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文章數：34 |
 TANG Zhan 湯棧套餐划算嗎？ 》台中公益路餐廳大賞｜10家特色名店推薦 |
| 時事評論｜兩岸 2025/11/18 23:25:24 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
身為一個熱愛美食、喜歡在城市裡挖掘驚喜的人，臺中公益路一直是我最常出沒的地方之一。這條路可說是「臺中人的美食戰場」，從精緻西餐到創意火鍋，從日式丼飯到義式早午餐，每走幾步，就會有完全不同的特色料理餐廳。 這次我特別花了一整個月，實際造訪了公益路上十間口碑不錯的餐廳。有的是網友熱推的打卡名店，也有隱藏在巷弄裡的小驚喜。我以環境氛圍、口味表現、價格CP值與再訪意願為基準，整理出這篇實測評比。希望能幫正在猶豫去哪裡吃飯的你，找到那一間「吃完會想再來」的餐廳。 評比標準與整理方向
這次我走訪的10家餐廳橫跨不同料理類型，從高質感牛排館到巷弄系早午餐，每一間都有自己獨特的風格。為了讓整體比較更客觀，我依照以下四大面向進行評比，並搭配實際用餐體驗來打分。
整體而言，我希望這份評比不只是「哪家好吃」，而是幫你在不同情境下（約會、家庭聚餐、朋友小聚、商業午餐）都能快速找到合適的選擇。畢竟，美食不只是味覺的滿足，更是一段段與朋友共享的生活記憶。 10間臺中公益路餐廳評比懶人包公益路向來是臺中人聚餐的首選地段，從火鍋、燒肉到中式料理與早午餐，每走幾步就有驚喜。以下是我實際造訪過的10間代表性餐廳清單，橫跨平價、創意、高級各路風格。
一頭牛日式燒肉｜炭香濃郁的和牛饗宴，約會聚餐首選
走在公益路上，很難不被 一頭牛日式燒肉 的木質外觀吸引。低調卻不失質感的門面，搭配昏黃燈光與暖色調的內裝，讓人一進門就感受到濃濃的日式職人氛圍。店內空間不大，但桌距規劃得宜，每桌皆設有獨立排煙設備，烤肉時完全不怕滿身油煙味。 餐點特色
一頭牛的靈魂，絕對是他們招牌的「三國和牛拼盤」。 用餐體驗整體節奏掌握得非常好。店員會在你剛想烤下一片肉時貼心遞上夾子、幫忙換烤網，讓人完全不用分心。整場用餐過程就像一場表演，從視覺、嗅覺到味覺都被滿足。 綜合評分
地址：408臺中市南屯區公益路二段162號電話：04-23206800 官網：http://www.marihuana.com.tw/yakiniku/index.html 小結語一頭牛日式燒肉不僅是「吃肉的地方」，更像是一場五感盛宴。從進門那一刻到最後一道甜點，都能感受到他們對細節的用心。 TANG Zhan 湯棧｜文青系火鍋代表，麻香湯底與視覺美感並重
在公益路這條美食戰線上，TANG Zhan 湯棧 是讓人一眼就會想走進去的那一種。 餐點特色
湯棧最有名的當然是它的「麻香鍋」。 用餐體驗整體氛圍比一般火鍋店更有質感。 綜合評分
地址：408臺中市南屯區公益路二段248號電話：04-22580617 官網：https://www.facebook.com/TangZhan.tw/ 小結語TANG Zhan 湯棧 把傳統火鍋做出新的樣貌保留臺式鍋物的溫度，又結合現代風格與細節服務，讓吃鍋這件事變得更有品味。 如果你想找一間兼具「好吃、好拍、好放鬆」的火鍋店，湯棧會是公益路上最有風格的選擇之一。 NINI 尼尼臺中店｜明亮寬敞的義式早午餐天堂
如果說前兩間是肉食愛好者的天堂，那 NINI 尼尼臺中店 絕對是想放鬆、聊聊天的好地方。餐廳外觀以白色系與大片玻璃窗為主，陽光灑進室內，讓人一踏入就有種度假般的輕盈感。假日早午餐時段特別熱鬧，建議提早訂位。 餐點特色
NINI 的菜單融合義式與臺灣人口味，選擇多樣且份量十足。主打的 松露燉飯 濃郁卻不膩口，米芯保留微Q口感；而 香蒜海鮮義大利麵 則以新鮮白蝦、花枝與淡菜搭配微辣蒜香，口感層次豐富。 用餐體驗店內氣氛輕鬆不拘謹，無論是一個人帶電腦工作、或朋友聚餐，都能找到舒服角落。餐點上桌速度穩定，服務人員態度親切、補水與收盤都非常主動。整體節奏讓人覺得「時間變慢了」，很適合想遠離忙碌日常的人。 綜合評分
地址：40861臺中市南屯區公益路二段18號電話：04-23288498 小結語NINI 尼尼臺中店是一間能讓人放下手機、慢慢吃飯的餐廳。餐點不追求浮誇，而是以「剛剛好」的份量與風味，陪伴每個平凡午後。如果你在找一間能邊吃邊聊天、拍照也漂亮的早午餐店，NINI 會是你在公益路上最不費力的幸福選擇。 加分100%浜中特選昆布鍋物｜平價卻用心的湯頭系火鍋，家庭聚餐好選擇
在公益路這條高質感餐廳林立的戰場上，加分100%浜中特選昆布鍋物 走的是截然不同的路線。它沒有浮誇的裝潢、也沒有高價位的套餐，但靠著實在的湯頭與親切的服務，默默吸引許多回頭客。每到用餐時間，總能看到家庭或情侶三兩成群地圍著鍋邊聊天。 餐點特色
主打 北海道浜中昆布湯底，湯頭清澈卻不單薄，越煮越能喝出海藻與柴魚的自然香氣。 用餐體驗整體氛圍偏家庭取向，桌距寬敞、座位舒適，帶小孩來也不覺擁擠。店員態度親切，補湯、收盤都很勤快，給人一種「被照顧著」的安心感。 綜合評分
地址：403臺中市西區公益路288號電話：0910855180 小結語加分100%浜中特選昆布鍋物是一間「不浮誇、但會讓人想再訪」的火鍋店。它不追求豪華擺盤，而是用最簡單的湯頭與新鮮食材，傳遞出家常卻不平凡的溫度。 印月餐廳｜中式料理的藝術演繹，宴客與家庭聚會首選
說到臺中公益路的中式料理代表，印月餐廳 絕對是榜上有名。這間開業多年的餐廳以「中菜西吃」的概念聞名，把傳統中式料理以現代手法重新詮釋。從建築外觀到餐具擺設，每個細節都散發著低調的典雅氣息。 餐點特色
印月最令人印象深刻的是他們將傳統中菜融入創意手法。 用餐體驗服務方面完全對得起餐廳的高級定位。從入座、點餐到上菜節奏，都拿捏得恰如其分。每道菜都會有服務人員細心介紹食材與吃法，讓人感受到「被款待」的尊榮感。 綜合評分
地址：408臺中市南屯區公益路二段818號電話：0422511155 小結語印月餐廳是一間「不只吃飯，更像品味生活」的地方。 KoDō 和牛燒肉｜極致職人精神，專為儀式感與頂級味覺而生
若要形容 KoDō 和牛燒肉 的用餐體驗，一句話足以總結——「像在欣賞一場關於肉的表演」。 餐點特色
這裡主打 日本A5和牛冷藏肉，以「精切厚燒」的方式呈現。 用餐體驗KoDō 的最大特色是「儀式感」。 綜合評分
地址：403臺中市西區公益路260號電話：0423220312 官網：https://www.facebook.com/kodo2018/ 小結語KoDō 和牛燒肉不是日常餐廳，而是一場體驗。 永心鳳茶｜在茶香裡用餐的優雅時光，臺味早午餐的新詮釋
走進 永心鳳茶公益店，彷彿進入一間有氣質的茶館。 餐點特色
永心鳳茶的餐點結合中式靈魂與西式擺盤，無論是「炸雞腿飯」還是「紅玉紅茶拿鐵」，都能讓人感受到熟悉卻不平凡的味道。 用餐體驗店內服務人員態度溫和，對茶品介紹詳盡。上餐節奏剛好，不急不徐。 綜合評分
地址：40360臺中市西區公益路68號三樓(勤美誠品)電話：0423221118 小結語永心鳳茶讓人重新定義「臺味」。 三希樓｜老饕級江浙功夫菜，穩重又帶人情味的中式饗宴
位於公益路上的 三希樓 是許多臺中老饕的口袋名單。 餐點特色
三希樓的菜色以 江浙與港式料理 為主，兼顧傳統與現代風味。 用餐體驗三希樓的服務給人一種老派但貼心的感覺。 綜合評分
地址：408臺中市南屯區公益路二段95號電話：0423202322 官網：https://www.sanxilou.com.tw/ 小結語三希樓是一間「吃得出功夫」的餐廳。 一笈壽司｜低調奢華的無菜單日料，職人手藝詮釋旬味極致
在熱鬧的公益路上，一笈壽司 低調得幾乎不顯眼。 餐點特色
一笈壽司採 Omakase（無菜單料理） 形式，每一餐都由主廚根據當日食材設計。 用餐體驗整場用餐約90分鐘，節奏緩慢但沉穩。 綜合評分
地址：408臺中市南屯區公益路二段25號電話：0423206368 官網：https://www.facebook.com/YIJI.sushi/ 小結語一笈壽司是一間真正讓人「放慢呼吸」的餐廳。 茶六燒肉堂｜人氣爆棚的和牛燒肉聖地，肉香與幸福感同時滿分
若要票選公益路上「最難訂位」的餐廳，茶六燒肉堂 絕對名列前茅。 餐點特色
