我 的 第一篇做文. ▶️. ®️
今天我終於擺脫我的寒假作業了噢對了！這是我第一次寫日記喔！好啦！我要繼續講了：
，我就可以看鬼滅之刃了！
。我真的想不到靈感了，我要去玩玩具了 bye-bye
我抓到寫作文的訣竅了，下次我一定能寫得很好。
2021年2月20日
Lixu 日記 2021/02/21
噢對了！這是我第一次寫日記喔！好啦！我要繼續講了：
，我就可以看鬼滅之刃了！
。我真的想不到靈感了，我要去玩玩具了 bye-bye
我抓到寫作文的訣竅了，下次我一定能寫得很好。
2020年1月17日
近況 - 2020
好一段時間沒有更新了，一開始寫這部落格是一個同事建議我把FB上的病情記錄下來，放在部落格上比較容易被Google算法找到，也許茫茫人海中會有人需要這些資訊
所以記得一開始除了想要紀錄病情與當下心境，其實也想要幫助一些還在病情初期需要詳細資訊的人，沒想到就這樣也還真的認識了幾個病友，也加入了一個FB社團想做一些貢獻，算是意外的收穫。
關於近況呢，老實說很不錯，應該說算是這兩年最好的一段時間。在半導體業，身體不好還真的很難撐下去。
2016年做完腰椎錐間盤手術到現在，忍過初期的那段恢復期，慢慢習慣後，脊椎好一陣子沒有劇痛了，也不再有睡到痛醒的情形。
而眩暈的部份，2017年開始SSP後，眩暈慢慢收斂到可以勉強恢復可自行開車上下班的狀況，雖然偶發性的會有眩暈發作，頻率與強度都在可接受的範圍，而我也按照Stephen Spring的建議，積極的處理舊牙套內牙根尖發炎的情形，花了不少錢打開牙套重作顯微根管也重作新的牙套，慢慢撥時間處理到現在，也只剩一顆臼齒還沒做。雖然沒有證據說眩暈跟牙根慢性發言有關聯，但我總覺得積極去處理身體慢性發炎對身體健康總是好的。
說到慢性發炎，看了一些書，有一段時間也嘗試理解"腸漏症"與"腸腦軸線"的概念，做了慢性過敏的檢查(IgG)，發現自己對某些食物有慢性過敏，所以就慢慢避開這些食物，開始吃一些對腸道有幫助的益生菌。同樣，沒有證據顯示眩暈跟腸漏有關，但正視這些飲食習慣的問題，調整腸道菌種 也總是不錯的。
而這些事情也不是說做就做 做了就會看到效果，而是有恆心有耐性有紀律的慢慢做，身體狀況是不會騙人的，有什麼慢慢的改變 這些感受自己最清楚。
那為什麼說最近的狀況是近期最好的呢，其實一直到2019年，眩暈還是維持某個頻率每幾天就來一次，但強度勉強算是吃止暈藥可以維持工作開會等等。但2019年底，因緣際會李丞永醫師又聯絡上我，把懶惰的我叫去台中安律診所一趟，他說他離開慈濟以後一直有記得我的事情 (真是感動，因為我也才去慈濟門診兩次)，所以我就又厚著臉皮去找李醫師幫忙，不意外的當天在診所點滴治療就睡了個好覺，更神奇的是，說也奇怪吃了這次李醫師的藥以後，我平常不離身的止暈藥就很少有機會拿出來吃了。現在也是維持吃李醫師的藥，持續觀察中
那如果有人問我推不推SSP，我一樣是不推，因為真的是太貴了，即使當時也許是歸功於SSP把我從休兵狀態推回工作崗位，但我真的無法推薦任何人去跟這位老兄接觸，他貴就算了人又怪，連話都沒辦法好好講。(我這就不透露花多少錢了)
李醫師就不一樣，會殷殷切切關心你，可以聽你說話半小時再為你調整用藥的配方。他說他小小的診所裡，看盡人生百態，管你是達官顯貴販夫走卒，遇到耳鳴眩暈一樣是志氣消沉抑鬱寡歡，而他就聽這些病人說著這些人生故事久病纏身，說著. 聽著，這些病人就都帶著滿滿的充實感離開，也會懷抱著希望回到這個診所
而有時候我覺得，人生活著不就只是為了一個希望嗎
所以記得一開始除了想要紀錄病情與當下心境，其實也想要幫助一些還在病情初期需要詳細資訊的人，沒想到就這樣也還真的認識了幾個病友，也加入了一個FB社團想做一些貢獻，算是意外的收穫。
關於近況呢，老實說很不錯，應該說算是這兩年最好的一段時間。在半導體業，身體不好還真的很難撐下去。
2016年做完腰椎錐間盤手術到現在，忍過初期的那段恢復期，慢慢習慣後，脊椎好一陣子沒有劇痛了，也不再有睡到痛醒的情形。
而眩暈的部份，2017年開始SSP後，眩暈慢慢收斂到可以勉強恢復可自行開車上下班的狀況，雖然偶發性的會有眩暈發作，頻率與強度都在可接受的範圍，而我也按照Stephen Spring的建議，積極的處理舊牙套內牙根尖發炎的情形，花了不少錢打開牙套重作顯微根管也重作新的牙套，慢慢撥時間處理到現在，也只剩一顆臼齒還沒做。雖然沒有證據說眩暈跟牙根慢性發言有關聯，但我總覺得積極去處理身體慢性發炎對身體健康總是好的。
說到慢性發炎，看了一些書，有一段時間也嘗試理解"腸漏症"與"腸腦軸線"的概念，做了慢性過敏的檢查(IgG)，發現自己對某些食物有慢性過敏，所以就慢慢避開這些食物，開始吃一些對腸道有幫助的益生菌。同樣，沒有證據顯示眩暈跟腸漏有關，但正視這些飲食習慣的問題，調整腸道菌種 也總是不錯的。
而這些事情也不是說做就做 做了就會看到效果，而是有恆心有耐性有紀律的慢慢做，身體狀況是不會騙人的，有什麼慢慢的改變 這些感受自己最清楚。
那為什麼說最近的狀況是近期最好的呢，其實一直到2019年，眩暈還是維持某個頻率每幾天就來一次，但強度勉強算是吃止暈藥可以維持工作開會等等。但2019年底，因緣際會李丞永醫師又聯絡上我，把懶惰的我叫去台中安律診所一趟，他說他離開慈濟以後一直有記得我的事情 (真是感動，因為我也才去慈濟門診兩次)，所以我就又厚著臉皮去找李醫師幫忙，不意外的當天在診所點滴治療就睡了個好覺，更神奇的是，說也奇怪吃了這次李醫師的藥以後，我平常不離身的止暈藥就很少有機會拿出來吃了。現在也是維持吃李醫師的藥，持續觀察中
那如果有人問我推不推SSP，我一樣是不推，因為真的是太貴了，即使當時也許是歸功於SSP把我從休兵狀態推回工作崗位，但我真的無法推薦任何人去跟這位老兄接觸，他貴就算了人又怪，連話都沒辦法好好講。(我這就不透露花多少錢了)
李醫師就不一樣，會殷殷切切關心你，可以聽你說話半小時再為你調整用藥的配方。他說他小小的診所裡，看盡人生百態，管你是達官顯貴販夫走卒，遇到耳鳴眩暈一樣是志氣消沉抑鬱寡歡，而他就聽這些病人說著這些人生故事久病纏身，說著. 聽著，這些病人就都帶著滿滿的充實感離開，也會懷抱著希望回到這個診所
而有時候我覺得，人生活著不就只是為了一個希望嗎
2017年9月9日
關於Stephen Spring Protocol
Some interesting material from Stephen Spring
Backup from here
http://archive.is/m4yUq
==========================================
Thanks to Angelea for bringing this to my attention.
Many of you have probably read this, but I wanted to post it for newbies or people with questions about Spring's treatment. It's from a long thread on the MDUK (Meniere's Disease United Kingdom) forum about a year ago. There's a lot of dissension from certain forum members, as there is on our forum--people calling him a charlatan, etc. But keep an open mind and forget that.
I extracted Stephen's comments, which are pretty detailed, and put them into a bulleted list below.
If you want to read the whole thread, I included the link:
Stephen Spring, Meniere’s researcher, Sydney Australia
Comments from thread on the Meniere’s Disease United Kingdom web forum
The entire thread can be accessed at http://www.mduk.org/index.php?topic=4341.0
• I was once the VP of the Meniere’s Research Fund at Sydney Uni and former sufferer.
I spent 7 years researching the medical literature. In essence, I connected the dots of thousands of research studies to conclude what I have written to you above. MD is an infection with particular characteristics including immune dysfunction. This causes cytokine controlled inflammation cascades that will render the endolymphatic sac inoperable and thus causes the hydrops causing MD symptoms. This mechanism has been, in part, proven recently at Sydney Uni.
