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141: 名無しさん 2022/03/17(木) 22:19:27.74
血の斬撃とかに怒るのは分かるけど霜弱くなって起こってるやつマジでおるの?

155: 名無しさん 2022/03/17(木) 22:20:35.04
>>141
霜はろくに使ってなかったし別にやな
もっと他に強い戦技あるしなんなら猟犬ステップで十二分に強い

183: 名無しさん 2022/03/17(木) 22:23:16.22
>>141
霜踏みを主力として攻略してきたならキレるやつおるやろうけどナーフ入りは確実やったからそこまでやな

178: 名無しさん 2022/03/17(木) 22:23:02.99
「霜踏みつえー!これ絶対修正されるわ!!」
皆ネタで言ってて楽しんでた
いや実際強かったけどそれも含めて楽しんでた
でも空気読めないチー牛みたいなフロムがニチャついてマジで修正
ユーザーに楽しませる気ないんだなあって

203: 名無しさん 2022/03/17(木) 22:24:31.29
>>178
霜踏みなんて所詮育成終わるまでの繋ぎでキャラが育てばみんな特化ビルドに旅立っていくのにな
ワイも特大二刀に移行してからは1回も使ってないし
それすら許せなかったんか…

189: 名無しさん 2022/03/17(木) 22:23:29.77
ワイは霜踏みとかスリップダメージとか使うとつまらんくなるから使わんのだけど
それが弱体化されて怒るってことは簡単なゲームにしてくれないと困るってことなんかな

263: 名無しさん 2022/03/17(木) 22:29:45.13
悪りぃ、あいつ(霜踏み)の事忘れらんねえわ…

やっぱ辛えわ…

346: 名無しさん 2022/03/17(木) 22:36:38.16
>>263
(霜降り)のとこすげえ滑ってる

277: 名無しさん 2022/03/17(木) 22:31:26.25
霜踏み写し身使わないまま弱体されてしまったから一回くらい使っとけばよかったな

326: 名無しさん 2022/03/17(木) 22:35:04.54
王朝稼ぎは神の遺剣使えばええやん 霜踏むより早い

333: 名無しさん 2022/03/17(木) 22:35:34.56
霜踏み写し身使ってみたけどナーフされたとはいえまだ強いな
元がどれだけぶっ壊れだったか分かる

引用元:https://swallow.5ch.net/test/read.cgi/livejupiter/1647522014/

この件についてどう思う?

コメント一覧
  1. 名無しさん より:

    霜踏とかは対人要素がある以上調整するのは分かるけど写身とかを弱体するのはライト層離れるからいい調整とは思えないな

  2. 名無しさん より:

    霜踏みの冷気ダメージは下がってないから攻略には問題ない

  3. 名無しさん より:

    強ボスとはまだやってないが写身まだ強いだろ
    ぶっ壊れ遺灰が超強遺灰になっただけじゃね

  4. 名無しさん より:

    神肌のふたりだけに使ってたけど、やっぱつれぇわ。

  5. 名無しさん より:

    トロコンしてから弱体化したから別に怒らないよ

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    This evaluation summarizes latest progress within the development of myostatin inhibitors for the therapy of muscle wasting disorders.

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    In brief, if you need to develop muscle tissue, you need to control myostatin and enhance follistatin.
    In truth, some research implies that myostatin actively triggers muscle atrophy (muscle
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    Secondly, scientists consider that myostatin inhibition may also prevent muscle loss that occurs because
    of other ailments. For instance, deleting the genes concerned in producing myostatin within the hearts of mice prevented the extreme muscle and weight reduction caused by coronary heart failure [11].
    Under is a listing of pathways myostatin inhibition may target,
    based mostly on the available research.
    Increased levels of ActRIIB in quick muscle fiber varieties could partly explain the predominant impacts of HS in fast versus slow muscle
    fibers73. Inhibiting this signaling pathway with a soluble
    decoy ActRIIB receptor induces hypertrophy in a fiber-type independent manner74
    and prevents limb immobilization muscle atrophy, but not denervation atrophy75.
    Our use of a decoy receptor, which inhibits myostatin together with Activin A and other ligands, seems
    to more fully prevent muscle atrophy, a minimum of in the TA, then inhibiting myostatin alone,
    as in our examine. Signaling with Activin A
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    Second, caution is needed in the interpretation of findings completely
    drawn from circulating biomarkers when employing "local" disuse models, such as knee brace immobilization. Certainly, disuse effects are expected mostly
    at an area muscle degree and outcomes obtained from systemic biomarkers could also
    be affected by the relatively low muscle mass present process unloading/immobilization (one leg only).
    Due to the COVID-19 outbreak and the poor compliance with wearing a knee brace, we couldn't analyze the whole number of members deliberate to have a medium effect dimension of power (S1
    File) and recognize that our findings are restricted to younger males.

