Phylogeny of the genus Tordylium (Tordylineae,Apioideae, Apiaceae) inferred from morphological data

Tordylium is a medium‐sized genus characterized by an annual habit, 1–3‐pinnate leaves, dorsally compressed mericarps, and thickened mericarp margins. Eighteen Tordylium species occur in Turkey, of which seven are endemic. Although the morphology of the genus is well known, evolutionary relationships among its species have never been evaluated. In this study, phylogenetic relationships within Tordylium are investigated using parsimony analysis based on morphological data from 17 ingroup and 15 outgroup taxa from Turkey. The results indicate that Tordylium is paraphyletic due to the inclusion of Ormosciadium. Further, it suggests that Hasselquistia, Condylocarpus and Ainsworthia are nested within Tordylium, confirming their current taxonomic treatment as synonyms. Within the paraphyletic Tordylium, two major clades are apparent, but these clades are not compatible with the current sub‐generic classification. Tordylium lanatum, T. aegyptiacum and T. elegans, which have dimorphic mericarps, form a monophyletic subclade. In addition, it is suggested that T. aegaeum should be accepted as a distinct species rather than as a synonym of T. pestalozzae.     

Polyribosomes of Escherichia coli. I. Isolation of polysomes from a complex of DNA and membrane

Summary The distribution of pulse labeled RNA, pulse labeled protein, soluble enzyme (-galactosidase) and polyribosomes between low speed (10 min 20000xg) supernatant and pellet of E. coli lysates was examined. This distribution was greatly changed by addition of deoxyribonuclease to the lysing medium. Large amounts of polysomes sedimented with DNA at low centrifugal forces. A complex of membrane, DNA, polyribosomes and RNA polymerase could be separated from unlysed cells by surcrose gradient centrifugation. The polysomes present in this complex (Polysomes II) were separated from the polysomes which were found in the cytoplasma (Polysomes I). Polysomes II contain very few ribosomal subunits and 70S ribosomes.     

How is the relationship between TWIST-1 and BCR-ABL1 gene expressions in chronic myeloid leukaemia patients?

Background: The activation and increased expression of BCR-ABL1 lead to malignant chronic myelogenous leukaemia (CML) cells, as well as the resistance to antitumour agents and apoptosis inducers. Moreover, TWIST-1 protein is a prognostic factor of leukemogenesis, and its level is raised in CML patients with cytogenetic resistance to imatinib. So, there is a likely relationship between BCR-ABL1 and TWIST-1 genes.

Objective: The aim of the study was to assess the relationship between TWIST-1 and BCR-ABL1 expressions.

Methods: Peripheral blood samples were obtained from 44 CML patients under treatment and also from ten healthy subjects as normal controls. The expression of TWIST-1 and BCR-ABL1 genes was measured using real-time PCR, and ABL1 was used as the reference gene. The gene expression was evaluated by REST software.

Results: The expression levels of TWIST-1 and BCR-ABL1 genes in CML patients was changed 40.23?±?177.75-fold and 6?±?18-fold, respectively.

Discussion: No significant relationship was observed between the expressions of TWIST-1 and BCR-ABL1 genes. All patients with TWIST-1 expression levels?≥100-fold had failure of response to treatment.

Conclusion: The probability of the relationship between BCR-ABL1 and TWIST-1 is still debatable, and the average of TWIST-1 expression has been higher in patients without response to treatment. Definitive conclusion needs further investigations.     

