Uterine Rbpj is required for embryonic-uterine orientation and decidual remodeling via Notch pathway-independent and -dependent mechanisms

Coordinated uterine-embryonic axis formation and decidual remodeling are hallmarks of mammalian post-implantation embryo development. Embryonic-uterine orientation is determined at initial implantation and synchronized with decidual development. However, the molecular mechanisms controlling these events remain elusive despite its discovery a long time ago. In the present study, we found that uterine-specific deletion of Rbpj, the nuclear transducer of Notch signaling, resulted in abnormal embryonic-uterine orientation and decidual patterning at post-implantation stages, leading to substantial embryo loss. We further revealed that prior to embryo attachment, Rbpj confers on-time uterine lumen shape transformation via physically interacting with uterine estrogen receptor (ERα) in a Notch pathway-independent manner, which is essential for the initial establishment of embryo orientation in alignment with uterine axis. While at post-implantation stages, Rbpj directly regulates the expression of uterine matrix metalloproteinase in a Notch pathway-dependent manner, which is required for normal post-implantation decidual remodeling. These results demonstrate that uterine Rbpj is essential for normal embryo development via instructing the initial embryonic-uterine orientation and ensuring normal decidual patterning in a stage-specific manner. Our data also substantiate the concept that normal mammalian embryonic-uterine orientation requires proper guidance from developmentally controlled uterine signaling.     

医院感染多重耐药革兰阴性杆菌耐消毒剂基因的检测分析

目的研究医院感染多重耐药革兰阴性杆菌耐消毒剂基因qac E△1-sul1存在情况。方法采用聚合酶链反应(PCR)技术检测qac E△1-sul1基因。结果 201株多重耐药革兰阴性杆菌对阿莫西林和头孢类等抗菌药物多数耐药率均达到50%以上,但对碳青霉烯类仍高度敏感。qac E△1-sul1基因的总检出率为40.80%,其中产超广谱β-内酰胺酶(ESBLs)大肠埃希菌、产ESBLs肺炎克雷伯菌、多重耐药鲍曼不动杆菌、多重耐药的铜绿假单胞菌qac E△1-sul1检出率分别为34.78%、44.23%、58.91%和31.25%。结论医院感染患者临床分离多重耐药革兰阴性杆菌耐消毒剂基因qac E△1-sul1携带率较高,加强多重耐药革兰阴性杆菌对消毒剂耐药性的监测,对临床合理使用消毒剂具有重要意义。     

HYPERSENSITIVE TO HIGH LIGHT1 Interacts with LOW QUANTUM YIELD OF PHOTOSYSTEM II1 and Functions in Protection of Photosystem II from Photodamage in Arabidopsis

Under high-irradiance conditions, plants must efficiently protect photosystem II (PSII) from damage. In this study, we demonstrate that the chloroplast protein HYPERSENSITIVE TO HIGH LIGHT1 (HHL1) is expressed in response to high light and functions in protecting PSII against photodamage. Arabidopsis thaliana hhl1 mutants show hypersensitivity to high light, drastically decreased PSII photosynthetic activity, higher nonphotochemical quenching activity, a faster xanthophyll cycle, and increased accumulation of reactive oxygen species following high-light exposure. Moreover, HHL1 deficiency accelerated the degradation of PSII core subunits under high light, decreasing the accumulation of PSII core subunits and PSII–light-harvesting complex II supercomplex. HHL1 primarily localizes in the stroma-exposed thylakoid membranes and associates with the PSII core monomer complex through direct interaction with PSII core proteins CP43 and CP47. Interestingly, HHL1 also directly interacts, in vivo and in vitro, with LOW QUANTUM YIELD OF PHOTOSYSTEM II1 (LQY1), which functions in the repair and reassembly of PSII. Furthermore, the hhl1 lqy1 double mutants show increased photosensitivity compared with single mutants. Taken together, these results suggest that HHL1 forms a complex with LQY1 and participates in photodamage repair of PSII under high light.     

