|
|
文章數:88 |
NINI 尼尼台中店商務聚餐適合嗎?》台中公益路美食巡禮|10家好吃到想回訪 |
| 休閒生活|旅人手札 2026/04/20 15:30:35 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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 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%浜中特選昆布鍋物好吃嗎? 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。一笈壽司適合約會嗎? 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。一頭牛日式燒肉公司聚餐適合嗎? 下一餐,不妨從這10家開始。印月餐廳節慶時段會不會太難訂位? 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。TANG Zhan 湯棧商務聚餐適合嗎? 如果你有私心愛店,也歡迎留言分享,一笈壽司人潮很多嗎? 你的推薦,可能讓我下一趟美食旅程變得更精彩。TANG Zhan 湯棧清淡口味適合嗎? A recent study uncovers a direct link between the protein p53 and autism-like behavior in mice, revealing its crucial role in managing sociability, repetitive actions, and learning and memory related to the hippocampus. New findings shed light on the link between the TP53 protein-coding gene and neurodevelopmental and psychiatric conditions such as autism spectrum disorder. Researchers have established that the protein p53 plays a crucial role in managing sociability, repetitive behavior, and learning and memory related to the hippocampus in mice. This finding sheds light on the connection between the TP53 protein-coding gene and neurodevelopmental and psychiatric conditions such as autism spectrum disorder. “This study shows for the first time that p53 is linked directly to autism-like behavior,” said Nien-Pei Tsai, an associate professor of molecular and integrative biology at the University of Illinois Urbana-Champaign and a researcher at the Beckman Institute for Advanced Science and Technology. Researchers at the University of Illinois Urbana-Champaign’s Beckman Institute for Advanced Science and Technology led by Professor Nien-Pei Tsai (right) and Kwan Young Lee have established the protein p53 as critical for regulating sociability, repetitive behavior, and hippocampus-related learning and memory in mice, illuminating the relationship between the protein-coding gene TP53 and neurodevelopmental and psychiatric disorders like autism spectrum disorder. Credit: University of Illinois/L. Brian Stauffer In living systems, genes act as a biological version of binary code, using the letters A, C, G, and T instead of ones and zeroes to spell out cellular marching orders. Some genes — called coding genes — instruct cells to create proteins with specific functions. For example, the gene TP53 instructs cells to create the protein p53; its job is to regulate how other genes are expressed. In this study, Tsai and his colleagues lowered hippocampal p53 levels in mice, looking for changes in gene expressions related to behavior. They observed that the decreased p53 levels: Promoted repetitive behavior in mice. Reduced sociability in mice. Impaired hippocampus-dependent learning and memory, especially in male mice. The researchers also observed that p53 levels were elevated after a period of active communication between hippocampal neurons called long-term potentiation. Flexible neuron firing — known as plasticity — is related to positive learning and memory outcomes. Nien-Pei Tsai, a researcher at the Beckman Institute for Advanced Science and Technology at the University of Illinois Urbana-Champaign, led a team of researchers to establish the protein p53 as critical for regulating sociability, repetitive behavior, and hippocampus-related learning and memory in mice, illuminating the relationship between the protein-coding gene TP53 and neurodevelopmental and psychiatric disorders like autism spectrum disorder. Credit: University of Illinois Urbana-Champaign School of Molecular and Cellular Biology In a 2018 study, Tsai and his colleagues identified p53 as a key protein involved in the irregular brain cell activity seen in ASD and epilepsy. In future studies, they aim to explore how p53 coordinates the expression of those autism-linked genes to guide behavior. Reference: “Tumor suppressor p53 modulates activity-dependent synapse strengthening, autism-like behavior and hippocampus-dependent learning” by Kwan Young Lee, Haohan Wang, Yeeun Yook, Justin S. Rhodes, Catherine A. Christian-Hinman and Nien-Pei Tsai, 28 September 2023, Molecular Psychiatry. DOI: 10.1038/s41380-023-02268-9 The study was funded by the National Institutes of Health. In wild-type plant cells, lattice-bound Msd1 (filled green circle) recruits cytoplasmic Wdr8 (open green circle) to form a heteromeric complex, which is translocated to and associated with a microtubule nucleation complex (orange) on a preexisting microtubule (green line). After nucleation of a daughter microtubule, Msd1-Wdr8 stabilizes the base of the Y-shaped nucleation structure and then recruit katanin (red) to sever the basal end of the daughter microtubule. Credit: Takashi Hashimoto Researchers from Nara Institute of Science and Technology find that an anchoring