Fast seedling root growth leads to competitive superiority of invasive plants

The competitive superiority of invasive plants plays a key role in the process of plant invasions, enabling invasive plants to overcome the resistance of local plant communities. Fast aboveground growth and high densities lead to the competitive superiority of invasive species in the competition for light. However, little is understood of the role belowground root competition may play in invasion. We conducted an experiment to test the effect of root growth on the performance of an invasive shrub Cassia alata, a naturalized, non-invasive shrub Corchorus capsularis, and a native shrub Desmodium reticulatum. We compared seedling growth of the three species and their competitive ability in situ. The roots of the C. alata seedlings grew much faster than those of C. capsularis and D. reticulatum during the entire growth period although C. alata had shorter shoots than D. reticulatum. Furthermore, C. alata showed an apparent competition advantage compared to the other two species as evidenced by less biomass reduction in intraspecific competition and higher competitive effects in interspecific competition. Our study reveals that fast seedling root growth may be important in explaining the competitive advantages of invasive plants. Future studies should pay more attention to the belowground traits of invasive plants, the trade-off between shoot and root growth, and the role of root competition in affecting the population dynamics of invasive plants and the structures of invaded communities.     

Discovery of 3-(4-sulfamoylnaphthyl)pyrazolo[1,5-a]pyrimidines as potent and selective ALK2 inhibitors

The pyrazolo[1,5-a]pyrimidine LDN-193189 is a potent inhibitor of activin receptor-like kinase 2 (ALK2) but is nonselective for highly homologous ALK3 and shows only modest kinome selectivity. Herein, we describe the discovery of a novel series of potent and selective ALK2 inhibitors by replacing the quinolinyl with a 4-(sulfamoyl)naphthyl, yielding ALK2 inhibitors that exhibit not only excellent discrimination versus ALK3 but also high kinome selectivity. In addition, the optimized compound 23 demonstrates good ADME and in vivo pharmacokinetic properties.     

Changes in fatigue,autonomic functions,and blood biomarkers due to sitting isometric yoga in patients with chronic fatigue syndrome

Background

In a previous randomized controlled trial, we found that sitting isometric yoga improves fatigue in patients with chronic fatigue syndrome (CFS) who are resistant to conventional therapy. The aim of this study was to investigate possible mechanisms behind this finding, focusing on the short-term fatigue-relieving effect, by comparing autonomic nervous function and blood biomarkers before and after a session of isometric yoga.

Methods

Fifteen patients with CFS who remained symptomatic despite at least 6 months of conventional therapy practiced sitting isometric yoga (biweekly 20 min practice with a yoga instructor and daily home practice) for eight weeks. Acute effects of sitting isometric yoga on fatigue, autonomic function, and blood biomarkers were investigated after the final session with an instructor. The effect of a single session of sitting isometric yoga on fatigue was assessed by the Profile of Mood Status (POMS) questionnaire immediately before and after the session. Autonomic nervous function (heart rate (HR) variability) and blood biomarkers (cortisol, DHEA-S, TNF-α, IL-6, IFN-γ, IFN-α, prolactin, carnitine, TGF-β1, BDNF, MHPG, and HVA) were compared before and after the session.

Results

Sitting isometric yoga significantly reduced the POMS fatigue score (p?<?0.01) and increased the vigor score (p?<?0.01). It also reduced HR (p?<?0.05) and increased the high frequency power (p?<?0.05) of HR variability. Sitting isometric yoga increased serum levels of DHEA-S (p?<?0.05), reduced levels of cortisol (p?<?0.05) and TNF-α (p?<?0.05), and had a tendency to reduce serum levels of prolactin (p?<?0.1). Decreases in fatigue scores correlated with changes in plasma levels of TGF-β1 and BDNF. In contrast, increased vigor positively correlated with HVA.

Conclusions

A single session of sitting isometric yoga reduced fatigue and increased vigor in patients with CFS. Yoga also increased vagal nerve function and changed blood biomarkers in a pattern that suggested anti-stress and anti-inflammatory effects. These changes appear to be related to the short-term fatigue-relieving effect of sitting isometric yoga in patients with CFS. Furthermore, dopaminergic nervous system activation might account for sitting isometric yoga-induced increases in energy in this patient population.

Trial registration

University Hospital Medical Information Network (UMIN CTR) UMIN000009646. Registered Dec 27, 2012.

