Ngày 04/06/2017, tại lễ trao giải “Thương hiệu xuất sắc – Excellent Brand 2017” do Hội sở hữu trí tuệ TP.HCM tổ chức, Công ty TNHH TM FEATERA 3H GLOBAL được vinh dự đứng trong hàng ngũ 10 thương hiệu sản phẩm xuất sắc, nhận được sự tin tưởng của người tiêu dùng trong cả nước.
Excellent Brand – giải thưởng mang tầm quốc tế
Excellent Brand là giải thưởng được tổ chức thường niên nhằm tìm ra những thương hiệu xuất sắc, đóng góp vào sự phát triển của quốc gia và mang đến những lợi ích thiết thực cho người tiêu dùng. Để nhận được giải thưởng này, các thương hiệu – doanh nghiệp phải trải qua quá trình khảo sát và đánh giá theo quy trình Thương hiệu xuất sắc EBI (Excellent Brand Index) của Mỹ.
Bà Hoàng Thị Mỹ Liên – Giám đốc thị trường Cty Featera 3H Global (người đứng thứ 2, hàng trên cùng từ trái qua) trong lễ trao giải “Thương hiệu xuất sắc năm 2017” tại Nhà hát Quân đội Tp.HCM
Năm 2017, chương trình được tổ chức bởi Hội Sở hữu Trí tuệ TP.HCM phối hợp thực hiện cùng Tạp chí Doanh Nghiệp và Đầu tư mạng doanh nghiệp Sài Gòn dưới sự giám sát của hiệp hội AQA – International (Hiệp hội các nhà đánh giá quốc tế Mỹ) và Bộ Khoa học và Công Nghệ. Ban tổ chức đã khảo sát và đánh giá một cách kỹ lưỡng độ tín nhiệm của khách hàng, đánh giá tín nhiệm và truyền thông cùng uy tín, mức độ thực hiện cam kết của doanh nghiệp trước khi chính công bố. Các thương hiệu và doanh nghiệp đạt giải thưởng là những cái tên đã khẳng định được tên tuổi và tầm ảnh hưởng của mình cả trong và ngoài nước.
Dinh dưỡng Featera 3H Global đạt giải thưởng “Thương hiệu xuất sắc”
Cty TNHH TM Featera 3H Global là doanh nghiệp chuyên nghiệp phân phối các sản phẩm dinh dưỡng chất lượng cao và ưu việt. Với dòng sản phẩm dinh dưỡng chăm sóc máu và tế bào Nature Power.
Nature Power gồmcó:
Dòng Sản Phẩm Dinh Dưỡng Tế Bào – Máu Nature Power
Cúp và Giấy Chứng Nhận Giải Thưởng “Thương hiệu xuất sắc năm 2017”
N1: bổ sung dinh dưỡng toàn diện cho tế bào, chiết xuất từ hơn 100 loại rau củ quả trái cây.
N2: tăng năng lượng, tăng oxy máu, giúp máu lưu thông, chiết xuất từ các loại thảo dược,
N3: Bổ sung khoáng chất cần thiết cho tế bào, giúp cơ thể đào thải độc tố.
Sản phẩm được sản xuất theo công nghệ Đức, đặt nhà máy sản xuất tại Quốc Đảo Đài Loan nơi có ngành trồng trọt trái cây với cộng nghệ tiên tiến và an toàn.
Nature Power là sản phẩm bổ sung dinh dưỡng toàn diện chăm sóc các tế bào và hệ thống mạch máu.
Đồng thời với công nghệ hấp thụ thông qua niêm mạc có tại lưỡi, thực quản, dạ dày, ruột non đi thẳng vào máu, giúp cảm nhận sản phẩm chỉ sau 3-5 phút sau khi sử dụng. Và dinh dưỡng của Nature Power sẽ tập trung chăm sóc các tế bào yếu (cơ quan yếu) giúp hồi phục sức khỏe nhanh chóng.
Hiện nay sản phẩm đã được bán ở 4 quốc gia: NewZealand, Đài Loan, Indonesia và Việt Nam.
Trụ sở chính Featera 3H Việt Nam đặt tại Tòa nhà The UseFull, số 654 Lạc Long Quân, P.9, Q.Tân Bình, Tp.HCM.
Tại Việt Nam sản phẩm đã có mặt tại các tỉnh thành như: Tp.HCM, Hà Nội, Đà Nẵng, Huế, Nha Trang, Buôn Mê Thuột, Vũng Tàu, Biên Hòa, Bình Dương, Bình Phước, Long An,…. Tiến đến xây dựng hệ thống phân phối trên 63 tỉnh thành.
