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Menya amagambo y’indirimbo « UMUGABO W’INGANZWA » -Inanga ya Sofiya Nzayisenga!

May 18, 2024
professormaurice
886 Comments
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HAKIZIMANA Maurice

Amagambo(lyrics) y’ indirimbo gakondo « UMUGABO W’INGANZWA » -Inanga ya Sofiya Nzayisenga! Muryoherwe!

II Ushaka kunkurikira kuri Whatsapp https://whatsapp.com/channel/0029VaCyM5ILdQejDYwQ2b2u/ II Ushaka kunkurikira kuri facebook: https://www.facebook.com/professormaurice/

Ati Ndi Inganzwa, ndi Ingangare

Ndi ikubitwa ntitake iya rukingamubiri nitwaza

Ntutarabuke ni njye muco w’incungurabuzima !

Karame mugore mwiza utantukira ubusa

Uko niko bucya kabiri yitaba umugore hhhmmmm

Umugabo uhora aganzwa ntagira umujinya

N’umugore we ugasanga yarabyohotseho hhhmmmm

Iyo amubwiye iryo ashaka ahora amwumva vuba

Ati karame mugore mwiza utantukira ubusa

Namuhamagara nabi akitaba atyo

Ati karame mugore mwiza utantukira ubusa hmmmm

Umusore w’intabwirwa yubatse urugo

Ajya gusaba umukobwa yikundiye ubwe

Umukobwa ngo abamuzi bazabimenye

Niko kunyura hirya bajya kwica ubukwe hmmmm

Bati Urya mukobwa w’ingare wamukundiye iki

Ushobora kukuganza akajya kwaka ishema

Ukaba utaye agaciro ka nyirurugo hmmmm

Umuburiye amuhana akajya amwima amatwi

Bigaturuka ku bwiza yamukurikiyeho

Akaba agira ngo uburanga ni bwo bugore

Naho uw’ubuziranenge ntakamenye ko

Umutimanama atari imisaya!

Amurongoje agahato atitondeye ibye

Ati umugore yangaza biturutse kuki ?

Icyo bita kuganza njye ncyita ububwa hmmmm

Kubimwereka neza yamushatse uburyo

Amucisha makeya akajya amwiga umuco

Ngo bamare nko kubyarana abana bane

Aba yamushyikiriye akajya amutuma inkwi

Atavoma n’amazi akamuraza ubusa hmmmm

Yasigaye nta jambo aho abandi bari

Uretse kwihonga nk’uruhatswemo hmmmm

Ndetse n’uwo bahuye akamuyagira ibye

Ati

“Nta mibereho yanjye ubu ntako meze

Dore iryo nikoreye uko ryankozeho

Umugore nizaniye ni we unjyeze ku buce hmmmm

Igituma ingeso angirira zampugije urugo

Ni uko mpinguka ntashye ntarwiriwemo

Ati Segatindi, Segahinga wari wagiye he ?

Nti aho niriwe hose, dore ntahanye inkwi hmmmm

Neza ngirango mubajije nanjye aho yahoze

Nti weho se Nyirumushyashya wari wagiye he ?

Ati ujye umenya Secyobo ntukambaze utyo !

Aho nirirwa hose uba uhashakira iki

Ko ali kwa mubyara wanjye kwa Munyampame

Aho nirirwa hose uba uhashakira iki

Ko ali kwa mubyara wanjye kwa Munyampame

Urebe uko kuganza bihuza umugore

Ubu Nyirumushyashya ntazi icyo maze

Hali n’abagabo bandi yigerekeyeho

Iyo mpingutse iwanjye bateretse inzoga

Njya kwinjira mu nzu hali nk’icyo mbaza

Ati wowe ubu turaheje usubire mu rugo hmmmm

Haracyariho ibanga mba mbwira nshuti

Ndetse mfasha uyu mwana nganire na yo hmmmm

Ninyiherekeza itashye sinzaza vuba

Urebe agashyiga kawe ku ishyiga rihera

Urebe utuboga twawe ku mbehe rusate hmmmm

U(ra)zanywe umutero ntunywere inzoga

Uzanywe n’umujagwe ntunywere amata

Kandi uzarye ibijumba ntundire imboga hmmmm

Urebe igifuma cyawe undindire izi fuku

Urebe ubuhiri bwawe usanganire ihene

Tora agaheto kawe ungire mu murima

Ujye kuharasira isandi zamariye uburo hmmmm

Uribuke ingasire unsere aya masaka

Utore n’igisabo uncundire aya mata

Urebe n’agatebo ube uyora iri vu

Uzakuke, ukubure, nzagaruka aha ejo hmmmm

Nti aho wamugore we ubu wiroye ute ?

