基于音节聚类分析的被动声学监测技术及其在鸟类监测中的应用

被动声学监测通过分析鸟鸣声信息来实现物种识别,为鸟类多样性监测提供了一种切实可行的技术方案。由于鸟种的鸣声复杂多变,如何通过声纹快速准确辨别物种,分析鸟类丰度,降低对人工操作的需求等技术难题,成为基于声纹的鸟类多样性监测所面临的挑战。本文提出了基于音节聚类的鸟类鸣声监测框架:首先通过音高、频率平坦度等音频特征在声纹数据中提取音节,然后通过无监督表征学习与狄利克雷过程(Dirichlet process)混合模型对音节进行深度无监督聚类训练,完成音节聚类和自动音节种类推断。分析结果表明,本文提出的基于音节聚类的鸟类鸣声监测框架在处理开源数据集白腰文鸟(Lonchura striata)的曲目时可获得接近90%的聚类准确率。在此基础上,本研究对2022年4-5月在广州市白云山公园固定监测点所录制的10种鸟类鸣声进行了无监督的音节聚类分析,验证了本文所提出的基于音节聚类的鸟类鸣声监测框架的有效性:本技术不仅可以支持快速鸟类物种识别,还可以统计和分析不同物种鸟鸣在时间、频度、数量上的变化。这些结果表明,基于音节聚类的鸟类鸣声监测框架可以显著降低对人工标注训练数据的要求,克服传统鸟鸣物种识别框架...     

On CD28/CD40 ligand costimulation, common gamma-chain signals, and the alloimmune response

Activation and robust expansion of naive T cells often require T cell costimulatory signals and T cell growth factors. However, the precise growth and costimulation requirements for activation and expansion of CD4(+) and CD8(+) T cells in vivo in allograft response are still not clearly defined. In the present study, we critically examined the role of CD28/CD40 ligand (CD40L) costimulation and the common gamma-chain (gamma(c)) signals, a shared signaling component by receptors for all known T cell growth factors (i.e., IL-2, IL-4, IL-7, IL-9, IL-15, IL-21), in activation and expansion of CD4(+) and CD8(+) T cells in the allogeneic hosts. We found that CD28/CD40L costimulation and the gamma(c) signals are differentially involved in proliferation and clonal expansion of CD4(+) and CD8(+) T cells in response to alloantigen stimulation. CD8(+) T cells are highly dependent on the gamma(c) signals for survival, expansion, and functional maturation, whereas in vivo expansion of alloreactive CD4(+) T cells is largely gamma(c) independent. T cell costimulation via CD28 and CD40L, however, is necessary and sufficient for activation and expansion of CD4(+) T cells in vivo. In a skin transplant model, blocking both CD28/CD40L and the gamma(c) pathways induced prolonged skin allograft survival. Our study provides critical insights that the CD4 and CD8 compartments are most likely governed by distinct mechanisms in vivo, and targeting both costimulatory and gamma(c) signals may be highly effective in certain cytopathic conditions involving activation of both CD4(+) and CD8(+) T cells.     

Improved DNA purification with quality assurance for evaluation of the microbial genetic content of constructed wetlands

Efficient isolation of target DNA is a crucial first step of DNA-based metagenomic analyses of environmental samples. Insufficient quantity and purity of DNA isolated using commercial kits result in missing genetic information, especially for large-diameter substrates in constructed wetlands (CWs). Here, we addressed this problem by devising a cost-effective calcium chloride lysozyme-sodium dodecyl sulfate (SDS) method (CCLS), with key improvements in the steps of humic acid removal and cell lysis. The buffer comprising Tris, EDTA, Na₂O₂P₇ and PVPP (TENP), and skim milk, could reduce adsorption between microorganisms and substrates, and calcium chloride precipitated and removed over 94% of humic acid. This humic acid removal step, when compared to the PowerSoil DNA kit (MO BIO Laboratories Inc.) (MBKIT), significantly enhanced the DNA purity (A260/230) from 0.68 to 1.63 (p < 0.01). When gentle and extended cell lysis in CCLS replaced the short but violent bead-beating in the MBKIT, DNA yield and the amount of lysed bacteria detected by quantitative real-time polymerase chain reaction (qPCR) on average increased by 2 and 4 folds, respectively, compared to that obtained using the MBKIT (p < 0.01). Furthermore, the full-length bacterial 16S rRNA gene and nirK gene from denitrifying microorganisms were successfully amplified from CCLS-generated DNA. Additionally, bacterial diversity indices of richness, Shannon, and evenness examined by denaturing gradient gel electrophoresis (DGGE) increased by 75, 30, and 7%, respectively, by CCLS compared to that using the MBKIT. Hence, the CCLS method enables improved evaluation of microbial density and diversity in CW systems.