茶六主打 和牛燒肉套餐，價格約落在 $700–$1000 間，份量與品質兼具。 用餐體驗茶六的服務效率相當高。店員親切、換網勤快、補水速度快，整場用餐流程流暢無壓力。 綜合評分
地址：403臺中市西區公益路268號電話：0423281167 官網：https://inline.app/booking/-L93VSXuz8o86ahWDRg0:inline-live-karuizawa/-LUYUEIOYwa7GCUpAFWA 小結語茶六燒肉堂用「穩定品質＋輕奢氛圍」抓住了臺中年輕族群的心。 吃完10家公益路餐廳後的心得與結語吃完這十家餐廳後，臺中公益路不只是一條美食街，而是一段生活風景線。 有的餐廳講究細膩與儀式感，像 一頭牛日式燒肉 與 一笈壽司，讓人感受到食材最純粹的美好 有的則以親切與溫度打動人心，像 加分昆布鍋物、永心鳳茶，讓人明白吃飯不只是為了飽足，而是一種被照顧的幸福。 而像茶六燒肉堂、TANG Zhan 湯棧 這類人氣名店，則用穩定的品質與熱絡的氛圍，成為許多臺中人心中「想吃肉就去那裡」的代名詞。 這十家店，構成了公益路最動人的縮影 有華麗的，也有溫柔的；有傳統的，也有創新的。 每一家都在自己的風格裡發光，讓人吃到的不只是料理，而是一種生活的溫度與節奏。 對我而言，這不僅是一場美食旅程，更是一趟關於「臺中味道」的回憶之旅。 FAQ：關於臺中公益路美食常見問題Q1：公益路哪一區的餐廳最集中？ Q2：需要提前訂位嗎？ 最後的話若要用一句話形容這趟美食之旅，我會說： 加分100%浜中特選昆布鍋物適合跨年聚餐嗎？ 如果你也和我一樣喜歡用味蕾探索一座城市，那就把這篇公益路美食攻略收藏起來吧。三希樓平日好排隊嗎？ 無論是約會、慶生、家庭聚餐，或只是想犒賞一下辛苦的自己——這條路上永遠會有一間剛剛好的餐廳在等你。永心鳳茶口味偏臺式還是日式？ 下一餐，不妨從這10家開始。一笈壽司適合約會嗎？ 打開手機、約上朋友，讓公益路成為你生活裡最容易抵達的小確幸。永心鳳茶單點比較好嗎？ 如果你有私心愛店，也歡迎留言分享，NINI 尼尼臺中店小孩適合去嗎？ 你的推薦，可能讓我下一趟美食旅程變得更精彩。一笈壽司好吃嗎？ The image shows fear memory neurons (red) among all prefrontal cortex neurons (blue). Credit: Cho lab, UC Riverside A study conducted by UC Riverside researchers on mice may pave the way for new innovative treatments for individuals with PTSD. A mouse study from the University of California, Riverside, published in Nature Neuroscience, has uncovered the basic mechanisms that drive the brain to consolidate remote fear memories of traumatic events from the past, ranging from a few months to decades ago. The study shows that remote fear memories from the distant past are permanently stored in the connections between memory neurons in the prefrontal cortex (PFC). “It is the prefrontal memory circuits that are progressively strengthened after traumatic events and this strengthening plays a critical role in how fear memories mature to stabilized forms in the cerebral cortex for permanent storage,” said Jun-Hyeong Cho, an associate professor of molecular, cell and systems biology, who led the study. “Using a similar mechanism, other non-fear remote memories could also be permanently stored in the PFC.” Transition from Hippocampus to Prefrontal Cortex The brain uses distinct mechanisms to store recent versus remote fear memories. Previous studies have suggested that while the initial formation of fear memory involves the hippocampus, it progressively matures with time and becomes less dependent on the hippocampus. Much research now explains how recent fear memory is stored, but how the brain consolidates remote fear memories is not well understood. The researchers focused on the PFC, a part of the cerebral cortex that has been implicated in remote memory consolidation in previous studies. “We found a small group of nerve cells or neurons within the PFC, termed memory neurons, were active during the initial traumatic event and were reactivated during the recall of remote fear memory,” Cho said. “When we selectively inhibited these memory neurons in the PFC, it prevented the mice recalling remote but not recent fear memory, suggesting the critical role of PFC memory neurons in the recall of remote fear memories.” In the experiments, the mice received an aversive stimulus in an environment called a context. They learned to associate the aversive stimulus with the context. When exposed to the same context a month later, the mice froze in response, indicating they could recall remote fear memories. The researchers showed that connections (synapses) between memory neurons in the PFC, termed prefrontal memory circuits, were gradually strengthened with time after fear learning, and such strengthening helped