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Dysfunction of mitochondria as the basis of Parkinson’s disease

control. Antioxid Redox Signal. 2011;14(10):1929-38; DOI:10.1089/ars.2010.3799. 94. Rakovic A, Shurkewitsch K, Seibler P, Grünewald A, Zanon A, Hagenah J, Krainc D, Klein C. Phosphatase and tensin homolog (PTEN)-induced putative kinase 1 (PINK1)-dependent ubiquitination of endogenous Parkin attenuates mitophagy: Study in human primary fibroblasts and induced pluripotent stem cell-derived neurons. J Biol Chem. 2013;288(4):2223-37; DOI:10.1074/jbc.M112.391680. 95. Wang X, Petrie T, Liu Y, Liu J, Fujioka H, Zhu X. Parkinson’s disease-associated DJ-1 mutations

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Circulating miR-210 and miR-1246 as potential biomarkers for differentiating hepatocellular carcinoma from metastatic tumors in the liver

British Journal of Cancer 2013 108 3 644 52 52 Kim G, An HJ, Lee MJ, Song JY, Jeong JY, Lee JH, Jeong HC. Hsa-miR-1246 and hsa-miR-1290 are associated with stemness and invasiveness of non-small cell lung cancer. Lung Cancer (Amsterdam, Netherlands) 2016; 91: 15–22. 10.1016/j.lungcan.2015.11.013 Kim G An HJ Lee MJ Song JY Jeong JY Lee JH Jeong HC. Hsa-miR-1246 and hsa-miR-1290 are associated with stemness and invasiveness of non-small cell lung cancer Lung Cancer (Amsterdam, Netherlands) 2016 91 15 22 53 Wang S, Zeng Y, Zhou JM, Nie SL, Peng Q, Gong J, Huo JR

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Thiol-disulphide homeostasis in essential thrombocythemia patients

is high in ET patients ( 2 , 3 ). ET is a disease with bone marrow myeloproliferation in which monoclonal proliferation of megakaryocytes is more distinct. Although the pathogenesis of ET is not clearly known, 90% of cases have acquired somatic driver mutations such as JAK2, CALR, and MPL. Hypersensitivity to cytokines such as erythropoietin (EPO), thrombopoietin (TPO), interleukin 3 (IL-3) and stem cell factor (SCF) is known in the etiopathogenesis of ET. Increased free radicals are also known to increase the risk of genetic mutation in neoplastic processes ( 4

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Interaction of apelin, elabela and nitric oxide in schizophrenia patients

burden of schizophrenia in the United States was $156 billion ( 2 ). Elabela (ELA) is a peptide of 32 amino acids that activates the apelin receptor (APJ) ( 5 , 6 ). It plays a role in various biological events such as self-renewing human embryonic stem cells in embryonic and adult periods, endoderm differentiation, cardiac morphogenesis, bone formation, regulation of blood pressure, water and food intake ( 7 ). ELA appears in many tissues including the APJ such as placenta, heart, kidney, lung, liver, brain, skeletal muscle, gastrointestinal system ( 8 ). Before

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Association of overexpressed MYC gene with altered PHACTR3 and E2F4 genes contributes to non-small cell lung carcinoma pathogenesis

, optimize treatments and enable monitoring disease progression and response to therapy. Molecules that regulate cellular processes essential for maintaining malignant phenotype, such as c-Myc oncogene, stand out as promising candidates to serve as molecular markers. This nuclear phosphoprotein functions as transcriptional regulator of multiple genes and controls cell proliferation, induces apoptosis, and regulates stemness, senescence, metabolism and genome stability ( 4 ). Its expression is deregulated in number of human cancers including breast cancer, Burkitt

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Mouse (Mus musculus) embryonic cerebral cortex cell death caused by carbofuran insecticide exposure

carcasses ( 20 ). In 2001, a flower plantation in Ecuador was contaminated by CF. There were some babies born with impaired reflex and motor functions. During their childhood, the effect of CF contamination was brain development dysfunctions, such as poor concentration and memory ( 8 ). CF, a potential environmental xenobiotic, has the ability to cross the blood–brain barrier and to adversely influence brain functions ( 6 ). Like organophosphate, CF ingestion by gavage may cause significant oxidative damage to the cerebral cortex, cerebellum, and brain stem. Cerebral

