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  MS-ihmisten kannattaa huolehtia D-vitamiinin saannista
1  Yleinen / MS-diagnoosi / Re: MS-taudin tunnottomuus
 Pvm: Tänään - 07:58:08 
Keskustelun aloitti kipe | Kirjoittaja VPS358  
Tervetuloa foorumille.

Valitettavasti MS on tautina niin monimuotoinen, että yksittäisistä oireista ei oikein voi päätellä juuta eikä jaata.
MS-diagnoosina on usein "löyhässä hirressä", eli vaatii jopa vuosien kehityksen ja odottelun.

"Savolainen" vastaus:
Suottaapi tuo olla, mutta ihan yhtä hyvin suottaa olla olemati.

Näihin olet tietenkin tutustunut:

T: Vesku

2  Yleinen / MS-diagnoosi / MS-taudin tunnottomuus
 Pvm: Eilen - 13:59:54 
Keskustelun aloitti kipe | Kirjoittaja kipe  
Hei. Olen 20-vuotias nainen. Minulla on tällä hetkellä menossa MS-tauti epäily ja haluaisin teiltä kysyä minkälaista on MS-taudin tunnottomuus? Onko se siis sellaista, että kosketus ei tunnu ollenkaan vai kihelmöintiä vai miten kuvailisit sitä?
Minulla siis siksi epäillään sitä, koska vasen puoleni on ”puutunut”. Kasvoista, jalasta ja sormenpäistä. Puuttuminen kuitenkaan ei ole joka päiväistä ja saattaa kestää esim muutaman tunnin vain. Onko tämä tyypillistä MS-taudille? Minulle on todettu vaikea masennus ja ahdistuneisuushäiriö.

3  Yleinen / MS-jutut / Re: Tupakkakuoriaiset
 Pvm: 06.01.2019 - 21:38:40 
Keskustelun aloitti Neilikkamies | Kirjoittaja Neilikkamies  
Feromoniansa on roikkunut nyt kolme viikkoa keittiön kattolampussa eikä mitään ole jäänyt kiinni. Oletan, että tämä oli väärä hälytys ja näkemäni pari ötökkää ovat jotain muuta kuin tupakkakuoriaisia. Kuoriaisten jäljitys ja hävitys olisi ollut viheliäisitä, koska normaalillakin näöllä munia ja toukkia on vaikea nähdä saati sitten, jos on heikko näkö.

4  Tutkimus / Tutkimus / Re: Krooniset bakteeri-infektiot
 Pvm: 06.01.2019 - 00:38:44 
Keskustelun aloitti HopeSprings | Kirjoittaja HopeSprings  
Fungi cause brain infection and impair memory in mice


January 4, 2019

Fungal infections are emerging as a major medical challenge, and a team led by researchers at Baylor College of Medicine has developed a mouse model to study the short-term consequences of fungal infection in the brain.

The researchers report in the journal Nature Communications the unexpected finding that the common yeast Candida albicans, a type of fungus, can cross the blood-brain barrier and trigger an inflammatory response that results in the formation of granuloma-type structures and temporary mild memory impairments in mice. Interestingly, the granulomas share features with plaques found in Alzheimer's disease, supporting future studies on the long-term neurological consequences of sustained C. albicans infection.

"An increasing number of clinical observations by us and other groups indicates that fungi are becoming a more common cause of upper airway allergic diseases such as asthma, as well as other conditions such as sepsis, a potentially life-threatening disease caused by the body's response to an infection," said corresponding author Dr. David B. Corry, professor of medicine-immunology, allergy and rheumatology and Fulbright Endowed Chair in Pathology at Baylor College of Medicine.

Importantly, explains Corry, fungal infections causing airway allergic diseases and sepsis have been associated with increased risk for dementia later.

"These observations led us to investigate the possibility that fungus might produce a brain infection and, if so, the consequences of having that kind of infection," said Corry, who also is a member of the Dan L Duncan Comprehensive Cancer Center.

The researchers began their investigation by developing a mouse model of a low-grade fungus infection with the common yeast C. albicans that would not cause severe disease, but might carry implications for brain function. They tested several doses and finally settled on one dose of 25,000 yeasts.

They injected C. albicans into the blood stream of mice and were surprised to discover that the yeast can cross the blood-brain barrier, a robust protective mechanism the brain employs to exclude all kinds of large and small molecules, as well as a number of microorganisms that can potentially damage the brain.

"We thought that yeast would not enter the brain, but it does," Corry said. "In the brain, the yeast triggered the activity of microglia, a resident type of immune cell. The cells became very active 'eating and digesting' the yeast. They also produced a number of molecules that mediated an inflammatory response leading to the capture of the yeasts inside a granule-type structure inside the brain. We called it fungus-induced glial granuloma, or FIGG."

