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排序方式: 共有140条查询结果,搜索用时 15 毫秒
21.
22.
Dorian Salin Pierre-Jean Arnoux Kambiz Kayvantash Michel Behr 《Computer methods in biomechanics and biomedical engineering》2016,19(14):1578-1582
In the field of biomechanics, the offer of models which are more and more realistic requires to integrate a physiological response, in particular, the controlled muscle bracing and the reflexes. The following work aims to suggest a unique methodology which couples together a sensory and motor loop with a finite element model. Our method is applied to the study of the oscillation of the elbow in the case of a biceps brachial stretch reflex. The results obtained are promising in the purpose of the development of reactive human body models. 相似文献
23.
Maria Weinert Tharakeswari Selvakumar Travis S. Tierney Kambiz N. Alavian 《Journal of visualized experiments : JoVE》2015,(96)
Degeneration of mesencephalic dopaminergic (mesDA) neurons is the pathological hallmark of Parkinson’s diseae. Study of the biological processes involved in physiological functions and vulnerability and death of these neurons is imparative to understanding the underlying causes and unraveling the cure for this common neurodegenerative disorder. Primary cultures of mesDA neurons provide a tool for investigation of the molecular, biochemical and electrophysiological properties, in order to understand the development, long-term survival and degeneration of these neurons during the course of disease. Here we present a detailed method for the isolation, culturing and maintenance of midbrain dopaminergic neurons from E12.5 mouse (or E14.5 rat) embryos. Optimized cell culture conditions in this protocol result in presence of axonal and dendritic projections, synaptic connections and other neuronal morphological properties, which make the cultures suitable for study of the physiological, cell biological and molecular characteristics of this neuronal population. 相似文献
24.
Gray JP Alavian KN Jonas EA Heart EA 《American journal of physiology. Endocrinology and metabolism》2012,303(2):E191-E199
NADPH is an important component of the antioxidant defense system and a proposed mediator in glucose-stimulated insulin secretion (GSIS) from pancreatic β-cells. An increase in the NADPH/NADP(+) ratio has been reported to occur within minutes following the rise in glucose concentration in β-cells. However, 30 min following the increase in glucose, the total NADPH pool also increases through a mechanism not yet characterized. NAD kinase (NADK) catalyzes the de novo formation of NADP(+) by phosphorylation of NAD(+). NAD kinases have been shown to be essential for redox regulation, oxidative stress defense, and survival in bacteria and yeast. However, studies on NADK in eukaryotic cells are scarce, and the function of this enzyme has not been described in β-cells. We employed INS-1 832/13 cells, an insulin-secreting rat β-cell line, and isolated rodent islets to investigate the role of NADK in β-cell metabolic pathways. Adenoviral-mediated overexpression of NADK resulted in a two- to threefold increase in the total NADPH pool and NADPH/NADP(+) ratio, suggesting that NADP(+) formed by the NADK-catalyzed reaction is rapidly reduced to NADPH via cytosolic reductases. This increase in the NADPH pool was accompanied by an increase in GSIS in NADK-overexpressing cells. Furthermore, NADK overexpression protected β-cells against oxidative damage by the redox cycling agent menadione and reversed menadione-mediated inhibition of GSIS. Knockdown of NADK via shRNA exerted the opposite effect on all these parameters. These data suggest that NADK kinase regulates intracellular redox and affects insulin secretion and oxidative defense in the β-cell. 相似文献
25.
Razia Sultana Bina Shaheen Siddiqui Kambiz Taraz Herbert Budzikiewicz Jean-Marie Meyer 《Biometals》2000,13(2):147-152
From Pseudomonas putida CFML 90-51 – a hospital isolate – a pyoverdine was obtained which is characterized by the unusual linkage by the -rather than the -amino group of Lys in the peptide chain. The structure elucidation by spectroscopic methods and degradation reactions is reported. 相似文献
26.
Saumitri Bhattacharyya Jeremy Keirsey Beatriz Russell Juraj Kavecansky Kate Lillard-Wetherell Kambiz Tahmaseb John J. Turchi Joanna Groden 《The Journal of biological chemistry》2009,284(22):14966-14977
The BLM helicase associates with the telomere structural proteins TRF1 and
TRF2 in immortalized cells using the alternative
lengthening of telomere (ALT) pathways. This work
focuses on identifying protein partners of BLM in cells using ALT. Mass
spectrometry and immunoprecipitation techniques have identified three proteins
that bind directly to BLM and TRF2 in ALT cells: telomerase-associated protein
1 (TEP1), heat shock protein 90 (HSP90), and topoisomerase IIα
(TOPOIIα). BLM predominantly co-localizes with these proteins in foci
actively synthesizing DNA during late S and G2/M phases of the cell
cycle when ALT is thought to occur. Immunoprecipitation studies also indicate
that only HSP90 and TOPOIIα are components of a specific complex
containing BLM, TRF1, and TRF2 but that this complex does not include TEP1.
TEP1, TOPOIIα, and HSP90 interact directly with BLM in vitro
and modulate its helicase activity on telomere-like DNA substrates but not on
non-telomeric substrates. Initial studies suggest that knockdown of
BLM in ALT cells reduces average telomere length but does not do so
in cells using telomerase.Bloom syndrome
(BS)4 is a genetic
disease caused by mutation of both copies of the human BLM gene. It
is characterized by sun sensitivity, small stature, immunodeficiency, male
infertility, and an increased susceptibility to cancer of all sites and types.