My protocol simply addresses the immune dysfunction and the infection and restores normal function. If you are in Sydney, you can get tested at the Sydney Cochlea Implant Centre.
• Md is an infection of the malt, the mucosa associated lymphatic system. The malt is a bit like an immune system within an overall, serum or blood immune system. Malt covers the throat, sinuses, gut, nose, tonsils, vagina etc with a continual mucus blanket, reacting to and washing away, sweeping away, sneezing away, snotting away etc nasty viruses and bugs. One aspect of a very complex chain is that the malt presents fragments of bugs to the serum immune that does a whole bunch of stuff to use that information so specialised immune cells called T cells learn about that particular bug out of millions we live with. This is the basis of vaccination or delayed immune response. If the bug strikes again, the immune system memory kicks in and cells for that bug rapidly multiply and outpace the infection.
The endolymphatic sac controls fluid pressure and volume of one inner ear compartment that connects the cochlea for hearing and semi circular canals for balance and the utricle for acceleration and deacceleartion. The endolymphatic sac is also the immune defence organ of the ear. It is the interface between blood immune system and the malt. To keep it very simple here, the sac stuffs up in md, it can no longer process infection, the fluid swells the compartment. This is hydrops. Unknown reasons for Hydrops is md but pagets, aied, cholesteoma, syphilis, trauma, otitis etc can all cause hydrops, transient or permanent.
Thus, you need to correct the serum immune system which corrects the malt which corrects the hydrops and remove the infection. Up to a point, the sac will repair itself and so symptoms go away. My tinnitus is not complete silence, but close to it for example.
This is all confirmed with tests as everyone has a slightly differing immune profile. A vaccine and antinfectives are used. Chronic infections take a long time to resolve, at least 36-48 weeks.
• The idea of pathogens exploiting weakness in one part of the human immune system is hardly new, AIDS victims don’t die of AIDS. They die because they cannot fight multiple infections. Cystic fibrosis gene defect won’t kill you if you don’t get infections. MD is mainly an acquired immune defect.
• MD is idiopathic hydrops. This is really when, the treating doctor does not know or cannot work out what it is that caused the Hydrops. It does not mean that no one knows or never will. That’s the start point.
Hydrops is a dynamic concept. The endolymphatic sac is a dynamic organ. The entire inner ear is a stable organ with parameters governing fluid control such as volume but it is also dynamic enough so that when under stress conditions, the endolymphatic sac can work and the hearing and balance still functions. Hydrops can be measured and when the hydrops is present and there are symptoms, there are different signals to when there it is not.
Many things can “cause” hydrops, it can be transient or it can eventually become so severe that the inner ear will no longer function. Hydrops for some people is a minor nuisance, for others it’s a permanent and chronic misery.
If the doctor does not go through the known things that can cause hydrops, or does not test for hydrops, or is lazy or other reasons, the patient is left wondering. In other words there are many variables that can contribute to a diagnoses of MD (“You have hydrops I think, but I don’t know what causes it or how to treat it madam and because its idiopathic in my eyes, you have Meniere’s Disease.") This includes the doctor’s attitude, experience and many other factors. It also implies a correct diagnose because the person might have what is termed autoimmune inner ear disease, cholesteoma, sac tumor and others which can cause hydrops too and are treated differently depending on the doctor’s point of view.