Mục tiêu của FEATERA 3H là trở thành một trong những thương hiệu dinh dưỡng hàng đầu Việt Nam.
Công ty này hội thảo toàn lừa đảo không. Nếu uống mấy cái sản phẩm này vào mà hết ung thư, hết tiểu đường này nọ thì xin lỗi mấy cái bệnh viện nó đóng của lâu rồi….
Thực phẩm chức năng mà lúc nào hội thảo cũng nói cái kiểu như thuốc thần chữa được bách bệnh! Nào là ông này ung thư uống vào khỏi, bà này bị viêm gan B uống vào hết! Không biết thuê đội ngũ lên tự nhận mình bị bệnh xong hết đấy mất bao nhiêu tiền.
Intensive cyclic bodily exercise induced significant lower
of IgG and IgA in blood serum of the athletes. These researchers concluded that both supplements contributed
to restoration of the lowered IgG and IgA, while the working capacity of the athletes grew by 10 to 15% [20].
Moreover, Chermnykh et al [5] compared beta-ecdysterone with dianabol which is an especially powerful anabolic steroid, suggesting each beta-ecdysterone and dianabol increased the dimensions and energy of the muscular tissues.
These researchers concluded that ecdysterone had a higher anabolic action on the contractile proteins of the skeletal muscles than dianabol.
Throughout fetal improvement, muscle fiber
formation occurs, and MSTN mRNA is very expressed within the developing skeletal muscle.
In mice, expression begins around 9.5 days post-coitum (dpc) and
peaks at roughly 14.5 dpc, indicating its crucial function in regulating early muscle development [30].
Members reported to the Human Performance Lab at a pre-scheduled time in the morning.
Upon arrival participants have been weighed and then, after 5 min of
seated relaxation, coronary heart price and blood strain had been assessed within the seated place.
Subsequent, venous blood and muscle biopsy samples have been obtained,
after which the members carried out a 30 s Wingate anaerobic cycle test.
After resting, the participants carried out a peak oxygen uptake assessment
utilizing a cycle ergometer. Post-testing classes were completed between 48 and 72
h after the ultimate coaching session. These advantages emphasize YK11’s ability to
spice up bone energy, assist muscular development, and improve total power and performance throughout coaching.
Users frequently expertise a big increase in power within a couple of weeks after beginning a cycle.
There are quite so much of open supply and licensed digital screening software/tools
available, and every has its personal constraints that have to
be overcome to forestall the manufacturing of erroneous conclusions or artifacts (Gimeno et
al., 2019). For VS, licensed software program corresponding to Molecular Working
Environment (MOE) (Vilar et al., 2008), and the GLIDE module in Schrodinger (Bhachoo and Beuming,
2017) as nicely as open access tools such as Autodock Vina
(Trott and Olson, 2010), are generally used. Uralensis is native to Asia and is used as
a medicinal herb, sweetener, and in conventional Chinese medicine
(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 muscle tissue (Lee et al., 2021b).
Uralensis-derived compounds have therapeutic potential for the management of muscle-related issues.
To that impact, glucose is first metabolised to pyruvate via glycolysis and may subsequently enter the mitochondria for additional metabolism
throughout the TCA cycle. The important upregulation of MAPLC3B (a key gene in cell autophagy) observed within the present research further support
this notion. Apparently, UA can activate AMPK [38], a common regulator
of each autophagy and GLUT4 expression [39, 40], which may present
the mechanism by which UA exerts its dual results on glucose uptake and mitochondrial function.
In both cachexia and PEW definitions, mid-arm muscle circumference area is a
criterion, Table 1. Contrary to PEW, muscle functional measures together with fatigue or muscle power, are thought of diagnostic standards for cachexia [13].
Total, Koppe et al. acknowledged that PEW is equivalent
to cachexia and needs to be substituted by “kidney illness cachexia” which could be less complicated.
They also suggested that the definition of cachexia ought to be expanded to include inadequate protein consumption and fat
loss [13]. The term “cachexia” comes from the Greek kakos,
“bad” and hexis, “condition/state” [16]. Concerning the
discrepancies between cachexia and protein-energy wasting (PEW) in CKD,
the diagnostic standards recommended by the Society on Sarcopenia, Cachexia, and Losing Problems for
cachexia are similar to these of the PEW, though not similar.
Elevated angiotensin ranges 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, whereas concurrently reducing circulatory IGF-1 concentrations,
a principal reason for muscle mass discount [96].
