Caryological study on four Hesperis L. (Cruciferae) taxa from the Diaplictos (Dvorák) Dvorák section in Turkey

This study examined chromosome numbers and karyotypes of four taxa, Hesperis novakii Dvorák, H. bottae Fourn., H. balansae Fourn. and H. syriaca (DC.) Dvorák, from naturally growing Diaplictos (Dvorák) Dvorák section, which is represented by only these four taxa in Turkey, in the genus Hesperis. H. novakii and H. syriaca have 2n=14 chromosomes, H. bottae and H. balansae have 2n=12 chromosomes in somatic cells. Total chromosome lengths are 5.37 mum and 2.17 mum in H. novakii, 5.38 mum and 2.70 mum in H. bottae, 9.59 mum and 4.28 mum in H. balansae, 4.88 mum and 2.32 mum in H. syriaca (no. 4969), 7.89 mum and 3.44 mum in H. syriaca (no. 4971). The karyotypes are as follows: H. novakii consists of 3m+1sm+1st+2T, H. bottae consists of 4m+2st, H. balansae consists of 4m+2sm, H. syriaca (no. 4969) consists of 3m+1sm+1st+2T and H. syriaca (no. 4971) consists of 3m+1sm+1st+2T chromosome pairs. Results were discussed from a cytological and taxonomical point of view.     

Molecular mechanism by which palmitate inhibits PKR autophosphorylation

PKR (double-stranded RNA-activated protein kinase) is an important component of the innate immunity, antiviral, and apoptotic pathways. Recently, our group found that palmitate, a saturated fatty acid, is involved in apoptosis by reducing the autophosphorylation of PKR at the Thr451 residue; however, the molecular mechanism by which palmitate reduces PKR autophosphorylation is not known. Thus, we investigated how palmitate affects the phosphorylation of the PKR protein at the molecular and biophysical levels. Biochemical and computational studies show that palmitate binds to PKR, near the ATP-binding site, thereby inhibiting its autophosphorylation at Thr451 and Thr446. Mutation studies suggest that Lys296 and Asp432 in the ATP-binding site on the PKR protein are important for palmitate binding. We further confirmed that palmitate also interacts with other kinases, due to the conserved ATP-binding site. A better understanding of how palmitate interacts with the PKR protein, as well as other kinases, could shed light onto possible mechanisms by which palmitate mediates kinase signaling pathways that could have implications on the efficacy of current drug therapies that target kinases.     

Determination of stress responses induced by aluminum in maize (Zea mays)

To assess the alternative responses to aluminum toxicity, maize (Zea mays L. cv Karadeniz y?ld?z?) roots were exposed to different concentrations of AlCl3 (150, 300 and 450 μM). Aluminum reduced the root elongation by 39.6% in 150 μM, 44.1% in 300 μM, 50.1% in 450 μM AlCl3 after 96 h period. To correlate the root elongation with the alternative stress responses including aluminum accumulation, lipid peroxidation, mitotic abnormalities, reduction of starch content, intracellular Ca2+ accumulation, callose formation, lignin deposition and peroxidase activity, cytochemical and biochemical tests were performed. The results indicated that aluminum accumulation and lipid peroxidation were observed more densely on the root cap and the outer cortex cells. In addition to morphological deformations, cytochemical analysis displayed cellular deformations. Furthermore, mitotic abnormalities were observed such as c-mitosis, micronuclei, bi- and trinucleated cells in aluminum treated root tips. Aluminum treatment induced starch reduction, callose formation, lignin accumulation and intracellular Ca2+ increase. Moreover, the peroxidase activity increased significantly by 3, 4.4 and 7.7 times higher than in that of control after 96 h, respectively. In conclusion, aluminum is significantly stressful in maize culminating in morphological and cellular alterations.     

Elevated S100B and Neuron Specific Enolase Levels in Patients with Migraine-without Aura: Evidence for Neurodegeneration?

Although migraine has mainly been considered as a benign disease, there is cumulative evidence of silent changes in the brain, brainstem, or cerebellum and subtle subclinical cerebellar dysfunction. In this study, in order to investigate a possible neuronal and/or glial damage at the cellular level in migraine, we measured and compared serum levels of S100B which is a protein marker of glial damage or activation, and neuron specific enolase (NSE) which is a marker of neuronal damage, in migraine patients and control subjects. Serum levels of S100B and NSE were measured in blood samples from 41 patients with migraine-without aura taken during a migraine attack (ictal) and in the attack-free period between migraine attacks (interictal) and 35 age- and sex-matched controls. Patients with migraine-without aura had significantly higher ictal serum levels of S100B and NSE (P < 0.05, for both) than control subjects; whereas in the interictal phase, there was a significant increment only in S100B levels (P < 0.05) compared to controls. On the other hand, serum levels of S100B and NSE in ictal and interictal blood samples did not differ significantly. The findings of increased ictal serum S100B and NSE levels together with increased interictal levels of S100B suggested that migraine might be associated with glial and/or neuronal damage in the brain and a prolonged disruption of blood–brain barrier. Increased interictal serum levels of S100B might point out to an insidious and slow damaging process in migraine patients.     

