是否有人能否提供相關原始論文---避免失智 染唇皰疹3天內投藥
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是否有人能否提供相關原始論文---避免失智 染唇皰疹3天內投藥
我只查到一些關於老鼠的動物實驗
不曉得其他醫師有較詳細的原始論文
避免失智 染唇皰疹3天內投藥
〔記者鍾麗華/台北報導〕研究指出,唇皰疹病毒與阿茲海默症(老人失智症)有關。根據統計,有八成的人曾感染過唇皰疹,潛伏的罹病風險不小,醫師建議,民眾罹患唇皰疹時,最好在發病三天內投以抗病毒藥物,才能抑制病毒複製。健保已開始給付唇皰疹抗病毒外用藥,更有效的口服藥物則仍須自費。
淡水馬偕紀念醫院小兒科主治醫師林達雄指出,國外已有不少研究證實,唇皰疹病毒與失智症有關,腦細胞中的「β糊蛋白」(beta amyloid protein)斑塊堆積,是造成失智症的主要原因之一,科學家在九十%的失智症患者腦中的β糊蛋白中發現唇皰疹病毒的DNA。
林達雄強調,十四歲到五十九歲的民眾,有八成都感染過唇皰疹,尤其七個月大到六歲的兒童最容易感染皰疹病毒,一般小朋友感染都是給予緩解症狀的治療方式,但他認為,應該投以口服抗病毒藥物,才能減少病毒複製,殘存在體內,否則恐成為四、五十年後,造成失智症的風險。
台安醫院皮膚科主治醫師陳眉穎表示,相關研究報告出爐後,不少門診病人會主動要求給予抗病毒藥物。不過,唇皰疹病程約七天,最好在水泡剛出現,發病三天內就投藥,把握黃金治療期,等到水泡全部長出來,再以抗病毒藥治療的效果有限,反而是以症狀緩解的消炎、止痛藥為主。
陳眉穎強調,一旦感染皰疹病毒,病毒就會終生潛藏於人體的神經節內,如果免疫力下降、壓力大、天冷溫差大使身體抵抗力降低、熬夜等,就會再度發病,兒童可能經由父母親的餵食、親吻時遭傳染,而抗病毒藥主要是讓病毒不要繼續複製、抑制病毒繁殖。
不曉得其他醫師有較詳細的原始論文
避免失智 染唇皰疹3天內投藥
〔記者鍾麗華/台北報導〕研究指出,唇皰疹病毒與阿茲海默症(老人失智症)有關。根據統計,有八成的人曾感染過唇皰疹,潛伏的罹病風險不小,醫師建議,民眾罹患唇皰疹時,最好在發病三天內投以抗病毒藥物,才能抑制病毒複製。健保已開始給付唇皰疹抗病毒外用藥,更有效的口服藥物則仍須自費。
淡水馬偕紀念醫院小兒科主治醫師林達雄指出,國外已有不少研究證實,唇皰疹病毒與失智症有關,腦細胞中的「β糊蛋白」(beta amyloid protein)斑塊堆積,是造成失智症的主要原因之一,科學家在九十%的失智症患者腦中的β糊蛋白中發現唇皰疹病毒的DNA。
林達雄強調,十四歲到五十九歲的民眾,有八成都感染過唇皰疹,尤其七個月大到六歲的兒童最容易感染皰疹病毒,一般小朋友感染都是給予緩解症狀的治療方式,但他認為,應該投以口服抗病毒藥物,才能減少病毒複製,殘存在體內,否則恐成為四、五十年後,造成失智症的風險。
台安醫院皮膚科主治醫師陳眉穎表示,相關研究報告出爐後,不少門診病人會主動要求給予抗病毒藥物。不過,唇皰疹病程約七天,最好在水泡剛出現,發病三天內就投藥,把握黃金治療期,等到水泡全部長出來,再以抗病毒藥治療的效果有限,反而是以症狀緩解的消炎、止痛藥為主。
陳眉穎強調,一旦感染皰疹病毒,病毒就會終生潛藏於人體的神經節內,如果免疫力下降、壓力大、天冷溫差大使身體抵抗力降低、熬夜等,就會再度發病,兒童可能經由父母親的餵食、親吻時遭傳染,而抗病毒藥主要是讓病毒不要繼續複製、抑制病毒繁殖。
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Re: 是否有人能否提供相關原始論文---避免失智 染唇皰疹3天內投藥
動物實驗
The effects of antiviral therapy on the distribution of herpes simplex virus type 1 to ganglionic neurons and its consequences during, immediately following and several months after treatment
http://vir.sgmjournals.org/cgi/content/full/81/10/2385
Famciclovir and Valaciclovir Differ in the Prevention of Herpes Simplex Virus Type 1 Latency in Mice: a Quantitative Study
http://aac.asm.org/cgi/content/full/42/7/1555
Persistence of Infectious Herpes Simplex Virus Type 2 in the Nervous System in Mice after Antiviral Chemotherapy
http://aac.asm.org/cgi/content/full/44/1/97
The effects of antiviral therapy on the distribution of herpes simplex virus type 1 to ganglionic neurons and its consequences during, immediately following and several months after treatment
http://vir.sgmjournals.org/cgi/content/full/81/10/2385
Famciclovir and Valaciclovir Differ in the Prevention of Herpes Simplex Virus Type 1 Latency in Mice: a Quantitative Study
http://aac.asm.org/cgi/content/full/42/7/1555