In summary, CKD ends in elevated levels of angiotensin II
in the physique, 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 muscles.
There had been no significant variations in body or gastrocnemius muscle weights between peptide-injected and non-injected muscles,
which could probably be attributed to the truth that the
peptide-injected mice experiments were carried out after a short interval
(7 days). MSCs are liable for the upkeep and restoration of SM following damage and express nuclear Pax7,
which regulates MYOD and MYF5 [32,33].
Testing of myostatin inhibitors in animal fashions of muscular dystrophy
[34] has shown typically optimistic results on muscle mass however inconsistent results
on muscle perform and histopathology [reviewed in [35▪]].
ActRIIB-Fc or ActRIIB shRNA given to mdx mice, a
well used however not best model of human muscular dystrophy
[36,37▪▪], produced will increase in muscle mass and complete pressure but
particular pressure was unchanged [38,39▪,40]. In contrast, a current study reported an increase in specific force of the soleus muscle in mdx mice after long-term
exposure to a myostatin propeptide [41]. Studies with myostatin inhibitors haven’t proven any improvement on eccentric contraction-induced drive drop, a key
measure of myofiber structural integrity [40,42,43].
Research has demonstrated that the insulin/insulin-like growth
issue 1 (IGF-1)-dependent mammalian target of rapamycin (mTOR) pathway is
a vital participant in the growth or atrophy of human skeletal muscle.
In CKD, hindering anabolic agents, corresponding to IGF-1/insulin factor may lead to diminished Akt-mTOR signaling,
which promotes muscle protein degradation [29]. Moreover, myostatin serves
as a major negative modulator of muscle volume, which is elevated in individuals with CKD.
Activin A receptor kind IIB (ActRIIB), the
cell surface receptor for this protein, which is generally transcripted in human muscle cells, phosphorylates and
prompts numerous transcription variables, including Smad2,
three, and Smad2/4 family. Smad2/4 complex is then translocated to the nucleus, directly influencing protein losing.
On the opposite hand, the phosphorylation of Smad2/Smad3 results in a further decrease in p-Akt, hence perpetuating the cycle of muscle protein breakdown [30].
New research have additionally established an emergent function for microRNAs (miRNAs) in skeletal
muscle wasting in CKD patients.
It also focuses on findings in myostatin biology
that will have implications for the development of antimyostatin therapies.
Clients are glad with the muscle power and restoration advantages of the
dietary complement. The product speeds up muscle restoration, making their workouts easier and permitting them to maintain muscle mass.
Two traits of senescent MPCs most likely result in the frequent description of CKD
as an inflammatory persistent condition. Initially, senescent
cells exhibit resistance to apoptosis, resulting in their continued existence
in the senescent part. Secondly, they formulate an SASP
characterised by sustained cytokine technology [57].
The train test was carried out until the participant was no longer capable of keep a cycling cadence
above 40 revolutions per minute. This examine utilized a double-blind, randomized, placebo-controlled parallel
design. Individuals were randomly assigned to the EPI group or PLA group whereas finishing a 4 weeks anaerobic and cardio cycle training protocol.
Individuals accomplished a familiarization session, a pre-testing session, a cycle training protocol, and a post-testing session in the course of the course of the examine.
When cortisol regulation is interrupted, it can impact many body techniques and cause extreme joint pain.
Taking nutrients during post-cycle therapy may
help to minimize this unfavorable effect. Epi Cat by Blackstone
Labs doesn’t have quite as many evaluations, nevertheless it incorporates
each epicatechin and green tea leaf extract which might maximize power
and blood circulate throughout your workout for better
outcomes.
The concern with MYO-X was that it just didn’t seem to translate to extra muscle in real-world observational research.
Technically there’s 4 supplements I’ll speak about here, and although there’ll undoubtedly be more to come back sooner or later, these are of specific relevance to this dialogue.
Male and feminine bodybuilders can get big, but the elite professionals
of the heaviest weight class usually stay within a few pounds of every other at their peak.
By No Means delay or disregard seeking professional
medical advice out of your physician or another certified healthcare supplier due to something you have learn on SelfHacked.
We understand that reading particular person, real-life experiences can be a helpful resource, but it is by no means an different choice to skilled medical advice, diagnosis,
or remedy from a professional healthcare supplier.
Our science group is put by way of the strictest vetting course
of in the health trade and we often reject candidates who have written articles
for most of the largest well being web sites that are deemed trustworthy.
Our science staff must cross lengthy technical science checks, troublesome logical reasoning and reading comprehension tests.
