Najava 7. Memorijalni turnir “Akademik Prof. dr. Nijaz Duraković”

2,582 Comments / Memorijal Prof.dr. Nijaz Duraković / By

Šahovski klub Sarajevo u saradnji sa Fakultetom političkih nauka (FPN) Univerziteta u Sarajevu organizuje u nedjelju 02. februara 2020. godine, 7. Memorijalni šahovski turnir “Akademik Prof. Dr. Nijaz Duraković”. 

Turnir se igra u znak sjećana na dugogodišnjeg profesora FPN-a i istaknutog društveno-političkog radnika. Šahovski klub Sarajevo u saradnji sa Fakultetom političkih nauka Sarajevo u proteklih šest godina organizovao je memorijalni šahovski turnir kulturnih i javnih radnika u spomen na akademika prof.dr. Nijaza Durakovića, koji je svojim djelovanjem zadužio i Grad Sarajevo i Bosnu i Hercegovinu u cjelini. Svojim aktivnostima i naučnim djelovanjem akademik prof.dr. Nijaz Duraković uvijek se borio i isticao Bosnu i Hercegovinu kao cjelovitu zemlju svih njenih naroda, a bio je i veliki zaljubljenik u šahovsku igru. Na prethodnih šest memorijalnih turnira nastupilo je preko 100 istaknutih kulturnih i javnih radnika Grada Sarajeva i Bosne i Hercegovine.

Početak turnira je planiran u 12 sati u prostorijama Fakulteta političkih nauka u ulici Skenderija broj 72. Organizatori su obezbjedili značajne nagrade za najuspješnije takmičare i to: redovne nagrade za prvih sedam mjesta i posebne nagrade za najuspješnije kulturne i javne radnike iz oblasti diplomatije, politike, medija, zdravstva, obrazovanja, kulture i sporta.

Turnir je pozivnog karaktera, a učešće mogu uzeti samo osobe koje su dobile poziv od organizatora.

Turnir se igra po “Švicarskom sistemu” uz tempo igre od 15 minuta po igraču.

Sudije Memorijala su Mirza Miralem (internacionalni sudija) i Zlatko Miladinović (nacionalni sudija).

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    Myostatin circulates in two types, latent and energetic, and
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    thereby initiating signaling, together with the pathways activating UPS and inhibiting myogenesis [8].
    In the current examine, the molecular kinetics of myostatin exercise between blood and muscle at the cellular degree are unclear.

    Sarcoplasmic hypertrophy is when glycogen storage increases the size of the
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    midpoint between the patella and the higher trochanter of
    the femur at a depth between 1 and a pair of cm primarily based on previously-used procedures (20).
    The same leg and general location (determined by pre-biopsy markings) was biopsied at every testing session.
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    and II), and cortisol (control I and II). The dietary supplements were prepared in capsule form and packaged in generic bottles for double blind administration by MuscleTech Research & Growth, Inc., (Mississauga, ON).
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    AICAR was also reported to enhance exercise capability in mice
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    The mechanisms of MSTN-induced SM loss are mediated by decreased protein synthesis and/or enhanced
    protein catabolism (Elliott et al., 2012). MSTN decreases protein synthesis by inhibiting the
    Akt/mTOR signaling pathway and induces muscle
    atrophy by selling the transcriptions of atrophy-related genes (atrogenes).
    MSTN signaling pathways may be divided into Smad and non-Smad mediated pathways (Figure 1).

    The extracellular matrix (ECM) is a complex structure comprised of
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    Myostatin, also referred to as growth differentiation issue 8 (GDF-8),
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    result of they reduce the functioning of myostatin, the protein that causes muscles to atrophy.
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    The researchers did in-vitro research on the results
    of leucine, HMB and creatine on muscle cells. The body produces barely more myostatin as we age from our 30s to late 50s, making it harder to construct muscle mass [12].

    Therefore, myostatin inhibitors have been an emphasis of research regarding sarcopenia (age-related muscle
    wasting), muscular dystrophy, and different musculoskeletal circumstances.
    Notably, the variations in outcomes stem from the differing protein consumptions throughout the studies.

    In a pilot examine on 106 HD patients, McKeaveney et al. (2020)
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    Nonetheless, the impression of FOR supplementation on circulating myostatin and muscle tissue-level variations throughout
    muscle disuse in humans is unknown. In this examine,
    we used a extremely particular anti-myostatin peptibody inhibitor of myostatin to
    evaluate the function of myostatin signaling in hindlimb suspension muscle pathology.
    Myostatin is important to the steadiness of protein synthesis and degradation in skeletal muscle, thus myostatin-inhibiting-therapeutics hold promise to mitigate the deleterious results
    of disuse. Deletion of Mstn in hindlimb unloaded mice resulted in comparable muscle atrophy as wild-type mice47,
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    Administration of an anti-myostatin antibody attenuated skeletal muscle
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    Myostatin inhibition has also demonstrated therapeutic
    potential in more complex mouse models involving muscle wasting with issues including
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    option for lost muscle mass and function in spaceflight.