Persistence of Infectious Herpes Simplex Virus Type 2 in the Nervous System in Mice after Antiviral Chemotherapy
http://aac.asm.org/cgi/content/full/44/1/97
- joelin
- 科主任級
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Re: 是否有人能否提供相關原始論文---避免失智 染唇皰疹3天內投藥
http://www3.interscience.wiley.com/jour ... 1&SRETRY=0
MA Wozniak, AP Mee and RF Itzhaki. Herpes simplex virus type I DNA is located within Alzheimer's disease amyloid plaques. The Journal of Pathology, Volume 217, Issue 1 , Pages131 - 138 DOI: 10.1002/path.2449
http://www.prohealth.com/library/showar ... ibid=14172
[Note: Herpes simplex virus type 1 (HSV-1) is most commonly known as the virus that causes “cold sores” or “fever blisters” on the mouth. Worldwide, some 75% to 95% of adults carry the virus, which is "an infection for life."]
The brains of Alzheimer's disease sufferers are characterized by amyloid plaques and neurofibrillary tangles. However, the cause(s) of these features and those of the disease are unknown, in sporadic cases. We previously showed that herpes simplex virus type 1 is a strong risk factor for Alzheimer's disease when in the brains of possessors of the type 4 allele of the apolipoprotein E gene (APOE-e4), and that Beta-amyloid, the main component of plaques, accumulates in herpes simplex virus type 1-infected cell cultures and mouse brain.
The present study aimed to elucidate the relationship of the virus to plaques by determining their proximity in human brain sections.
We used in situ polymerase chain reaction to detect herpes simplex virus type 1 DNA, and immunohistochemistry or thioflavin S staining to detect amyloid plaques.
We discovered a striking localization of herpes simplex virus type 1 DNA within plaques. In Alzheimer's disease brains:
• 90% of the plaques contained the viral DNA
• And 72% of the DNA was associated with plaques;
In aged normal brains, which contain amyloid plaques at a lower frequency:
• 80% of plaques contained herpes simplex virus type 1 DNA
• But only 24% of the viral DNA was plaque-associated (p < 0.001). [Probability that this finding would result by chance less than 1 in 1,000.]
We suggest that this is because in aged normal individuals, there is a lesser production and/or greater removal of Beta-amyloid (ABeta), so that less of the viral DNA is seen to be associated with ABeta in the brain.
Our present data - together with our finding of ABeta accumulation in herpes simplex virus type 1-infected cells and mouse brain - suggest that this virus is a major cause of amyloid plaques and hence probably a significant aetiological factor in Alzheimer's disease.
