Search

Variability of North Tropical Atlantic (NTA) sea surface temperature (SST), characterized by a near-uniform warming at its positive phase, is a consequential mode of climate variability. Modulated by El Niño-Southern Oscillation (ENSO) and the North Atlantic Oscillation, NTA warm anomalies tend to induce La Niña events, droughts in Northeast Brazil, increased frequency of extreme hurricanes, and phytoplankton blooms in the Guinea Dome. Future changes of NTA variability could have profound socioeconomic impacts yet remain unknown. Here, we reveal a robust intensification of NTA variability under greenhouse warming. This intensification mainly arises from strengthening of ENSO-forced Pacific-North American pattern and tropospheric temperature anomalies, as a consequence of an eastward shift of ENSO-induced equatorial Pacific convection and of increased ENSO variability, which enhances ENSO influence by reinforcing the associated wind and moist convection anomalies. The intensification of NTA SST variability suggests increased occurrences of extreme NTA events, with far-reaching ramifications.

Abstract Background In nature, mussel adhesive proteins (MAPs) show remarkable adhesive properties, biocompatibility, and biodegradability. Thus, they have been considered promising adhesive biomaterials for various biomedical and industrial applications. However, limited production of natural MAPs has hampered their practical applications. Recombinant production in bacterial cells could be one alternative to obtain useable amounts of MAPs, although additional post-translational modification of tyrosine residues into 3,4-dihydroxyphenyl-alanine (Dopa) and Dopaquinone is required. The superior properties of MAPs are mainly attributed to the introduction of quinone-derived intermolecular cross-links. To solve this problem, we utilized a co-expression strategy of recombinant MAP and tyrosinase in Escherichia coli to successfully modify tyrosine residues in vivo. Results A recombinant hybrid MAP, fp-151, was used as a target for in vivo modification, and a dual vector system of pET and pACYC-Duet provided co-expression of fp-151 and tyrosinase. As a result, fp-151 was over-expressed and mainly obtained from the soluble fraction in the co-expression system. Without tyrosinase co-expression, fp-151 was over-expressed in an insoluble form in inclusion bodies. The modification of tyrosine residues in the soluble-expressed fp-151 was clearly observed from nitroblue tetrazolium staining and liquid-chromatography-mass/mass spectrometry analyses. The purified, in vivo modified, fp-151 from the co-expression system showed approximately 4-fold higher bulk-scale adhesive strength compared to in vitro tyrosinase-treated fp-151. Conclusion Here, we reported a co-expression system to obtain in vivo modified MAP; additional in vitro tyrosinase modification was not needed to obtain adhesive properties and the in vivo modified MAP showed superior adhesive strength compared to in vitro modified protein. It is expected that this co-expression strategy will accelerate the use of functional MAPs in practical applications and can be successfully applied to prepare other Dopa/Dopaquinone-based biomaterials.

Abstract Background Information on the health-related quality of life (HRQoL) of patients with genital warts (GW) in populations in mainland China is still limited. The aim of the study was to use a generic instrument to measure the impact of genital warts on HRQoL in men and women in this setting. Methods A multi-centre hospital-based cross-sectional study across 18 centers in China was conducted to interview patients using the European quality of life-5 dimension (EQ-5D) instrument; respondents' demographic and clinical data were also collected. Results A total of 1,358 GW patients (612 men, 746 women) were included in the analysis, with a mean age of 32.0 ± 10.6 years. 56.4% of the patients reported some problems in the dimension of Anxiety/Depression (highest), followed by Pain/Discomfort (24.7%) and Mobility (3.5%). The overall visual analogue scale (VAS) score of the study population was found to be 65.2 ± 22.0, and the EQ-5D index score was found to be 0.843 ± 0.129 using Japanese preference weights (the Chinese preference was unavailable yet). Patients with lower VAS means and EQ-5D index scores were more often female, living in urban area, and suffering multiple GW (all p values < 0.05), but the values did not differ notably by age (p values > 0.05). Conclusions The HRQoL of patients with GW was substantially lower, compared to a national representative general population in China (VAS = ~80); the findings of different subgroups are informative for future GW prevention and control efforts.

