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Genetic

جمع کنیم ،بریم


آقا این چه وضعشه......این چه وبلاگیه..........نه فعالیتی نه بازدیدی نه نظری.....آخه آدم به چی دل خوش کنه که مطلب بزاره

اول فک کردم اکثر شما مثه همه  زیاد با مطالب علمی حال نمیکنین.....ولی بعد که دقت کردم متوجه شدم با اون پست هایی که غیرعلمی هم هستن همین برخورد میشه........مشکل اینه که نمیایین به وبلاگ سر نمیزنین

من به نشانه اعتراض  دیگه مطلب نمیزارم!(حالا نه که خیلی مهمه.... تازه اصلا اگه کسی همین مطلب هم بخونه)


منبع : خودم

+ نوشته شده در  یکشنبه 1391/03/07ساعت 10:3 PM  توسط آرش درزیان رستمی  | 

E. Coli Bacteria Becomes Factory for Sugar-Modified Proteins to Make Cheaper, Faster Pharmaceuticals



 

Escherichia coli -- a bacteria considered the food safety bane of restaurateurs, grocers and consumers -- is a friend. Cornell University biomolecular engineers have learned to use E. coli to produce sugar-modified proteins for making pharmaceuticals cheaper and faster.

Matthew DeLisa, Cornell associate professor of chemical and biomolecular engineering, and his research team, now have published a novel method for engineering human therapeutic glycoproteins simply and quickly by using E. coli bacteria as a platform. Their methods are now being developed and commercialized through a startup company, Glycobia Inc., which recently took up residence in Cornell's McGovern Family Center for Venture Development in the Life Sciences. While there are no firm plans yet, the professor hopes that within a year, testing this kind of pharmaceutical could be done at the Weill Cornell Medical College in Manhattan.

 

Glycoproteins are proteins that are modified at specific amino acid "acceptor" sites with complex carbohydrate structures, or oligosaccharides -- a basic human chemical reaction that's essential to life. That's why specifically designed, genetically engineered glycoproteins are so commonly used as drugs -- they bind to certain protein receptor sites and, for example, block cancer cells from multiplying. Among glycoproteins used to treat diseases today are monoclonal antibodies and interferons.

Current manufacturing methods rely mainly on costly, time-consuming mammalian culture cells, such as the Chinese Hamster Ovary (CHO) cell line. The process is also susceptible to viral contamination, further driving up production cost. In fact in 2009, another biopharmaceutical company temporarily shut down its plant after such a contamination occurred.

The Cornell research uses a method to assemble a synthetic pathway for the simple and quick production of a glycoprotein that forms the basis of many of today's therapeutic protein drugs, including, for example, the protein GCase, used in a drug that treats Gaucher's disease. To do so, they artificially introduced the machinery of glycosylation -- the chemical process by which proteins become glycoproteins -- into E. colicells, rather than animal cells.

The synthetic pathway they designed, which can be tailored to many amino acid acceptor sites to make different drugs, starts with native enzymes in E. coli. Added to that was a mixture of four enzymes taken from yeast cells, which triggered the biosynthesis of a specific glycan (sugar structure) that resembles the core structure found in virtually all eukaryotic glycans. A fifth enzyme from the bacterium, Campylobacter jejuni, transferred these core glycans to pre-engineered protein acceptor sites, resulting in the desired glycoproteins.

DeLisa and his colleagues are now working to improve their approach that they call "glycans by design" -- using the enzyme-based protein production method to specifically tailor sugar structures to make many different glycans and glycoproteins.

The National Institutes of Health, the National Science Foundation, and the New York State

Office of Science, Technology and Academic Research funded the work.

 

ScienceDaily (Mar. 26, 2012) 

 


+ نوشته شده در  جمعه 1391/03/05ساعت 10:7 AM  توسط آرش درزیان رستمی  | 

What is MicroRNA?

 

 

MicroRNAs are a class of post-transcriptional regulators. They are short ~22 nucleotide RNA sequences that bind to complementary sequences in the 3’ UTR of multiple target mRNAs, usually resulting in their silencing. MicroRNAs target ~60% of all genes, are abundantly present in all human cells and are able to repress hundreds of targets each. These features, coupled with their conservation in organisms ranging from the unicellular algae Chlamydomonas reinhardtii to mitochondria, suggest they are a vital part of genetic regulation with ancient origins.

