When Landscaping Goes Bad: The Incipient Invasion of Mahonia bealei in the Southeastern United States

Woodlots are forest islands embedded within an urban matrix, and often represent the only natural areas remaining in suburban areas. Woodlots represent critical conservation areas for native plants, and are important habitat for wildlife in urban areas. Invasion by non-indigenous (NIS) plants can alter ecological structure and function, and may be especially severe in remnant forests where NIS propagule pressure is high. Woody shrubs in the Family Berberidaceae have been well documented as invaders of the forest–urban matrix in North America. Mahonia bealei (Berberidaceae) is a clonal shrub native to China, and is a popular ornamental in the Southeastern United States. Mahoni bealei is listed as “present” on some local and state floras, but almost nothing is known regarding its invasion potential in the United States. We sampled 15 woodlots in Clemson, South Carolina, to assess the invasion of M. bealei and other woody non-indigenous species (NIS). M. bealei invaded 87% of the woodlots surveyed and species richness of NIS on these woodlots varied from 5 to 14. Stepwise-multiple regression indicated that less canopy cover and older M. bealei predicted greater abundance of M. bealei , and that not all subdivisions were equally invaded (P < 0.0001; r² = 0.88). The impact of M. bealei on native flora and fauna may be considerable, and it is likely to continue to spread in the Southeastern United States. M. bealei should be recognized as an aggressive invader in the Southeastern United States, with the potential for negative impacts on native flora and fauna.     

Identification of copy number variants in children and adolescents with autism spectrum disorder: a study from Turkey

Molecular Biology Reports - Copy number variants (CNVs) play a key role in the etiology of autism spectrum disorder (ASD). Therefore, recent guidelines recommend chromosomal microarrays (CMAs) as...     

Shedding light on the EpCAM: An overview

The epithelial cell adhesion molecule (EpCAM) is a Type I transmembrane superficial glycoprotein antigen that is expressed on the surface of basolateral membrane of multiple epithelial cells with some exceptions such as epidermal keratinocytes, hepatocytes, thymic cortical epithelial cells, squamous stratified epithelial cells, and myoepithelial cells that do not express the molecule. The molecule plays a pivotal role in the structural integrity, adhesion of the epithelial tissues and their interaction with the underlying layers. EpCAM prevents claudin-7 and claudin-1 molecules from degradation, thereby, decreasing the number of tight junctions and cellular interconnections, and promoting the cells toward carcinogenic transformation. Moreover, the mutations in the EpCAM gene lead to congenital tufting enteropathy, severe intestinal epithelium homeostasis disorders, and Lynch and Lynch syndrome. Overexpression of EpCAM on stem cells of some cancers and the presence of this molecule on circulating tumor cells (CTCs) makes it a promising candidate for cancer diagnosis as well as tracing and isolation of CTCs.     

Association Between Hypertension in Healthy Participants and Zinc and Copper Status: a Population-Based Study

Biological Trace Element Research - The prevalence of hypertension (HTN) is increasing globally. It has been shown that there is an association between micronutrient deficiency and HTN. In the...     

Therapeutic potency of oncolytic virotherapy–induced cancer stem cells targeting in brain tumors,current status,and perspectives

Brain tumors are the most common form of solid tumors in children and is presently a serious therapeutic challenge worldwide. Traditional treatment with chemotherapy and radiotherapy was shown to be unsuccessful in targeting brain tumor cancer stem cells (CSCs), leading to recurrent, treatment-resistant secondary malignancies. Oncolytic virotherapy (OV) is an effective antitumor therapeutic strategy which offers a novel, targeted approach for eradicating pediatric brain tumor CSCs by utilizing mechanisms of cell killing that differ from conventional therapies. A number of studies and some clinical trials have therefore investigated the effects of combined therapy of radiations or chemotherapies with oncolytic viruses which provide new insights regarding the effectiveness and improvement of treatment responses for brain cancer patients. This review summarizes the current knowledge of the therapeutic potency of OVs-induced CSCs targeting in the treatment of brain tumors for a better understanding and hence a better management of this disease.     

Contractile responses of the human umbilical artery to KCl and serotonin in Ca-free medium and the effects of levcromakalim

It is known that K(ATP) channel openers inhibit the release and refilling of Ca(2+) from intracellular stores. The present study was designed to test the effects of levcromakalim in human umbilical artery (HUA) rings stimulated by serotonin (5-HT) and KCl in Ca-free medium. Umbilical cords were obtained at vaginal or cesarean deliveries from healthy, term pregnancies. After the isolation, HUA rings were placed in organ baths in solution with indomethacin (10(-5) M) and N(G)-nitro-L-arginine methyl ester (L-NAME) (10(-3) M) at 37 degrees C and aerated with 95% O(2) and 5% CO(2) for the measurement of isometric force. In Ca-free solution with Ethylene glycol-bis (ss-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) (2 mM) the contractions produced by 5-HT (10(-6) M) and KCl (40 mM) decreased significantly. Afterwards, HUA rings were treated with 5-HT and KCl in repeated manner in Ca-free medium. In contrast to KCl, 5-HT induced contractions reduced in each application, progressively. Levcromakalim (10(-4) M) abolished the contractions elicited by 5-HT. On the other hand, levcromakalim had a little but significant inhibitory effect on KCl induced contraction in Ca-free medium. These results suggest that Ca(2+) is not the only transduction pathway in KCl produced contractions of HUA smooth muscle cells.     

