.رابطه بین کمبود ویتامین D و انتی بادی ضد مخمر نان و بیمارهای نقص ایمنی با فاکتور رشد میدکین growth factor midkine (MK) .

Midkine in vitamin D deficiency and its association with anti-Saccharomyces cerevisiae antibodies

AUTHOR(S)
Serinkan Cinemre, F.; Cinemre, Hakan; Karacaer, Cengiz; Aydemir, Birsen; Nalbant, Ahmet; Kaya, Tezcan; Tamer, Ali
PUB. DATE
February 2016
SOURCE
Inflammation Research;Feb2016, Vol. 65 Issue 2, p143
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
Objectives and design: The growth factor midkine (MK) is a protein that is involved in cancer, inflammation, immunity. Vitamin D is a potent immunomodulator. Anti-Saccharomyces cerevisiae antibody (ASCA) is reported in autoimmune disorders, some of which are among the causes of vitamin D deficiency. 
 The objective of this study was to investigate a possible association of MK and ASCA with vitamin D deficiency. Materials and methods: 208 adults presented to internal medicine outpatient clinic for history and physical examination has been studied. Serum biochemistry, vitamin D, MK, ASCA-IgG and -IgA, IL-1β, IL-6, IL-8, TNF-α, PDGF, VEGF were obtained. Results: Vitamin D deficiency was 74.2 %. Serum MK level was significantly higher in vitamin D-deficient compared to vitamin D-sufficient individuals (1138.1 ± 262.8 vs 958.6 ± 189 pg/mL, respectively; P < 0.009). Serum MK levels were also significantly higher in both ASCA-IgG and -IgA positives compared to negatives (1318.5 ± 160.3 vs 1065.5 ± 256.1, P = 0.008 and 1347.7 ± 229.7 vs 1070.1 ± 250.9 pg/mL, P = 0.011, respectively). Vitamin D was significantly lower in ASCA positives ( P = 0.044).Vitamin D showed positive correlation with IL-1β ( r 0.338, P < 0.009) and negative correlation with VEGF ( r −0.366, P < 0.004). Conclusions: MK was significantly elevated in vitamin D deficiency and associated with ASCA positivity which was significantly increased in vitamin D deficiency. These findings suggested that molecular mechanism of vitamin D deficiency may be related with some inflammatory processes.
پروتینی به نام فاکتور رشد میدکین   growth factor midkine (MK) در  بدن است که جلوی التهاب اندام ها و سرطان را می گیرد در کسی که کمبود ویتامین D دارد  سیستم دفاعی بدن در برابر سرطان ومخمر نان  و بیماری های اتوایمون به درستی عمل نمی کند  و ریسک سرطان و بیماری های مزمن بالا می رود  در ضمن زمانی که شما کمبود ویتامین D دارید ماده ای ضد مخمر نان در بدن شما  ایجاد می شود که  ایین انتی بادی ضد مخمر نان بعد ها ممکن است سرطان کولون و التهابات مختلف بدهد  مثل بیماری های خود ایمنی ارتریت روماتید ام اس و دیگر بیماریها می شود

تغییرات ژنتیکی بر روی مخمرنان(ساکارومایسس سرویزیه ) برای نسل کشی انسانها را چه کسانی انجام دادند / / Saccharomyces cerevisiae /Yeast, the Spam Filter

 تغییرات ژنتیکی بر روی مخمرنان(ساکارومایسس سرویزیه ) برای نسل کشی  انسانها را چه کسانی انجام دادند / / 