MicroRNAs were first discovered in 1993 by Victor Ambros, Rosalind Lee and Rhonda Feinbaum during a study into development in the nematode Caenorhabditis elegans (C. elegans) regarding the gene lin-14. This screen led to the discovery that the lin-14 was able to be regulated by a short RNA product from lin-4, a gene that transcribed a 61 nucleotide precursor that matured to a 22 nucleotide mature RNA which contained sequences partially complementary to multiple sequences in the 3’ UTR of the lin-14 mRNA. This complementarity was sufficient and necessary to inhibit the translation of lin-14 mRNA. Retrospectively, this was the first microRNA to be identified, though at the time Ambros et al speculated it to be a nematode idiosyncrasy.

It was only in 2000 when let-7 was discovered to repress lin-41, lin-14, lin28, lin42 and daf12 mRNA during transition in developmental stages in C. elegans and that this function was phylogenetically conserved in species beyond nematodes, that it became apparent the short non-coding RNA identified in 1993 was part of a wider phenomenon.

Since then over 4000 miRNAs have been discovered in all studied eukaryotes including mammals, fungi and plants. More than 700 miRNAs have so far been identified in humans and over 800 more are predicted to exist.

Comparing miRNAs between species can even be used to delineate molecular evolutionary history on the basis that the complexity of an organisms phenotype may reflect that of the microRNA found in the genotype.

When the human genome project mapped its first chromosome in 1999, it was predicted it would contain over 100,000 protein coding genes. However, only around 20,000 were eventually identified (International Human Genome Sequencing Consortium, 2004) and for a long time much of the non-protein-coding DNA was considered "junk", though conventional wisdom holds that much if not most of the genome is functional. Since then, the advent of sophisticated bioinformatics approaches combined with genome tiling studies examining the transcriptome, systematic sequencing of full length cDNA libraries and experimental validation (including the creation of miRNA derived antisense oligonucleotides called antagomirs) have revealed that many transcripts are for non protein coding RNA of which many new classes have been deducted such as snoRNA and miRNA. Unfortunately, the rate of validation of microRNA targets is substantially more time consuming than that of predicting sequences and targets.

Due to their abundant presence and far-reaching potential, miRNAs have all sorts of functions in physiology, from cell differentiation, proliferation, apoptosis to the endocrine system, haematopoiesis, fat metabolism, limb morphogenesis. They display different expression profiles from tissue to tissue, reflecting the diversity in cellular phenotypes and as such suggest a role in tissue differentiation and maintenance
.


ادامه مطلب
+ نوشته شده در  سه شنبه 1391/02/05ساعت 12:33 PM  توسط آرش درزیان رستمی  | 

Processes Leading to Acute Myeloid Leukemia Discovered

ScienceDaily (Jan. 30, 2012) — Researchers at UC Santa Barbara have discovered a molecular pathway that may explain how a particularly deadly form of cancer develops. The discovery may lead to new cancer therapies that reprogram cells instead of killing them. The findings are published in a recent paper in the Journal of Biological Chemistry.


The UCSB research team described how a certain mutation in DNA disrupts cellular function in patients with acute myeloid leukemia (AML). The researchers were prompted to study this process by another research team's discovery that AML patients have a mutation in a certain enzyme, which was reported in the New England Journal of Medicine. The enzyme is a protein called DNMT3A, which leads to changes in how the DNA of AML patients is methylated, or "tagged." Norbert Reich, professor in the Department of Chemistry and Biochemistry at UCSB, was already studying that particular enzyme with his research group, so they began to study the disease process of AML at the cellular level.

Reich explained that tagging is a way of reading DNA at the cellular level. This falls within an area of study called epigenetics, a process that occurs "on top" of genetics. Each person has approximately 200 types of cells, all with the same DNA, and these must be controlled in different ways. "There is an enzyme -- a protein -- that tags DNA and controls which of the genes in your cells, your DNA, gets turned on and off," said Reich. "So you have 20,000 genes, and you have to control them differently in your brain than in your liver."

Reich explained that there is current interest in this broader field of epigenetics as a direction for the treatment of cancer. "There's definitely the idea that this may be a new way of developing therapeutics, because you don't have to kill the cancer cell," said Reich. "Almost every cancer therapy that's out there works on the principle that a cancer cell needs to be killed."

With epigenetics, instead of only having DNA sequence coding for certain genes, there is an epigenetic process, with another layer of information on top of the genetic process. In this case, that information is the tagging by the methyl groups.