Urambwiriza iy’ubuja nk’uwarwinjiyemo

Nzagukubita ugende nishakire undi

Ati erega wowe nawe ntubura ibyo uvuga

Ati urambwira iryo jambo nta soni ufite

Rihamya kunsenda utibereyeho ? hmmmm

Aho wareba nabi njyewe uko mbibona

Ni wowe ushobora gusohoka nkarusigaramo hmmmm

Ubwo abandi imiryango bakoraniye iwe

Urya mugore w’ingare wamujyanaga he ?

Nti icyo umugabo wese ashakire umugore

Aba yifuza inkunga izamura urugo

*N’ingaruka mbi yindi yayimenya ate hmmmm

Ko nagize imana imungezaho

Iyamusubiza iyo avuye nayibona he ? hmmmm

Kumva no kureba iyi nanga,kanda hano: Sophie Nzayisenga

Iyi si!

HAKIZIMANA Maurice: II Kunkurikira kuri  Whatsapp https://whatsapp.com/channel/0029VaCyM5ILdQejDYwQ2b2u II Ushaka kunkurikira kuri facebook: https://www.facebook.com/professormaurice/

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    MSTN ranges. On average, human serum MSTN levels are around 5–10 ng/ml,
    whereas mice exhibit concentrations exceeding one hundred ng/ml, up to a 20-fold distinction [105, 106].

    In addition, ghrelin has been proven to prevent muscle atrophy in rats by enhancing AKT phosphorylation, suppressing the MSTN pathway,
    and activating myogenin and MyoD (Chen et al., 2015). Ghrelin formulations for parenteral administration are being developed (Garin et al., 2013).
    Nonetheless, administration by injection over prolonged periods can outcome in poor affected person compliance and remedy failure, and ghrelin is prone to enzymatic breakdown in blood when delivered intravenously (Brimijoin et al.,
    2016). Ghrelin liposomes coated with chitosan are being developed for
    nose-to-brain administration for the treatment of
    cachexia (Salade et al., 2017).
    Primary human myogenic cultures have been derived from skeletal muscle
    biopsies of eight wholesome adults. After differentiation,
    myotubes were treated with 0.002, 1 and 50 µM UA or automobile for twenty-four h.

    Basal and insulin-stimulated glucose uptake was measured using tritiated deoxy-D-glucose,
    while amino acid-stimulated protein synthesis was estimated utilizing
    the surface sensing of translation (SuNSET) method. Expression of myostatin and glucose transporters was quantified by
    way of real-time PCR. FST-related gene (FLRG) also referred to as FSTL3 protein, exhibits excessive
    homology to a 10-cysteine repeat of FST.
    Myokines are known to be concerned in MSC activation and regulate their main functions, for example, they increase
    proliferation and differentiation rates (Mandai et al., 2017).
    Intracellular aggregation of methylglyoxal, a
    precursor of superior glycation end-products (AGEs), and
    subsequent glycation of biomolecules impaired ECM remodeling, and curcumin and gingerol have
    been reported to scale back the impression of AGE on myoblasts (Baig et al.,
    2017). Furthermore, enhanced AGE manufacturing and consequent RAGE (AGE receptor)-AGE interaction hinders the
    muscle improvement program. We additionally discovered by in silico evaluation that
    the MSTN-ACVRIIB interplay is reduced by curcumin or gingerol.
    Protein-ligand (curcumin/gingerol and MSTN) and protein-protein interactions (MSTN and ACVRIIB) studies
    have been carried out to discover the impact of curcumin and gingerol in the
    myogenesis processes. However, the free vitality of MSTN to ACVRIIB binding fell to −46.55 and −47.26, correspondingly, for MSTN-curcumin and MSTN-gingerol complexes,
    exhibiting that curcumin and gingerol intrude with MSTN-ACVRIIB interaction (Baig
    et al., 2017). Other TGF-β superfamily members, in addition to MSTN,
    are documented to be effective unfavorable muscle regulators, notably “activin A” being the second unfavorable
    muscle regulator.
    Li-hua Yao () must be contacted if someone needs to
    request the data from this examine. This part collects any information citations, data
    availability statements, or supplementary supplies included on this article.
    The data offered on this study are available on this article and the accompanying Supplementary Supplies.
    In summary, MIFs promote myoblast proliferation, myogenic differentiation, and muscle regeneration by upregulating muscle regulatory genes.
    On the opposite hand, they inhibit proliferation and adipogenic differentiation by downregulating adipogenic regulatory genes.

