Beschreibung: The Alfred Wegener Institute Climate Model (AWI‐CM) participates for the first time in the Coupled Model Intercomparison Project (CMIP), CMIP6. The sea ice‐ocean component, FESOM, runs on an unstructured mesh with horizontal resolutions ranging from 8 to 80 km. FESOM is coupled to the Max Planck Institute atmospheric model ECHAM 6.3 at a horizontal resolution of about 100 km. Using objective performance indices, it is shown that AWI‐CM performs better than the average of CMIP5 models. AWI‐CM shows an equilibrium climate sensitivity of 3.2°C, which is similar to the CMIP5 average, and a transient climate response of 2.1°C which is slightly higher than the CMIP5 average. The negative trend of Arctic sea‐ice extent in September over the past 30 years is 20–30% weaker in our simulations compared to observations. With the strongest emission scenario, the AMOC decreases by 25% until the end of the century which is less than the CMIP5 average of 40%. Patterns and even magnitude of simulated temperature and precipitation changes at the end of this century compared to present‐day climate under the strong emission scenario SSP585 are similar to the multi‐model CMIP5 mean. The simulations show a 11°C warming north of the Barents Sea and around 2°C to 3°C over most parts of the ocean as well as a wetting of the Arctic, subpolar, tropical, and Southern Ocean. Furthermore, in the northern middle latitudes in boreal summer and autumn as well as in the southern middle latitudes, a more zonal atmospheric flow is projected throughout the year.

Beschreibung: An abundance of evidence indicates that the tropics are expanding. Despite many attempts to decipher the cause, the underlying dynamical mechanism driving tropical expansion is still not entirely clear. Here, based on observations, multimodel simulations from the Coupled Model Intercomparison Project phase 5 (CMIP5) and purposefully designed numerical experiments, the variations and trends of the tropical width are explored from a regional perspective. We find that the width of the tropics closely follows the displacement of oceanic midlatitude meridional temperature gradients (MMTG). Under global warming, as a first‐order response, the subtropical ocean experiences more surface warming because of the mean Ekman convergence of anomalously warm water. The enhanced subtropical warming, which is partially independent of natural climate oscillations, such as the Pacific Decadal Oscillation, leads to poleward advance of the MMTG and drives the tropical expansion. Our results, supported by both observations and model simulations, imply that global warming may have already significantly contributed to the ongoing tropical expansion, especially over the ocean‐dominant Southern Hemisphere.

Beschreibung: Multimodel Arctic Ocean “climate response function” experiments are analyzed in order to explore the effects of anomalous wind forcing over the Greenland Sea (GS) on poleward ocean heat transport, Atlantic Water (AW) pathways, and the extent of Arctic sea ice. Particular emphasis is placed on the sensitivity of the AW circulation to anomalously strong or weak GS winds in relation to natural variability, the latter manifested as part of the North Atlantic Oscillation. We find that anomalously strong (weak) GS wind forcing, comparable in strength to a strong positive (negative) North Atlantic Oscillation index, results in an intensification (weakening) of the poleward AW flow, extending from south of the North Atlantic Subpolar Gyre, through the Nordic Seas, and all the way into the Canadian Basin. Reconstructions made utilizing the calculated climate response functions explain ∼50% of the simulated AW flow variance; this is the proportion of variability that can be explained by GS wind forcing. In the Barents and Kara Seas, there is a clear relationship between the wind‐driven anomalous AW inflow and the sea ice extent. Most of the anomalous AW heat is lost to the atmosphere, and loss of sea ice in the Barents Sea results in even more heat loss to the atmosphere, and thus effective ocean cooling. Release of passive tracers in a subset of the suite of models reveals differences in circulation patterns and shows that the flow of AW in the Arctic Ocean is highly dependent on the wind stress in the Nordic Seas.

Beschreibung: Background: High-risk human papillomavirus type 16 (HPV16) is a risk factor for cervical cancer. Previous studies suggest that polymorphisms in the E6 gene or the long control region(LCR)of HPV16 may alter the oncogenic potential of the virus. The aims of this study were to investigate the genetic variations of HPV16 E6 gene and LCR in isolates from Chinese population and correlation of the E6 and LCR polymorphisms with disease status of infected patients. Methods: HPV16 positive endocervical specimens were collected from 304 women living in Northeast of China. Sequences of E6 gene and LCR were analyzed by PCR-sequencing. Results: Two lineages were found in the populations, including EUR lineage and As lineage. Based on the HPV16 prototype, the most frequent variation in the E6 gene was T178A/G (48.7%), followed by mutations of G94A (12.2%) and T350G (9.9%). The rank orders of incidence of E6 variations in amino acid were as follows: D25E (46.3%), L83V (9.9%) and H78Y (4.3%). Nucleotide variations in LCR were found in all the 304 isolates from HPV16 positive cervical samples. The most commonly observed LCR variations were the transition replacement G7193T, 7434CIns, G7521A and 7863ADel (100%). The As lineage was associated with HPV persistent infections and with disease status of 〉=CIN2,3. The EUR lineage variants showed a negative trend of association with the severity of 〉=CIN2,3. Among 41 variations found in LCR, 25 (61.0%) were located at the binding sites for transcription factors. Occurrence of 〉=CIN2,3 was significantly associated with the mutations of R10G/L83V in E6 and the C7294T co-variation in LCR, after adjusting for ages of infected patients. Conclusions: Associations between As lineage and HPV persistent infections, and with disease status of 〉=CIN2,3, and an association between the EUR lineage and negative trend of association with the severity of 〉=CIN2,3 were found in this study. An association between a co-variation of R10G/L83V in E6 and C7294T in LCR and an increased risk for developing CIN-2,3 was found in a HPV16 infected population of Chinese women. These findings indicate that HPV16 polymorphism influences development of CIN-2,3.