"If you really think about it, this is part of the answer as to how your cells can be so different and yet they all have the same DNA," said Reich. "You have the same genome in every one of your cells, but you do not have the same epigenome, which is basically the methylation pattern, the tagging pattern. That is different in every type of your cells. And the way this relates back to cancer, with leukemia, in those patients, the tagging is messed up. The patterns are not correct. Our big contribution to that is we've explained how the mutations in the enzyme could lead to that disruption of the tagging pattern."

The UCSB group developed a test to demonstrate that the mutant enzymes in AML can only work on DNA for short distances. As a result, the precise methylation patterns of a healthy cell are disturbed, resulting in genes being turned on at the wrong place and time, which in turn can initiate the growth of cancerous cells.

The team found that the mutation AML patients have causes a certain complex of four proteins to be disrupted. "The surprise was that the disruption doesn't stop the enzyme from being active; it doesn't stop the enzyme from tagging the DNA," said Reich. "Instead, it stops the way it can do it. Instead of going to your DNA and tagging an entire region of chromosome, it goes there, does one thing, and leaves. That process, that change, is what we see in the AML patients. So we think we have a molecular explanation for this disease."

Reich said that the currently prescribed drug Vidaza works by affecting the same enzyme that is mutated in AML. There is interest in the pharmaceutical industry in developing other therapeutics to target the enzymes responsible for tagging the DNA. These epigenetic inhibitors would reprogram rather than kill the cell.

Traditional cancer therapies use radiation and chemotherapy to remove or kill cancer cells. "The problem with that is that cancer cells are often very subtly different from normal cells," said Reich. "So you have one of the most difficult therapeutic challenges known to man, which is to distinguish between two human cells -- one that's cancerous and one that's not. Instead of killing the cell, the notion is that if you could just reprogram the cell, then it goes back to being normal. You intercept the cancer development. This is still an aspiration; it hasn't been achieved really, but that's what attracts people to the field of epigenetic-based therapies, because of the prospect of not ".having to kill cells

.

+ نوشته شده در  جمعه 1390/11/14ساعت 0:24 AM  توسط آرش درزیان رستمی  | 

The Man Who Would Stop Time


Bill Andrews has spent two decades unlocking the molecular mechanisms of aging. His mission: to extend the human life span to 150 years--or die trying


Bill Andrews’s feet are so large, he tells me, that back when he was 20 he was able to break the Southern California barefoot-waterskiing distance record the first time he put skin to water. Then he got ambitious and went for the world speed record. When the towrope broke at 80 mph, he says, “they pulled me out of the water on a stretcher.”

The soles of the size-15 New Balances that today shelter those impressive feet strike a steady clap-clap on the macadam as Andrews and I lope down a path along the Truckee River that takes us away from the clutter of cut-rate casino hotels, strip malls and highway exit ramps that is downtown Reno, Nevada. Andrews, 59, is a lean 6-foot-3 and wears a close-cropped salt-and-pepper Vandyke and, for today’s outing, a silver running jacket, nicely completing a package that suggests a Right Stuff–era astronaut. He is in fact one of the better ultramarathoners in America. I am an out-of-shape former occasional runner, so it gives me pause to listen as Andrews describes his racing exploits. “I can run 100 miles, finish, turn around, and meet friends of mine on the course who are still coming in,” he says. “I’ve been in many races where I’m stepping over bodies of people who have collapsed, and I’m feeling great.”

"I want to cure my aging, my friends' and family's aging, my investors' aging, and I want to make a ton of money," Andrews says.

His return to running after a middle-aged break was, he says, inspired by a revelation he had at a time when he and a small team of scientists at his biotech start-up, Sierra Sciences, had been working 14 to 18 hours a day in the lab for five years, rather obsessively pursuing a particular breakthrough. Finally, his doctor told him he was headed for an early grave. “I thought, god, I don’t want to cure aging and then drop dead,” Andrews says.

That would indeed be ironic. Because Andrews does intend to cure aging. This stated ambition induces in some listeners the suspicion that Andrews might suffer from delusions of grandeur, but he has a scientific pedigree that insists he be taken seriously. Unlike his friend Aubrey de Grey, the University of Cambridge longevity theorist who relentlessly generates media attention with speculations that straddle the border between science and science fiction, Andrews is an actual research scientist, a top-drawer molecular biologist.