Heat shock protein 27 as a neuroprotective biomarker and a suitable target for stem cell therapy and pharmacotherapy in ischemic stroke

Ischemic stroke is a major common cause of death and long‐term disability worldwide. Several pathophysiological events including excitotoxicity, oxidative/nitrative stress, inflammation, and apoptosis are involved in ischemic injuries. Recently, the molecular mechanisms involved in cerebral ischemia through a focus on a member of small heat shock proteins family, Hsp27, has been developed. Notably, following exposure to ischemia, Hsp27 expression in the brain could be increased rather than the normal condition and it may play an important role in neuroprotection after ischemic stroke. The neuroprotection effects of Hsp27 may arise from its anti‐oxidant, anti‐inflammatory, anti‐apoptotic, and chaperonic properties. Moreover, some therapeutic strategies such as stem cell therapy and pharmacotherapy have been developed with Hsp27 targeting. In this review, we describe the function and structure of Hsp27 and its possible role in neuroprotection after ischemic stroke. Finally, we present current studies in stroke therapy, which focused on Hsp27 targeting.     

The roles of polyamines in microorganisms

Polyamines are small polycations that are well conserved in all the living organisms except Archae, Methanobacteriales and Halobacteriales. The most common polyamines are putrescine, spermidine and spermine, which exist in varying concentrations in different organisms. They are involved in a variety of cellular processes such as gene expression, cell growth, survival, stress response and proliferation. Therefore, diverse regulatory pathways are evolved to ensure strict regulation of polyamine concentration in the cells. Polyamine levels are kept under strict control by biosynthetic pathways as well as cellular uptake driven by specific transporters. Reverse genetic studies in microorganisms showed that deletion of the genes in polyamine metabolic pathways or depletion of polyamines have negative effects on cell survival and proliferation. The protein products of these genes are also used as drug targets against pathogenic protozoa. These altogether confirm the significant roles of polyamines in the cells. This mini-review focuses on the differential concentrations of polyamines and their cellular functions in different microorganisms. This will provide an insight about the diverse evolution of polyamine metabolism and function based on the physiology and the ecological context of the microorganisms.     

The genetic factors contributing to hypospadias and their clinical utility in its diagnosis

Hypospadias is among the most common congenital malformations in male neonates. It results from abnormal penile and urethral development, but is a multifactorial disorder that is highly heterogeneous, with several genetic and environmental determinants. Monogenic and chromosomal abnormalities are present in approximately 30% of cases, although the genetic factors contributing to hypospadias remain unknown in 70% of cases. While defects in androgen synthesis can lead to this malformation, mutational analyses have shown several genes, such as sonic hedgehog, fibroblast growth factors, bone morphogenetic proteins, homeobox genes, and the Wnt family, are involved in the normal development of male external genitalia. Mutations in the genes of penile development (e.g., HOX, FGF, Shh) and testicular determination (e.g., WT1, SRY), luteinizing hormone receptor, and androgen receptor have also been proposed to be implicated in hypospadias. Here we review the recent advances in this field and discuss the potential genes that could determine the risk of hypospadias.     

Quantitative proteomics analysis of human endothelial cell membrane rafts: evidence of MARCKS and MRP regulation in the sphingosine 1-phosphate-induced barrier enhancement

Endothelial cell barrier dysfunction results in the increased vascular permeability observed in inflammation, tumor metastasis, angiogenesis, and atherosclerosis. Sphingosine 1-phosphate (S1P), a biologically active phosphorylated lipid growth factor released from activated platelets, enhances the endothelial cell barrier integrity in vitro and in vivo. To begin to identify the molecular mechanisms mediating S1P induced endothelial barrier enhancement, quantitative proteomics analysis (iTRAQ) was performed on membrane rafts isolated from human pulmonary artery endothelial cells in the absence or presence of S1P stimulation. Our results demonstrated that S1P mediates rapid and specific recruitment (1 microM, 5 min) of myristoylated alanine-rich protein kinase C substrate (MARCKS) and MARCKS-related protein (MRP) to membrane rafts. Western blot experiments confirmed these findings with both MARCKS and MRP. Finally, small interfering RNA-mediated silencing of MARCKS or MRP or both attenuates S1P-mediated endothelial cell barrier enhancement. These data suggest the regulation of S1P-mediated endothelial cell barrier enhancement via the cell specific localization of MARCKS and MRP and validate the utility of proteomics approaches in the identification of novel molecular targets.