Corry and his colleagues also tested the animals' memory in both yeast-infected and non-infected mice. They found that infected mice had impaired spatial memory, which reversed when the infection cleared.

The mice cleared the yeast infection in about 10 days; however, the microglia remained active and the FIGGs persisted well past this point, out to at least day 21. Intriguingly, as the FIGGs formed, amyloid precursor proteins accumulated within the periphery and amyloid beta molecules built up around yeast cells captured at the center of FIGGs. These amyloid molecules are typically found in plaques that are the trademark of Alzheimer's disease.

"These findings suggest that the role fungi play in human illness potentially goes well beyond allergic airway disease or sepsis," Corry said. "The results prompted us to consider the possibility that in some cases, fungi also could be involved in the development of chronic neurodegenerative disorders, such as Alzheimer's, Parkinson's and multiple sclerosis. We are currently exploring this possibility."

"For these reasons, if we better understand how our immune system deals with this kind of constant threat and what are the weaknesses in our immunological armor that occur with aging that allow fungal disease to take root, then we would likely increases the possibility of finding ways to fight back, " Corry said.

5  Tutkimus / Tutkimus / Re: Suolistobakteerit, myeliini ja aivotoiminta
 Pvm: 04.01.2019 - 22:32:28 
Keskustelun aloitti HopeSprings | Kirjoittaja HopeSprings  
Gut immune cells cut inflammation in multiple sclerosis


January 3, 2019
Researchers at the University of Toronto and UC San Francisco have discovered that the intestine is the source of immune cells that reduce brain inflammation in people with multiple sclerosis (MS), and that increasing the number of these cells blocks inflammation entirely in a preclinical model of the disease.

The cells in question are plasma cells -- white blood cells that originate as B cells in the bone marrow but change their behavior when triggered by microbes in the gut. Studying mice and samples from human MS patients, the researchers found that plasma cells that reside in the gut and produce Immunoglobulin A (IgA) antibodies appear to migrate to the central nervous system and produce an anti-inflammatory effect during MS flare-ups.

MS is an autoimmune disease, driven by other types of immune cells (including B and T cells) that attack myelin, the protective coating that surrounds nerve fibers. Recent clinical studies have shown drugs that target B cells mitigate MS, while those that target plasma cells make the disease worse. The current study offers an explanation for these divergent results.

"We already knew what was and was not working in the clinic," says Jen Gommerman, PhD, a professor of immunology at the University of Toronto and the senior author on the study. "But here we've uncovered the molecular and cellular mechanism at play. It's a kind of reverse translation approach, which highlights the importance of the gut-brain axis in MS and other autoimmune conditions."

The results were published online January 3, 2019 in Cell.

Canada and the U.S. have among the highest rates of MS in the world, with around three in every thousand individuals affected. Symptoms can include fatigue, poor coordination, tingling, organ problems and cognitive impairment. There is no cure, although quicker diagnoses and better drugs have improved outcomes significantly in the last 15 years.

"IgAs comprise 80 per cent of all antibodies in the body, yet their exact function is still not fully understood," says Sergio Baranzini, PhD, a co-author on the paper who is a professor of neurology in the UCSF Weill Institute for Neurosciences. "Showing that IgA-producing B cells can travel from the gut to the brain opens a new page in the book of neuroinflammatory diseases and could be the first step towards producing novel treatments to modulate or stop MS and related neurological disorders."

The lead authors on the work are postdoctoral fellows Olga Rojas, PhD, and Elisa Porfilio, PhD, from the Gommerman lab at the University of Toronto and Anne-Katrin Pröbstel, MD, from the Baranzini lab at UCSF. In a moment of scientific serendipity, they recently presented their research at the same conference and realized their results aligned. The researchers began to collaborate, and Pröbstel and colleagues in the Baranzini lab were able to show that the Gommerman lab's findings in mice had parallels to human MS patients.

Specifically, the UCSF team found evidence that IgA was decreased in fecal samples from patients with active MS neuroinflammation, suggesting that the inflammation-suppressing cells had been recruited to help fight the patients' disease.

One promising aspect of the new research is that increasing the number of IgA plasma cells that migrate from the gut to the brain eradicated neuroinflammation in mice. A therapeutic approach might aim to expand the number of these cells in the gut, enabling a plentiful supply that could move to the brain and dampen inflammation.

"As a clinician-scientist, it is exciting that our experiments linking preclinical animal models to the biology we see in real MS patients may have uncovered a general mechanism for how the immune system counteracts inflammation," said UCSF's Pröbstel. "Until now, no one has really studied these IgA-producing plasma cells in the context of disease, but we are now examining them in detail in patients with MS to begin to understand how we might manipulate them to help treat neuroinflammatory disease."