In the 1990s, as the director of molecular biology at the Bay Area biotech firm Geron, Andrews helped lead a team of researchers that, in alliance with a lab at the University of Colorado, just barely beat out the Massachusetts Institute of Technology in a furious, near-decade-long race to identify the human telomerase gene. That this basic science took on the trappings of a frenzied Great Race is a testament to the biological preciousness of telomerase, an enzyme that maintains the ends of our cells’ chromosomes, called telomeres. Telomeres get shorter each time a cell divides, and when they get too short the cell can no longer make fresh copies of itself. If we live long enough, the tissues and organ systems that depend on continued cell replication begin to falter: The skin sags, the internal organs grow slack, the immune-system response weakens such that the next chest cold could be our last. But what if we could induce our bodies to express more telomerase? We’ll see, because that is what Andrews intends to do.

Andrews had scheduled this afternoon’s run as an 18-miler, but he graciously downscaled those ambitions on my behalf long before we set out from the parking lot of the Grand Sierra Resort Hotel. Four miles in, he’s hardly winded—and I’m out of gas. As we make our way back to his car, he consults his training watch and informs me that our pace was an almost respectable 8:40, excepting the latter stretches when I walked, pushing our average up to 10 minutes a mile.

The embrace of fitness has for Andrews a telomeric logic. Make poor lifestyle choices, and you’re likely to die of heart disease or cancer or something well before your telomeres would otherwise become life-threateningly short. But for the aerobicized Andrews, for anyone who takes reasonable care of himself, a drug that activates telomerase might slow down the baseline rate at which the body falls apart. Andrews likens the underlying causes of aging, free radicals and the rest, to sticks of dynamite, with truncated telomeres being the stick with the shortest fuse. “I believe there’s a really good chance that if we defuse that stick,” he says, “and the person doesn’t smoke and doesn’t get obese, it wouldn’t be surprising if they lived to be 150 years old. That means they’re going to have 50 more years to be around when somebody solves the other aging problems.”

But in his race to cure aging, Andrews may himself be running out of time. The stock-market crash of 2008 nearly wiped out two investors who had until then been his primary funders. Without the money to continue refining the nearly 40 telomerase-activating chemicals he and his team had already discovered, Andrews made the decision last September to cut a deal with John W. Anderson, the founder of Isagenix, an Arizona-based “network marketing” supplement company. This month, Isagenix will launch an anti-aging product containing several natural compounds that Sierra Sciences has verified to have “telomere-supporting” properties. It’s not the powerful drug Andrews originally envisioned, but he says he believes it will promote “health and well-being” and just possibly generate enough cash to underwrite the expensive “medicinal chemistry” required to come up with a more fully developed anti-aging compound—one attractive enough to bring in a billionaire or a Big Pharma partner with pockets deep enough to take a drug candidate through the FDA’s time-consuming and fabulously expensive approval process.

“I want to cure my aging,” Andrews tells me, “my friends’ and family’s aging, my investors’ aging, their friends’ and families’ aging, and make a ton of money. And I want to cure everybody else’s aging too—I put that probably equal to making a ton of money."



برچسب‌ها: The Man Who Would Stop Time
+ نوشته شده در  پنجشنبه 1390/10/29ساعت 5:20 PM  توسط آرش درزیان رستمی  | 

خبرای جدید

سلام بر همگی

میدونم که بعضی هاتون نمی دونین ،پس بدونین!

قابل توجه داوطلبان آزمون کارشناسی ارشد:  سازمان سنجش و آموزش کشور  آخرین تغییرات در مواد امتحانی و ضرایب دروس آزمون کارشناسی ارشد سال 1391 برای گرایش های مختلف رشته زیست شناسی را به شرح زیر اعلام کرده است:

کد رشته

رشته امتحانی

مواد امتحانی و ضرایب

 

 

 

x

زیست شناسی- علوم گیاهی

- فیزیولوژی گیاهی

- سیستماتیک- اکولوژی گیاهی

- زیست شناسی تکوینی گیاهی

1- زبان عمومی و تخصصی،2- مجموعه زیست شناسی (شامل: گیاهی، جانوری، میکروبی، سلولی، مولکولی، ژنتیک، بیوشیمی، بیوفیزیک،اکولوژی و تکامل)، 3- فیزیولوژی گیاهی، 4- سیستماتیک گیاهی، 5- تکوین گیاهی (ریخت شناسی، تشریح، ریخت زائی و اندام زائی)

ضرایب به ترتیب دروس:

1- فیزیولوژی گیاهی                      (2، 3، 4، 2 و 2)

2- سیستماتیک- اکولوژی گیاهی      (2، 3، 2، 4 و 2)

3- زیست شناسی تکوینی گیاهی    (2، 3، 2، 2 و 4)

 

 