Some hydrops is so mild and transient that the patient thinks they can control it with diet. Some doctors and even support groups say salt retains fluid in the inner ear but in reality there is very little evidence for this, but if that gives the person some degree of control (even though it is unlikely to long term, there is nothing wrong thinking it will) it does no harm and gets the patient out the office.
Some people take larger and larger amounts of antihistamines to help themselves and some people simply walk up the treatment ladder to get worse and worse and have surgery.
My work has investigated the immunological basis for hydrops that can arise after a number of common events that lead to it. This is simply another way of looking at hydrops initiation and is something that many doctors do not know how to do. I provide the tools so that doctors and patient can work on the problem together. As is understandable, some doctors will not help and one or two can be hostile, others will help and others are keen to learn more and for some doctors it is waaay above them because its not the specialty. As is also understandable, some people with MD react the same way.
My protocol will not, for instance remove hydrops that is being "fed" with an undetected neuroma. It will not reverse destructive surgery. It will not resurrect hearing when a congenital (unformed sac or valve of Bast for example) or genetic problem (IPEX syndrome or immunoglobulin or complement fixation defect) but it does explain in many cases why someone can be normal one week and chronically ill the next. It is simply another reason to define more finely the nature of hydrops so that its not idiopathic and can be treated correctly and the person not left wondering. MD is idiopathic hydrops. This is really when, the treating doctor does not know or cannot work out what it is that caused the Hydrops. It does not mean that no one knows or never will. That’s the start point.
• As explained above, many foreign-to-the-body proteins (mycoplasama, bacteria, viruses, L-Form cysts etc called antigens) can create hydrops. Hydrops creates the symptoms doctors called MD.
As explained above, the infection is in the MALT. The MALT is a connected to, but distinct part of the immune system. It relies on its antigenic information from the blood and lymphatic system.
Hydrops is a problem of the endolymphatic sac. That organ is defender of the inner ear. When antigens get into the inner ear, it reacts to communicate with the MALT and lymph (that’s why its endoLYMPHATIC) so release antibodies and summons T cells etc and produce inflammation so that the infection can be cleared (see above). It does this with cell to cell communication of messenger proteins and some are called cytokines.
Hydrops is caused by antigens, but which ones? There are thousands of types and thousands of antiifectives. Identification has proved impossible in the living. The difficulty is that the inner ear is TOTALLY INACCESSIBLE AND VERY, VERY SENSITIVE.
Let’s say a female goes to the MALT doctor and says I have a dull ache in my pelvis and my vagina itches and is discharging. The doctor can order imagery of the sore region to detect inflammation, can swab the vaginal wall to send the swab off to culture (to incubate any infection in a broth at a lab and thus identify the infection if there is one) and isolate the part of the MALT that is the problem. The doctor could, after narrowing down the region, use a speculum and knife on a probe to cut a tiny piece of tissue, say at the entrance of the fallopian tube. Then too send if off to be cultured. Out of the hundreds of antibiotics on the market, one can be chosen if it is say, for example, a bacterial infection. No point taking a blood sample because the infection is not in the blood clinically and may be in levels undetectable.
Contrast that to inner ear inflammation/hydrops. If the doctor opens the inner ear in any way, it loses its fluid and goes deaf. No doctor will do that. So they look at the eardrum. If they see no signs of infection, they say you don’t have one. They will not take a swab of anything as you cannot get close to it easily, even via the Eustachian tube, nor do they see any reason to. No point in taking a blood sample, there is no blood borne infection. “Sorry, its idiopathic.”
However, MD (because the endolyphatic sac is the INTERFACE ORGAN FROM THE MALT TO THE BLOOD/LYMPH) leaves a particular basic immunological footprint in blood draw (also in mucus, but that's another story altogether). The blood tests identify that footprint. From the same way an archeologist can tell from a footprint roughly, and sometimes very accurately what species gave rise to it, the same can be said with some types of antigens that can manifest in a cytokine profile from blood tests. In combination with a viral panel and full blood count, it is possible to identify certain infectious elements that can be addressed.
As noted above, none of that means that finding viral particles in inner ears of dead MD'rs prove MD is caused by a virus and antivirals will fix it. As everyone who tries antivirals eventually finds out.
Backup from here
http://archive.is/m4yUq
==========================================
Thanks to Angelea for bringing this to my attention.
Many of you have probably read this, but I wanted to post it for newbies or people with questions about Spring's treatment. It's from a long thread on the MDUK (Meniere's Disease United Kingdom) forum about a year ago. There's a lot of dissension from certain forum members, as there is on our forum--people calling him a charlatan, etc. But keep an open mind and forget that.
I extracted Stephen's comments, which are pretty detailed, and put them into a bulleted list below.
If you want to read the whole thread, I included the link:
Stephen Spring, Meniere’s researcher, Sydney Australia
Comments from thread on the Meniere’s Disease United Kingdom web forum
The entire thread can be accessed at http://www.mduk.org/index.php?topic=4341.0
• I was once the VP of the Meniere’s Research Fund at Sydney Uni and former sufferer.
I spent 7 years researching the medical literature. In essence, I connected the dots of thousands of research studies to conclude what I have written to you above. MD is an infection with particular characteristics including immune dysfunction. This causes cytokine controlled inflammation cascades that will render the endolymphatic sac inoperable and thus causes the hydrops causing MD symptoms. This mechanism has been, in part, proven recently at Sydney Uni.
My protocol simply addresses the immune dysfunction and the infection and restores normal function. If you are in Sydney, you can get tested at the Sydney Cochlea Implant Centre.