They point to the usage of antiviral agents to treat the disease and possibly of vaccination to prevent it.
Source: The Journal of Pathology, Jan 2009;217(1)pp 131-138. PMID: 18973185, by Wozniak MA, Mee AP, Itzhaki RF, Faculty of Life Sciences, University of Manchester, UK; Department of Medicine, Manchester Royal Infirmary, UK. [E-mail: ruth.itzhaki@manchester.ac.uk]
MA Wozniak, AP Mee and RF Itzhaki. Herpes simplex virus type I DNA is located within Alzheimer's disease amyloid plaques. The Journal of Pathology, Volume 217, Issue 1 , Pages131 - 138 DOI: 10.1002/path.2449
http://www.prohealth.com/library/showar ... ibid=14172
[Note: Herpes simplex virus type 1 (HSV-1) is most commonly known as the virus that causes “cold sores” or “fever blisters” on the mouth. Worldwide, some 75% to 95% of adults carry the virus, which is "an infection for life."]
The brains of Alzheimer's disease sufferers are characterized by amyloid plaques and neurofibrillary tangles. However, the cause(s) of these features and those of the disease are unknown, in sporadic cases. We previously showed that herpes simplex virus type 1 is a strong risk factor for Alzheimer's disease when in the brains of possessors of the type 4 allele of the apolipoprotein E gene (APOE-e4), and that Beta-amyloid, the main component of plaques, accumulates in herpes simplex virus type 1-infected cell cultures and mouse brain.
The present study aimed to elucidate the relationship of the virus to plaques by determining their proximity in human brain sections.
We used in situ polymerase chain reaction to detect herpes simplex virus type 1 DNA, and immunohistochemistry or thioflavin S staining to detect amyloid plaques.
We discovered a striking localization of herpes simplex virus type 1 DNA within plaques. In Alzheimer's disease brains:
• 90% of the plaques contained the viral DNA
• And 72% of the DNA was associated with plaques;
In aged normal brains, which contain amyloid plaques at a lower frequency:
• 80% of plaques contained herpes simplex virus type 1 DNA
• But only 24% of the viral DNA was plaque-associated (p < 0.001). [Probability that this finding would result by chance less than 1 in 1,000.]
We suggest that this is because in aged normal individuals, there is a lesser production and/or greater removal of Beta-amyloid (ABeta), so that less of the viral DNA is seen to be associated with ABeta in the brain.
Our present data - together with our finding of ABeta accumulation in herpes simplex virus type 1-infected cells and mouse brain - suggest that this virus is a major cause of amyloid plaques and hence probably a significant aetiological factor in Alzheimer's disease.
They point to the usage of antiviral agents to treat the disease and possibly of vaccination to prevent it.
Source: The Journal of Pathology, Jan 2009;217(1)pp 131-138. PMID: 18973185, by Wozniak MA, Mee AP, Itzhaki RF, Faculty of Life Sciences, University of Manchester, UK; Department of Medicine, Manchester Royal Infirmary, UK. [E-mail: ruth.itzhaki@manchester.ac.uk]
最後由 joelin 於 週二 2月 24, 2009 12:05 am 編輯,總共編輯了 1 次。
儒 學 身 能
道 修 靈 淨
佛 悟 心 空
道 修 靈 淨
佛 悟 心 空
- joelin
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Re: 是否有人能否提供相關原始論文---避免失智 染唇皰疹3天內投藥
'http://www.ihmf.org/journal/download/83pyles(64)vol864.pdf'
'http://www.eurekalert.org/pub_releases/2003-08/aha-ilt081303.php'
'http://www.eurekalert.org/pub_releases/2003-08/aha-ilt081303.php'
最後由 joelin 於 週二 2月 24, 2009 11:36 am 編輯,總共編輯了 1 次。
儒 學 身 能
道 修 靈 淨
佛 悟 心 空
道 修 靈 淨
佛 悟 心 空
-
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Re: 是否有人能否提供相關原始論文---避免失智 染唇皰疹3天內投藥
2001年就有paper
謝謝joelin
謝謝joelin
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- 來自: 山水之地
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Re: 是否有人能否提供相關原始論文---避免失智 染唇皰疹3天內投藥
不好意思
希望能提供有
治療HSV type I 感染能有效降低Alzheimer's disease的論文
希望能提供有
治療HSV type I 感染能有效降低Alzheimer's disease的論文
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- V1
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- 來自: 島南
Re: 是否有人能否提供相關原始論文---避免失智 染唇皰疹3天內投藥
這篇先參考看看
下面只有摘要
http://www.ncbi.nlm.nih.gov/pubmed/1922 ... d_RVDocSum
Alzheimer's Disease-Specific Tau Phosphorylation is Induced by Herpes Simplex Virus Type 1.Wozniak MA, Frost AL, Itzhaki RF.
