this study, four RAPD (randomly amplified polymorphic DNA) markers linked to FHB resistance were obtained and one was cloned and sequenced. F7 recombinant inbred lines (RILs) were derived from the F1 of the cross Ning894037 (resistant)/Alondra (susceptible) by the single-seed descent method. Scab resistance of F7 RILs was evaluated in the greenhouse by injecting conidiospores into a central floret. Scab symptoms were evaluated on the 21st day after inoculation. Disease severity was assessed as the percentage of infected spikelets/spike. The F7 RIL population displayed a normal distribution, transgressive segregation and significant variation for FHB severity. DNA from resistant and susceptible parents was analyzed with 520 RAPD primers. Four markers (S1384-640,S1360-600, S1319-350,S1319-820) linked to FHB resistance were obtained. DNA of S1384-640 was recovered, subjected to re-amplification by using S1384 primer and the same protocol as for RAPD analysis and identified the rightness. The PCR product of S1384-640 was ligated into the pUCm-T vector, and cloned into fresh competent cells of Escherichia coli strain DH5alpha RAPD analysis showed that the inserts of the recombinant plasmids were DNA of S1384-640. The sequencing result showed that the cloned fragment was 648 bp.  相似文献   
994.
995.

Background

Microalbuminuria and subsequent progression to proteinuria and nephropathy is associated with increased oxidative stress, increased inflammatory cytokines and increased cardiovascular (CVD) risk. The common functional IL-6 -174G>C gene variant is also associated with elevated levels of inflammatory cytokines and CVD risk.

Methods

The aim of this study was to examine the association between the IL-6 -174G>C gene variant with plasma total antioxidant status (TAOS) in 552 subjects with type 2 diabetes in relation to urinary protein excretion.

Results

In subjects free from CVD, there was a significant interaction between urinary protein excretion (normoalbuminuria/ microalbuminuria/proteinuria) and the -174C allele (compared to -174GG) in determining plasma TAOS (p value for interaction = 0.03). In the -174C allele carriers there was a significant association between plasma TAOS and urinary protein excretion: normalbuminuria v microalbuminuria v proteinuria: 44.30% ± 11.32 vs. 39.74% ± 14.83 vs. 37.93% ± 16.42, ANOVA p = 0.025. In those with CVD, no interaction or association was observed with the -174C allele (p = 0.246).

Conclusion

The IL-6 -174G>C gene variant is associated with differences in plasma oxidative stress in response to altered protein excretion in subjects with type 2 diabetes.  相似文献   
996.
We previously demonstrated prolonged, profound CD4+ T-lymphopenia in rheumatoid arthritis (RA) patients following lymphocyte-depleting therapy. Poor reconstitution could result either from reduced de novo T-cell production through the thymus or from poor peripheral expansion of residual T-cells. Interleukin-7 (IL-7) is known to stimulate the thymus to produce new T-cells and to allow circulating mature T-cells to expand, thereby playing a critical role in T-cell homeostasis. In the present study we demonstrated reduced levels of circulating IL-7 in a cross-section of RA patients. IL-7 production by bone marrow stromal cell cultures was also compromised in RA. To investigate whether such an IL-7 deficiency could account for the prolonged lymphopenia observed in RA following therapeutic lymphodepletion, we compared RA patients and patients with solid cancers treated with high-dose chemotherapy and autologous progenitor cell rescue. Chemotherapy rendered all patients similarly lymphopenic, but this was sustained in RA patients at 12 months, as compared with the reconstitution that occurred in cancer patients by 3–4 months. Both cohorts produced naïve T-cells containing T-cell receptor excision circles. The main distinguishing feature between the groups was a failure to expand peripheral T-cells in RA, particularly memory cells during the first 3 months after treatment. Most importantly, there was no increase in serum IL-7 levels in RA, as compared with a fourfold rise in non-RA control individuals at the time of lymphopenia. Our data therefore suggest that RA patients are relatively IL-7 deficient and that this deficiency is likely to be an important contributing factor to poor early T-cell reconstitution in RA following therapeutic lymphodepletion. Furthermore, in RA patients with stable, well controlled disease, IL-7 levels were positively correlated with the T-cell receptor excision circle content of CD4+ T-cells, demonstrating a direct effect of IL-7 on thymic activity in this cohort.  相似文献   
997.
998.