Beschreibung: Drought stress is one of the most adverse environmental constraints to plant growth and productivity. Comparative proteomics of drought-tolerant and sensitive wheat genotypes is a strategy to understand the co...

Beschreibung: Background: Batch effect is one type of variability that is not of primary interest but ubiquitous in sizable genomic experiments. To minimize the impact of batch effects, an ideal experiment design should ensure the even distribution of biological groups and confounding factors across batches. However, due to the practical complications, the availability of the final collection of samples in genomics study might be unbalanced and incomplete, which, without appropriate attention in sample-to-batch allocation, could lead to drastic batch effects. Therefore, it is necessary to develop effective and handy tool to assign collected samples across batches in an appropriate way in order to minimize batch effects. Results: We describe OSAT (Optimal Sample Assignment Tool), a bioconductor package designed for automated sample-to-batch allocations in genomics experiments. Conclusions: OSAT is developed to facilitate the allocation of collected samples to different batches in genomics study. Through optimizing the even distribution of samples in groups of biological interest into different batches, it can reduce the confounding or correlation between batches and the biological variables of interest. It can also optimize the homogeneous distribution of confounding factors across batches. It can handle challenging instances where incomplete and unbalanced sample collections are involved as well as ideally balanced designs.

Beschreibung: Background: Gankyrin was originally purified and characterized as the p28 component of the 26S proteasome, and later identified as an oncogenic protein in hepatocellular carcinomas (HCC). It has recently been found to be highly expressed in several other malignancies, and compelling evidence show gankyrin plays important roles in tumorigenesis. However, its mechanism of action remains unclear. Methods: In order to further clarify the functions of gankyrin and better understand its molecular mechanisms, we generated a gankyrin null cell line, HCT116 gankyrin[MINUS SIGN]/[MINUS SIGN] , by targeted homologous recombination in human colon cancer cells, and then employed two-dimensional electrophoresis (2-DE) based proteomic approaches followed by MS identification to investigate alterations in the proteome due to the gankyrin knockout. Western blot and qRT-PCR assays were also used to examine the protein and mRNA levels of some identified proteins. Results: Compared with wild-type control cells, gankyrin null cells were impaired in terms of their proliferation, migration and anchorage-independent growth. A total of 21 altered proteins were identified, which included 18 proteins that had not previously been reported to be related to gankyrin. Notably, eight metastasis-related proteins were identified. Western blot analyses confirmed that the changes in three examined proteins were consistent with 2-DE gel analysis. Conclusions: In summary, we have generated a useful cell tool to clarify the functions of gankyrin. Our proteomic data provide novel information to better understand the roles and underlying mechanisms by which gankyrin is involved in tumorigenesis and cancer metastasis.

Beschreibung: Background: RNA binding proteins (RBPs) play a fundamental role in posttranscriptional control of gene expression. Different RBPs have oncogenic or tumor-suppressive functions on human cancers. RNPC1 belongs to the RNA recognition motif (RRM) family of RBPs, which could regulate expression of diverse targets by mRNA stability in human cancer cells. Several studies reported that RNPC1 played an important role in cancer, mostly acting as an oncogene or up-regulating in tumors. However, its role in human breast cancer remains unclear. Methods: In the present study, we investigated the functional and mechanistic roles of RNPC1 in attenuating invasive signal including reverse epithelial-mesenchymal transition (EMT) to inhibit breast cancer cells aggressiveness in vitro. Moreover, RNPC1 suppress tumorigenicity in vivo. Further, we studied the expression of RNPC1 in breast cancer tissue and adjacent normal breast tissue by quantitative RT-PCR (qRT-PCR) and Western blot. Results: We observed that RNPC1 expression was silenced in breast cancer cell lines compared to breast epithelial cells. More important, RNPC1 was frequently silenced in breast cancer tissue compared to adjacent normal breast tissue. Low RNPC1 mRNA expression was associated with higher clinical stages and mutp53, while low level of RNPC1 protein was associated with higher lymph node metastasis, mutp53 and lower progesterone receptor (PR). Functional assays showed ectopic expression of RNPC1 could inhibit breast tumor cell proliferation in vivo and in vitro through inducing cell cycle arrest, and further suppress tumor cell migration and invasion partly through repressing mutant p53 (mutp53) induced EMT. Conclusions: Overall, our findings indicated that RNPC1 had a potential function to play a tumor-suppressor role which may be a potential marker in the therapeutic and prognostic of breast cancer.