@구글 크롬 플래시(Adobe Flash Player) 차단 해제 하는 방법!!참고
컴퓨터에서 Chrome을 엽니다.
오른쪽 상단에서 더보기 더보기 다음 설정을 클릭합니다.
하단에서 고급을 클릭합니다.
'개인정보 및 보안'에서 사이트 설정을 클릭합니다.
상단에서 사이트의 플래시 실행 차단(권장)을 사용 중지합니다.
@설치 문제 | Flash Player | Windows 7 이하....Adobe 지원 검색
적용 대상: Flash Player....최종 게시일: 2019년 6월 17일
이 단계별 안내서를 사용하여 Windows 7 이하 시스템에서의 Adobe Flash Player 설치 문제를 해결하십시오. Adobe Flash Player 문제를 해결하는 데 도움이 되는 유용한 리소스 링크를 찾으십시오.
Adobe Flash Player 설치에 문제가 있습니까? 문제를 파악하고 해당 해결방법을 시도해 보십시오.
1. 컴퓨터에 Flash Player가 이미 설치되어 있는지 확인했습니까? [지금확인]클릭
2. 브라우저를 닫으라는 메시지가 표시됩니까?
Internet Explorer에서는 설치를 계속하려면 설치 프로그램에서 브라우저를 닫아야 합니다.
[다음 지침..클릭]을 따르십시오.
또한, 응용 프로그램에서 이미 설치되어 있는 Flash Player 버전을 사용 중인 경우에는 Flash Player 설치 프로그램이 제대로 실행되지 않습니다. 이러한 경우 열려 있는 응용 프로그램을 모두 닫고 다시 시도하십시오.
3. 브라우저에 Flash Player가 활성화되어 있는지 확인했습니까?
Internet Explorer의 경우 Internet Explorer에 대해 Flash Player 활성화를 참조하십시오.
Firefox(모든 OS)의 경우 Firefox에 대해 Flash Player 활성화를 참조하십시오.
Mac OS에 있는 Safari의 경우 Safari에 대해 Flash Player 활성화를 참조하십시오.
Google Chrome의 경우 Chrome에 대해 Flash Player 활성화를 참조하십시오.
Opera의 경우 Opera에 대해 Flash Player 활성화를 참조하십시오.
4. ActiveX 문제가 포함된 오류가 표시됩니까?
Flash Player가 제대로 작동하도록 ActiveX 필터링을 비활성화합니다.
IE9, IE10 및 IE11에서 'ActiveX 필터링' 설정 또는 해제 방법을 참조하십시오.
5. 설치 프로그램에서 설치를 시작했습니까?
다운로드가 완료되면 Flash Player 설치 프로그램에서 설치를 시작하라는 메시지를 표시합니다. 표시되지 않는 경우, Downloads 폴더에서 바로 설치 프로그램을 시작할 수 있습니다.
Flash Player를 다운로드한 후에 브라우저를 모두 닫습니다.
Flash Player 설치 파일을 찾습니다. 달리 지정하지 않은 한 이 파일은 Downloads 폴더에 저장되어 있습니다.
설치 프로그램 파일을 두 번 클릭하여 Flash Player 설치를 시작합니다.
다운로드한 파일 찾기에 대한 자세한 내용은 Microsoft 도움말에서 다운로드한 파일 찾기 및 웹에서 파일 다운로드를 참조하십시오.
6. 권한 문제가 발생합니까?
Flash Player 설치 후 컴퓨터를 다시 시작하기 전까지는 모든 것이 제대로 작동합니다. 다시 시작하고 나면 웹 페이지에서 Flash Player를 다시 설치하라는 메시지를 표시합니다.
Flash Player 관련 Windows 권한 문제를 해결하려면 어떻게 합니까?
7. Flash Player 설치 프로그램이 실행되지 않습니까?
설치 프로그램의 디지털 인증서(sha256)와 호환되도록 운영 체제를 업데이트해야 할 수도 있습니다. 다음 운영 체제를 업데이트해야 합니다.
Windows XP 운영 체제가 Windows XP이고 서비스 팩 2 이하를 실행 중인 경우 서비스 팩 3으로 업그레이드합니다.
Windows Vista 운영 체제가 Windows Vista SP2인 경우 Microsoft 지원에서 운영 체제에 맞는 업데이트를 다운로드합니다.
Windows Server 2008 운영 체제가 Windows Server 2008 SP2인 경우 Microsoft 지원에서 운영 체제에 맞는 업데이트를 다운로드합니다.
==문제가 계속 발생합니까?
Adobe Flash Player를 설치하는 데 계속 문제가 있는 경우 설치 프로그램을 다운로드해 보십시오.
Internet Explorer용 Flash Player - ActiveX
Firefox용 Flash Player - NPAPI
Opera 및 Chromium 기반 브라우저용 Flash Player - PPAPI
Flash Player 설치 및 업데이트 - FAQ
포럼의 전문가에게 질문하기
자주 발생하는 문제
The Importance of SIRT1
SIRT enzymes “turn off” certain genes that promote aging, such as those involved in inflammation, fat synthesis and storage, and managing blood sugar levels.