the PFC permanently store remote fear memories. Extinction of Fear and Prefrontal Memory Circuits Next, to extinguish the remote fear memory in the mice, the researchers repeatedly exposed the mice to the same fear-predictive context but without the aversive stimulus. The result was a reduced fear response to the context. “Interestingly, the extinction of remote fear memory weakened the prefrontal memory circuits that were previously strengthened to store the remote fear memory,” Cho said. “Moreover, other manipulations that blocked the strengthening of the PFC memory circuits also prevented the recall of remote fear memory.” Cho explained that a dysregulation of fear memory consolidation can lead to chronic maladaptive fear in PTSD, which affects about 6% of the population at some point in their lives. “Considering that PTSD patients suffer from fear memories formed in the distant past, our study provides an important insight into developing therapeutic strategies to suppress chronic fear in PTSD patients,” he said. Next, Cho’s team plans to selectively weaken the prefrontal memory circuits and examine whether this manipulation suppresses the recall of remote fear memories. “We expect the results will contribute to developing a more effective intervention in PTSD and other fear-related disorders,” Cho said. Reference: “Neocortical synaptic engrams for remote contextual memories” by Ji-Hye Lee, Woong Bin Kim, Eui Ho Park, and Jun-Hyeong Cho, 23 December 2022, Nature Neuroscience. DOI: 10.1038/s41593-022-01223-1 The study was funded by the National Institutes of Mental Health. UMD-led study revealed age-related changes to the DNA of bats related to longevity. Clockwise from top left: common vampire bat, (G. Wilkinson), greater horseshoe bat, Rhinolophus ferrumequinum (G. Jones), velvety free-tailed bat, bat, (S. Puechmaille), and greater mouse-eared (M. Tschapka). All can live 30 years or longer except greater mouse-eared, which only lives to 6 years of age. Credit: G. Wilkinson, G. Jones, S. Puechmaille, M. Tschapka UMD-led research identifies age-related changes to DNA and reveals longevity-related differences between bat species. A new study led by University of Maryland and UCLA researchers found that DNA from tissue samples can be used to accurately predict the age of bats in the wild. The study also showed age-related changes to the DNA of long-lived species are different from those in short-lived species, especially in regions of the genome near genes associated with cancer and immunity. This work provides new insight into causes of age-related declines. This is the first research paper to show that animals in the wild can be accurately aged using an epigenetic clock, which predicts age based on specific changes to DNA. This work provides a new tool for biologists studying animals in the wild. In addition, the results provide insight into possible mechanisms behind the exceptional longevity of many bat species. The study appears in the March 12, 2021, issue of the journal Nature Communications. “We hoped that these epigenetic changes would be predictive of age,” said Gerald Wilkinson, a professor of biology at UMD and co-lead author of the paper. “But now we have the data to show that instead of having to follow animals over their lifetime to be sure of their age, you can just go out and take a tiny sample of an individual in the wild and be able to know its age, which allows us to ask all kinds of questions we couldn’t before.” How DNA Methylation Tells Time