Masaki Jiatian, Fu Jidong, Paul delgado-Olguin, Vasante Weidansen, Yohei Hayashi, benoit Bruno, deepak srivastava.
On August 6th, American and Japanese researchers published a paper in the online edition of Cell magazine, saying that they successfully cultivated cardiomyocytes by implanting certain Gata4, Mef2c and Tbx5 genes into fibroblasts. Researchers have found that in the heart of mouse embryos, three genes are essential to produce cardiomyocytes. By implanting these three genes into fibroblasts, you can get myocardial cells that drive the heartbeat. Compared with culturing cardiomyocytes with induced pluripotent stem cells (iPS cells), this method is safer and simpler.
Tian, the head of the study, said: "Whether human cardiomyocytes can be produced in the same way in the future will be confirmed. If feasible, patients with myocardial infarction will not need thoracotomy, but only need to introduce these genes, so that fibroblasts there can directly generate healthy myocardial cells. "
2. Rat pancreas was produced in mice by injecting pluripotent stem cells into interspecific blastocysts.
Linjun Xiao Hiroshi, Satoshi Yamaguchi Zhi, Hamanaka Shinai, Kato Hui, Yamazaki Yusuke, Tsuda Cheng, Sato Hideyoshi, Li Yunzhu, Akiichi Sumi, A.S. Knisely, etc.
On September 3rd, the latest headline of Cell was interdisciplinary organogenesis. Researchers from the Institute of Medicine, University of Tokyo, Japan, successfully used rat iPS cells (induced pluripotent stem cells) to culture mouse pancreas, which was the first experiment that successfully used cells from different animals to generate internal organs.
Nakauchi Hiroshi, a well-known stem cell research expert at the University of Tokyo, led the study. In the same period, Cell magazine also published a review article by Davor Solter of Singapore Institute of Medical Biology.
The purpose of regenerative medicine is to obtain organs from patients' pluripotent stem cells. The latest article injected rat iPS cells into mouse embryonic balls to produce functional rat pancreas in mice lacking pancreas, which opened up a new way for regenerative medicine to treat diabetes.
Under normal circumstances, fertilized eggs of animals undergo repeated cell division to produce various internal organs of organisms, but researchers have changed this process: they mated female and male mice with genetically altered genes to obtain fertilized eggs of mice that cannot produce pancreas independently. Three days later, they injected 10 to 15 iPS cells extracted from the tail of rats into mouse fertilized eggs that had split into embryos, and finally cultivated a mouse with rat pancreas.
The researchers experimented with about 150 mice, but only one adult mouse was obtained. The results showed that the pancreatic cells of mice were the same as those of rats, and the blood sugar level remained normal. At present, regenerative medicine research using induced pluripotent stem cells mainly focuses on the repair of organs and tissues. Although the research on organ culture in vivo by this stem cell is still in its infancy, the related research results bring new hope to the research in the field of regenerative medicine.
Although mice and rats belong to vertebrates, mammals, rodents and rodents in biological taxonomy, the former belongs to Zokor, while the latter belongs to Rattus and Rattus. Both of them are widely used in genetic research.
3.p53-induced overall gene repression in p53 reaction mediated by non-coding RNA between large genes.
Maite Huarte, Mitchell Guttman, David Feldser, Manuel Garber, Magdalena J. Koziol, Daniela Kenzelmann-Broz, Ahmad M. Khalil or Zuk, Ido Amit, Michal Rabani and others.
Researchers from Harvard Medical School, Massachusetts Institute of Technology, Stanford University and other places have discovered a new class of large-chain noncoding RNAs (lincRNAs) regulated by p53. Both the study of p53 as a star gene and the analysis of long-chain noncoding RNAs provide important information. This research achievement appeared on the cover of Cell magazine.
The research was led by the famous young scientist John Ryan. Dr. John Rinn devoted himself to RNA research, and in 2009, he was named as an American young talent. The growth of this scientific community is quite tortuous: skateboarding and skiing once occupied all his life. It was not until he was studying at the University of Minnesota in the United States that he began to immerse himself in biology classes and gradually realized that he was not only talented in science, but actually he liked science very much.
Dr. John Rinn discovered thousands of new forms of RNA, called large amounts of inserted noncoding RNA or LINCs. Later, it was proved that these newly discovered RNA not only played an auxiliary role in gene regulation, but also directly directed the whole play.