When proteins are undergoing stress, acetyl groups are added to proteins as a response to changes induced by inflammation and oxidation.
Sirtuins (like SIRT1) remove these acetyl groups to keep the protein in service longer than usual, while simultaneously stabilizing the charge state of the carbon backbone in protein to resist any further changes in their shape. This allows your cellular proteins to live longer and you can save energy on other processes.
Excessive blue light is capable of loosening cytochrome c from the mitochondria, which makes the electron flow less efficient. Red light causes tight binding to remain to cytochrome c in mitochondria and this allows electrons to continue to flow normally to oxygen, which lowers free radical production per oxygen molecule.
SIRT1 powerfully reverses leptin resistance .
SIRT1 (and PGC-1a) also make you more sensitive to T3 , which is also a problem in CFS – indicated by the fact that people feel cold and have symptoms of low T3 (symptoms that are worse than their numbers reveal).
SIRT1 increases estrogen function (estrogen receptor signaling) .
Resveratrol and SIRT1 make you more sensitive to vitamin D – it potentiates the vitamin D receptor (VDR) [4, 5].
SIRT1 inhibits IGF-1 .
SIRT1 inhibits mTOR .
SIRT1 protects you from nitric oxide. Nitric oxide is damaging but it can also be good. When you have good SIRT1 levels and activity, nitric oxide will stimulate DNA repair genes (via deacetylation of FoxO1). Otherwise, nitric oxide will stimulate genes that will cause the cell to self-destruct .
SIRT1 probably overall increases adiponectin release from fat cells. It decreases adiponectin by decreasing PPAR gamma in these cells , however, it increases adiponectin by increasing Foxo1 [10, 11, 12].
A reduction in SIRT 1 and SIRT 3 enzymes leads to:
Neurodegeneration in the brain
Vascular inflammation, producing damage to blood vessels that can result in stroke or heart attack
Increased fat storage in the liver, which can lead to fatty liver disease (NAFLD)
Increased fat production and deposition in white adipose tissue, the primary fat storage form found in dangerous belly fat
Insulin resistance, preventing cells from appropriately removing glucose from the blood, producing higher blood sugar levels and leading directly to metabolic syndrome
Fatigue, loss of muscle strength, and fatty infiltration of muscles resulting in reduced fatty acid oxidation (“burning”), thereby depriving muscles of their normal sources of energy.
Molecular Pathways Activated by SIRT1:
SIRT1 causes the activation (by deacetylation) PPAR-alpha, PGC-1a, LXR , MAO-A, FOXOs – FOXO1a, Foxo3 , UCP2, FGF-21 , PXR (overall increase production/activity) [16, 17]. FXR (deacetylation allows to bind with RXR-a, DNA binding, and transactivation activity)  – can also inhibit FXR .
Deacetylation of Androgen Receptors and Estrogen Receptor-a by SIRT1 causes these hormones to have less cancer growth properties .
SIRT1 deacetylates and inhibits NF-kB, STAT3, and MMP9 . SIRT1 deacetylation degrades PER2 .
SIRT1 Deacetylates the following other proteins not listed: Hif-1α, Hif-2a, HSF1, Bax, Ku70, b-catenin, E2F1, Myc, TORC2, SREBP, PER2, CLOCK .
SIRT1 and The Circadian Rhythm
Not taking care of your circadian rhythm properly is also a root cause of chronic health issues because your circadian rhythm gets deregulated (mainly by not enough sun in the day and too much artificial lighting at night).
The enzyme that makes NAD+ (NAMPT) is under circadian control  and is produced by CLOCK and BMAL1.
When your circadian rhythm isn’t working, NAD+ levels are not regulated properly and that means SIRT1 (and SIRT3) isn’t either regulated properly since NAD+ is needed to activate SIRT1 & 3.
SIRT1 regulates the strength (amplitude) and the duration of circadian gene expression in the retina by removing acetyl groups from key circadian clock regulators, such as BMAL1 and PER2.
In aged mice, SIRT1 levels in the SCN (circadian command center) are decreased, as are those of BMAL1 and PER2, causing a longer circadian period, a more disrupted activity pattern, and an inability to adapt to changes in the light entrainment schedule. Young mice lacking brain SIRT1 have similar effects to these aging-dependent circadian changes, whereas mice that overexpress SIRT1 in the brain are protected from the effects of aging (25).
We start getting to feedback loops, where not taking care of your circadian rhythm, hypoxia, excess carbs, and energy imbalance go on to cause an even more deregulated system and you get lower levels of SIRT1.
This is why ALL CFS sufferers that I’ve seen have a messed up circadian rhythm/SCN.
Negatives of SIRT1
The way to look at these negatives is:
Most of the time, biology deals with tradeoffs.
SIRT1 effects are tissue dependent. So even though SIRT1 levels may correlate in one tissue to another, the levels are different.
The cellular environment matters. If SIRT1 is high AND you have certain other genes switched on, then SIRT1 will matter. Otherwise, it won’t. I see this with many other pathways.
SIRT1 is supposed to be cycled in a circadian manner. Chronically high levels could produce a different effect.