• Md is an infection of the malt, the mucosa associated lymphatic system. The malt is a bit like an immune system within an overall, serum or blood immune system. Malt covers the throat, sinuses, gut, nose, tonsils, vagina etc with a continual mucus blanket, reacting to and washing away, sweeping away, sneezing away, snotting away etc nasty viruses and bugs. One aspect of a very complex chain is that the malt presents fragments of bugs to the serum immune that does a whole bunch of stuff to use that information so specialised immune cells called T cells learn about that particular bug out of millions we live with. This is the basis of vaccination or delayed immune response. If the bug strikes again, the immune system memory kicks in and cells for that bug rapidly multiply and outpace the infection.
The endolymphatic sac controls fluid pressure and volume of one inner ear compartment that connects the cochlea for hearing and semi circular canals for balance and the utricle for acceleration and deacceleartion. The endolymphatic sac is also the immune defence organ of the ear. It is the interface between blood immune system and the malt. To keep it very simple here, the sac stuffs up in md, it can no longer process infection, the fluid swells the compartment. This is hydrops. Unknown reasons for Hydrops is md but pagets, aied, cholesteoma, syphilis, trauma, otitis etc can all cause hydrops, transient or permanent.
Thus, you need to correct the serum immune system which corrects the malt which corrects the hydrops and remove the infection. Up to a point, the sac will repair itself and so symptoms go away. My tinnitus is not complete silence, but close to it for example.
This is all confirmed with tests as everyone has a slightly differing immune profile. A vaccine and antinfectives are used. Chronic infections take a long time to resolve, at least 36-48 weeks.
• The idea of pathogens exploiting weakness in one part of the human immune system is hardly new, AIDS victims don’t die of AIDS. They die because they cannot fight multiple infections. Cystic fibrosis gene defect won’t kill you if you don’t get infections. MD is mainly an acquired immune defect.
• MD is idiopathic hydrops. This is really when, the treating doctor does not know or cannot work out what it is that caused the Hydrops. It does not mean that no one knows or never will. That’s the start point.
Hydrops is a dynamic concept. The endolymphatic sac is a dynamic organ. The entire inner ear is a stable organ with parameters governing fluid control such as volume but it is also dynamic enough so that when under stress conditions, the endolymphatic sac can work and the hearing and balance still functions. Hydrops can be measured and when the hydrops is present and there are symptoms, there are different signals to when there it is not.
Many things can “cause” hydrops, it can be transient or it can eventually become so severe that the inner ear will no longer function. Hydrops for some people is a minor nuisance, for others it’s a permanent and chronic misery.
If the doctor does not go through the known things that can cause hydrops, or does not test for hydrops, or is lazy or other reasons, the patient is left wondering. In other words there are many variables that can contribute to a diagnoses of MD (“You have hydrops I think, but I don’t know what causes it or how to treat it madam and because its idiopathic in my eyes, you have Meniere’s Disease.") This includes the doctor’s attitude, experience and many other factors. It also implies a correct diagnose because the person might have what is termed autoimmune inner ear disease, cholesteoma, sac tumor and others which can cause hydrops too and are treated differently depending on the doctor’s point of view.
Some hydrops is so mild and transient that the patient thinks they can control it with diet. Some doctors and even support groups say salt retains fluid in the inner ear but in reality there is very little evidence for this, but if that gives the person some degree of control (even though it is unlikely to long term, there is nothing wrong thinking it will) it does no harm and gets the patient out the office.
Some people take larger and larger amounts of antihistamines to help themselves and some people simply walk up the treatment ladder to get worse and worse and have surgery.
My work has investigated the immunological basis for hydrops that can arise after a number of common events that lead to it. This is simply another way of looking at hydrops initiation and is something that many doctors do not know how to do. I provide the tools so that doctors and patient can work on the problem together. As is understandable, some doctors will not help and one or two can be hostile, others will help and others are keen to learn more and for some doctors it is waaay above them because its not the specialty. As is also understandable, some people with MD react the same way.
My protocol will not, for instance remove hydrops that is being "fed" with an undetected neuroma. It will not reverse destructive surgery. It will not resurrect hearing when a congenital (unformed sac or valve of Bast for example) or genetic problem (IPEX syndrome or immunoglobulin or complement fixation defect) but it does explain in many cases why someone can be normal one week and chronically ill the next. It is simply another reason to define more finely the nature of hydrops so that its not idiopathic and can be treated correctly and the person not left wondering. MD is idiopathic hydrops. This is really when, the treating doctor does not know or cannot work out what it is that caused the Hydrops. It does not mean that no one knows or never will. That’s the start point.
• As explained above, many foreign-to-the-body proteins (mycoplasama, bacteria, viruses, L-Form cysts etc called antigens) can create hydrops. Hydrops creates the symptoms doctors called MD.
As explained above, the infection is in the MALT. The MALT is a connected to, but distinct part of the immune system. It relies on its antigenic information from the blood and lymphatic system.
Hydrops is a problem of the endolymphatic sac. That organ is defender of the inner ear. When antigens get into the inner ear, it reacts to communicate with the MALT and lymph (that’s why its endoLYMPHATIC) so release antibodies and summons T cells etc and produce inflammation so that the infection can be cleared (see above). It does this with cell to cell communication of messenger proteins and some are called cytokines.
Hydrops is caused by antigens, but which ones? There are thousands of types and thousands of antiifectives. Identification has proved impossible in the living. The difficulty is that the inner ear is TOTALLY INACCESSIBLE AND VERY, VERY SENSITIVE.
Let’s say a female goes to the MALT doctor and says I have a dull ache in my pelvis and my vagina itches and is discharging. The doctor can order imagery of the sore region to detect inflammation, can swab the vaginal wall to send the swab off to culture (to incubate any infection in a broth at a lab and thus identify the infection if there is one) and isolate the part of the MALT that is the problem. The doctor could, after narrowing down the region, use a speculum and knife on a probe to cut a tiny piece of tissue, say at the entrance of the fallopian tube. Then too send if off to be cultured. Out of the hundreds of antibiotics on the market, one can be chosen if it is say, for example, a bacterial infection. No point taking a blood sample because the infection is not in the blood clinically and may be in levels undetectable.