A key next step for the researchers is to figure out what microbes in the gut promote the generation of immunosuppressive IgA plasma cells. "If we can understand what these cells are reacting to, we can potentially treat MS by modulating our gut commensals," says Gommerman, referring to the bacteria that live in the healthy gut. "That might be easier than getting drugs into the brain, which is a strategy that hasn't always worked in MS."

The study also raises questions about the microbiome and lifestyle choices. Do certain lifestyles nudge some people toward a gut microbiome that allows immunosuppressive plasma cells to flourish? Are specific foods conducive to creating that environment and if so, might a drug or supplement mimic the effect? Genetics are just one factor that affect susceptibility to MS; the current study highlights how non-genetic factors may confer disease resistance.

Gommerman plans to pursue the basic science behind these questions, working with Baranzini and other research groups to bring the findings into the clinical realm. "There is something very critical about how the gut and brain are connected, and we're starting to unravel the molecular threads behind that clinical observation," she says. "It's a great example of how fast science can move."

6  Hoito / Lääkitys / Re: Tecfidera
 Pvm: 31.12.2018 - 17:25:13 
Keskustelun aloitti Gwbh | Kirjoittaja vanilla  
Viruslääkekuuri tehosi, ja patti iholla tasoittui. Minulla on aikoinaan tutkittu tämä rakkulapatin aiheuttaja, se on vesirokkovirus, eli iholla on Herpes  Simplex. Voihan tietenkin jotain uuttakin tulla, niinkuin nämä muut läiskät...

Lopetin Tecfideran, kun oli niin outo olo, ja halusin, että virus talttuu kunnolla. Kuulosti sen verran pelottavalta, kun neurologi sanoi, että on olemassa vaara, että se leviää keskushermostoon.

7  Hoito / Lääkitys / Re: Tecfidera
 Pvm: 28.12.2018 - 19:48:53 
Keskustelun aloitti Gwbh | Kirjoittaja Red Kite  
Kuulostaa kyhmyruusulta. Se tekee noita punaisia, vähän hilseilevia läiskiä, jotka tummuvat ajan myötä. Omat eivät juuri kutisseet, lähinnä särkivät. Reseptivahvuinen kortisoni nopeutti läiskien lähtöä. Kuukauden tauon jälkeen läiskät olivat lähes kadonneet, yhdestä jäi pysyvä arpi. Niitä oli polvesta pyrstön päälle koko reiden mitalta, vitsailin että näyttää isolle leoparditatskalle.  Virnistys Nyt on pysynyt vuoden verran kokonaan poissa, viimeksi, reilu vuosi sitten ei tosiaan tarvittu tauotustakaan.

8  Hoito / Lääkitys / Re: Tecfidera
 Pvm: 28.12.2018 - 00:44:35 
Keskustelun aloitti Gwbh | Kirjoittaja vanilla  
Itselläni on ihoon tullut sinne tänne vaalean punertavia hiukan hilseileviä läikkiä, jotka kutiavat armottomasti. Myös lääkkeestä johtuva punottaminen ja kihelmöinti on voimakasta, siihen liittyy myös hirveä kutina, tekisi mieli juuriharjalla hangata ihoa. Herään siihen yölläkin.

Pakaraani ilmestyi myös Herpes Simples (siis huuliherpestä vastaava rakkulaihottuma), se on aina aika ajoin tullut, jos on sairas tai muu stressi on iskenyt. En ole siihen koskaan kummemmin suhtautunut, koska se on aina parissa päivässä parantunut. Tämä oli pari päivää ennen Joulua, ja  silloin sattui olemaan neuron kontrolli. Näytin pattia, ja heti piti aloittaa viruslääkitys, koska se oli hirveän näköinen.

Myös Tecfideran jatkaminen on nyt mietinnässä, sen joudun itse ratkaisemaan, koska jäljelle jää vaihtoehtona vain lääkkeettömyys. Neurogi melkein suositteli sitä...

9  Hoito / Lääkitys / Re: Tecfidera
 Pvm: 27.12.2018 - 17:31:25 
Keskustelun aloitti Gwbh | Kirjoittaja Red Kite  
vanilla kirjoitti on 26.12.2018 - 23:47:28:
Onko kellään tullut iho-oireita Tecfiderasta?

Kahteen kertaan on ollut kyhmyruusua, ensimmäisellä kerralla kun koko reisi oli läiskikäs, TEcfidera tauotettiin kuukaudeksi.

10  Hoito / Lääkitys / Re: Tecfidera
 Pvm: 26.12.2018 - 23:47:28 
Keskustelun aloitti Gwbh | Kirjoittaja vanilla  
Onko kellään tullut iho-oireita Tecfiderasta?