    In-depth evaluation of the bindings between MSTN and the activin kind IIB receptor (ACVRIIB) or FMOD showed that the residues at
    positions 22–31 of MSTN had been predominantly concerned
    with both interactions. Computational alanine scanning of MSTN–FMOD and MSTN–ACVRIIB complexes confirmed
    that MSTN residues on this area had been major contributors to ACVRIIB and FMOD binding (Supplementary Tables
    S1–S3).
    Final however not least, EP1LOGUE features a proprietary
    vasodilating and nitric oxide-boosting formulation of gallate-enhanced oligomers derived from grape seeds and marketed
    as 10x extra powerful than the basic citrulline. This means better blood move
    to the muscular tissues – and thus enhanced
    supply of epicatechin and urolithin B. In quick, if you need to grow
    muscular tissues, you have to control myostatin and improve follistatin.
    Extra studies are needed to fully probe the mechanisms underlying muscle loss
    using the hindlimb unloading mannequin. Yet hindlimb suspension is a posh model that mimics sure
    features of spaceflight where muscle contraction and movement can nonetheless occur7.
    Hindlimb suspension additionally creates a head-down tilt condition, causing
    a cephalic fluid shift similar to that which happens in astronauts.
    Stress is elevated via activation of the hypothalamic-pituitary-adrenal (HPA) axis resulting in elevated glucocorticoids, primarily corticosterone13.
    Suspended mice lose up to 10% of their physique weight in the first two days of suspension9.

    Fasting causes muscle atrophy without will increase
    in the glucocorticoid corticosterone14,15.
    Thus, taking an epicatechin complement can ostensibly increase skeletal muscle mass, energy, and endurance.
    Myostatin is a human growth issue that forestalls excessive
    muscle development, and abnormally high ranges can cause the lack of muscle mass.
    Despite the lack of proper knowledge, myostatin has become a scorching matter amongst
    athletes and bodybuilders, who declare that inhibiting it can enhance
    muscle progress. Skeletal muscle is a plastic tissue that adapts its
    structure and metabolism in response to a number of internal and external variables,
    notably mechanical load and protein ingestion [1]. Loss of muscle mass and performance occurs rapidly with muscle disuse inherent to bed relaxation and single-leg immobilization [2, 3], which finally ends up in impaired functional
    capability, insulin resistance, and an increased risk for morbidity and mortality [4].

    Satisfactory progress, and repair of skeletal muscle depending
    on the kind of cells. SCs are a subpopulation of skeletal
    muscle progenitors and are situated beneath the basal lamina of
    myocytes. In wholesome circumstances, these cells keep inactive until
    encountering an activating stimulus corresponding to injury or exercise which ends
    up in the initiation of the cell cycle and differentiation to myoblasts, selling the regeneration or growth
    of myocytes [93]. It has been demonstrated that individuals with CKD possess a smaller amount of SCs
    in their skeletal muscle and the remaining SCs have abnormal perform, reducing the
    regenerative capacity of their skeletal muscle [94].
    All of those mentioned alterations contribute to the method of muscle losing in CKD sufferers.