Contrast that to inner ear inflammation/hydrops. If the doctor opens the inner ear in any way, it loses its fluid and goes deaf. No doctor will do that. So they look at the eardrum. If they see no signs of infection, they say you don’t have one. They will not take a swab of anything as you cannot get close to it easily, even via the Eustachian tube, nor do they see any reason to. No point in taking a blood sample, there is no blood borne infection. “Sorry, its idiopathic.”
However, MD (because the endolyphatic sac is the INTERFACE ORGAN FROM THE MALT TO THE BLOOD/LYMPH) leaves a particular basic immunological footprint in blood draw (also in mucus, but that's another story altogether). The blood tests identify that footprint. From the same way an archeologist can tell from a footprint roughly, and sometimes very accurately what species gave rise to it, the same can be said with some types of antigens that can manifest in a cytokine profile from blood tests. In combination with a viral panel and full blood count, it is possible to identify certain infectious elements that can be addressed.
As noted above, none of that means that finding viral particles in inner ears of dead MD'rs prove MD is caused by a virus and antivirals will fix it. As everyone who tries antivirals eventually finds out.
2017年7月26日
關於國小數學
大叔碎碎念 關於國小數學
最近不知道為什麼常常想到一個老話題，事情是這樣的，一個媽媽在某社團分享了一張圖片是關於他小學的孩子在學校考卷上答了一個問題，明明答的方式正確，但被老師打叉。這個問題印象中是這樣：
"小明跟發哥的雜貨店買了5顆光碟機IC，一顆IC價錢是2塊錢，請問小明花了多少錢？"
結果小孩的答案是 5 X 2 = 10 元 (然後上面被畫了一個大紅叉)
然後老師的答案是 2 X 5 = 10 元
OK，我想你應該猜的到底下的留言應該是幹聲連連，說什麼老師莫名其妙什麼的，然後就有老師出來解釋說：這是在建立孩子解讀題目以及乘數/被乘數的觀念，要告訴孩子 "單位量×單位數＝總量"
所以
2 X 5 =10元 代表你用2塊之單價買了5顆IC
但我想，難道我們的數學教育不能引導孩子解釋成 "買了5顆2塊錢的IC"嗎？我的意思是說，為什麼一定要遵守"單位量×單位數＝總量"這個沒有科學概念的說明式，如果硬要照這樣教，那麼比較妥善的說明式是
5[顆] X 2 [元/每顆] = 10 元
2 [元/每顆] X 5[顆] = 10 元
兩者都對
也就是要求直接把單位寫上來，這樣一來純量交換率不會被破壞，也同時讓孩子知道單位的重要性，更重要的是當孩子學到除法與分式的時候他會知道[顆]是可以跟著算式一起被相消的，學校該教的是這樣的真理，不會因為時間的過去才發現今是昨非，更不需要在那邊咬文嚼字然後沒事找事做
純量的乘法有交換性，我相信每個數學老師都有大學數學系或是相關學歷，難道這些老師在說服自己接受"單位量×單位數＝總量"這個說明式的時候，心裡沒有痛苦的矛盾感嗎？難道這種教育方式不是間接的告訴孩子：即使是真理 也可以今是昨非，而且現在又不是在教孩子向量或是張量，有必要讓孩子的數學表達跟生活經驗充滿了矛盾嗎？當你用這種尺度去作為數學教育的度量衡，那麼你期待教出來的孩子要怎麼用正確的數學態度去解釋所有的生活行為？
OK這只是一個問題，其他不少留言才更讓我傻眼了，有家長說:"數學這麼計較幹嘛啦，我以前數學很爛，現在還不是月入X萬，而且離開學校以後根本就用不到數學，數學又不能拿來賺錢，現在手機這麼發達拿出來按一下就知道答案了啦，學什麼數學"。這種"數學無用論"留言讓我覺得很心裡很憂鬱
我憂鬱的並不是 "對啊數學真的沒有用 我還花這麼多時間學 ，根本浪費時間"，而是憂鬱: 在台灣，基礎學問的重要性被忽視與踐踏的程度，事實上這些忽視與踐踏的人都是曾經在學校學過這些學科然後靠著這些分數畢業拿到文憑的人，為什麼這些人會這麼輕視數學？
首先 台灣的教育並沒有好好的區分 "算術 與 數學"，讓很多人在畢業若干年後只記得"算術"，而根本忘記數學，很多人會說"學算術就夠用了啊，學什麼一元二次方程式, 二元一次方程式啊？會這些真的用不到又不能賺錢啊"
其實生活在現代，數學真真實實的存在你生活裡的每一處
你每天乘坐的各種交通工具如果沒有數學，你每天出門根本都是在自殺；你每天用的GPS如果沒有數學，不會看地圖的你根本永遠到不了目的地；隨便把一根USB裝置插上電腦這過程有數學；你家會有電也是數學；引擎內燃機有數學；潮潮最愛的唉鳳溝溝肉裏面是滿到多出來的數學。
不要再告訴你的孩子學數學不能賺錢了，會這樣想的人你一定永遠都想不到用數學賺錢的人到底從你身上賺了多少錢
#小弟數學沒有很好不要噹我啦
最近不知道為什麼常常想到一個老話題，事情是這樣的，一個媽媽在某社團分享了一張圖片是關於他小學的孩子在學校考卷上答了一個問題，明明答的方式正確，但被老師打叉。這個問題印象中是這樣：