The researchers looked at DNA from 712 bats of known age, representing 26 species, to find changes in DNA methylation at sites in the genome known to be associated with aging. DNA methylation is a process that switches genes off. It occurs throughout development and is an important regulator for cells. Overall, methylation tends to decrease throughout the genome with age. Using machine learning to find patterns in the data, the researchers found that they could estimate a bat’s age to within a year based on changes in methylation at 160 sites in the genome. The data also revealed that very long-lived bat species exhibit less change in methylation overall as they age than shorter-lived bats. Wilkinson and his team then analyzed the genomes of four bat species — three long-lived and one short-lived — to identify the specific genes present in those regions of the genome where age-related differences in methylation correlated with longevity. They found specific sites on the genome where methylation was more likely to increase rather than decrease with age in the short-lived bats, but not in long-lived bats, and that those sites were located near 57 genes that mutate frequently in cancerous tumors and 195 genes involved in immunity. Genetic Clues to Longevity and Cancer Resistance “What’s really interesting is that the sites where we found methylation increasing with age in the short-lived bats are near genes that have been shown to be involved in tumorigenesis — cancer — and immune response,” Wilkinson said. “This suggests there may be something to look at in these regions regarding mechanisms responsible for longevity.” Wilkinson said analyzing methylation may provide insight into many age-related differences between species and lead to a better understanding of the causes for age-related declines across many species. “Bats live a long time, and yet their hearing doesn’t decay with age, the way ours does,” he said. “You could use this method to see whether there are differences in methylation that are associated with hearing. There are all kinds of questions like this we can ask now.” Reference: “DNA methylation predicts age and provides insight into exceptional longevity of bats” by Gerald S. Wilkinson, Danielle M. Adams, Amin Haghani, Ake T. Lu, Joseph Zoller, Charles E. Breeze, Bryan D. Arnold, Hope C. Ball, Gerald G. Carter, Lisa Noelle Cooper, Dina K. N. Dechmann, Paolo Devanna, Nicolas J. Fasel, Alexander V. Galazyuk, Linus Günther, Edward Hurme, Gareth Jones, Mirjam Knörnschild, Ella Z. Lattenkamp, Caesar Z. Li, Frieder Mayer, Josephine A. Reinhardt, Rodrigo A. Medellin, Martina Nagy, Brian Pope, Megan L. Power, Roger D. Ransome, Emma C. Teeling, Sonja C. Vernes, Daniel Zamora-Mejías, Joshua Zhang, Paul A. Faure, Lucas J. Greville and Steve Horvath, 12 March 2021, Nature Communications. DOI: 10.1038/s41467-021-21900-2 In addition to Wilkinson, co-authors of the paper from UMD include current postdoctoral associate Danielle M. Adams (Ph.D. ’19, biological sciences) and former graduate students Bryan Arnold (Ph.D. ’11, behavior, ecology, evolution, and systematics), now an associate professor at Illinois College; and Gerald Carter (Ph.D., ’15, biology), now an assistant professor at Ohio State University; Edward Hurme (Ph.D. ’20, biological sciences), now a postdoctoral associate at the University of Konstanz in Germany. This work was supported by a grant from the Paul G. Allen Frontiers Group. The content of this article does not necessarily reflect the view of