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New & Noteworthy

Yeast, the Spam Filter

November 11, 2015
magine what our email inboxes would look like if we didn’t have spam filters! To find the meaningful emails, we’d have to wade through hundreds of messages about winning lottery tickets, discount medications, and other things that don’t interest us.
When it comes to sorting out meaningful mutations from meaningless variation in human genes, it turns out that our friend S. cerevisiae makes a pretty good spam filter. And as more and more human genomic sequence data are becoming available every day, this is becoming more and more important.
For example, when you look at the sequence of a gene from, say, a cancer cell, you may see many differences from the wild-type gene. How can you tell which changes are significant and which are not?
SuperBud to the rescue! Because many human proteins can work in yeast, simple phenotypes like viability or growth rate can be assayed to test whether variations in human genes affect the function of their gene products. This may be one answer to the increasingly thorny problem of variants of uncertain significance—those dreaded VUS’s.
In a new paper in GENETICS, Hamza and colleagues systematically screened for human genes that can replace their yeast equivalents, and went on to test the function of tumor-specific variants in several selected genes that maintain chromosome stability in S. cerevisiae. This work extends the growing catalog of human genes that can replace yeast genes.
More importantly, it also provides compelling evidence that yeast can help us tell which mutations in a cancer cell are driver mutations, the ones that are involved in tumorigenesis, and which are the passenger mutations, those that are just the consequence of a seriously messed up cell. Talk about a useful filter!
The researchers started by testing systematically for human genes that could complement yeast mutations. Other groups have done similar large-scale screens, but this study had a couple of different twists.
Previous work from the Hieter lab had identified genes in yeast that, when mutated, made chromosomes unstable: the CIN (Chromosome INstability) phenotype. Reduction-of-function alleles of a significant fraction (29%) of essential genes confer a CIN phenotype. The human orthologs of these genes could be important in cancer, since tumor cells often show chromosome rearrangements or loss. 
So in one experiment, Hamza and colleagues focused specifically on the set of CIN genes, starting with a set of 322 pairs of yeast CIN genes and their human homologs. They tested functional complementation by transforming plasmids expressing the human cDNAs into diploid yeast strains that were heterozygous null mutant for the corresponding CIN genes. Since all of the CIN genes were essential, sporulating those diploids would generate inviable spores—unless the human gene could step in and provide the missing function.
In addition to this one-to-one test, the researchers cast a wider net by doing a pool-to-pool transformation. They mixed cultures of diploid heterozygous null mutants in 621 essential yeast genes, and transformed the pooled strains with a mixture of 1010 human cDNAs. This unbiased strategy could identify unrecognized orthologs, or demonstrate complementation between non-orthologous genes.
In combination, these two screens found 65 human cDNAs that complemented null mutations in 58 essential yeast genes. Twenty of these yeast-human gene pairs were previously undiscovered.
The investigators looked at this group of “replaceable” yeast genes as a whole to see whether they shared any characteristics. Most of their gene products localized to the cytoplasm or cytoplasmic organelles rather than to the nucleus. They also tended to have enzymatic activity rather than, for example, regulatory roles. And they had relatively few physical interactions.
So yeast could “receive messages” from human genes, allowing us to see their function in yeast. But could it filter out the meaningful messages—variations that actually affect function—from the spam? 
The authors chose three CIN genes that were functionally complemented by their human orthologs and screened 35 missense mutations that are found in those orthologs in colorectal cancer cells. Four of the human missense variants failed to support the life of the corresponding yeast null mutant, pointing to these mutations as potentially the most significant of the set.
Despite the fact that these mutations block the function of the human proteins, a mutation in one of the yeast orthologs that is analogous to one of these mutations, changing the same conserved residue, doesn’t destroy the yeast protein’s function. This underscores that whenever possible, testing mutations in the context of the entire human protein is preferable to creating disease-analogous mutations in the yeast ortholog.
Another 19 of the missense mutations allowed the yeast mutants to grow, but at a different rate from the wild-type human gene. (Eighteen conferred slower growth, but one actually made the yeast grow faster!)
For those 19 human variants that did support life for the yeast mutants, Hamza and colleagues tested the sensitivity of the complemented strains to MMS and HU, two agents that cause DNA damage. Most of the alleles altered resistance to these chemicals, making the yeast either more or less resistant than did the wild-type human gene. This is consistent with the idea that the cancer-associated mutations in these human CIN gene orthologs affect chromosome dynamics.
As researchers are inundated by a tsunami of genomic data, they may be able to turn to yeast to help discover the mutations that matter for human disease. They can help us separate those emails touting the virtues of Viagra from those not-to-be-missed kitten videos. And when we know which mutations are likely to be important for disease, we’re one step closer to finding ways to alleviate their effects. 
by Maria Costanzo, Ph.D., Senior Biocuration Scientist, SGD

کمبود «ویتامین D» احتمال گرایش به اعتیاد را بالا می برد ...