     

Mechanisms Orchestrating Mitochondrial Dynamics for Energy Homeostasis

To maintain homeostasis, every cell must constantly monitor its energy level and appropriately adjust energy, in the form of ATP, production rates based on metabolic demand. Continuous fulfillment of this energy demand depends on the ability of cells to sense, metabolize, and convert nutrients into chemical energy. Mitochondria are the main energy conversion sites for many cell types. Cellular metabolic states dictate the mitochondrial size, shape, function, and positioning. Mitochondrial shape varies from singular discrete organelles to interconnected reticular networks within cells. The morphological adaptations of mitochondria to metabolic cues are facilitated by the dynamic events categorized as transport, fusion, fission, and quality control. By changing their dynamics and strategic positioning within the cytoplasm, mitochondria carry out critical functions and also participate actively in inter-organelle cross-talk, assisting metabolite transfer, degradation, and biogenesis. Mitochondrial dynamics has become an active area of research because of its particular importance in cancer, metabolic diseases, and neurological disorders. In this review, we will highlight the molecular pathways involved in the regulation of mitochondrial dynamics and their roles in maintaining energy homeostasis.     

Subchronic Arsenism Disorders mRNA Expression of Cytokines and Immunoglobulins in the Intestinal Tract of the Cock

Provision of feed containing arsenic may cause intestinal flora imbalance and consequently, the dysfunction of immunological protection of the cock. To understand the intricate tuning of immune responses in the intestinal tract elicited by subchronic arsenism, a cock model (1-day-old Hy-line cocks) was established by subjecting cocks to different environmentally relevant concentrations of arsenic in the diet for 90 days. Intestinal cytokine and immunoglobulin (Ig) messenger RNA (mRNA) expression levels were determined using real-time PCR on days 30, 60, and 90. Results showed that, compared to those of the control groups, the mRNA levels of interleukin (IL)-1β, IL-2, IL-4, and interferon (IFN)-γ displayed increases on day 30 then decreases on days 60 and 90 dose-dependently in every tissue. Except for the decrease in the jejunum, the mRNA levels of IL-6 and IL-8 were increased in the duodenum, ileum, cecum, and rectum. However, the mRNA levels of IL-12β decreased in every tissue and every time point compared to those of the control groups. In contrast, chicks showed considerably higher expression levels of IgA, IgM, and IgG after exposure to arsenic. These results demonstrated that immune strategies of cocks were disturbed when suffered from subchronic arsenism, at least on the intestinal level.     

Effects of sap velocity on the daytime increase of stem CO2 efflux from stems of Schima superba trees

Stem CO₂ efflux (E _s) has been estimated from a temperature-related equation, but sap flux often affects measurements of E _s, which leads to misunderstanding real stem respiration. In order to observe the relationship between E _s and stem temperature and to analyze the effect of sap velocity on E _s, stem temperature, E _s and sap flux were measured from a subtropical Schima superba plantation in South China on three trees for consecutive 3 days in July and October 2009. Stem temperature, E _s and sap velocity were significantly higher in July than in October. Stem temperature could explain 17–41 and 54–75% variations of E _s in July and October, respectively. A negative relationship between E _s and stem temperature was found during 1800–2300 hours in July. The daytime E _s was 9.2, 4.3 and 2.4% higher than the predicted for three trees in July, and this occurred only on Tree 1 in October. Sap velocity was positively correlated with E _s for three trees in July, and the increase of E _s with the increase of sap velocity was only observed on Tree 1 in October. These results demonstrated that the occurrence of sap flux could account for the increase of daytime E _s, and the effect of sap velocity on E _s varied with the seasons from the S. superba stem.     

LncRNA TUG1 alleviates cardiac hypertrophy by targeting miR-34a/DKK1/Wnt-β-catenin signalling

The current study was designed to explore the role and underlying mechanism of lncRNA taurine up-regulated gene 1 (TUG1) in cardiac hypertrophy. Mice were treated by transverse aortic constriction (TAC) surgery to induce cardiac hypertrophy, and cardiomyocytes were treated by phenylephrine (PE) to induce hypertrophic phenotype. Haematoxylin-eosin (HE), wheat germ agglutinin (WGA) and immunofluorescence (IF) were used to examine morphological alterations. Real-time PCR, Western blots and IF staining were used to detect the expression of RNAs and proteins. Luciferase assay and RNA pull-down assay were used to verify the interaction. It is revealed that TUG1 was up-regulated in the hearts of mice treated by TAC surgery and in PE-induced cardiomyocytes. Functionally, overexpression of TUG1 alleviated cardiac hypertrophy both in vivo and in vitro. Mechanically, TUG1 sponged and sequestered miR-34a to increase the Dickkopf 1 (DKK1) level, which eventually inhibited the activation of Wnt/β-catenin signalling. In conclusion, the current study reported the protective role and regulatory mechanism of TUG1 in cardiac hypertrophy and suggested that TUG1 may serve as a novel molecular target for treating cardiac hypertrophy.