this organization. Researchers at UC Santa Barbara have developed a method to significantly enhance the efficiency of CRISPR/Cas9 gene editing without using viral material for the delivery of the genetic template. The method, as outlined in a paper published in Nature Biotechnology, employs interstrand crosslinks to stimulate homology-directed repair, a step in the gene editing process, increasing the efficiency threefold without raising mutation frequencies. These crosslinks, usually used in cancer chemotherapy, were found to boost the cell’s natural repair mechanisms and improve the likelihood of successful gene editing. Scientists have enhanced the efficiency of CRISPR/Cas9 gene editing by threefold using interstrand crosslinks, without resorting to viral material for delivery. This approach boosts the cell’s natural repair mechanisms, allowing for more accurate and efficient gene editing, potentially improving disease research and preclinical work. Gene editing is a powerful method for both research and therapy. Since the advent of the Nobel Prize-winning CRISPR/Cas9 technology, a quick and accurate tool for genome editing discovered in 2012, scientists have been working to explore its capabilities and boost its performance. Researchers in the University of California, Santa Barbara biologist Chris Richardson’s lab have added to that growing toolbox, with a method that increases the efficiency of CRISPR/Cas9 editing without the use of viral material to deliver the genetic template used to edit the target genetic sequence. According to their new paper published in the journal Nature Biotechnology, their method stimulates homology-directed repair (a step in the gene editing process) by approximately threefold “without increasing mutation frequencies or altering end-joining repair outcomes.” “We’ve found a chemical modification that improves non-viral gene editing and also discovered an intriguing new type of DNA repair,” Richardson said. Find, Cut and Paste The CRISPR/Cas9 method works by capitalizing on a defense technique employed by bacteria against viral attackers. To do this, the bacteria snip a piece of the invading virus’s genetic material, and incorporate it into their own in order to recognize it later. Should the bacteria get reinfected, they can target the now-familiar genetic sequences for destruction. In gene editing, this process uses the enzyme Cas9 as molecular “scissors” to snip sequences it recognizes, guided by the CRISPR system. This cut is also an opportunity to replace the severed genes with similar (homologous) but improved ones, utilizing the cell’s natural repair mechanisms. If successful, the cell should have modified expressions and functions thereafter. CRISPR (short for “clustered regularly interspaced short palindromic repeats”) is a technology that research scientists use to selectively modify the DNA of living organisms. CRISPR was adapted for use in the laboratory from naturally occurring genome editing systems found in bacteria. To deliver the repair template DNA to the nucleus of the cell where its genetic material lives, oftentimes viruses are used. While they are effective, the researchers say, viral workflows “are expensive, difficult to scale, and potentially toxic to cells.” Nonviral templates are potentially less expensive and more scalable, although researchers still must overcome efficiency and toxicity barriers. In their study, the Richardson Lab found that introducing interstrand crosslinks into the workflow increased