In additional contrast to earlier studies (12, 24), our results indicated no effect on myostatin gene
expression after 4 weeks of supplementation. In this research, we sought to further
elucidate the position of the myostatin pathway in the etiology of hindlimb suspension-induced muscle loss.
In addition, protein synthesis and degradation pathways have been studied to ascertain how
skeletal muscle mass was influenced by myostatin inhibition during unloading.
The U.S. healthcare cost of sarcopenia was estimated in 2000 at ~$20 billion and
is growing because the population ages [13]. In a recent evaluation, current non-exercise
based therapy options have been mentioned including nutritional dietary supplements, hormone remedy (testosterone, estrogens,
growth hormone), vitamin D, angiotensin changing enzyme inhibitors and creatine [13].
Modifications in accessible floor space (ASA) confirmed
the residues on this region of MSTN exhibited maximum ASA modifications after binding
with FMOD or ACVRIIB. Statements regarding supplement advantages have
not been evaluated by the Meals and Drug Administration. Clear Labs merchandise
are not supposed to diagnose, deal with, cure, or stop
any disease.
By blocking MSTN action, these inhibitors could improve muscle development, improve energy expenditure, and enhance insulin sensitivity, providing a promising strategy
to combating diabetes-related health situations. In contrast to HS mice,
the myostatin inhibitor had pronounced anabolic results
in normally loaded controls. Lean mass and hindlimb muscle plenty elevated, aside from the
small postural muscle tissue. Due to the fiber-type specificity of myostatin signaling12, the
predominantly slow fiber varieties within the soleus are unlikely to learn from myostatin inhibition. Nevertheless, in unsuspended mice handled
with the drug, the in vitro soleus tetanic force production increased.
Understanding the position of myostatin has vital implications for developing therapies to deal
with muscle losing ailments and enhancing athletic efficiency.
MSTN is known to work together with FST, GASP-1, GASP-2, decorin, FMOD,
and FLRG, which are collectively known as MIPs.
These proteins inhibit the formation of mature MSTN advanced and intrude with complicated formation between MSTN and ACVRIIB.
Designing short peptides primarily based on the make-up of MIPs provides
a possible means of efficient MSTN inhibitors,
and a few studies indicate that these inhibitory peptides have therapeutic potential for the
remedy of a spread of muscular dystrophies (Tsuchida, 2008).
FS I-I (MSTN-specific inhibitor derived from FST)
supplies an instance of an FST-derived inhibitory
peptide and increased SM mass in mdx/FS I-I mice and decreased
cell infiltration into muscles (Tsuchida, 2008).
This study was funded by a analysis grant from MuscleTech Research & Improvement, Inc., (Mississauga,
ON) to Baylor College. Researchers within the ESNL independently
collected, analyzed and interpreted the results from this research and don’t have any financial
pursuits in the results of this examine. Presentation of outcomes on this research does not represent endorsement by
Baylor University or its authors of the dietary supplements investigated.
The manuscript should describe a technically sound piece
of scientific research with data that supports the conclusions.
Experiments will need to have been performed rigorously, with applicable controls,
replication, and sample sizes. In whole, 24 individuals were recruited,
and 22 completed the protocol; 2 participants dropped out due to the Covid-19 outbreak.
Of the participants who accomplished the study, 2 participants in the PLA-SUPP have
been excluded as a result of poor compliance with sporting the
knee brace through the immobilization part (S1 File).
Nonetheless, there are a number of potential downsides to myostatin inhibition in people looking for athletic enhancement.
Creatine and follistatin dietary supplements have not
been permitted by the FDA for medical use.
Laws set manufacturing standards for them however don’t assure that they’re safe or effective.
Some scientists assume myostatin inhibition must be additional
researched for doubtlessly preventing weight problems and diabetes [29, 26].
This impact has largely been seen in animal studies
on follistatin, a pure hormone that inhibits myostatin [26, 27, 28].
Users shouldn’t disregard, or delay in acquiring,
medical advice for any medical condition they could have and may search the help of their
health care professionals for any such conditions.
The extra I research and learn about the human physique (there is,
it appears, too much data for one lifetime), the more I see all of
it come right down to steadiness. We seem to have all
we’d like in the form of creatine, leucine, HMB along with resistance training itself.
That stated, we additionally can’t rule out the likelihood
that some new scientific analysis somewhere will result in better/different technology.
For occasion, MSTN propeptide has demonstrated efficacy as a selected
inhibitor but has yet to obtain medical attention. Although MSTN inhibition has yet
to totally understand its promise as a muscle-enhancing drug, there is nonetheless ample
potential for refinement in its therapeutic applications and drug designs.