     

Is inflammation the cause of pre-eclampsia?

It has been proposed that either excessive inflammation or an imbalance in angiogenic factors cause pre-eclampsia. In the present review, the arguments for and against the role of inflammation and/or angiogenic imbalance as the cause of pre-eclampsia are discussed on the basis of the Bradford-Hill criteria for disease causation. Although both angiogenic imbalance and systemic inflammation are implicated in pre-eclampsia, the absence of temporality of inflammatory markers with pre-eclampsia challenges the concept that excessive inflammation is the cause of pre-eclampsia. In contrast, the elevation of anti-angiogenic factors that precede the clinical signs of pre-eclampsia fulfils the criterion of temporality. The second most important criterion is the dose-response relationship. Although such a relationship has not been proven between pro-inflammatory cytokines and pre-eclampsia, high levels of anti-angiogenic factors have been shown to correlate with increased incidence and disease severity, hence satisfying this condition. Finally, as the removal of circulating sFlt-1 (soluble Fms-like tyrosine kinase receptor-1) from pre-eclamptic patients significantly improves the clinical outcome, it fulfils the Hill's experiment principle, which states that removal of the cause by an appropriate experimental regimen should ameliorate the condition. In contrast, treatment with high doses of corticosteroid fails to improve maternal outcome in pre-eclampsia, despite suppressing inflammation. Inflammation may enhance the pathology induced by the imbalance in the angiogenic factors, but does not by itself cause pre-eclampsia. Development of therapies based on the angiogenic and cytoprotective mechanisms seems more promising.     

Lower Levels of Expression of FATA2 Gene Promote Longer Siliques with Modified Seed Oil Content in Arabidopsis thaliana

Fatty acyl thioesterases control the termination of intraplastidial fatty acid synthesis by hydrolyzing fatty acyl-ACP complexes. The fatty acyl thioesterase A (FATA) gene family in Arabidopsis comprises two members, i.e., FATA1 and FATA2. Previous studies have shown that FATAs display high specificity for unsaturated fatty acids. However, the expression pattern and individual roles of these two FATA genes remains unknown. In this study, we initially studied the expression patterns of FATA1 and FATA2 in various organs of Arabidopsis and we found that FATA1 was expressed at low level in all organs examined and FATA2 was detected in all organs examined, with especially high accumulation in siliques. The transient expression of a FATA2-eGFP fusion in Arabidopsis green leaf protoplasts showed that FATA2 was localized in chloroplasts. A T-DNA insertion mutant line of FATA2 (named fata2) was obtained and used for phenotypic observation. Semiquantitative RT-PCR assay showed that the expression level of FATA2 decreased significantly in fata2 compared with that in wild type. Furthermore, fata2 mutants produced longer siliques with more seeds, whereas seed size was slightly smaller than that of wild type. Compositional analysis of seed oil revealed that, except for a subtly decreased C24:0 and unchanged C22:0 level, all other fatty acids were increased by between 10 and 60 % in fata2 dry seeds compared with those in wild-type. Taken together, our results indicate that FATA2 plays important roles in lipid metabolism in seeds and in silique development in Arabidopsis thaliana.     

Human adipose tissue endothelial cells promote preadipocyte proliferation

Adipogenesis is preceded by development of a microvascular network, and optimal functioning of adipose tissue as an energy store and endocrine organ is dependent on extensive vascularization. We have examined the role of endothelial cell-derived factors that influence the proliferation of human preadipocytes. Microvascular endothelial cells and preadipocytes were isolated from human omental and subcutaneous adipose tissue biopsies by use of a developed procedure of collagenase digest, immunoselection, and differential trypsinization. Conditioned medium from microvascular endothelial cell cultures promoted the proliferation of preadipocytes (P = <0.001) and (to a lesser extent) other cell types. No depot-specific differences in mitogenic capacity of microvascular endothelial cell medium or of preadipocyte response were observed. These results indicate that adipose tissue endothelial cells secrete soluble adipogenic factor(s).