homology directed repair dramatically. “Every workflow that we have put this approach into has worked better by roughly threefold,” Richardson said. Interstrand crosslinks are lesions that keep the double strands of a DNA helix tethered to each other, making them unable to replicate. Cancer chemotherapies use this mechanism to interrupt tumor growth and kill cancer cells. Added to a homology directed repair template, however, these crosslinks were found to stimulate the cell’s natural repair mechanisms and increase the likelihood of editing success. “Basically, what we’ve done is taken this template DNA and damaged it,” Richardson said. “We’ve in fact damaged it in the most severe way I can think of. And the cell doesn’t say, ‘Hey this is junk; let me throw it away.’ What the cell actually says is, ‘Hey this looks great; let me stick it into my genome.’” The result is a highly efficient and minimally error-prone nonviral system of gene editing. Their discovery, like many breakthroughs in science, was actually something of a happy accident. While working to purify proteins to study DNA repair, graduate student researcher and lead author Hannah Ghasemi noted unanticipated changes to the outcomes of their experiments. “We were introducing these chemical modifications to the DNA templates in order to be able to pull them out of the cells and see what proteins were bound to them, and I was just checking to see if this modification had somehow affected the editing in any capacity,” she said. “I was expecting to either see no change or that it actually might have negatively affected the editing.” What she found instead was a positive effect, up to three times the editing activity of the uncrosslinked controls. Furthermore, the team found that even with the increase in edits — and therefore the chances for errors — there was no increase in mutation frequency. They are still investigating the specific mechanisms leading to this result, but they have ideas. “What we think happens is that the cell detects and tries to repair the damaged DNA that we’ve added this crosslink to,” Richardson said. “And in doing so, it delays the cell past a checkpoint where it would normally stop this recombination process. And so by prolonging the amount of time that it takes the cell to do this recombination, it makes it more likely that the edits will go to completion.” Studying this new process could also lead to a better understanding about how cells detect editing reagents and how they “decide” to accept them or not, he said. This method will find the most use in ex-vivo gene editing applications, according to the team, that is, in the realm of disease research and preclinical work. “We can more effectively knock down genes and insert things into genomes to study systems outside of the human body in a lab setting,” Ghasemi said. This development allows them to more efficiently build disease models and test hypotheses about how diseases work, which could lead to better clinical and therapeutic approaches. Reference: “Interstrand crosslinking of homologous repair template DNA enhances gene editing in human cells” by Hannah I. Ghasemi, Julien Bacal, Amanda C. Yoon, Katherine U. Tavasoli, Carmen Cruz, Jonathan T. Vu, Brooke M. Gardner and Chris D. Richardson, 27 February 2023, Nature Biotechnology. DOI: 10.1038/s41587-022-01654-y RRG455KLJIEVEWWF 永心鳳茶肉質如何？ 》台中公益路吃爆指南｜10家餐廳逐間介紹一頭牛日式燒肉價格合理嗎？ 》台中公益路美食巡禮｜10家好吃到想回訪印月餐廳有什麼推薦搭配？ 》台中公益路聚餐推薦｜10大類型餐廳評比 |
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