Mechanistically, MSTN inhibition interacts with insulin sensitivity and obesity via both skeletal muscle-dependent and impartial mediation. The major phenotypic change accompanying MSTN suppression is an increase in skeletal muscle,
which partitions nutrients away from adipose tissue to support energy necessities
for muscle development. Skeletal muscle is the primary site for insulin-mediated glucose uptake
through glucose transporter kind 4 (GLUT4) protein [127].
There are many commonalities at the molecular degree within the pathways in skeletal muscle that lead to atrophy, whether or not it’s in the context of most cancers cachexia or other noncancer muscle wasting conditions.
The mechanisms regulating skeletal muscle mass have just
lately been reviewed [17–21]. Myostatin, a member of the TGFβ superfamily
of growth elements, is a highly conserved adverse regulator of
skeletal muscle mass that’s upregulated in plenty of circumstances of muscle losing.
Numerous induced or natural circumstances leading to myostatin deficiency end in elevated muscle mass and strength in normal animals and have
been proven to deal with or stop a range of muscle losing
conditions.
Dietary support to counter disuse atrophy has included supplementation with
important amino acids [5] or omega-3 fatty acids [6], which have been shown to
mitigate disuse-induced atrophy. Further work is warranted to establish effective methods to take care
of muscle mass and function during disuse, leveraging key
molecular targets. There is limited analysis involving isolated (–)-epicatechin supplementation with
train in healthy grownup populations. Research is required to examine the consequences of (–)-epicatechin on train performance utilizing totally different dosing
methods of (–)-epicatechin. Since (–)-epicatechin is the
first flavanol found in cocoa and is often consumed in much smaller doses, it might be useful to
review the consequences of the whole cocoa extract instead of one isolated flavanol as was used in the current research.
Decroix et al. (35) discovered that acute supplementation of
cocoa flavanols had no impact on cyclists’ time trials, however did positively
have an result on oxidative capability in the identical
cyclists.
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Dietary Supplements like epicatechin and quercetin may complement your efforts however aren’t miraculous options.
No single methodology, including drugs, can be thought-about the
best way to inhibit myostatin universally.
ACE-083, a FST-based fusion protein during which FST291 is coupled to a human IgG Fc domain [81],
is an alternate version of ACE-031 developed by Acceleron Pharma for the remedy of FSHD and Charcot-Marie-Tooth illness
(CMT). Notably, ACE-083 is designed to act regionally by
way of intramuscular administration and its treatment effectively induced localized muscle hypertrophy and focal improvement in pressure era without systemic results in wild-type mice and mouse fashions for CMT
and DMD [81]. In a section 1 research carried out on wholesome
postmenopausal ladies, ACE-083 injection ( mg) into muscular tissues resulted in significant targeted muscle growth with no change in energy [82].
Unfortunately, section 2 scientific trials in patients with FSHD and
CMT had been lately terminated because of failure in achieving useful improvements, shutting
down additional growth of ACE-083. One of the most potent methods to
inhibit myostatin signaling was demonstrated utilizing the soluble type of ACVR2B receptor.
In 2013, the Food and Drug Administration (FDA)
granted the breakthrough therapy designation to bimagrumab for sIBM.
In a part 2 clinical trial performed in topics older than sixty five years with sarcopenia, remedy with bimagrumab (30 mg/kg) for 16 weeks significantly improved thigh muscle
quantity, gait pace, and 6-min strolling distance
[76]. Nevertheless, a further dose vary finding research (6 monthly doses
of 70, 210, or seven-hundred mg) in patients with sarcopenia resulted in 2 deaths in the highest-dosage group,
halting the development of bimagrumab as a therapy for sarcopenia.
In a part 2 scientific trial involving wholesome
younger men who had been placed in a cast for
two weeks to induce disuse atrophy, a single injection (30 mg/kg) of bimagrumab significantly accelerated thigh muscle quantity recovery [77].
Moreover, a section 2 scientific trial in continual obstructive
pulmonary illness (COPD) patients with cachexia demonstrated a big improve in thigh muscle volume, however
not 6-min stroll distance, after 2 injections of bimagrumab (30 mg/kg) [78].
Myostatin circulates in two forms, latent and energetic,
and solely activated C-terminal myostatin, after proteolytic processing, can bind to the ActRIIB, thereby initiating signaling, including the pathways activating UPS and inhibiting myogenesis [8].
In the current research, the molecular kinetics of myostatin exercise between blood and muscle at the cellular degree are unclear.
References:
Types of steroid pills