complex stabilizes microtubule creation sites within plant cells, then recruits katanin — named after the katana sword — to cut new microtubules. The katana, a Japanese sword, may be thought of solely as a weapon used by the samurai. But researchers from Japan have discovered that not only do plants wield their own katanas within their cells, they recruit them to specific locations within those cells to do their work. In a study published in Nature Communications, researchers from Nara Institute of Science and Technology have revealed that the enzyme katanin, which is named after the katana, is used by an anchoring complex to cut microtubules at specific locations of the framework within individual plant cells. Katanin severs microtubules in cells, which is an important step in cell division and central to the development of many organisms, including plants and animals. Microtubules form part of the cytoskeleton, a complex network of protein filaments found in all cells. The severing performed by katanin enables mobility, which is important during development, and treadmilling — a phenomenon where one end of a filament lengthens as the other shrinks, which results in a section of filament that seems to ‘move’ like a treadmill. “Katanin severs microtubules at specific locations in plant and animal cells, and this leads to active reorganization of the microtubule cytoskeleton,” says senior author of the study Takashi Hashimoto. “But the mechanisms for targeting this extraordinary enzyme at specific sites within the cell are not well understood — these are what we wanted to investigate.” The team’s genetic and cell biology research results showed that the microtubule anchoring complex Msd1-Wdr8 is used to stabilize microtubule nucleation sites (where microtubules are formed) in plant cells to prevent early release of the new microtubules (called ‘daughter microtubules’). But in a seemingly counterintuitive twist, Msd1-Wdr8 then turns around and recruits katanin to the same location to enable the efficient release of daughter microtubules. “These ‘glue-and-cut’ functions performed by Msd1-Wdr8 and their effects on microtubule stability may seem confusing at first, but they probably enable strict control of microtubule release by the katanin activity,” explains Hashimoto. This study will inform future research on whether the Msd1-Wdr8 complex in animal cells also recruits katanin, and whether other sites use similar mechanisms for the stabilization and release of daughter microtubules. The results of this study will be of interest to cell biologists, especially those working on cytoskeletons, in plants and other organisms. Reference: “An anchoring complex recruits katanin for microtubule severing at the plant cortical nucleation sites” by Noriyoshi Yagi, Takehide Kato, Sachihiro Matsunaga, David W. Ehrhardt, Masayoshi Nakamura and Takashi Hashimoto, 17 June 2021, Nature Communications. DOI: 10.1038/s41467-021-24067-y Researchers from the Salk Institute, in a global collaboration, have produced a detailed atlas of human brain cells by analyzing over half a million cells. The study, part of the NIH’s BRAIN Initiative, marks a pivotal shift in understanding brain cell diversity and function. The new research, part of the NIH BRAIN Initiative, paves the way toward treating, preventing, and curing brain disorders. Salk Institute researchers, as part of a larger collaboration with research teams around the world, analyzed more than half a million brain cells from three human brains to assemble an atlas of hundreds of cell types that make up a human brain in unprecedented detail. The research, published in a special issue of the journal Science on October 13, 2023, is the first time that techniques to identify brain cell subtypes originally developed and applied in mice have been applied to human brains. “These papers represent the first tests of whether these approaches can work in human brain samples, and we were excited at just how well they translated,” says Professor Joseph Ecker, director of Salk’s Genomic Analysis Laboratory and a Howard Hughes Medical Institute investigator. “This is really the beginning of a new era in brain science, where we will be able to better understand how brains develop, age, and are affected by disease.” The BRAIN Initiative and Brain Cell Diversity The new work is part of the National Institute of Health’s Brain Research Through Advancing Innovative Neurotechnologies Initiative, or The BRAIN Initiative, an effort launched in 2014 to describe the full plethora of cells—as characterized by many different techniques—in mammalian brains. Salk is one of three institutions awarded grants to act as central players in generating data for the NIH BRAIN Initiative Cell Census Network, BICCN. An abstract representation of cell diversity