Recent studies show that SIRT1 can increase Th17 cells (by deacetylating RORγt), which are inflammatory. Inhibition of SIRT1 suppresses multiple sclerosis .
SIRT1 increased the cytokine TNF (in response to LPS), IL-6 and IL-8 in the tissue of patients with rheumatoid arthritis .
SIRT1 decreases Nrf2-related gene production since acetylation allows Nrf2 to bind to DNA better and produce antioxidant genes .
SIRT1 decreases beta cell proliferation in the pancreas (GLP-1 blocks SIRT1 deacetylation of FoxO1) . Beta cells release insulin, so reduced beta cells can contribute to diabetes, but SIRT1 has many other anti-diabetic actions.
SIRT1 inhibition with nicotinamide is being investigated as an anti-tumor agent because SIRT1 promotes cell survival over apoptosis, which can increase cancer in some ways and also block the ability of chemotherapy to kill cancer .
SIRT1 can contribute to cancer by inhibiting DNA repair enzymes (including p53, BRCA1&2, Ku70) and the apoptosis proteins .
Specifically, SIRT1 deacetylates p53, which decreases its ability to function as an anti-tumor protein .
Since SIRT1 lowers IGF-1 and its receptors, it can cause some downsides to less IGF-1, including less neuroprotection and more likely for your neurons to die .
SIRT1 overproduction can impair liver regeneration to a degree .
More SIRT1 in CD4+ cells increases Lupus risk [34, 35]
How to Activate SIRT1
Anything that increases NAD+, will increase SIRT1 activity. So I won’t list the ones listed above.
According to Kruse, SIRT1 and NAD+ provide that fine control through the special properties of DHA.
Increasing DHA is the best way to increase SIRT1 because it works together with it to modulate the immune system and improve your mitochondria.
DHA increases SIRT1 in the blood vessels, which increase Nitric Oxide (eNOS) .
DHA decreases macrophage inflammation and inhibits Nf-kB via increasing SIRT1 in macrophages (DHA decreases inflammation via other mechanisms as well) . DHA decreases COX-2 inflammation and insulin resistance also through SIRT1 (in colon cells) .
DHA increases SIRT1 in the hippocampus and reverses the cognitive decline in a bunch of disease states. Several epidemiological studies have shown that low blood DHA levels are associated with cognitive deficits in healthy elderly subjects and also in patients suffering from neurodegenerative disorders. Additionally, DHA enhances performance in learning and memory tasks in aged animals, and it also improves cerebral blood flow (which is lacking in CFS sufferers) .
DHA supplementation is effective in reversing the reduction of sirt1 levels in rats with mild traumatic brain injury .
Ideally, you want to get DHA from fish, but supplements are certainly better than nothing. I use them a little in addition to a lot of seafood.
Cold, forskolin, and adrenaline increase SIRT1 activity by increasing cyclic AMP and this is independent of NAD+ levels [41, 42].
We evolved to have this as a more rapid way to activate metabolism than by slowly increasing NAD+ levels. There are many other benefits to these as well.
Cold [41, 42]
Sun (Nitric Oxide) 
Fructose – In the liver, fructose increased SIRT1 production and activity 
Extra Virgin Olive Oil 
Nicotinamide Riboside 
EGCG/ Tea (cells) 
Forskolin [41, 42]
Vitamin D (active form calcitriol) 
Lipoic Acid 
Pau Darco/Beta Lapachone 
Gotu Kola 
Grape Seed Extract 
LLLT (infrared) 
Bitter melon  – normalizes SIRT1
Lycopene – metabolite increases SIRT1 production and activity 
Metformin – increases SIRT1 production and activity 
Adrenaline [41, 42]
Hydrogen Peroxide 
Hydrogen Sulfide 
PDE5 inhibitors 
PON1 , BMAL1 , Other: FOXO3a, c-Myc, PARP inhibition
How to Increase NAD+, Which Activates SIRT1
Calorie restriction 
Nicotinamide Riboside 
AMPK activation  – AMPK increases SIRT1 activity by increasing cellular NAD+levels (increases NAMPT ). SIRT1 activation also stimulates fatty acid oxidation and indirectly activates AMPK.
Pau Darco/Beta Lapachone 
Malic acid 
Niacinamide – low doses 
Lithium inhibits mir-34a, which inhibits NAMPT, the enzyme that makes NAD+ [79, 80] So lithium should technically increase NAMPT and NAD+ by taking the breaks away from its production.
Succinic acid, to a lower degree than malic acid 
Tryptophan and Aspartic acid are fuel for NAD+ , but we usually get enough dietary amino acids if you eat adequate protein.
Melatonin [31, 83]
IFNy [84, 85], CIITA 
Nicotinamide – at higher doses 
CLA (supplement) 
The variation rs12778366 is found in the SIRT1 gene. About 80% of the global population has “TT”, while 18% have CT.
It’s thought that the C allele causes increased gene production of SIRT1 .
People with the C allele have an almost 30% reduced risk of dying during an 18-year follow-up study in the general population [91, 92].
TT was at a higher risk for diabetes .
People with a C allele had better glucose tolerance indicated by 0.34 mmol/l lower glucose levels . Obese people with the C allele especially had better glucose tolerance .