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Therapy-related myelodysplastic syndrome after successful treatment of acute promyelocytic leukemia: case report and literature review

Abstract

In the 2016 revision of the World Health Organization classification the term therapy-related myeloid neoplasia (t-MN) defines a subgroup of acute myeloid leukemia (AML) comprising patients who develop myelodysplastic syndrome (MDS-t) or acute myeloid leukemia (AML-t) after treatment with cytotoxic and/or radiation therapy for various malignancies or autoimmune disorders. We report the case of a 36 year old patient with t-MN (t-MDS) after achieving complete remission (CR) of a PML-RARA positive acute promyelocytic leukemia (APL) at 32 months after diagnosis. Initially classified as low risk APL and treated according to the AIDA protocol - induction and 3 consolidation cycles - the patient achieved a complete molecular response in September 2013 and started maintenance therapy. On follow-up PML-RARA transcript remained negative. In January 2016 leukopenia and thrombocytopenia developed and a peripheral blood smear revealed hypogranular and agranular neutrophils. Immunophenotyping in the bone marrow aspirate identified undifferentiated blast cells that did not express cytoplasmic myeloperoxidase. The cytogenetic study showed normal karyotype. The molecular biology tests not identified PMLRARA transcript. A diagnosis of t-MDS (AREB-2 - WHO 2008) was established. Treatment of AML was started with 2 “3+7” regimens and 1 MEC cycle. Two months from diagnosis, while in CR, an allogeneic HSCT from an unrelated HLA compatible donor was performed after myeloablative regimen. An unfavorable clinical evolution was followed by death on day 9 after transplantation. The occurrence of t-MNs during CR of APL represents a particular problem in terms of follow-up and differential diagnosis of relapse and constitutes a dramatic complication for a disease with a favorable prognosis.

This work was supported by the grants PN 41-087 /PN2-099 from the Romanian Ministry of Research and Technology

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Performance and Genetic Parameters of Somatic and Zygotic Progenies of Coastal Douglas-fir at 71/2-Years across Washington and Oregon, USA

References ADAMS, W. T. and D. G. JOYCE (1990): Comparison of selection methods for improving volume growth in young coastal Douglas-fir. Silvae Genet. 39: 219-226. BALTUNIS, B. S., D. A. HUBER, T. L. WHITE, B. GOLDFARB and H. E. STELZER (2005): Genetic effects of rooting loblolly pine stem cuttings from a partial diallel mating design. Can. J. For. Res. 35: 1098-1108. BENOWICZ, A., S. C. GROSSNICKLE and Y. A. EL-KASSABY (2002): Field assessment of Douglas-fir somatic and zygotic seedlings with respect to gas

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Acquisition and Expansion of Adult Rat Bone Marrow Multipotent Mesenchymal Stromal Cells

REFERENCES 1. Animal Protection Act of Slovakia No. 15/1995, part 39 (In Slovak), 1250—1255. 2. Caplan, A. I., Dennis, J. E., 2006: Mesenchymal stem cells as trophic mediators. J. Cell. Biochem. , 98, 1076—1084. 3. Chesier, S. H., Kalani, M. Y. S., Lim, M., Ailles, L., Huhn, S. L., Weissman, I. L., 2009: A neurosurgeon’s guide to stem cells, cancer stem cells, and brain tumor stem cells. Neurosurgery , 65, 237—250. 4. Čížková, D., Rosocha, J., Vanický, I., Jergová, S., Čížek, M., 2006: Transplants of human mesenchymal stem cells

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Growth Performance and Heritability Estimation of Acacia crassicarpa in a Progeny Trial in eastern Thailand

References Arnold RJ and E Cuevad (2003) Genetic variation in early growth, stem straightness and survival in A. crassicarpa, A. mangium and Eucalyptus urophylla in Nukindon Province, Philippines. Journal of Tropical Forest Sciences 15 (2): 332-351. Awang K, NA Shukor and AL Senin (1995) Two-year performance of Acacia crassicarpa provenances at Serdang, Malaysia. Pertanika J. Trop. Agric. Sci. 18(3): 177-181. Holland BJ, WE Nyquist and CT Cervantes-Martinez (2003) Estimating and interpreting heritability for plant breeding [online] pp. 9-112. In

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