In the latest article, Dr. John Rinn's team and other colleagues discovered a new long-chain non-coding RNA regulated by p53. The so-called long-chain non-coding RNA is an RNA molecule whose transcript length exceeds 200nt. They do not encode protein, but regulate the gene expression level in different levels in the form of RNA (epigenetic regulation, transcriptional regulation and post-transcriptional regulation, etc.). ).
4. Reversing cancer cachexia and muscular atrophy through ActRIIB antagonism can prolong the survival time.
Wang, Lu, Guo, Jiao Qingsheng, Rosenfeld, Boone, Simone, etc.
Researchers have found a molecule in mice that can completely reverse the destructive muscle loss associated with advanced cancer and prolong the survival time of cancer animals. This molecule can be used as bait to block the activity of myostatin, a key muscle growth inhibitor. The binding of myostatin to bait molecules is "cleared", so it cannot bind to its normal receptor to start muscle degeneration.
The destructive loss of cancer muscle, also known as cachexia, is the cause of death of 30% cancer patients. At present, it is not clear how cancer causes cachexia and how cachexia leads to the decline of patients' function. Scientists believe that it is caused by a series of related molecular signals. "It controls muscle mass in a negative way," said Han Hanqing, the initiator of this study.
Han and his research team hope to find the signal pathway related to cancer cachexia and block it to achieve the purpose of treating patients. Studies have confirmed that blocking myostatin signaling pathway can promote muscle growth. Studies have confirmed that activin A, which is closely related to myostatin, is highly expressed in some cancer patients.
"We randomly selected a large number of cancer cell lines cultured in vitro and found that 1/3 secreted a large amount of activin A," Han said. "This leads us to believe that activin A overexpressed in cancer must have some systemic functions."
Researchers have created a soluble activin A receptor-like molecule, which is thought to affect myostatin and activin A signaling pathways, that is, an antibody with activin receptor characteristics. This decoy molecule blocks the activation of the receptor by clearing the ligand.
Injecting this soluble molecule into the muscles of normal mice alone can promote muscle accumulation within a week or two. When it was given to mice transplanted with colon cancer cells, although the tumor continued to grow, its muscle mass returned to normal. Surprisingly, all animals that did not receive soluble molecular therapy died within 40 days after cancer cell implantation, while half of the animals in the treatment group survived within the same time. The research paper was published in the journal Cell.
This is not the first time that Han's team has tried to treat muscular atrophy through myostatin signal. Molecular biologist Sai Li Zhen of Johns Hopkins University in Baltimore, Maryland, discovered myostatin gene in 1997, and determined its function of regulating skeletal muscle. Li said; "There is indeed a lot of data to prove that this signal path is beneficial. But in fact, it is not surprising that destroying the myostatin signaling pathway leads to strong muscle regeneration, because other studies have confirmed that this signaling pathway has extreme side effects on muscle growth. "
5.GPR 120 is an ω-3 fatty acid receptor, which mediates effective anti-inflammatory and insulin sensitization.
Dayounoh, Saswata Talukdar, Eun Ju Bae, Takeshi Imamura, Hidetaka Morinaga, Fan Wuqiang, Li, Wendell J. Lu, Steven M. Watkins, Jerrold M. Olefsky.
6. Another splicing network links cell cycle control with apoptosis.
Michael J Moore, Qingqing Wang, Keller J Kennedy, Pamela A Silver.
7. Dendritic function of Tau mediates amyloid β toxicity in mouse model of Alzheimer's disease.
Lars M. Ittner, Yazi D. Ke, Yang Qiyu Deleru, Mian Bi, Amadeus Gladbach, Janet van Eersel, Heidrun W? Lfing, Billy C. Chieng, MacDonald J. Christie, Ian A. Napier, etc.
8. The language of histone crosstalk
Li Zhengxin, Edwin Smith, Ali Shirati Failde.
9. Activate specific apoptotic caspase with engineered small molecule activating protease.
Daniel Gray, Sammy Mareuse, James Wells.
10. Immunoproteasome keeps the balance in protein during the oxidative stress induced by interferon.
Ulrike Seifert,Lukasz P. Bialy,Frédéric Ebstein,Dawadschargal Bech-Otschir,Antje Voigt,Friederike Schr? Ter, Timour Prozorovski, Nicole Lange, Janos Steffen, Melanie Rieger, etc.
An article *** 10, hope to adopt.
The following is a paper I compiled for your little monkey for your reference.
The relations