    Oxidative stress results from an imbalance
    between the antioxidant protection system and ROS production of
    reactive oxygen species, leading to neuronal death or neurodegeneration. The
    Nrf2/Keap1 signalling pathway is a crucial
    regulatory pathway concerned in antioxidant responses.
    Nuclear issue erythroid 2-related issue 2 (Nrf2) is a redox-sensitive transcription factor that
    induces the expression of several antioxidant proteins.
    These antioxidant proteins are identified to minimize back the mobile
    harm attributable to oxidative stress7. Overexpression of the Nrf2 downstream gene heme oxygenase 1 (HO-1) additionally
    enhances anti-fatigue effects and responses to oxidative
    stress8. Therefore, antioxidant remedy concentrating on Nrf2 and HO-1 might successfully forestall exercise-induced fatigue and studying and memory impairment.

    This research was funded by a research grant from MuscleTech Research & Development, Inc., (Mississauga,
    ON) to Baylor College. Researchers in the ESNL independently collected, analyzed and interpreted the results from this research and have no financial interests within the outcomes of this research.

    Presentation of outcomes in this study doesn’t represent endorsement
    by Baylor University or its authors of the supplements investigated.

    An in vivo useful assay to quantify the pressure produced predominately by the hindlimb
    muscular tissues, the “Hindlimb Exertion Pressure Test” (HEFT), was
    carried out as previously described76. Briefly, HEFT evaluates dominant hindlimb muscles used during an evoked
    escape response (electrical stimulus, 1.5 mA, 0.three s administered to the tail) and
    was designed as a substitute for the more conventional grip
    strength measurement. Two stimuli are utilized to the tail (with a 2 min rest) which is affixed to a force transducer; the force
    responses were recorded through a customized developed Labview™
    v7.1 (National Devices Corporation, Austin, TX) code.
    Soleus MHC-I and MHC-IIa fiber CSA significantly decreased with hindlimb suspension, in vehicle-treated groups (NS-P vs HS-P), by −48.4% and −45.8%, respectively.

    AICAR was also reported to reinforce exercise capability in mice by ~44% but
    has poisonous effects [14]. The improvement of novel and protected therapies is thus, warranted given the
    typical older population profile of topics with sarcopenia
    and likely indefinite interval of remedy. Epi is a naturally occurring flavanol found in cacao and green tea and has been orally ingested
    safely by people for a lot of centuries.
    There are a wide selection of open supply and licensed digital screening software/tools obtainable, and each has its personal
    constraints that should be overcome to forestall the manufacturing of erroneous conclusions or artifacts (Gimeno
    et al., 2019). For VS, licensed software program such
    as Molecular Working Environment (MOE) (Vilar et al., 2008), and the GLIDE
    module in Schrodinger (Bhachoo and Beuming, 2017) as nicely as
    open access instruments such as Autodock Vina (Trott and Olson, 2010), are commonly used.

    Uralensis is native to Asia and is used as a medicinal herb, sweetener,
    and in conventional Chinese drugs (Ji et al., 2016).
    In addition, liquiritigenin, tetrahydroxymethoxychalcone, and licochalcone B isolated from the EtOAc fraction of G.
    Uralensis enhanced myoblast proliferation and differentiation,
    and liquiritigenin enhanced muscle regeneration in injured muscles (Lee et al., 2021b).
    Uralensis-derived compounds have therapeutic potential for
    the management of muscle-related problems.
    This evaluate particulars the mechanisms behind myostatin’s operate and the various inhibitors which have been examined preclinically and clinically.

    It additionally examines the challenges encountered in medical translation, including issues with drug specificity, differences in serum myostatin concentrations
    between animal models and humans, and the necessity of neural
    enter for useful enhancements. Moreover, we discover promising avenues of research beyond muscle dystrophies,
    particularly in the therapy of metabolic syndromes and orthopedic issues.
    Insights from these various applications suggest that myostatin inhibition may hold the potential for addressing a broader vary of pathologies,
    offering new instructions for therapeutic development. In abstract, blocking myostatin signaling using
    an anti-myostatin-specific peptibody solely partially mitigated muscle atrophy and practical power following 14 days of
    hindlimb suspension of male mice. Extra direct comparisons between spaceflight and hindlimb suspension will
    be required to completely assess the utility of the suspension model to deal
    with spaceflight musculoskeletal problems. Outcomes from this examine also recommend that
    there could presumably be therapeutic potential for myostatin inhibition in disuse muscle
    losing and possibly even in astronauts assigned to long-duration area missions.