 

y

زیست شناسی- علوم جانوری

- فیزیولوژی جانوری

- بیوسیستماتیک جانوری

- زیست شناسی تکوینی جانوری

1- زبان عمومی و تخصصی،2- مجموعه زیست شناسی (شامل: گیاهی، جانوری، میکروبی، سلولی، مولکولی، ژنتیک، بیوشیمی، بیوفیزیک،اکولوژی و تکامل)، 3- فیزیولوژی جانوری، 4- جانور شناسی، 5- تکوین جانوری (بافت شناسی و جنین شناسی)

ضرایب به ترتیب دروس:

1- فیزیولوژی جانوری                        (2، 3، 4،  2و 2)

2-بیو سیستماتیک جانوری                (2، 3، 2، 4 و 2)

3- زیست شناسی تکوینی جانوری      (2، 3، 2، 2 و 4)

 

 

 

 

z

زیست شناسی- علوم سلولی و مولکولی

- علوم سلولی و مولکولی

- ژنتیک

- میکروبیولوژی

- بیوشیمی

- بیوفیزیک

- زیست فناوری(گرایش میکروبی)

1- زبان عمومی و تخصصی،2- مجموعه زیست شناسی (زیست شناسی: گیاهی، جانوری، میکروبی، سلولی، مولکولی، ژنتیک، بیوشیمی، بیوفیزیک،اکولوژی و تکامل)، 3- ژنتیک، 4- بیوشیمی، 5- سلولی و مولکولی، 6- میکروبیولوژی، 7- مجموعه ویروس شناسی، قارچ شناسی و ایمنی شناسی، 8- بیوفیزیک

ضرایب به ترتیب دروس:

1- علوم سلولی و مولکولی      (2، 3، 2، 2، 4، 2، 1 و 0)

2- ژنتیک                            (2، 3، 4، 2، 2، 2، 0 و 1)

3- میکروبیولوژی                    (2، 3، 2، 2، 1، 4، 2 و 0)

4- بیوشیمی                       (2، 3، 2، 4، 2، 1، 0 و 2)

5- بیوفیزیک                         (2، 3، 1، 2، 3، 1، 0 و 4)

6- بیوتکنولوژی میکروبی           (2، 3، 3، 2، 0، 3، 2 و 1)

 

 

من از وقتی که یادمه هر چی طرح جدیده بوده روی ما آزمایش شده.....

اونی که این کارو کردی به روح اعتقاد داری؟!

+ نوشته شده در  چهارشنبه 1390/07/06ساعت 9:34 PM  توسط آرش درزیان رستمی  | 

توالی یابی دی ان ای DNA Sequencing



سلام

از اونجایی که این ترم بیوشیمی داریم گفتم تا یه مطلب که مربوط به همین درس است بزارم تا شاید مفید باشه.

این متنی که در ادامه مطلب میزارم مراحل توالی یابی دی ان ای است که از تو دانشگاه میشیگان برداشتمش!

متاسفانه دانشگاه های آمریکا مطالبشونو به زبان شیرین پارسی منتشر نمیکنند به همین دلیل متن لاتینه و  لازمه که یه نمه لغت بلد باشین ...خوده متن ساده اس ولی شاید اصطلاحاتی داشته باشه که باهاش آشنا نباشین....من لینک های کمکی لازم رو میزارم ...........ولی اگه حال متن اصلی خوندنو ندارین و کلا حال نمیکنین با این مطلب!!! یه سر برین به کتاب های بیوشیمی ترجمه شده بزنین حتما در این مورد توضیح دادن....توصیه من اینه که بدشه های خوبی باشین و همینی که گذاشتمو بخونین! یه فرآیند خیلی جالبیه که بعد از این که کاملا فهمیدینش کلیب ا خودتون حال میکنین که از همچین چیز باحالی سر در آوردین!


ادامه مطلب
+ نوشته شده در  شنبه 1390/06/12ساعت 9:54 PM  توسط آرش درزیان رستمی  | 

توجه !                                                                                        توجه!

با سلام خدمت بچه های زرنگی که واسه تقویت پایشون درسارو پاس نمیکنن(نه اینکه بیفتن)

تمام کسائیکه «شیمی آلی۲» پاس نکردن   سعی کنن۲۰٬۱۹٬ شهریور بیان دانشگاه تا یه تقاضا پر

بشه واسه مدیر گروه تا بلکه موافقت کنن برا ترم مهر «شیمی آلی ۲  »ارائه بشه و بتونیم با

میکروب هم نیاز کنیم .

حالا هرکسم اینو میخونه به اونایی که افتادن حتما بگه .از ما گفتن بود (وگرنه ما که پاس کردیم).