"小明跟發哥的雜貨店買了5顆光碟機IC，一顆IC價錢是2塊錢，請問小明花了多少錢？"
結果小孩的答案是 5 X 2 = 10 元 (然後上面被畫了一個大紅叉)
然後老師的答案是 2 X 5 = 10 元
OK，我想你應該猜的到底下的留言應該是幹聲連連，說什麼老師莫名其妙什麼的，然後就有老師出來解釋說：這是在建立孩子解讀題目以及乘數/被乘數的觀念，要告訴孩子 "單位量×單位數＝總量"
所以
2 X 5 =10元 代表你用2塊之單價買了5顆IC
但我想，難道我們的數學教育不能引導孩子解釋成 "買了5顆2塊錢的IC"嗎？我的意思是說，為什麼一定要遵守"單位量×單位數＝總量"這個沒有科學概念的說明式，如果硬要照這樣教，那麼比較妥善的說明式是
5[顆] X 2 [元/每顆] = 10 元
2 [元/每顆] X 5[顆] = 10 元
兩者都對
也就是要求直接把單位寫上來，這樣一來純量交換率不會被破壞，也同時讓孩子知道單位的重要性，更重要的是當孩子學到除法與分式的時候他會知道[顆]是可以跟著算式一起被相消的，學校該教的是這樣的真理，不會因為時間的過去才發現今是昨非，更不需要在那邊咬文嚼字然後沒事找事做
純量的乘法有交換性，我相信每個數學老師都有大學數學系或是相關學歷，難道這些老師在說服自己接受"單位量×單位數＝總量"這個說明式的時候，心裡沒有痛苦的矛盾感嗎？難道這種教育方式不是間接的告訴孩子：即使是真理 也可以今是昨非，而且現在又不是在教孩子向量或是張量，有必要讓孩子的數學表達跟生活經驗充滿了矛盾嗎？當你用這種尺度去作為數學教育的度量衡，那麼你期待教出來的孩子要怎麼用正確的數學態度去解釋所有的生活行為？
OK這只是一個問題，其他不少留言才更讓我傻眼了，有家長說:"數學這麼計較幹嘛啦，我以前數學很爛，現在還不是月入X萬，而且離開學校以後根本就用不到數學，數學又不能拿來賺錢，現在手機這麼發達拿出來按一下就知道答案了啦，學什麼數學"。這種"數學無用論"留言讓我覺得很心裡很憂鬱
我憂鬱的並不是 "對啊數學真的沒有用 我還花這麼多時間學 ，根本浪費時間"，而是憂鬱: 在台灣，基礎學問的重要性被忽視與踐踏的程度，事實上這些忽視與踐踏的人都是曾經在學校學過這些學科然後靠著這些分數畢業拿到文憑的人，為什麼這些人會這麼輕視數學？
首先 台灣的教育並沒有好好的區分 "算術 與 數學"，讓很多人在畢業若干年後只記得"算術"，而根本忘記數學，很多人會說"學算術就夠用了啊，學什麼一元二次方程式, 二元一次方程式啊？會這些真的用不到又不能賺錢啊"
其實生活在現代，數學真真實實的存在你生活裡的每一處
你每天乘坐的各種交通工具如果沒有數學，你每天出門根本都是在自殺；你每天用的GPS如果沒有數學，不會看地圖的你根本永遠到不了目的地；隨便把一根USB裝置插上電腦這過程有數學；你家會有電也是數學；引擎內燃機有數學；潮潮最愛的唉鳳溝溝肉裏面是滿到多出來的數學。
不要再告訴你的孩子學數學不能賺錢了，會這樣想的人你一定永遠都想不到用數學賺錢的人到底從你身上賺了多少錢
#小弟數學沒有很好不要噹我啦
2017年7月2日
Stephen Spring Protocol 進度報告 (持續更新中)
Stephen Spring Protocol 進度報告 2017/07/02 - update to 2017/07/26
之前我的梅尼爾氏症(MD)病況已經在下列這篇文章的前言中有敘述到https://allenmeniere.blogspot.tw/2017/01/43441810-reviewent-currently-there-is.html
簡單來說我的MD發作程度已經讓我沒辦法工作賺錢，現在已經留停在家休養，家裡經濟也呈現斷炊的狀態，為了拯救全家的命運，後來努力在網路上找尋國外資訊，輾轉得知關於Stephen Spring這個人的資訊(也看到了一些關於他的爭議)，他有一個網站，有興趣可以點進去看看。總之，在死馬當活馬醫的狀況下，後來我決定跟他合作看看。
因為必須要跟Stephen Spring簽一張NDA才能正式進行SSP treatment，所以我不能在部落格上寫出SSP進行的細節，這篇文主要只是紀錄我在開始與進行SSP過程中的一些大事紀時間點與病情變化。
2017/01/01, 決定開始用email跟Stephen諮詢他對MD研究的看法,主要是我提問關於與他合作的模式, 付費方式, 需要做什麼樣的檢查才能確認我是他的target, 以及SSP treatment的副作用, 這個過程差不多花了兩個禮拜，在這之前眩暈的發作頻率大約是一周2~3次
2017/01/13, 我根據在網路上蒐集到的資訊判斷思考後，決定告知SS我要嘗試SSP並且開始進行一連串的檢查(想當然爾健保不給付, 前前後後跑醫院和醫檢所大約花了一萬五)
2017/02/14, SS認為我的狀況屬於他的防守範圍，答應會寄MeniVac給我，這期間我已經開始使用抗HSV病毒藥物Valtrex進一個半月了(依照國外研究建議的劑量)，但沒什麼進展，眩暈發作頻率仍然是一週兩到三次
2017/04/10, 收到第1批MeniVac, 這段期間仍然持續吃Valtrex，但眩暈一樣一週兩到三次
2017/04/12, 開始第1次服用MeniVac
2017/05/08, 服用大約1個月(用量約2罐)，眩暈一樣一週兩到三次，有時候似乎變嚴重了，嚴重到每天1次，因為手上只剩下1罐，所以下訂單請SS再寄一批給我
2017/05/24, 第1批買的3罐已經用完了，但遲遲不見新的一批寄來, 此時眩暈大約減緩到一周一次 (似乎是有好轉的預兆？)，發作的強度似乎有降低，天旋地轉的程度似乎沒有之前嚴重了, 此時因為反正MeniVac沒得吃，所以我把之前買了沒用的左旋離胺酸+B12來搭配Valtrex一起用
2017/05/30, 端午節連假回高雄，回程在高鐵上發作，一路吐回家，此時眩暈大約一周一次
2017/06/10, 眩暈發作，與上次眩暈發作大約10天了，似乎眩暈發作間隔又拉長了，且眩暈強度又再降低，服用Diazepam與Meclizine後不至於到吐的程度，但這次發作完，左耳的低頻一直處於聽不到的狀態，低頻耳鳴也持續嗡嗡作響
2017/06/13, 終於第2批MeniVac寄來了，左旋離胺酸+B12仍然沒有中斷，持續搭著服用
2017/07/02, 一直到做紀錄的今天，這接近三周的時間都沒有眩暈發作，且低頻聽力與低頻耳鳴用一種非常緩慢的速度在緩解，漸漸的低頻耳鳴不見了，低頻聽力也慢慢聽的到了，剩下高頻的eeeee耳鳴，但還在可以接受的範圍，這應該是從去年發病以來，維持不發作的時間最長的一次，希望可以保持下去