    Subjects signed an knowledgeable consent that was permitted
    by the Institutional Evaluate Board for Human topics prior to participation. Every subject completed a
    private info sheet and a regular medical historical past kind verified by a registered nurse.
    Topics have been free from any major metabolic issues (i.e.
    coronary heart disease, diabetes, thyroid disease, etc.) as nicely as main musculoskeletal issues
    that might intervene with their capacity to workout and/or full the exams during the three
    testing sessions. Topics were not permitted in the examine if they’d taken any
    self-reported ergogenic dietary supplements (i.e. creatine,
    androstendione, myostatin inhibitors, pro-hormones, and so forth.) within six months previous to the onset of the examine.

    The use, distribution or copy in different forums is permitted, supplied the unique author(s) and
    the copyright owner(s) are credited and that the unique publication in this journal is cited,
    in accordance with accepted tutorial follow. No use, distribution or reproduction is permitted which doesn’t comply with these phrases.
    Get unique health tips, early entry to new products, and special discounts—straight to your inbox.

    Dietary Supplements like epicatechin and quercetin may complement
    your efforts but are not miraculous solutions. No single method, including tablets, may be
    thought-about the easiest way to inhibit myostatin universally.

    Structural perception of binding between totally
    different MIPs and MSTN ought to open new doorways to the design of higher therapeutic
    peptide candidates. Although no drugs have but been developed to prevent
    muscle degeneration, we believe that research efforts concentrating on MSTN will
    end in therapies that attenuate muscle degeneration and enhance the standard of life in the aged and people affected by MD.
    Some ECM proteins bind and modulate the operate of MSTN, particularly fibromodulin (FMOD), decorin, fibronectin, and laminins (Miura et al., 2010).

    In addition, the mRNA and protein of FMOD, MSTN, and adipogenic markers (CD36, PPARγ, and CD163)
    had been significantly decreased in Ac-MIF1-treated cells, and
    FMOD and PPARγ mRNA and protein expression have been decreased in Ac-MIF2-NH2 (Figure 7B).

    Moreover, Smad2 and Smad3 mRNA expression was decreased in Ac-MIF-treated cells
    (Supplementary Determine S12). MSTN protein effects were observed in C2C12 cells after
    2 days of remedy in proliferation or myogenic differentiation media.
    Cell proliferation and fusion indices had been reduced by MSTN protein treatment (Supplementary
    Determine S1).
    Myostatin and activins (A and B) bind to the ActRIIA or
    ActRIIB receptor on the cell membrane and might signal via it.
    Inhibition of muscle hypertrophy and differentiation by
    myostatin occurs via Smad2/3 phosphorylation-dependent blockade of
    the AKT-mTOR pathway [180]. So that the remedy of muscle with myostatin or activin results in a decrease in the level
    of phosphorylated AKT. Easy blocking of myostatin was one
    of many first and most obvious therapeutic strategies to right muscle atrophy.
    Because clear hypertrophy was seen in myostatin-null
    animals and in humans who had been null for this ligand.
    Nevertheless, the level of myostatin reported in people is lower than the extent noticed in rodents.
    Therefore, it’s reasonable to ask the query that blocking myostatin alone can be effective or that we ought to always seek to inhibit other ligands that play a job in the adverse regulation of muscle mass by sending signals via the
    identical receptor.
    Indeed, MSTN-knockout mice exhibit upregulated
    GLUT1 (insulin-independent) and GLUT4 (insulin-dependent) proteins, leading to elevated glucose uptake [122].
    Conversely, energetic MSTN reduces GLUT4 expression and glucose uptake by way of muscle atrophy, inhibition of assorted
    insulin-related pathways, and downregulation of gene expression [128].
    MSTN inhibits the phosphorylation of insulin receptor substrate (IRS) proteins, which reduces the
    activation of phosphoinositide 3-kinase (PI3K) and downstream protein kinase B (Akt) [129].
    Akt promotes the translocation of GLUT4-containing vesicles to the plasma membrane of muscle cells in response to insulin [130].

    References:

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