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Understanding the roles of phenotypic plasticity in adaptive evolution has gained recognition for decades. Studies involving multiple taxa have shown that gene expression plasticity serves as “long-term memory” to facilitate re-adaptations to ancestral environments. Nevertheless, the general pattern and the underlying genetic basis of expression plasticity remain unclear. The transposable elements (TEs) play crucial roles in gene expression regulation and are widely distributed within the genome. Given this, we re-analyzed the transcriptomic data of chicken (Gallus gallus) generated from a reciprocal transplant experiment to examine whether expression shifts of TEs are involved in the re-adaptation process. Similar to the protein-coding genes, the plastic changes of TEs overwhelmingly exceed the genetic changes in the re-adaptation process. Further, the associated TEs co-expressed with diverse genes to perform a regulatory activity. Thus, our study supports the general function of phenotypic plasticity in adaptive evolution, and suggests a regulatory functions of TEs in this process.

Polycystic ovary syndrome (PCOS) is a disease related to reproductive endocrine abnormalities in women of reproductive age, often accompanied by metabolic diseases such as hyperandrogenemia, insulin resistance and dyslipidemia. However, the etiology and mechanism of PCOS are still unclear. In recent years, more and more studies have found that epigenetic factors play an important role in PCOS. DNA methylation is the most widely studied epigenetic modification. At present, changes of DNA methylation have been found in serum, ovarian, hypothalamus, skeletal muscle, adipose tissue of PCOS patients, and these changes are closely related to insulin resistance, lipid metabolism and follicular development of PCOS. Although the current research on DNA methylation in PCOS is not in-depth, it indicated up a good direction for future research on the etiology and mechanism of PCOS. This review discussed the relationship between DNA methylation and PCOS. It is expected to help accelerate the application of DNA methylation in the diagnosis and treatment of PCOS.

Skeletonization is employed to accelerate the multilevel fast multipole algorithm (MLFMA) solution of the method of moments matrix system arising from volume integral equations (VIEs). The acceleration is conducted in two aspects: 1) speedup of the calculation of near-field interactions of the MLFMA and 2) improvement of the iterative convergence. Numerical experiments indicate that the proposed algorithm can significantly reduce the runtime and memory usage without degrading the accuracy, in comparison with the VIE solver purely accelerated by the MLFMA. Additionally, for piecewise homogeneous complex plasmonic structures, the proposed algorithm can be more efficient and accurate than the commonly used surface integral equation solver.

The development of sensitive myocardial-specific cardiac biomarkers allows for detection of very small amounts of myocardial injury or necrosis. Myocardial injury (MI) as a prelude of the serious perioperative complication myocardial infarction, should be paid more attention, especially in elderly susceptible patients. Myocardial injury after abdominal surgery in elderly patients has not been described yet. The objectives of this study were to identify the incidence, predictors, characteristics and the impact of MI on outcome in elderly patients underwent abdominal surgery. Patients aged ≥ 65 who underwent abdominal surgery longer than 2 h between January 2016 and March 2017 were reviewed. Patients with peak troponin I level of 0.04 ng/ml or greater (abnormal laboratory threshold) within once-administration-period and without non-ischemia troponin elevation proof (e.g., sepsis) were assessed for characteristics and prognosis. Risk factors of MI were determined by multivariable regression. Among 285 patients with whole information, 36 patients (12.6%) suffered MI, only 2 patients (0.7%) fulfilled definition of myocardial infarction. With most of them occurred within first 7 days after surgery. Multivariable analysis showed that coronary artery disease (CAD) history [odds ratio (OR) 2.817, P = 0.015], non-laparoscopic surgery (OR 5.181, P = 0.030), blood loss ≥ 800 ml (OR 3.430, P = 0.008), non-venous maintain (OR 2.105, P = 0.047), and infection (OR 4.887, P = 0.008) as risk factors for MI. MI was associated with longer hospital stay (P = 0.006), more cardiac consultation (P = 0.011), higher infection(P = 0.016) and reoperation(P = 0.026) rate. MI is common in elderly patients who underwent abdominal surgery, while myocardial infarction is infrequent. They are both associated with risk factors and worse prognosis. MI deserves more attention especially in elderly patients. Troponin I measurement is a useful test after massive surgery, which can help risk-stratifying patients, effective preventing, prompt managing and predicting outcomes. Routine monitoring of cardiac biomarkers especially within 7 days after abdominal surgery in elderly patients is recommended.