Superresolution imaging reveals structural features of EB1 in microtubule plus-end tracking

Visualization of specific molecules and their interactions in real time and space is essential to delineate how cellular dynamics and the signaling circuit are orchestrated. Spatial regulation of conformational dynamics and structural plasticity of protein interactions is required to rewire signaling circuitry in response to extracellular cues. We introduce a method for optically imaging intracellular protein interactions at nanometer spatial resolution in live cells, using photoactivatable complementary fluorescent (PACF) proteins. Subsets of complementary fluorescent protein molecules were activated, localized, and then bleached; this was followed by the assembly of superresolution images from aggregate position of sum interactive molecules. Using PACF, we obtained precise localization of dynamic microtubule plus-end hub protein EB1 dimers and their distinct distributions at the leading edges and in the cell bodies of migrating cells. We further delineated the structure–function relationship of EB1 by generating EB1-PACF dimers (EB1^wt:EB1^wt, EB1^wt:EB1^mt, and EB1^mt:EB1^mt) and imaging their precise localizations in culture cells. Surprisingly, our analyses revealed critical role of a previously uncharacterized EB1 linker region in tracking microtubule plus ends in live cells. Thus PACF provides a unique approach to delineating spatial dynamics of homo- or heterodimerized proteins at the nanometer scale and establishes a platform to report the precise regulation of protein interactions in space and time in live cells.     

Evaluation of Angiogenesis in Non-small Cell Lung Carcinoma by CD34 Immunohistochemistry

The objective of the study was to investigate angiogenesis in non-small lung cancer by measuring the expression of CD34. Immunohistochemistry was used to detect CD34 at the endothelial cell surface in 81 surgically resected non-small cell lung cancer specimens. CD34 immunohistochemistry had high specificity and sensitivity with minimal background, which enabled efficient identification of CD34-positive staining. Statistical analysis showed that increased microvessel density (MVD) was closely correlated to tumor progression as reflected by the clinical stage (P < 0.05). However, MVD was not significantly associated with lymph node metastasis and other clinical and pathological features (P > 0.05). In conclusion, microvascular density may play an important role in the development and progression of lung cancer.     

Post‐heading heat stress and yield impact in winter wheat of China

Wheat is sensitive to high temperatures, but the spatial and temporal variability of high temperature and its impact on yield are often not known. An analysis of historical climate and yield data was undertaken to characterize the spatial and temporal variability of heat stress between heading and maturity and its impact on wheat grain yield in China. Several heat stress indices were developed to quantify heat intensity, frequency, and duration between heading and maturity based on measured maximum temperature records of the last 50 years from 166 stations in the main wheat‐growing region of China. Surprisingly, heat stress between heading and maturity was more severe in the generally cooler northern wheat‐growing regions than the generally warmer southern regions of China, because of the delayed time of heading with low temperatures during the earlier growing season and the exposure of the post‐heading phase into the warmer part of the year. Heat stress between heading and maturity has increased in the last decades in most of the main winter wheat production areas of China, but the rate was higher in the south than in the north. The correlation between measured grain yields and post‐heading heat stress and average temperature were statistically significant in the entire wheat‐producing region, and explained about 29% of the observed spatial and temporal yield variability. A heat stress index considering the duration and intensity of heat between heading and maturity was required to describe the correlation of heat stress and yield variability. Because heat stress is a major cause of yield loss and the number of heat events is projected to increase in the future, quantifying the future impact of heat stress on wheat production and developing appropriate adaptation and mitigation strategies are critical for developing food security policies in China and elsewhere.     

Outer Membrane Protein OmpW Is the Receptor for Typing Phage VP5 in the Vibrio cholerae O1 El Tor Biotype

Phage typing is used for the subtyping of clones of epidemic bacteria. In this study, we identified the outer membrane protein OmpW as the receptor for phage VP5, one of the typing phages for the Vibrio cholerae O1 El Tor biotype. A characteristic 11-bp deletion in ompW was observed in all epidemic strains resistant to VP5, suggesting that this mutation event can be used as a tracing marker in cholera surveillance.