Ubiquitination regulates the internalization, endolysosomal sorting, and signaling of the erythropoietin receptor

Ubiquitination is a common mechanism of down-regulation of mitogenic receptors. Here, we show that ubiquitination of the erythropoietin receptor (EpoR) at Lys(256) is necessary and sufficient for efficient Epo-induced receptor internalization, whereas ubiquitination at Lys(428) promotes trafficking of activated receptors to the lysosomes for degradation. Interestingly, EpoR that cannot be ubiquitinated has reduced mitogenic activities and ability to stimulate the STAT5, Ras/MAPK, and PI3K/AKT signaling pathways. We therefore propose that ubiquitination of the EpoR critically controls both receptor down-regulation and downstream signaling.     

Genetic Models of Apoptosis-Induced Proliferation Decipher Activation of JNK and Identify a Requirement of EGFR Signaling for Tissue Regenerative Responses in Drosophila

Recent work in several model organisms has revealed that apoptotic cells are able to stimulate neighboring surviving cells to undergo additional proliferation, a phenomenon termed apoptosis-induced proliferation. This process depends critically on apoptotic caspases such as Dronc, the Caspase-9 ortholog in Drosophila, and may have important implications for tumorigenesis. While it is known that Dronc can induce the activity of Jun N-terminal kinase (JNK) for apoptosis-induced proliferation, the mechanistic details of this activation are largely unknown. It is also controversial if JNK activity occurs in dying or in surviving cells. Signaling molecules of the Wnt and BMP families have been implicated in apoptosis-induced proliferation, but it is unclear if they are the only ones. To address these questions, we have developed an efficient assay for screening and identification of genes that regulate or mediate apoptosis-induced proliferation. We have identified a subset of genes acting upstream of JNK activity including Rho1. We also demonstrate that JNK activation occurs both in apoptotic cells as well as in neighboring surviving cells. In a genetic screen, we identified signaling by the EGFR pathway as important for apoptosis-induced proliferation acting downstream of JNK signaling. These data underscore the importance of genetic screening and promise an improved understanding of the mechanisms of apoptosis-induced proliferation.     

Genotoxic action of fungicide Conan 5FL (hexaconazole) on mammalian cells in vivo and in vitro

The genotoxic effects of fungicide Conan 5FL (containing 50 g/L hexaconazole) in mouse bone-marrow cells and human lymphocytes have been evaluated. Three different concentrations of Conan 5FL (17.50, 35.00 and 70.00 microg/mL for human lymphocytes and 17.50, 35.00 and 70.00 mg/kg for mouse bone marrow cells) were studied. Conan 5FL induced significant increases (except 17.50 mg/kg for mouse bone marrow) in the frequency of chromosomal aberrations (CAs) in both test systems. This fungicide caused structural and numerical abnormalities in both mammalian cells. These are sister chromatid union, chromatid and chromosome breaks, fragments, dicentric and ring chromosomes, and polyploidy. Significant increase was found in induction and in minimum-maximum numbers of sister chromatid exchanges (SCEs) at all treatments compared with the negative control. Conan 5FL did not affect the replication index (RI) in human lymphocyte cultures, however, it significantly decreased the mitotic index (MI) in all treatment concentrations in both test systems. Using of Conan 5FL should be reconsidered due to its possible cytotoxic, clastogenic and mutagenic effects.     

Surgical and Molecular Evaluation of Pediatric Hydatid Cyst Cases in Eastern Turkey

Cystic echinococcosis (CE) caused by Echinococcus granulosus is a major public health problem worldwide, including Turkey. The aim of the current study was to identify the strains and to estimate the potential risk factors of E. granulosus in operated pediatric cases in eastern Turkey. Ten pediatric patients (7 boys and 3 girls) living in rural areas, with ages ranging from 3 to 15 years old and various clinical histories, were included in this study. Eight patients had only liver hydatid cyst, while 1 patient had liver and lung hydatid cyst and the other liver, lung, and spleen, together. There were 2 ruptured liver cysts. After surgery, during follow-up, no increase was observed in hemagglutination levels, there were no mortalities, and there was no evidence of recurrence at 2 years post operation in all patients. Molecular analysis was performed on hydatid cyst samples obtained from the 10 pediatric cases. According to mt-12S rRNA PCR results, all cases were found to be G1/G3 cluster of E. granulosus sensu stricto.