Background The species-rich genus Impatiens is mainly distributed throughout much of tropical Africa, India, southwest Asia, southern China and Japan. There are more than 270 species recorded in China, most of which are restricted to the southwest. An unknown species of Impatiens was collected from Yunnan, southwest China. Results Impatiens pandurata Y. H. Tan & S. X. Yu, a new species of Balsaminaceae from Jinping County and Malipo County, Yunnan, China is similar to I. apalophylla and I. clavigera in having racemose inflorescences, 4 lateral sepals, hammer-shaped capsules and ellipsoid seeds, but differs in having leaves with oblanceolate blades aggregated at the top of the stem, 3–5-flowered racemes, a yellow lower sepal without reddish patches, yellowish flowers, and a dorsal petal with stalks at the base. Molecular phylogenetic analyses of sequences from both nuclear ribosomal and plastid genes confirm that this new species is distinct from morphologically similar species previously recorded. Conclusion With the support of careful morphological studies and phylogenetic analysis, I. pandurata is a species new to science. Electronic supplementary material The online version of this article (doi:10.1186/s40529-015-0108-4) contains supplementary material, which is available to authorized users.

In cancer cells, loss of E-cadherin gene expression caused dysfunction of the cell-cell junction system, triggering cancer invasion and metastasis. Therefore, E-cadherin is an important tumor-suppressor gene. To understand how E-cadherin gene expression is regulated in cancer cells, we have used E-cadherin-positive and -negative expressing cells to find out the possible up- or down regulating transcription factors in human E-cadherin regulatory sequences. Functional analysis of human E-cadherin regulatory sequences constructs indicated that AML1, Sp1, and p300 may play important roles in promoting E-cadherin expression. In addition, we found there are four HNF3-binding sites in human E-cadherin regulatory sequences. The exogenous HNF3 can enhance the E-cadherin promoter activity in metastatic breast cancer cells and the metastatic breast cancer cells stably transfected with HNF3 showed re-expression of E-cadherin. The HNF3 stable transfectants changed from mesenchymal-like into epithelial morphology. The transwell assays showed the re-expressed E-cadherin reduced cell motility of metastatic breast cancer cells. These results suggested HNF3 may play important roles in the upregulation of the E-cadherin promoter, with the consequent re-expression of E-cadherin, thus reducing the metastatic potential of breast cancer cells. These findings suggested HNF3 plays important roles in the upregulation of the E-cadherin gene and may be able to reduce the motility of metastatic breast cancer cells.

The activation of MAPK pathways in spinal cord and subsequent production of proinflammatory cytokines in glial cells contribute to the development of spinal central sensitization, the basic mechanism underlying bone cancer pain (BCP). Our previous study showed that spinal CXCL12 from astrocytes mediates BCP generation by binding to CXCR4 in both astrocyters and microglia. Here, we verified that CXCL12/CXCR4 signaling contributed to BCP through a MAPK-mediated mechanism. In naive rats, a single intrathecal administration of CXCL12 considerably induced pain hyperalgesia and phosphorylation expression of spinal MAPK members (including extracellular signal-regulated kinase, p38, and c-Jun N-terminal kinase), which could be partially prevented by pre-treatment with CXCR4 inhibitor AMD3100. This CXCL12-induced hyperalgesia was also reduced by MAPK inhibitors. In bone cancer rats, tumor cell inoculation into the tibial cavity caused prominent and persistent pain hyperalgesia, and associated with up-regulation of CXCL12 and CXCR4, activation of glial cells, phosphorylation of MAPKs, and production of proinflammatory cytokines in the spinal cord. These tumor cell inoculation-induced behavioral and neurochemical alterations were all suppressed by blocking CXCL12/CXCR4 signaling or MAPK pathways. Taken together, these results demonstrate that spinal MAPK pathways mediated CXCL12/CXCR4-induced pain hypersensitivity in bone cancer rats, which could be druggable targets for alleviating BCP and glia-derived neuroinflammation. Following tumor cell inoculation, chemokine CXCL12 from astrocytes spreads around the spinal environment, resulting in functional activation of CXCR4-expressing astrocytes and microglia. Once glia are activated, they may initiate MAPK (mitogen-activated protein kinase) pathways, and subsequently produce proinflammatory cytokines and chemokines. Among them, CXCL12 could reinforce the astrocytic and microglial activation in autocrine and paracrine manners. Such positive feedback loops sustain perseverant neuroinflammation, facilitate glial activation, and finally lead to bone cancer pain. IL = interleukin; TNF = tumor necrosis factor.