A replication-deficient murine gamma-herpesvirus blocked in late viral gene expression can establish latency and elicit protective cellular immunity

The human gamma-herpesviruses, EBV and Kaposi's sarcoma-associated herpesvirus, are widely disseminated and are associated with the onset of a variety of malignancies. Thus, the development of prophylactic and therapeutic vaccination strategies is an important goal. The experimental mouse gamma-herpesvirus, gammaHV68 (or MHV-68), has provided an in vivo model for studying immune control of these persistent viruses. In the current studies, we have examined infectivity, immunogenicity, and protective efficacy following infection with a replication-deficient gammaHV68 blocked in late viral gene expression, ORF31STOP. The data show that ORF31STOP was able to latently infect B cells. However, the anatomical site and persistence of the infection depended on the route of inoculation, implicating a role for viral replication in viral spread but not the infectivity per se. Furthermore, i.p. infection with ORF31STOP elicited strong cellular immunity but a non-neutralizing Ab response. In contrast, intranasal infection was poorly immunogenic. Consistent with this, mice infected i.p. had enhanced control of both the lytic and latent viral loads following challenge with wild-type gammaHV68, whereas intranasal infected mice were not protected. These data provide important insight into mechanisms of infection and protective immunity for the gamma-herpesviruses and demonstrate the utility of replication-deficient mutant viruses in direct testing of "proof of principal" vaccination strategies.     

Patterns in body mass distributions: sifting among alternative hypotheses

Understanding how animals interact with their environment is critical for evaluating, mitigating and coping with anthropogenic alteration of Earth's biosphere. Researchers have attempted to understand some aspects of these interactions by examining patterns in animal body mass distributions. Energetic, phylogenetic, biogeographical, textural discontinuity and community interaction hypotheses have been advanced to explain observed patterns. Energetic and textural discontinuity hypotheses focus upon the allometry of resource use. The community interaction hypothesis contends that biotic interactions within assemblages of species are of primary importance. Biogeographical and phylogenetic hypotheses focus on the role of constraints on the organization of communities. This paper examines and organizes these various propositions about species body mass distributions and discusses the multiple competing hypotheses, how their predictions vary, and possible methods by which the hypotheses can be distinguished and tested. Each of the hypotheses is partial, and explains some elements of pattern in body mass distributions. The scale of appropriate application, relevance and interpretation varies among the hypotheses, and the mechanisms underlying observed patterns are likely to be multicausal and vary with scale.     

Disruption of tubulin polymerization and cell proliferation by 1-naphthylarsonic acid

Arsenical compounds exhibit a differential toxicity to cancer cells. Microtubules are a primary target of a number of anticancer drugs, such as arsenical compounds. The interaction of 1-NAA (1-naphthylarsonic acid) has been investigated on microtubule polymerization under in vitro and cellular conditions. Microtubules were extracted from sheep brain. Transmission electron microscopy was used to show microtubule structure in the presence of 1-NAA. Computational docking method was applied for the discovery of ligand-binding sites on the microtubular proteins. Proliferation of HeLa cells and HF2 (human foreskin fibroblasts) was measured by the MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide] assay method following their incubation with 1-NAA. Fluorescence microscopic labelling was done with the help of α-tubulin monoclonal antibody and Tunel kit was used to investigate the apoptotic effects of 1-NAA on the HeLa cells. 1-NAA inhibits the tubulin polymerization by the formation of abnormal polymers having high affinity to the inner cell wall.     

A Potential Association between Helicobacter pylori CagA EPIYA and Multimerization Motifs with Cytokeratin 18 Cleavage Rate during Early Apoptosis

Background and Aims: Helicobacter pylori is a highly diverse pathogen, which encounters epithelial cells as the initial defense barrier during its lifelong infection. The structure of epithelial cells can be disrupted through cleavage of microfilaments. Cytokeratin 18 (CK18) is an intermediate filament, the cleavage of which is considered an early event during apoptosis following activation of effector caspases. Methods: Helicobacter pylori strains were isolated from 76 dyspeptic patients. cagA 3’ variable region and CagA protein status were analyzed by PCR and western blotting, respectively. Eight hours post‐co‐culture of AGS cells with different H. pylori strains, flow cytometric analysis was performed using M30 monoclonal antibody specific to CK18 cleavage‐induced neo‐epitope. Results: Higher rates of CK18 cleavage were detected during co‐culture of AGS cells with H. pylori strains bearing greater numbers of cagA EPIYA‐C and multimerization (CM) motifs. On the other hand, H. pylori strains with greater numbers of EPIYA‐B relative to EPIYA‐C demonstrated a decrease in CK18 cleavage rate. Thus, H. pylori‐mediated cleavage of CK18 appeared proportional to the number of CagA EPIYA‐C and CM motifs, which seemed to be downplayed in the presence of EPIYA‐B motifs. Conclusions: Our observation associating the heterogeneity of cagA variants with the potential of H. pylori strains in the induction of CK18 cleavage as an early indication of apoptosis in gastric epithelial cells supports the fact that apoptosis may be a type‐specific trait. However, additional cagA‐targeted experiments are required to clearly identify the role of EPIYA and CM motifs in apoptosis and/or the responsible effector molecules.