Hydrogen Sulfide Protects Damage From Methyl Viologen-Mediated Oxidative Stress by Improving Gas Exchange,Fluorescence Kinetics of Photosystem II,and Antioxidant System in Arabidopsis thaliana

Journal of Plant Growth Regulation - Considering the unfavorable impacts of methyl viologen-induced oxidative stress (MV1-2, 50 and 500 µM) on growth, gas exchange (intercellular CO2...     

Intercostal variation for age estimation--are the standards for the right 4th rib applicable for other ribs?

Age estimation of unknown skeletal remains is very important in forensic medicine. Morphologic methods are fast and easy to use for purpose of age determination. The sternal ends of the ribs are a reliable method of age estimation from late adolescence to old age. Iscan et al developed a phase analysis method for the right 4th rib that was sex and race specific. The purpose of this study is to determine the accuracy of the standards of age estimation from the right 4th and other rib using the phase analysis for the Turkish population. The sample consisted of right and left 3rd, 4th and 5th ribs from 34 Turkish women and 76 men. There were statistically significant variations found on the right 5th, left 3rd, 4th, and 5th ribs according to these standards in men for phases 5, 6, and 7. For women, all the right and left ribs included in this study were in concordance with right 4th rib standards in all phases.     

Meiotic state of bovine oocytes is regulated by interactions between cAMP,cumulus, and granulosa

Bovine oocytes are arrested at the prophase of first meiotic cell cycle. Meiosis resumes in oocytes of pre-ovulatory follicles upon LH surge. However, oocytes from secondary follicles spontaneously resume meiosis in the absence of hormones if removed from the follicle and cultured in vitro. The nature of meiotic arrestor in bovine follicles is poorly understood. In this study we investigated the role of cell-cell interactions between granulosa and cumulus cells and the oocyte in mediating maintenance of meiotic arrest by cAMP. We sorted oocytes as granulosa-cumulus oocyte complexes (GCOC) if surrounded with cumulus cells attached to a large granulosa investment or cumulus oocytes complexes (COC) if surrounded with cumulus cells only and investigated the role cAMP in maintenance of meiotic arrest in these oocytes under various conditions. In hormone- and serum-free medium both GCOC and COC enclosed oocytes resumed meiosis. When [cAMP](i) was elevated with addition of invasive adenylate cyclase (iAC) GCOC enclosed oocytes were maintained in the prophase with intact germinal vesicle (GV) while COC enclosed oocytes underwent GV breakdown (GVBD). iAC elevated [cAMP](i) in both types of oocytes to the same level. If oocytes were liberated from the cumulus and granulosa cells, they re-initiated meiosis in serum and hormone free medium, but remained in the GV stage if iAC was added to the medium. Untreated GCOC and COC enclosed oocytes extruded first polar body at the same frequency in hormone-supplemented media. GCOC and COC enclosed oocytes but not denuded oocytes (DO) cultured without somatic cells acquired developmental competence if cultured in hormone-containing medium. It is concluded that maintenance of meiotic arrest is regulated by the interplay of [cAMP](i), and cumulus and granulosa cells.     

Design of potent fluoro-substituted chalcones as antimicrobial agents

Owing to ever-increasing bacterial and fungal drug resistance, we attempted to develop novel antitubercular and antimicrobial agents. For this purpose, we developed some new fluorine-substituted chalcone analogs (3, 4, 9–15, and 20–23) using a structure–activity relationship approach. Target compounds were evaluated for their antitubercular efficacy against Mycobacterium tuberculosis H37Rv and antimicrobial activity against five common pathogenic bacterial and three common fungal strains. Three derivatives (3, 9, and 10) displayed significant antitubercular activity with IC₅₀ values of ≤16,760. Compounds derived from trimethoxy substituent scaffolds with monofluoro substitution on the B ring of the chalcone structure exhibited superior inhibition activity compared to corresponding hydroxy analogs. In terms of antimicrobial activity, most compounds (3, 9, 12–14, and 23) exhibited moderate to potent activity against the bacteria, and the antifungal activities of compounds 3, 13, 15, 20, and 22 were comparable to those of reference drugs ampicillin and fluconazole.     

The C-terminal peptide of thrombospondin-1 stimulates distinct signaling pathways but induces an activation-independent agglutination of platelets and other cells

A peptide from the C-terminal domain of thrombospondin-1 (4N1-1) has been proposed to stimulate platelet aggregation by a novel mechanism involving both an activation-independent agglutination and an activation-dependent, glycoprotein (GP) IIb/IIIa-mediated aggregation which involves GPVI signaling but does not involve CD47. The present study demonstrates that 4N1-1 stimulated a different pattern of signal transduction pathways than the GPVI agonist convulxin. Furthermore, 4N1-1-induced platelet aggregation was activation-independent and not dependent on GPVI or GPIIb/IIIa. Interestingly, 4N1-1 also stimulated activation-independent agglutination of different megakaryocytic and non-megakaryocytic cells. 4N1-1-induced cell agglutination but not platelet signaling was inhibited by anti-CD47 antibodies.     