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    It is best suited to start from a low dosage and then gradually improve to a better dosage
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    Some of the research suggests that follistatin 344 presents protection from breast most cancers.
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    It comprises 323 Amino acids, and a carbohydrate chain is connected to its
    core, making it a naturally occurring glycoprotein.
    With the exception of vitamin D, where a optimistic effect may be observed in these
    affected by a deficiency, the other treatments are famous to be both dangerous or unproven. Myostatin antagonists, peroxisomeproliferator-activated-receptor-δ agonists (GW1516) and adenosine monophosphate (AMP) activated protein kinase activators such as AICAR.

    GW1516 was examined in rodents outcomes show stimulated exercise capacity solely when used in combination with train [13].

    Elevated angiotensin levels diminish the satellite cell reservoir and impair muscle regeneration capability.
    Moreover, CKD stimulates the renin-angiotensin mechanism, which
    triggers caspase three in muscle tissue and promotes actin cleavage, thus precipitating
    muscle atrophy. Angiotensin II enhances muscle proteolysis by stimulating the UPS and the TGF-β
    course of, while concurrently lowering circulatory IGF-1 concentrations,
    a principal cause of muscle mass discount [96].
    In summary, CKD results in elevated ranges of angiotensin II in the
    body, contributing to skeletal muscle atrophy. After confirming the optimistic results of Ac-MIF1 and Ac-MIF2-NH2 on myogenesis, we
    investigated the regenerative potentials of these peptides in CTX-injected mouse gastrocnemius
    muscular tissues. There had been no significant variations in physique or gastrocnemius muscle weights between peptide-injected and non-injected
    muscles, which could probably be attributed to the fact that the peptide-injected mice experiments
    have been conducted after a short interval (7 days).
    MSCs are liable for the maintenance and recovery of SM following injury
    and specific nuclear Pax7, which regulates MYOD and MYF5 [32,33].

    Due to this limitation in study design, the authors can't determine with certainty whether the elevated myostatin focus occurred
    in the course of the immobilization phase or the recovery part, or each.

    This is especially relevant in mild of a recent 10-day mattress rest research that discovered
    an sudden increase in circulating myostatin after two
    days of recovery, but not during the unloading interval (Oranger
    et al., 2022). Why did the authors determine to not acquire blood
    samples on day 14 (onset of the immobilization phase) and day 28
    (end of the immobilization phase)?
    There are many commonalities at the molecular level within the pathways in skeletal muscle that
    lead to atrophy, whether it is in the context of cancer cachexia or different noncancer muscle losing conditions.
    The mechanisms regulating skeletal muscle mass have recently been reviewed [17–21].
    Myostatin, a member of the TGFβ superfamily of growth factors, is a highly conserved unfavorable regulator
    of skeletal muscle mass that is upregulated in many circumstances of muscle losing.
    Various induced or natural situations resulting in myostatin deficiency result in elevated muscle mass and power in regular
    animals and have been shown to deal with or prevent a spread of muscle losing situations.

    It additionally focuses on findings in myostatin biology which will have implications for the event of antimyostatin therapies.

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    Two traits of senescent MPCs probably lead to the
    common description of CKD as an inflammatory chronic condition. Initially, senescent cells exhibit
    resistance to apoptosis, resulting in their continued
    existence in the senescent phase. Secondly, they
    formulate an SASP characterized by sustained cytokine technology
    [57].
    Multiple myostatin-targeting methods corresponding to neutralizing antibodies,
    myostatin propeptides, soluble ACVR2A or ACVR2B receptors, and naturally-occurring antagonists (FST) have been developed, and those that have
    progressed into clinical trials are summarized in Desk 1.
    In the next part, the clinical progress of various myostatin inhibitors, their candidate targets, and potential unwanted effects might be mentioned.
    Targeting the myostatin processing pathway has been actively advised to be an efficient myostatin-inhibiting strategy to advertise muscle development.