=====================2017/07/26 update
2017/07/07 話真的不能說太早，07/02開始發燒，07/07我就也被傳染到也開始發燒，燒了四天以後看醫生說是流感，直接投克流感，這四天過程中又開始覺得耳悶 低頻聽不到了，
2017/07/15 眩暈又發作，之後又開始維持三四天一次的頻率到 07/26 ，不過暈的程度沒有之前嚴重，有時候三四個小時就過了，也不至於天旋地轉
2017/07/19 開始去大林慈濟看李醫師，當天就打了有名的慢點滴 (類固醇 + Diazepam + 心率調節藥物當作自律神經調節用) 口服藥物則是領了flunarizine + 舒安得(輕微的BZD藥物) ，感覺這個口服藥的組合跟楊怡和醫師開的 flunarizine + fludiazepam(中度的BZD藥物) 作用差不多，希望可以跟李醫師溝通不要打類固醇，因為類固醇有免疫抑制的作用，擔心會跟SSP起衝突。
2017年7月1日
Immulox與梅尼爾氏症的關聯
Immulox與梅尼爾氏症的關聯
從網路上可以找到梅尼爾的免疫治療 與 Immulox之間的有趣關聯
相關連結
http://baike.baidu.com/item/%E5%AF%8C%E8%84%AF%E6%B0%A8%E9%85%B8%E5%A4%9A%E8%82%BD
http://www.bio2u.us.com/%E7%B4%A0%E6%9D%90%E4%BB%8B%E7%B4%B9/item/aps-biogroup-immulox-%E7%9B%8A%E6%95%8F%E8%82%BD.html
http://www.choicesunlimited.ca/when-t1-t2-are-out-of-balance/
https://www.kingnet.com.tw/knNew/news/single-article.html?newId=7990
還是有點懶，細節之後有空再補上好了 @@
*首先兩者都是從牛乳製品中製造而來 (Immulox是從初乳的過慮製程而來)
*再者Immulox中的PRPs (富脯氨酸多肽)也同樣具備有特定的Th1/Th2平衡效果,
" In particular PRP are thought to modulate thymus function, specifically the T helper 1 / T helper 2 (Th1 / Th2) balance. "
from
http://calostart.com/app/docs/ALZHEIMER/CALOSTART-ALZHEIMER/CaloStart%20-%20THE%20EFFECT%20OF%20A%20COLOSTRUM%20EXTRACT%20OF%20PROLINE%20RICH%20POLYPEPTIDES.pdf
這跟某個梅尼爾氏症的免疫治療其假設為需要改變 T1/T2 balance的精神很類似
過敏與梅尼爾的關係?
Is Allergy Related to Meniere’s Disease?
原文： https://www.researchgate.net/publication/223136937_Is_Allergy_Related_to_Meniere's_Disease- 過敏與梅尼爾氏病的關係之前有跟大家分享國外許多研究對梅尼爾氏病的不同面向，有自體免疫, 過敏, 病毒, 壓力, 等等, 這篇論文則是review過敏這個因素，其中提到幾個重點跟大家分享
- In a large study, Derebery and Berliner investigated the prevalence of allergy in MD. In a survey of 734 patients with MD, concurrent allergic disease was found in 41 %.
*在一個大型的研究中，從734個MD病人當中survey，發現過敏在MD病人中的盛行率約為41%
*有過敏性鼻炎的人，可能會有氣喘,鼻瘜肉,中耳炎,或慢性鼻竇炎。而有氣喘與過敏性鼻炎的人則會有較高的食物過敏盛行率。在2000年的一份研究中指出在MD病人中，小麥是最常見的食物過敏原68%。麥膠蛋白被認為是造成小麥過敏的人們對"IgE誘導產生的過敏"(第1型過敏)最主要的原因
*Derebery等人認為有三種過敏機制可能造成梅尼爾症狀，第1種是IgE誘導的過敏反應在內淋巴囊造成局部發炎, 第2種是免疫複合物在內耳淋巴囊附近的微血管堆積造成局部發炎，有研究顯示MD病人的循環免疫複合物的檢驗結果比控制組高了21~96%, 第3種是病毒侵入造成內淋巴囊的輕微發炎反應
*Derebery等人建議病人使用過敏免疫治療(allergen immunotherapy)並且/或是移除過敏源，在113個接受治療的病人中，所有人都回報症狀有所改善
摘錄一些重點如下
- Likewise, in allergy-susceptible patients, an allergic response can evoke responses in distal sites.
- This likely occurs via an integration of neurological, immunologic, and allergic responses involved in inflammation.
- People with ARmay have asthma, nasal polyposis, otitis media, or chronicrhinosinusitis [36]. People with asthma and AR have a higherprevalence of food allergies, the estimated prevalence ofwhich in America is 3.5 % to 6 %
- Derebery and Berliner [18] in 2000 reported wheat as the most common food allergen found in patients with MD(68.2 %).
2000年的一份研究中指出在MD病人中，小麥是最常見的過敏原68%
- Gliadin is considered the major cause of IgE-mediated hypersensitivity in people with wheat allergy.