Comparison of long-term retinoic acid-based neural induction methods of bone marrow human mesenchymal stem cells

The differentiation of human mesenchymal stem cells (hMSCs) into neural cells in vitro provides a potential tool to be utilized for cell therapy of neurodegenerative disorders. Although previous studies repeated different protocols for the induction of neural cells from hMSCs in vitro, the results were not in complete agreement. In this study, we have attempted to compare three of these neural induction methods; retinoic acid (RA) treatment, RA treatment in serum reduced conditions, and treatment using other chemical compounds (dimethyl sulfoxide and potassium chloride) along with RA by real-time cell analysis and immunofluorescent staining of neural markers. RA treatment led to a slow progression of cells into neural-like morphology with the expression of neural protein neurofilament whereas reducing serum during RA treatment caused a much more extended differentiation process. Additionally, neural-like morphology was persistent in the later periods of differentiation in RA treatment. On the other hand, chemical induction caused cell shrinkages mimicking neural-like morphology in a short time and loss of this morphology along with increased cell death in later periods. Among the three methods compared, RA treatment was the most reliable one in terms of stability of differentiation and neural protein expressions.     

Effects of nicotine and vitamin E on glucose 6-phosphate dehydrogenase activity in some rat tissues in vivo and in vitro

Effects of nicotine, and nicotine + vitamin E on glucose 6-phosphate dehydrogenase (G-6PD) activity in rat muscle, heart, lungs, testicle, kidney, stomach, brain and liver were investigated in vivo and in vitro on partially purified homogenates. Supplementation period was 3 weeks (n = 8 rats per group): nicotine [0.5 mg/kg/day, intraperitoneal (ip)]; nicotine + vitamin E [75 mg/kg/day, intragastric (ig)]; and control group (receiving only vehicle). The results showed that nicotine (0.5 mg/kg, ip) inhibited G-6PD activity in the lungs, testicle, kidney, stomach and brain by 12.5% (p < 0.001), 48% (p < 0.001), 20.8% (p < 0.001), 13% (p < 0.001) and 23.35% (p < 0.001) respectively, and nicotine had no effects on the muscle, heart and liver G6PD activity. Also, nicotine + vitamin E inhibited G-6PD activity in the testicle, brain, and liver by 32.5% (p < 0.001), 21.5% (p < 0.001), and 16.5% (p < 0.001) respectively, and nicotine + vitamin E activated the muscle, and stomach G-6PD activity by 36% (p < 0.05), and 20% (p < 0.001) respectively. In addition, nicotine + vitamin E did not have any effects on the heart, lungs, and kidney G-6PD activity. In addition, in vitro studies were also carried out to elucidate the effects of nicotine and vitamin E on G-6PD activity, which correlated well with in vivo experimental results in lungs, testicles, kidney, stomach, brain and liver tissues. These results show that vitamin E administration generally restores the inactivation of G-6PD activity due to nicotine administration in various rat tissues in vivo, and also in vitro.     

p57kip2 regulates glial fate decision in adult neural stem cells

Our recent studies revealed p57kip2 as an intrinsic regulator of late gliogenesis and demonstrated that in oligodendroglial precursor cells p57kip2 inhibition leads to accelerated maturation. Adult neural stem cells have been described as a source of glial progenitors; however, the underlying mechanisms of cell fate specification are still poorly understood. Here, we have investigated whether p57kip2 can influence early events of glial determination and differentiation. We found that Sox2/GFAP double-positive cells express p57kip2 in stem cell niches of the adult brain. Short-hairpin RNA-mediated suppression of p57kip2 in cultured adult neural stem cells was found to strongly reduce astroglial characteristics, while oligodendroglial precursor features were increased. Importantly, this anti-astrogenic effect of p57kip2 suppression dominated the bone morphogenetic protein-mediated promotion of astroglial differentiation. Moreover, we observed that in p57kip2 knockdown cells, the BMP antagonist chordin was induced. Finally, when p57kip2-suppressed stem cells were transplanted into the adult spinal cord, fewer GFAP-positive cells were generated and oligodendroglial markers were induced when compared with control cells, demonstrating an effect of in vivo relevance.     

Ras links growth factor signaling to the cell cycle machinery via regulation of cyclin D1 and the Cdk inhibitor p27KIP1.

Activation of growth factor receptors by ligand binding initiates a cascade of events leading to cell growth and division. Progression through the cell cycle is controlled by cyclin-dependent protein kinases (Cdks), but the mechanisms that link growth factor signaling to the cell cycle machinery have not been established. We report here that Ras proteins play a key role in integrating mitogenic signals with cell cycle progression through G1. Ras is required for cell cycle progression and activation of both Cdk2 and Cdk4 until approximately 2 h before the G1/S transition, corresponding to the restriction point. Analysis of Cdk-cyclin complexes indicates that Ras signaling is required both for induction of cyclin D1 and for downregulation of the Cdk inhibitor p27KIP1. Constitutive expression of cyclin D1 circumvents the requirement for Ras signaling in cell proliferation, indicating that regulation of cyclin D1 is a critical target of the Ras signaling cascade.