    For example, transgenic mice carrying a mutation in the myostatin RSRR
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    by furin-like proteases, show enhanced muscular
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    It’s difficult to devour efficient quantities purely from diet, which is where
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    Formulation of dietary dietary supplements usually outpace the science behind their elements
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    advantages. Inhibiting myostatin is an instance of disinhibition — when a molecule that normally inhibits a pathway
    is inhibited by another molecule, an opposite impact results.
    In this case, the expression of myogenic elements increases when myostatin is inhibited.

    When myostatin binds to its receptor, ActRIIB, it prompts a mobile pathway referred
    to as Smad that blocks genes from transcribing myogenic components.

    Lately, we performed a VS-based analysis on recognized muscle-enhancing natural compounds for
    MSTN inhibitory exercise and identified curcumin and gingerol as candidates
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    The management group had a bigger vary and interquartile range in LOAD scores for all 3 time factors compared with the remedy group (Table 2).
    The resulting massive variance within the control group compared with the therapy group likely is
    the explanation for a statistical difference inside teams however not between groups.
    Therefore, this statistically significant distinction throughout the remedy group might not reflect a clinically
    related change.
    This examine examined 12-weeks of resistance training and cystoseira canariensis supplementation on serum levels of
    myostatin and muscle strength and body composition in twenty-two untrained males.
    Coaching consisted of three days per week utilizing 3 units of 6 to eight
    repetitions at 85–90% 1 RM. The researchers concluded that 12-weeks of heavy resistance coaching and 1200
    mg/d of cystoseira canariensis supplementation seemed to be ineffective
    at inhibiting serum myostatin and growing muscle strength and mass or lowering fat mass.
    The rationalization for the dramatic effects in animals while
    no observed effects in humans in all probability lies in the reality that myostatin particular antibodies were used in the animal model,
    while human models use sulfo-polysaccharides which are only
    marketed to bind to myostatin. Outcomes of this examine assist this prior report in that CSP3 supplementation had no vital results on body composition, coaching diversifications, or markers of anabolic/catabolic standing in resistance-trained males.

    It is unclear whether myostatin instantly affects fats and bone, or not directly through muscle.
    Whether through direct or indirect effects, myostatin inhibition appears to extend muscle and bone mass and decrease fats
    tissue-a combination that truly appears to be a holy grail.
    However, at this time, human data for each efficacy and security are extremely restricted.
    Moreover, whether elevated muscle mass additionally results in improved
    perform remains to be decided. Ultimately potential beneficial effects of myostatin inhibition will
    have to be determined based mostly on exhausting outcomes such as falls and fractures.

    Also, IL-15 remedy decreased muscle protein degradation and SM losing in an in vivo rat model of most cancers cachexia (Carbo et al., 2000).
    Furthermore, lowered exercise endurance has been reported
    in IL-15−/− mice, nevertheless, enhanced train induction has been found in SM-specific
    IL-15-transgenic mice (Quinn et al., 2013;
    Quinn et al., 2014). Altogether, the above research point out that IL-6,
    IL-15, and LIF appeared as an important myogenesis controllers, functioning during each
    myoblast proliferation and differentiation.
    Thus, Epi is the first compound ever noted, to favorably modulate both regulators of muscle development and counsel
    increases in power. From a biomedical perspective, myostatin inhibitors are a sort of drug
    that focus on myostatin, a protein concerned in regulating muscle development and growth.
    Myostatin inhibitors work by blocking the exercise of myostatin, which can result in increased muscle mass and power.
    These inhibitors have potential functions in treating
    muscle-wasting circumstances, such as muscular dystrophy, and can also be used to enhance muscle growth in athletes and bodybuilders.
    By inhibiting myostatin, these medicine can promote muscle hypertrophy
    and probably improve muscle perform.
    Focusing On the latent or pro-form of MSTN could offer superior efficacy and lowered cross-reactivity.

    Most inhibitors examined to date have targeted the mature form or employed
    broadly reactive receptor-based approaches. Numerous inhibition strategies with the potential for greater effectiveness remain unexplored in medical settings.

    References:

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