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Previous palaeoenvironmental reconstructions have implied that East Asia was dominated by a zonal climate pattern during the Eocene, with an almost latitudinal arid/semiarid band at ~ 30° N. However, this long-standing model has recently been challenged by growing body of multidisciplinary evidence. Some studies indicated that central China was characterized by climatic fluctuations between humid and drier conditions during the Early Eocene, akin to the present East Asian monsoon (EAM) regime. Using palynological assemblages in the Tantou Basin, central China, we quantitatively reconstructed climate changes from the Late Palaeocene to Early Eocene to better understand climate change in central China. Palynological assemblages revealed that the coniferous and broad-leaved mixed forest in this area received no less than 800 mm of annual precipitation and experienced a climate change from warm and wet to relatively cool and dry. According to palaeoclimate curves, a sudden climate change occurred in the Early Eocene, with the mean annual temperature and precipitation decreasing by 5.1 °C and 214.8 mm, respectively, and the climate became very similar to the present climate, which is controlled by the monsoon. Therefore, this significant climate change during the Early Eocene may signal the emergence of the EAM in East Asia.

Extracellular matrix (ECM) not only serves as a support for tumor cell but also regulates cell–cell or cell–matrix cross-talks. Collagens are the most abundant proteins in ECM. Several studies have found that certain collagen genes were overexpressed in gastric cancer (GC) tissues and might serve as potential biomarkers and therapeutic targets in GC patients. However, the expression patterns of all collagen family genes in GC tissue and their functions are still not clear. With RNA sequencing (RNA-Seq) data, microarray data, and corresponding clinical data obtained from TCGA, GTEx, and GEO databases, bioinformatics analyses were performed to investigate the correlation between the expression patterns of collagen family genes and GC progression. We found that quite many of the collagen family genes were overexpressed in GC tissues. The increase in mRNA expression of most of these overexpressed collagen genes happened between T1 and T2 stage, which indicates the significance of collagens in tumor enlargement of GC. Notably, the mRNA expressions of these differentially expressed collagens genes were highly positively correlated. The elevated expression of a large number of collagen genes in early T stage might greatly change the composition and structure organization of ECM, contributing to ECM remodeling in GC progression.

Fragile X syndrome (FXS), an X-chromosome linked intellectual disability, is the leading monogenetic cause of autism spectrum disorder (ASD), a neurodevelopmental condition that currently has no specific drug treatment. Building upon the demonstrated therapeutic effects on spatial memory of bryostatin-1, a relatively specific activator of protein kinase C (PKC)ε, (also of PKCα) on impaired synaptic plasticity/maturation and spatial learning and memory in FXS mice, we investigated whether bryostatin-1 might affect the autistic phenotypes and other behaviors, including open field activity, activities of daily living (nesting and marble burying), at the effective therapeutic dose for spatial memory deficits. Further evaluation included other non-spatial learning and memory tasks. Interestingly, a short period of treatment (5 weeks) only produced very limited or no therapeutic effects on the autistic and cognitive phenotypes in the Fmr1 KO2 mice, while a longer treatment (13 weeks) with the same dose of bryostatin-1 effectively rescued the autistic and non-spatial learning deficit cognitive phenotypes. It is possible that longer-term treatment would result in further improvement in these fragile X phenotypes. This effect is clearly different from other treatment strategies tested to date, in that the drug shows little acute effect, but strong long-term effects. It also shows no evidence of tolerance, which has been a problem with other drug classes (mGluR5 antagonists, GABA-A and -B agonists). The results strongly suggest that, at appropriate dosing and therapeutic period, chronic bryostatin-1 may have great therapeutic value for both ASD and FXS.

To investigate roaming paths planning for diagnosis of congenital heart diseases (CHD) using a cardiovascular virtual endoscopy (VE) system. Forty children were enrolled. VE system was applied to support in establishing a diagnosis. Performance in diagnosing CHDs by CT, VE using automatically planned roaming paths (VE-auto, objects were treated as left heart system and right heart system), VE using manually planned paths (VE-manual), and VE using automatically planned path for left heart system and manually planned path for right heart system (VE-combined) were studied and compared. Comparable accuracy of 93%, 93%, 95% and 95% was found by CT, VE-auto, VE-manual and VE-combined. However, in diagnosing tetralogy of Fallot, significantly higher performance was found by VEs, compared with CT. For VE-auto, poor performance with an accuracy of 85% and sensitivity of 22% was revealed in diagnosing muscular ventricular septal defect, compared with VE-manual and VE-combined. Compared with VE-manual, VE-combined illustrated comparable diagnostic accuracy on all CHDs; however, significantly smaller diagnostic time was utilized (P

With rapid spread of the urbanization, many environmental factors, such as climate, soil pH and nutrients have been changed. However, the plant pollination affected by urbanization was seldom conducted. Here, we studied the flower visitation rates, seed production, pollen limitation and flower morphological characters of Gentiana dahurica at 3 populations along an urban-peri-urban gradient around Xi’ning over 4 consecutive years, aiming to test the effects of urbanization on plant pollination service. Our results showed that the pollinator visit frequencies, interannual stability of pollinator assemblages and visit frequencies declined with the intensification of urbanization. As urbanization intensified, plant borne more flowers and the flower morphological sizes became “longer” (the length of flowers, filaments and styles were increased, but the width of flowers kept stable at the 3 populations); the flower duration, especially the female phase duration prolonged. The seed-set ratio of G. dahurica in natural condition decreased and more severe pollen limitation occurred in more urbanized populations. Also, an interannual variation of seed-set ratio and index of pollen limitation (IPL), which related with the variation of pollinator visit frequencies, were found in this study. These results suggest that the pollination service can be threatened by urbanization over a long-time interval for G. dahurica. This finding highlights the importance of pollinator affections acting on plant pollination system. Additionally, as pollinator assemblages and visit frequencies interannually changed, a long-time scale observation is needed to understand the plant-pollinator relationships.