Purpose

China is the world’s largest producer and consumer of refined and reclaimed copper because of the rapid economic and industrial development of this country. However, only a few studies have analyzed the environmental impact of China’s copper industry. The current study analyzes the life cycle environmental impact of copper production in China.

Methods

A life cycle impact assessment using the ReCiPe method was conducted to estimate the environmental impact of refined and reclaimed copper production in China. Uncertainty analysis was also performed based on the Monte-Carlo simulation.

Results and discussion

The environmental impact of refined copper was higher than that of reclaimed copper in almost all categories except for human toxicity because of the direct atmospheric arsenic emission during the copper recycling stage. The overall environmental impact for the refined copper production was mainly attributed to metal depletion, freshwater ecotoxicity, marine ecotoxicity, and water depletion potential impact. By contrast, that for the reclaimed copper production was mainly caused by human toxicity impact.

Conclusions

Results show that the reclaimed copper scenario had approximately 59 to 99% more environmental benefits than those of the refined copper scenario in most key categories except for human toxicity, in which a similar environmental burden was observed between both scenarios. The key factors that reduce the overall environmental impact for China’s copper industry include decreasing direct heavy metal emissions in air and water, increasing the national recycling rate of copper, improving electricity consumption efficiency, replacing coal with clean energy sources for electricity production, and optimizing the efficiency of copper ore mining and consumption.
  相似文献   
999.

Background

Planar cell polarity (PCP) is a phenomenon in which epithelial cells are polarized along the plane of a tissue. PCP is critical for a variety of developmental processes and is regulated by a set of evolutionarily conserved PCP signaling proteins. Many of the PCP proteins adopt characteristic asymmetric localizations on the opposing cellular boundaries. Currently, the molecular mechanisms that establish and maintain this PCP asymmetry remain largely unclear. Newly synthesized integral PCP proteins are transported along the secretory transport pathway to the plasma membranes. Once delivered to the plasma membranes, PCP proteins undergo endocytosis. Recent studies reveal insights into the intracellular trafficking of PCP proteins, suggesting that intracellular trafficking of PCP proteins contributes to establishing the PCP asymmetry.

Objective

To understand the intracellular trafficking of planar cell polarity proteins in the secretory transport pathway and endocytic transport pathway.

Methods

This review summarizes our current understanding of the intracellular trafficking of PCP proteins. We highlights the molecular mechanisms that regulate sorting of PCP proteins into transport vesicles and how the intracellular trafficking process regulates the asymmetric localizations of PCP proteins.

Results

Current studies reveal novel insights into the molecular mechanisms mediating intracellular trafficking of PCP proteins. This process is critical for delivering newly synthesized PCP proteins to their specific destinations, removing the unstable or mislocalized PCP proteins from the plasma membranes and preserving tissue polarity during proliferation of mammalian skin cells.

Conclusion

Understanding how PCP proteins are delivered in the secretory and endocytic transport pathway will provide mechanistic insights into how the asymmetric localizations of PCP proteins are established and maintained.
  相似文献   
1000.
Under current global warming, high‐elevation regions are expected to experience faster warming than low‐elevation regions. However, due to the lack of studies based on long‐term large‐scale data, the relationship between tree spring phenology and the elevation‐dependent warming is unclear. Using 652k records of leaf unfolding of five temperate tree species monitored during 1951–2013 in situ in Europe, we discovered a nonlinear trend in the altitudinal sensitivity (SA, shifted days per 100 m in altitude) in spring phenology. A delayed leaf unfolding (2.7 ± 0.6 days per decade) was observed at high elevations possibly due to decreased spring forcing between 1951 and 1980. The delayed leaf unfolding at high‐elevation regions was companied by a simultaneous advancing of leaf unfolding at low elevations. These divergent trends contributed to a significant increase in the SA (0.36 ± 0.07 days 100/m per decade) during 1951–1980. Since 1980, the SA started to decline with a rate of ?0.32 ± 0.07 days 100/m per decade, possibly due to reduced chilling at low elevations and improved efficiency of spring forcing in advancing the leaf unfolding at high elevations, the latter being caused by increased chilling. Our results suggest that due to both different temperature changes at the different altitudes, and the different tree responses to these changes, the tree phenology has shifted at different rates leading to a more uniform phenology at different altitudes during recent decades.  相似文献   
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