بسته بندی های رنگ وارنگ از ماده مخدر اسپایس با نام ها و اشکال زیبا برای بخور دادن به گاوهای مشکل پسند جهان در فروشگاها موجود است !.



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قابل توجه کسانی که دام داری دارند !

بخور اسپایس  برای طویله گاوهای شما  در بسته بندی های زیبا به تهران رسید  !

داداش یگهو گول بسته  بندی را نخوری ؟
روی اکثرا انها  به انگلیسی البته خیلی  ریز  نوشته : مصرف انسانی ندارد ؟Not for Human Consumption
حال این بسته بندهای زیبا و قشنگ  با وزن 1 تا 3 گرم  انهم  برای ماده ای که به عنوان کود شیمیایی و مواد صنعتی  بخور برای  دام  وارد می شود چرا باید  این همه اشکال قشنگ و رنگ وارنگ باشه   الله الم !

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  تازه وزن این ماده که به عنوان بخور برای طویله گاوها است چرا سه گرم است .
اخر  داخل  طویله به این بزرگی که من می بینم !این  سه گرم دود بشه که به  همه گاوها نمی رسه!

یعنی گاوها موقع خرید  می روند داخل فروشگاهای اسمارت  شاپ (هوشمند )  و  زمان  خرید از دیدن این عکس ها خوششون می اید و یکی را انتخاب می کنند و می خرند !
 بابا این خارجی ها گاوهاشون چقدر با هوشند !!

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 شاید یک گاوی یک زمانی  ارزو داشته مثلا فیدل کاسترو بشه و یک گاو  دیگر می خواسته  به جای گاو بودن میمون بشه !
به ما چه !

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گیاه کانابیس(ماری جوانا ) را در خارج  از ایران در بسیاری کشورها دام داری ها با مجوز دولت  برای خوراک گاو می کارند و گاو بعد از مصرف مخدر گل (ماری جوانا )اشتهای گاوی پیدا کند و کلی  چاق و چله میشه ! این هم بخور گاو است دیگه ؟
چقدر گاو های خارجی حال هول  می کنند !! خوب البته رئیس گاو داری   بعد  بیشتر از گاوها شیر می دوشه  و کلی سینه گاوها را فشار می دهد و گاو هم که تو عالم هپروت و نعشگی است حال هم می کنه !
شیر گاوه که تمام شد و مغزش هم توهم زد و دیوانه شد و جنون گاوی گرفت  رئیس گاو داری می برش برای ذبح کردن .
  و همه گاوهای ماریجوانای خورد و دود اسپایس گرفته  را پخ پخشون می کند و با گوشتش سوسیس کالباس یا بیفتک  درست می کنند
بیچاره گاوه خبر نداره اخر عاقبت این خوراک ماریجوانا دادن به جای علف  و این بخور اسپایس توی طویله   به جای بوی پشکل  اخر عاقبتش چیه !
خوب گاوه دیگه.
مثل ما و  بچه های ما که نیست ما می فهمیم  که گاو نیستیم چون  عقل و شعور داریم  
اما گاوه  که نمی فهمه گاوه !
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اقا توجه
این ها که بالا نوشتم  شوخی نبود !
  به راستی روی این بسته های زیبا با وزن بین 1 تا 5 گرم 10گرم  نوشته مصرف انسانی ندارد
Not for Human Consumption
و دارای یک ماده شیمیایی مخدر روانگردان است که صد برابر قویتر از مخدر گل  است
نام خیابانی این مواد  اسپایس یا ادویه است  و بیش از 3000 نوع بسته بندی به اشکال جالب دارد
  ماری جوانا صنعتی یعنی همان اسپایس خودمونه که صد برابر قویتر از مخدر گل است .
یک بار بزنی دیگر مخ بیمخ !
یعنی ادم با مصرف مخدر اسپایس تبدیل به گاو می شود !×!!