Transcription factors (TFs) are well-known important regulators in cell biology and tissue development. However, in mouse, one of the most widely-used model species, currently the vast majority of the known TFs have not been functionally studied due to the lack of sufficient annotations. To this end, we collected and analyzed the whole transcriptome sequencing data from more than 30 major mouse tissues and used the expression profiles to annotate the TFs. We found that the expression patterns of the TFs are highly correlated with the histology of the tissue types thus can be used to infer the potential functions of the TFs. Furthermore, we found that as many as 30% TFs display tissue-specific expression pattern, and these tissue-specific TFs are among the key TFs in their corresponding tissues. We also observed signals of divergent transcription associated with many TFs with unique expression pattern. Lastly, we have integrated all the data, our analysis results as well as various annotation resources to build a web-based database named mTFkb freely accessible at htt p://www.m yogenesisdb.org/mTFkb/. We believe that mTFkb could serve as a useful and valuable resource for TF studies in mouse.

Despite the therapeutic success of tenofovir (TFV) for treatment of HIV-1 infection, numerous cases of nephrotoxicity have been reported. Mitochondrial toxicity has been purported as the major target of TFV-associated renal tubulopathy but the underlying molecular mechanism remains unclear. In this report, we use metabolomics and proteomics with HK-2 cells and animal models to dissect the molecular pathways underlying nephropathy caused by TFV and its more toxic analog, adefovir (ADV). Proteomic analysis shows that mitochondrial chaperone TRAP1 and mtDNA replicating protein SSBP1 were significantly down-regulated in TFV and ADV treated HK-2 cells compared with controls. Transmission electron microscopy (TEM) revealed that TFV and ADV-treated HK-2 cells had accumulated glycogen, a phenotype that was also observed in mice treated with TFV and ADV. Analysis of the proteins in TCA cycle showed succinate dehydrogenase subunit B (SDHB) was nearly depleted in glucose oxidative phosphorylation pathway however certain enzymes in the glycolysis and glycogen synthesis pathway had elevated expression in TFV and ADV-treated HK-2 cells. These results suggest that TFV and ADV may cause mitochondrial dysfunction in renal tubular cells and reprogramming of glucose metabolism. The resulting glycogen accumulation may partially contribute to TFV and ADV induced renal dysfunction.

Transcription factor TBX1 plays a pivotal role in heart development and has been implicated in 22q11.2 deletion syndrome. The structure of this protein has been elucidated, and several mutations have been identified that disrupt TBX1 localization, DNA/protein-binding, or mRNA expression. This study reports a mutation in the TBX1 gene that leads to significantly reduced expression of the mutant protein. A total of 773 conotruncal heart defect patients and 516 unrelated healthy control individuals were enrolled, none of which harbored a 22q11.2 deletion or duplication. We identified a mutation, c.303-305delGAA, located in the third exon of TBX1 that does not disrupt TBX1 mRNA expression or DNA binding activity, but results in decreased TBX1 protein levels and transcriptional activity. Through protein degradation studies we demonstrated that TBX1 is degraded primarily in proteasomes. Although the c.303-305delGAA mutation leads to low levels of the mutant protein, we found that increased protein degradation was not the cause, and we hypothesize that an alternate mechanism, such as translational inhibition, may be the cause.

We propose a method for shortcut to adiabatic control of soliton matter waves in harmonic traps. The tunable interaction controlled by Feshbach resonance is inversely designed to achieve fast compression of soliton matter waves but within a short time, as compared to the conventional adiabatic compression. These results pave the way to control the nonlinear dynamics for matter waves and optical solitons by using shortcuts to adiabaticity., 8 pages, 5 figures, accepted for publication in Sci. Rep

With the application of advanced molecular cytogenetic techniques, the number of patients identified as having abnormal chromosome 8p has increased progressively. Individuals with terminal 8p deletion have been extensively described in previous studies. The manifestations usually include cardiac anomalies, developmental delay/mental retardation, craniofacial abnormalities, and multiple other minor anomalies. However, some patients with proximal deletion also presented with similar phenotypic features. Here we describe a female child with an 18.5-Mb deletion at 8p11.23–p22 that include the cardiac-associated loci NKX2-6 and NRG1. Further mutation screening of these two candidate genes in 143 atrial septal defect patients, two heterozygous mutations NKX2-6 (c.1A > T) and NRG1 (c.1652G > A) were identified. The mutations were described for the first time in patients with congenital heart disease (CHD). The c.1A > T NKX2-6 generated a protein truncated by 45 amino acids with a decreased level of mRNA expression, whereas the NRG1 mutation had no significant effect on protein functions. Our findings suggest that 8p21-8p12 may be another critical region for 8p-associated CHD, and some cardiac malformations might be due to NKX2-6 haploinsufficiency. This study also links the NKX2-6 mutation to ASD for the first time, providing novel insight into the molecular underpinning of this common form of CHD.