Faculty of Life Sciences, The University of Manchester, Manchester, UK.
Neurofibrillary tangles are one of the main neuropathological features of Alzheimer's disease (AD) and are composed of abnormally phosphorylated forms of a microtubule-associated protein called tau. What causes this abnormal phosphorylation is unknown. Our previous studies have implicated herpes simplex virus type 1 (HSV1) as an etiological agent in AD, and so we investigated whether infection with this virus induces AD-like tau phosphorylation. Here we demonstrate that HSV1 causes tau phosphorylation at several sites, including serine 202, threonine 212, serine 214, serine 396 and serine 404. In addition, we have elucidated the mechanism involved by showing that the virus induces glycogen synthase kinase 3beta and protein kinase A, the enzymes that cause phosphorylation at these sites. Our data clearly reveal the importance of HSV1 in AD-type tau phosphorylation, and support the case that the virus is a cause of the disease. Together with our previous data, our results point to the use of antiviral agents to slow the progression of the disease.
PMID: 19221424 [PubMed - in process]
Related ArticlesReviewCurrent advances on different kinases involved in tau phosphorylation, and implications in Alzheimer's disease and tauopathies. [Curr Alzheimer Res. 2005] Dephosphorylation of abnormal sites of tau factor by protein phosphatases and its implication for Alzheimer's disease. [Neurochem Int. 1995] Amyloid beta peptide induces tau phosphorylation and loss of cholinergic neurons in rat primary septal cultures. [Neuroscience. 2002] Kinases and phosphatases and tau sites involved in Alzheimer neurofibrillary degeneration. [Eur J Neurosci. 2007] ReviewPhysiology and pathology of tau protein kinases in relation to Alzheimer's disease. [J Biochem. 1997] » See Reviews... | » See All...
*****
發現這篇好像和joelin大大貼的是同一作者
下面只有摘要
http://www.ncbi.nlm.nih.gov/pubmed/1922 ... d_RVDocSum
Alzheimer's Disease-Specific Tau Phosphorylation is Induced by Herpes Simplex Virus Type 1.Wozniak MA, Frost AL, Itzhaki RF.
Faculty of Life Sciences, The University of Manchester, Manchester, UK.
Neurofibrillary tangles are one of the main neuropathological features of Alzheimer's disease (AD) and are composed of abnormally phosphorylated forms of a microtubule-associated protein called tau. What causes this abnormal phosphorylation is unknown. Our previous studies have implicated herpes simplex virus type 1 (HSV1) as an etiological agent in AD, and so we investigated whether infection with this virus induces AD-like tau phosphorylation. Here we demonstrate that HSV1 causes tau phosphorylation at several sites, including serine 202, threonine 212, serine 214, serine 396 and serine 404. In addition, we have elucidated the mechanism involved by showing that the virus induces glycogen synthase kinase 3beta and protein kinase A, the enzymes that cause phosphorylation at these sites. Our data clearly reveal the importance of HSV1 in AD-type tau phosphorylation, and support the case that the virus is a cause of the disease. Together with our previous data, our results point to the use of antiviral agents to slow the progression of the disease.