    An important progress element that controls the catabolic and anabolic processes in skeletal muscle is
    IGF-1 that stimulates muscle protein synthesis by stimulating the PI3K/AKT/mTOR axis [40].
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    A Number Of targets are phosphorylated by mTORC1, notably eukaryotic transcription factor 4E interacting protein 1 and its effector, 70-kDa ribosomal polypeptide S6 kinase
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    Scratch testing was performed on one hundred pc confluent
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    In the present research, our participants didn’t perform
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    Nonetheless, we discovered that along with enhancing myogenesis,
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    here we report that Ac-MIF1 and Ac-MIF2-NH2 peptides suppressed adipogenesis by
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    Ac-MIF1 or Ac-MIF2-NH2 were injected into gastrocnemius muscles and one day later cardiotoxin (CTX) was injected into the left and right muscles for 7 days.
    Gastrocnemius muscular tissues were then collected and muscle weights (g)
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    A specific pressure reduction is not observed when atrophied muscle, the predominant therapeutic target of
    myostatin inhibitor remedy, is made myostatindeficient.

    As CKD progresses to its latter phases, insulin resistance (IR), the first metabolic change within the situation,
    has become more and more frequent. In addition to its position in the metabolism of
    carbohydrates, insulin is taken into account a hormone with anabolic nature [82].
    Discount in the body’s reaction to insulin stimulation of target tissues,
    namely the muscle, adipose tissue, and liver is identified
    as IR. Research indicated a considerable correlation between the diploma of IR and muscle protein degradation in hemodialysis people devoid of diabetes [83].
    Patients with CKD had elevated concentrations of circulating proinflammatory mediators, such as IL-6, even through
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    of insulin resistance.
    Omega-3 has been linked to the biogenesis of mitochondria,
    selling NRF1 and NRF2, a outcome ascribed to enhanced transcription and deacetylation of PGC-1, initiated by SIRT1
    [187]. Animals with cancer cachexia treated with omega-3 exhibited an elevation in MAFbx and MuRF1 ranges, alongside a discount in the pro-inflammatory cytokine
    TNF-α [188]. However, research regarding the affect of several dietary elements
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    MSTN is expressed in adipose and muscle tissues and plays
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    Reportedly, MSTN regulates the adipogenesis of mesenchymal stem cells through the differentiation and dedication phases [22], and in animals, its deletion or inhibition enhances muscle mass and reduces fats
    mass [21]. Another novel discovering of this examine
    was that UA treatment decreased MSTN mRNA expression by ~ 14%.

    This research was funded by a analysis grant from MuscleTech Analysis & Growth,
    Inc., (Mississauga, ON) to Baylor University. Researchers in the ESNL
    independently collected, analyzed and interpreted the results from this research and don’t have any financial interests within the outcomes of this research.

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    the supplements investigated.
    To that effect, glucose is first metabolised to pyruvate by way of
    glycolysis and can subsequently enter the mitochondria for additional metabolism throughout the
    TCA cycle. The vital upregulation of MAPLC3B (a key gene in cell autophagy)
    observed within the current examine further assist this
    notion. Apparently, UA can activate AMPK [38], a common regulator
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    On the other hand, serum MSTN levels are elevated in aged people
    and inversely correlated with lean mass. This discordance may stem from the technical limitations of enzyme-linked immunosorbent assays or radioimmunoassays used to discriminate between lively and inactive
    MSTN or between MSTN and the same protein (GDF-11) (Yarasheski et al., 2002).

    In SM, although MSTN mRNA ranges aren’t correlated with age, MSTN protein ranges are elevated
    in aged subjects. Moreover, MSTN protein levels are higher in the muscle tissues of elderly males than in wholesome young males after acute muscle exercise
    (McKay et al., 2012). Sarcopenia is the results of
    a decline within the variety of motor models and muscle fiber atrophy
    and is extra prevalent today because of the increasing number of aged (Stoever et al.,
    2017). Though it is well known that reduced protein synthesis and/or elevated protein degradation induces SM atrophy, reports relating
    to the underlying molecular pathways are inconsistent.

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    balloon игра на деньги balloon казино Казино — РјРёСЂ азартных приключений.

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