The high incidence of spontaneous chromosome breakage and other unique
chromosomal anomalies in cells from BS patients indicate an increase in
homologous recombination in somatic cells
(1). Another notable feature of
non-immortalized and immortalized cells from BS individuals is the presence of
telomeric associations (TAs) between homologous chromosomes
(2). Work from our group and
others have suggested a role for BLM in recombination-mediated mechanisms of
telomere elongation or ALT (alternative lengthening of telomeres), processes
that maintain/elongate telomeres in the absence of telomerase
(3–5).
However, the exact mechanism by which BLM contributes to telomere stability is
unknown.Several proteins interact with and regulate BLM helicase activity,
including two telomere-specific proteins, TRF1 and TRF2
(6,
7). Although TRF2 stimulates
BLM unwinding of telomeric and non-telomeric 3′-overhang substrates,
TRF1 inhibits BLM unwinding of telomeric substrates. TRF2-mediated stimulation
of BLM helicase activity on a telomeric substrate is observed when TRF2 is
present in excess or with equimolar amount of TRF1 but not when TRF1 is
present in molar excess. Both proteins associate with BLM specifically in ALT
cells in vivo, suggesting their involvement in the ALT pathways. In
addition to TRF1 and TRF2, the telomere single-strand DNA-binding protein POT1
strongly stimulates BLM helicase activity on long telomeric forked duplexes
and D-loop structures (8).
Other proteins also play an important role in telomere maintenance in
telomerase-negative cells, including RAD50, NBS1, and MRE11, which co-localize
with TRF1 and TRF2 in specialized ALT-associated promyelocytic leukemia (PML)
nuclear bodies (APBs)
(9–11).
Thus, we hypothesize that BLM complex formation may be essential for the ALT
mechanism, and its modification may occur dynamically during the specific
nucleic acid transactions required to protect the telomere in cells using the
ALT pathways.This study has identified previously unknown protein partners of BLM and
TRF2 in ALT cells using double immunoprecipitation and mass spectrometry (MS).
These include telomerase-associated protein 1 (TEP1), heat shock protein 90
(HSP90), and topoisomerase IIα (TOPOIIα). These proteins associate
with BLM and TRF2 in cells using ALT but not in cells using telomerase and
directly interact with BLM in vitro. This complex of proteins
localizes to sites of new DNA synthesis in vivo in ALT cells,
suggesting a role in telomere maintenance. We also identified HSP90 and
TOPOIIα in another ALT-specific complex consisting of BLM, TRF1, and
TRF2 but not TEP1. In vitro analyses demonstrate that HSP90 inhibits
BLM helicase activity using both telomeric and non-telomeric substrates,
whereas TEP1 and TOPOIIα initially slow the kinetics of BLM unwinding
only using telomeric substrates. These findings suggest the presence of
dynamic BLM-associated ALT complexes that include previously unidentified
interacting proteins. The function of TEP1 in the BLM·TRF2 complex
remains unclear, although its previously described interaction with the RNA
subunit of telomerase (12)
suggests an interesting hypothesis of cross-talk between mechanisms of
telomere elongation. 相似文献
27.
Sepideh Torabi Matthias Wissuwa Manzar Heidari Mohammad‐Reza Naghavi Kambiz Gilany Mohammad‐Reza Hajirezaei Mansoor Omidi Bahman Yazdi‐Samadi Abdelbagi M. Ismail Ghasem Hosseini Salekdeh Dr. 《Proteomics》2009,9(1):159-170
Mineral deficiency limits crop production in most soils and in Asia alone, about 50% of rice lands are phosphorous deficient. In an attempt to determine the mechanism of rice adaptation to phosphorous deficiency, changes in proteome patterns associated with phosphorous deficiency have been investigated. We analyzed the parental line Nipponbare in comparison to its near isogenic line (NIL6‐4) carrying a major phosphorous uptake QTL (Pup1) on chromosome 12. Using 2‐DE, the proteome pattern of roots grown under 1 and 100 μM phosphorous were compared. Out of 669 proteins reproducibly detected on root 2‐DE gels, 32 proteins showed significant changes in the two genotypes. Of them, 17 proteins showed different responses in two genotypes under stress condition. MS resulted in identification of 26 proteins involved in major phosphorous deficiency adaptation pathways including reactive oxygen scavenging, citric acid cycle, signal transduction, and plant defense responses as well as proteins with unknown function. Our results highlighted a coordinated response in NIL in response to phosphorous deficiency which may confer higher adaptation to nutrient deficiency. 相似文献
28.
Shahrooz Vahedi Mehrnoosh Rajabian Arman Misaghian Daniel Grbec Horst H Simon Kambiz N Alavian 《Journal of biomedical science》2010,17(1):66
Background
Parkinson's disease is the second most common neurodegenerative disorder. The pathological hallmark of the disease is degeneration of midbrain dopaminergic neurons. Genetic association studies have linked 13 human chromosomal loci to Parkinson's disease. Identification of gene(s), as part of the etiology of Parkinson's disease, within the large number of genes residing in these loci can be achieved through several approaches, including screening methods, and considering appropriate criteria. Since several of the indentified Parkinson's disease genes are expressed in substantia nigra pars compact of the midbrain, expression within the neurons of this area could be a suitable criterion to limit the number of candidates and identify PD genes. 相似文献29.
30.