- Allergic reactions are considered to be one of the many causes of migraines. Numerous studies have reported an association between migraines and allergies. They found that the incidences of both allergy and migraine were significantly higher in the Meniere’s group and that the incidence of allergy in the MD migraine group was significantly higher than that in the group with MD alone.
- Derebery and Berliner [21] outlined three proposed mechanisms by which allergy can produce MD symptoms.
- The first mechanism, the endolymphatic sac, could be atarget organ of the allergic reaction. The antigen enters the endolymphatic sac andcauses an IgE-mediated degranulation of mast cells. Thisproduces a local inflammatory response that impairs theendolymphatic sac’s filtering function, and a buildup oftoxic metabolic products results, interfering with hair cell function. Histamine and other vasoactive mediators releasedin an allergic response elsewhere may also exert an effecton the well-vascularized fenestrated blood vessels of the endolymphatic sac, thereby affecting reabsorption.
- The second mechanism proposed is deposition of circu-lating immune complexes (CICs). These CICs are depositedand accumulate in the fenestrated blood vessels of the en-dolymphatic sac and stria vascularis. This results in inflam-mation and an increased permeability of the leaky capillariesthat surround the endolymphatic sac. The inflammationinterferes with the capability of the endolymphatic sac’shomeostasis function. Several studies demonstrated an in-crease in circulating immune complexes: 21 % to 96 % ofpatients with MD compared with controls
- The third mechanism is the viral antigen–allergic inter-action. This mechanism suggests that a viral insult canantigenically stimulate Waldeyer’s ring, with T-cell homingto the endolymphatic sac, causing a low-grade inflammatoryresponse. This impairs absorption of the endolymphatic sacbut does not produce symptoms. Then, later in life, anunknown trigger in the system stimulates excessive fluidproduction. Then, later in life, anunknown trigger in the system stimulates excessive fluidproduction. Derebery and Berliner [21] referenced howviruses are capable of exacerbating allergic symptoms by avariety of means, including causing histamine release,thought to be mediated by interferon. They can also damageepithelial surfaces, enhancing antigen entry and increasingresponsiveness of target organs to histamine. Derebery[22••]noted heat shock protein 70 (HSP70), an antibodyfrequently seen increased in both MD and autoimmuneinner ear disease, is often upregulated in viral infections. They concluded that patients with clinically “certain” MD do not have a significantly raised incidence of HSP70 antibodies.
- Derebery [19] (2000): 113 patients accepted treatment;all 113 reported improvementof symptoms after treatmentof allergy
- In Derebery’s clinicalexperience, patients who have both MD and allergybenefit from immunotherapy and/or dietary avoidanceof reactive food allergens. The symptoms of MD aregenerally better controlled, with fewer vertigo attacksand more stable hearing
- The association of allergy andMD is well-documented. At the present time, it is generallyaccepted that the cause of MD is likely to be multifactorial,consisting of an underlying genetic predisposition, com-bined with an extrinsic insult. Allergy may well be involvedin the final common inflammatory pathway in a selectsubpopulation of patients with MD
- 有點懶，之後再繼續讀這篇論文
關於第一二三型過敏反應的解釋 可參照這裡
https://smallcollation.blogspot.tw/2013/10/hypersensitivity.html#gsc.tab=0
"1.第Ⅰ型過敏反應－IgE誘導發生的過敏反應
造成第I型過敏反應的機制為：當過敏原第一次進入人體在與特定B細胞上的抗體結合後，會引起特定IgE的大量製造，分泌出的IgE與過敏原結合後，會附著在肥大細胞(Mast cell)表面的Fcε受體。當相同的過敏原再度入侵人體，過敏原和肥大細胞表面上的IgE結合，會誘發肥大細胞釋出發炎物質，如組織胺、介白素、細胞激素，造成紅腫發癢等症狀"
https://smallcollation.blogspot.tw/2013/10/hypersensitivity.html#gsc.tab=0
"1.第Ⅰ型過敏反應－IgE誘導發生的過敏反應
造成第I型過敏反應的機制為：當過敏原第一次進入人體在與特定B細胞上的抗體結合後，會引起特定IgE的大量製造，分泌出的IgE與過敏原結合後，會附著在肥大細胞(Mast cell)表面的Fcε受體。當相同的過敏原再度入侵人體，過敏原和肥大細胞表面上的IgE結合，會誘發肥大細胞釋出發炎物質，如組織胺、介白素、細胞激素，造成紅腫發癢等症狀"
"3.第Ⅲ型過敏反應－免疫複合體(immune complex)引發的過敏反應
...複合物如果沒有被清除，且在腎、血管壁、心臟瓣膜等處沉積，進而引發過度的免疫反應，如吞噬細胞企圖吞噬複合物，但複合物太大無法吞噬，於是釋放出酵素，導致發炎並造成該部位的傷害...複合物沉積的位置可以是全身性或局部性...造成的原因有可能是病患自己產生自體抗體與自體抗原形成免疫複合體而引發，如全身紅斑性狼瘡(systemic lupus erythematosus) 、類風濕關節炎的患者；或者是持續性感染，其抗原的量雖然不多，但一直存在，使得免疫複合物持續產生，並堆積在各個器官，如麻瘋病、瘧疾、B型肝炎"
...複合物如果沒有被清除，且在腎、血管壁、心臟瓣膜等處沉積，進而引發過度的免疫反應，如吞噬細胞企圖吞噬複合物，但複合物太大無法吞噬，於是釋放出酵素，導致發炎並造成該部位的傷害...複合物沉積的位置可以是全身性或局部性...造成的原因有可能是病患自己產生自體抗體與自體抗原形成免疫複合體而引發，如全身紅斑性狼瘡(systemic lupus erythematosus) 、類風濕關節炎的患者；或者是持續性感染，其抗原的量雖然不多，但一直存在，使得免疫複合物持續產生，並堆積在各個器官，如麻瘋病、瘧疾、B型肝炎"
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