PMID: 19221424 [PubMed - in process]
Related ArticlesReviewCurrent advances on different kinases involved in tau phosphorylation, and implications in Alzheimer's disease and tauopathies. [Curr Alzheimer Res. 2005] Dephosphorylation of abnormal sites of tau factor by protein phosphatases and its implication for Alzheimer's disease. [Neurochem Int. 1995] Amyloid beta peptide induces tau phosphorylation and loss of cholinergic neurons in rat primary septal cultures. [Neuroscience. 2002] Kinases and phosphatases and tau sites involved in Alzheimer neurofibrillary degeneration. [Eur J Neurosci. 2007] ReviewPhysiology and pathology of tau protein kinases in relation to Alzheimer's disease. [J Biochem. 1997] » See Reviews... | » See All...
*****
發現這篇好像和joelin大大貼的是同一作者
It is one thing to promise ,and
another to perform.
another to perform.
- yoyo
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Re: 是否有人能否提供相關原始論文---避免失智 染唇皰疹3天內投藥
汪威達 寫:我只查到一些關於老鼠的動物實驗
不曉得其他醫師有較詳細的原始論文
避免失智 染唇皰疹3天內投藥
〔記者鍾麗華/台北報導〕研究指出,唇皰疹病毒與阿茲海默症(老人失智症)有關。根據統計,有八成的人曾感染過唇皰疹,潛伏的罹病風險不小,醫師建議,民眾罹患唇皰疹時,最好在發病三天內投以抗病毒藥物,才能抑制病毒複製。健保已開始給付唇皰疹抗病毒外用藥,更有效的口服藥物則仍須自費。
..................................
有嗎??
我之前才被刪.....
80-90%的人都曾經得過HERPES, 從阿茲海默症病患腦組織裡找到HERPES VIRUS 的DNA好像也蠻合理的,但是就一定有關係嗎??
- Alex
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Re: 是否有人能否提供相關原始論文---避免失智 染唇皰疹3天內投藥
www.nhi.gov.tw/information/bulletin_fil ... 0970012754令-附件.DOC
「全民健康保險藥品給付規定」修正規定
第10章 抗微生物劑 Antimicrobial agents
(自97年12月1日生效)
修正後給付規定
10.7.5 Acyclovir外用軟膏製劑(97/12/1):限下列病例使用
1. 單純性疱疹(感染部位在頭頸部、生殖器周圍、嘴唇、口腔、陰部)3日內可使用acyclovir藥膏,每次給予藥量限5公克以內。
2. 口服、注射劑及外用藥膏擇一使用,不得合併使用。
「全民健康保險藥品給付規定」修正規定
第10章 抗微生物劑 Antimicrobial agents
(自97年12月1日生效)
修正後給付規定
10.7.5 Acyclovir外用軟膏製劑(97/12/1):限下列病例使用
1. 單純性疱疹(感染部位在頭頸部、生殖器周圍、嘴唇、口腔、陰部)3日內可使用acyclovir藥膏,每次給予藥量限5公克以內。
2. 口服、注射劑及外用藥膏擇一使用,不得合併使用。
莫欺少年窮
猛虎未出籠
待定出頭日
血色月朦朧
猛虎未出籠
待定出頭日
血色月朦朧
- yoyo
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Re: 是否有人能否提供相關原始論文---避免失智 染唇皰疹3天內投藥
太感謝Alex大師了!!
原來是12月才改的規定!!
我是去年10月份被刪的
以前報在簡表裡沒事
有一件和其他專案一起報就被..........
一直覺得很奇怪?常常同樣的藥以前在醫院開都ok
可是診所開就不行??
原來是12月才改的規定!!
我是去年10月份被刪的
以前報在簡表裡沒事
有一件和其他專案一起報就被..........
一直覺得很奇怪?常常同樣的藥以前在醫院開都ok
可是診所開就不行??
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- 註冊會員
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Re: 是否有人能否提供相關原始論文---避免失智 染唇皰疹3天內投藥
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