+ نوشته شده در  دوشنبه 1390/06/07ساعت 4:12 PM  توسط آرش درزیان رستمی  | 

ژن... Friends.....Facebook

ژنتیکدانان آلمانی به تازگی به روشی دست یافته اند که با استفاده از اون می شه اثرات ترکیبی ژن ها رو یه صفت چند ژنی نشون داد. این روش کمک میکنه که بفهمیم چطور ژنهای مختلف می تونند اثرات  همدیگه رو تقویت ، حذف و یا بپوشنند و محققان این ژنها  رو که در خیلی از موارد با همدیگه اثرگزارند ، هم ارز دوستان در جامعه مجازی FaceBook  می دونند.

برای پی بردن به ارتباط بین ترکیب ماده ژنتیک و صفاتی مثله استعداده یک بیماری ، محققان تفاوت های ژنتیکیه افرادی با یه بیماری خاص رو با افراد  سالم مقایسه کردن. این مطالعات خیلی از ژن ها رو به بیماری ها ربط داد ، ولی این ارتباط ها معمولا ضعیف و غیر واضع  بودند، شاید بخاطر این که ژنهای افراد معمولا به تنهایی کار نمیکنن ،تاثیرات یک ژن خاص میتونه به این که فرد چه ژن های دیگه ای رو حمل میکند وابسته باشه و روش جدید و توسعه یافته توسط این آلمانی ها که تکنیکی به نام " RNA interference " است ، اونا رو قادر می سازه تا اثرات ترکیبی این ژن ها بر همیدگر رو، آشکار و اندازه گیری کنند. RNA interference ؟!)

 اگر دو فرد در فیس بوک  دوستان مشترک زیادی داشته باشند. شانس اینکه این دو نفر همدیگر را بشناسند زیاده...حتی اگه آنها خودشان جزو دوستان فیس بوک هم دیگه نباشند ، به همین نحو ژن هایی که نمای برهمکنشی شبیه به هم دارند احتمالا تحت تاثیر اثرات یکدیگرند... واین محققان مفهمومی به نام 'friends' را ارائه دادند که به معنی ژن هایی است که احتمالا در فرایند های سلولی یکسان با همدیگه تاثیرگزارند. این یافته انشاالله  کمک میکنه در پیش بینی سرانجام بیمار و وفق دادن درمان ها برای بیماری هایی مثله سرطان(البته اگه درست ترجمه کرده باشم والا.....خب کمک نمیکنه به اینا!).


sciencedaily

متن اصلی رو ندارم...شرمنده...و.....هیچی...بیخیال.

+ نوشته شده در  شنبه 1390/05/08ساعت 6:54 PM  توسط آرش درزیان رستمی 

آمار زیستی

درود بر همکلاسی های ژنتیکی خودم

کلاس رفع اشکال آمار زیستی قرار شد تا سه شنبه ساعت یک و نیم تو علوم پایه برگزار شه البته مگر اینکه شما بخواین شنبه ساعت 8 الی 9 همچین کلاسی داشته باشین....می خواین؟

(راسی 4 شنبه نمیشه دکتر فتوکیان چهارشنبه دانشگاه نیس)



+ نوشته شده در  یکشنبه 1390/03/22ساعت 5:6 PM  توسط آرش درزیان رستمی  | 

biology jokes


یه چند تا جوک مربوط به زیست شناسی!(چون تو وبسایت های ایرانی همچین جوک های تخصصی! ای چیدا نمیشن برای همین رفتم سراغ خارجی هاش)



The Difference Between Dogs and Cats

A dog thinks: Hey, these people I live with feed me, love me, provide me with a nice warm, dry house, pet me, and take good care of me ... They must be gods!

A cat thinks: Hey, these people I live with feed me, love me, provide me with a nice warm, dry house, pet me, and take good care of me ... I must be a god!

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Genetics explain why you look like your father and if you don't why you should.

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What did the spinal chord say to when the others were too scared?
Answer: "I got your back bro..."

What did the 3 chromosomes in 21 say? 
Answer: You're going DOWN!! (reference to trsiomy 21)

How was testosterone allowed to influence and rule most of the body?
Answer: He promised CHANGE!

What did the Helicase say to the DNA?
Answer: I'ma rip you apart!!

What did the histone say to the DNA?
Answer: Now that's a wrap!

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ادامه مطلب
+ نوشته شده در  یکشنبه 1390/03/15ساعت 6:26 PM  توسط آرش درزیان رستمی  |