Abstract Airway remodeling and airway hyper-responsiveness are prominent features of asthma. Neurogenic inflammation participates in the development of asthma. Neurokinin substance P acts by binding to neurokinin-1 receptor (NK-1R). Airway smooth muscle cells (ASMC) are important effector cells in asthma. Increases in ASMC proliferation, migration, and cytoplasmic Ca2+ concentration are critical to airway remodeling and hyper-responsiveness. The effects of substance P on ASMC were investigated in Wistar rats challenged with a previously described asthmatic rat model. To exclude possible influences from other factors, the role of substance P was also investigated in primary cultured rat ASMC. Substance P and WIN62577-induced changes in cytoplasmic Ca2+ concentration were observed by fluorescence microscopy, and expression of Ca2+ homeostasis-regulating genes was assessed with real-time PCR. We found that cytoplasmic Ca2+ concentration increased in normal rat ASMC treated with substance P, but decreased in asthmatic rat ASMC treated with WIN62577, an antagonist of NK-1R. Real-time PCR analysis revealed increased Serca2 mRNA expression but decreased Ip3r mRNA expression after WIN62577 treatment in asthmatic rat ASMC. Flow cytometric analysis (FCM) revealed that most asthmatic rat ASMC stayed at G1 phase after combined treatment with WIN62577 and IL-13 in vitro. Transwell analysis suggested that ASMC migration was reduced after WIN62577 treatment. Therefore, we conclude that NK-1R is related to asthma mechanisms and a NK-1R antagonist downregulates calcium concentration in asthmatic ASMC by increasing Serca2 mRNA and decreasing Ip3r mRNA expression. The NK-1R antagonist WIN62577 inhibited ASMC IL-13-induced proliferation and ASMC migration in vitro and therefore may be a new therapeutic option in asthma.

Abstract Colloidal cubic silicon carbide (SiC) nanocrystals with an average diameter of 4.4 nm have been fabricated by anisotropic wet chemical etching of microsized cubic SiC powder. Fourier transform infrared spectra show that these cubic SiC nanocrystals contain carboxylic acid, SiH, CH, and CHx groups. UV/Vis absorption and photoluminescence (PL) spectroscopy clearly indicate that water and ethanol colloidal suspensions of the as-fabricated colloidal samples exhibit strong and above band gap blue and blue-green emissions. The cubic SiC nanocrystals show different surface charges in water and ethanol solutions due to the interaction of water molecules with polar Si-terminated surfaces of cubic SiC nanocrystals. The results explain the distinctive optical characteristics of colloidal cubic SiC nanocrystals in water and ethanol, and reveal that quantum confinement and surface charges play a great role in determining the optical characteristics of colloidal cubic SiC nanocrystals.

Abstract Background Cancer cells recurrently develop into acquired resistance to the administered drugs. The iatrogenic mechanisms of induced chemotherapy-resistance remain elusive and the degree of drug resistance did not exclusively correlate with reductions of drug accumulation, suggesting that drug resistance may involve additional mechanisms. Our aim is to define the potential targets, that makes drug-sensitive MCF-7 breast cancer cells turn to drug-resistant, for the anti-cancer drug development against drug resistant breast cancer cells. Methods Doxorubicin resistant human breast MCF-7 clones were generated. The doxorubicin-induced cell fusion events were examined. Heterokaryons were identified and sorted by FACS. In the development of doxorubicin resistance, cell-fusion associated genes, from the previous results of microarray, were verified using dot blot array and quantitative RT-PCR. The doxorubicin-induced expression patterns of pro-survival and pro-apoptotic genes were validated. Results YB-1 and ABCB5 were up regulated in the doxorubicin treated MCF-7 cells that resulted in certain degree of genomic instability that accompanied by the drug resistance phenotype. Cell fusion increased diversity within the cell population and doxorubicin resistant MCF-7 cells emerged probably through clonal selection. Most of the drug resistant hybrid cells were anchorage independent. But some of the anchorage dependent MCF-7 cells exhibited several unique morphological appearances suggesting minor population of the fused cells maybe de-differentiated and have progenitor cell like characteristics. Conclusion Our work provides valuable insight into the drug induced cell fusion event and outcome, and suggests YB-1, GST, ABCB5 and ERK3 could be potential targets for the anti-cancer drug development against drug resistant breast cancer cells. Especially, the ERK-3 serine/threonine kinase is specifically up-regulated in the resistant cells and known to be susceptible to synthetic antagonists.