in the brain. Individual nuclei are colored in the bright hues of t-SNE plots used in epigenomics analysis to distinguish individual brain cell types. Layers of background color represent the local environmental factors of each brain region that influence cell function. Credit: Michael Nunn Every cell in a human brain contains the same sequence of DNA, but in different cell types different genes are copied onto strands of RNA for use as protein blueprints. This ultimate variation in which proteins are found in which cells—and at what levels—allows the vast diversity in types of brain cells and the complexity of the brain. Knowing which cells rely on which DNA sequences to function is critical not only to understanding how the brain works, but also how mutations in DNA can cause brain disorders and, relatedly, how to treat those disorders. “Once we scale up our techniques to a large number of brains, we can start to tackle questions that we haven’t been able to in the past,” says Margarita Behrens, a research professor in Salk’s Computational Neurobiology Laboratory and a co-principal investigator of the new work. From Mice to Men: Adapting Research Techniques In 2020, Ecker and Behrens led the Salk team that profiled 161 types of cells in the mouse brain, based on methyl chemical markers along DNA that specify when genes are turned on or off. This kind of DNA regulation, called methylation, is one level of cellular identity. In the new paper, the researchers used the same tools to determine the methylation patterns of DNA in more than 500,000 brain cells from 46 regions in the brains of three healthy adult male organ donors. While mouse brains are largely the same from animal to animal, and contain about 80 million neurons, human brains vary much more and contain about 80 billion neurons. “It’s a big jump from mice to humans and also introduces some technical challenges that we had to overcome,” says Behrens. “But we were able to adapt things that we had figured out in mice and still get very high quality results with human brains.” Innovative Techniques and Collaborative Efforts At the same time, the researchers also used a second technique, which analyzed the three-dimensional structure of DNA molecules in each cell to get additional information about what DNA sequences are being actively used. Areas of DNA that are exposed are more likely to be accessed by cells than stretches of DNA that are tightly folded up. “This is the first time we’ve looked at these dynamic genome structures at a whole new level of cell type granularity in the brain, and how those structures may regulate which genes are active in which cell types,” says Jingtian Zhou, co-first author of the new paper and a postdoctoral researcher in Ecker’s lab. Other research teams whose work is also published in the special issue of Science used cells from the same three human brains to test their own cell profiling techniques, including a group at UC San Diego led by Bing Ren—also a co-author in Ecker and Behrens’ study. Ren’s team revealed a link between specific brain cell types and neuropsychiatric disorders, including schizophrenia, bipolar disorder, Alzheimer’s disease, and major depression. Additionally, the team developed artificial intelligence deep learning models that predict risk for these disorders. A diagram demonstrating how “barCodes” (“scMCodes”) can be used to identify and classify cell types in the brain. The image shows an anatomical brain cross section, an abstraction of the brain with regions represented as colored circles (blue, red, green, and yellow), and a barcode to represent the technique used by the scientists. Credit: Salk Institute Other groups in the global collaboration focused on measuring levels of RNA to group cells together into subtypes. The groups found a high level of correspondence in each brain region between which genes were activated, based on the DNA studies by Ecker and Behrens’ team, and which genes were found to be transcribed into RNA. The Road Ahead: More Discoveries Await Since the new Salk research was intended as a pilot study to test the efficacy of the techniques in human brains, the researchers say they can’t yet draw conclusions about how many cell types they might uncover in the human brain or how those types differ between mice and humans. “The potential to find unique cell types in humans that we don’t see in mice is really exciting,” says Wei Tian, co-first author of the new paper and a staff scientist in Ecker’s lab. “We’ve made amazing progress but there are always more questions to ask.” In 2022, the NIH Brain Initiative launched a new BRAIN Initiative Cell Atlas Network (BICAN), which will follow up the BICCN efforts. At Salk, a new Center for Multiomic Human Brain Cell Atlas funded through BICAN aims to study cells from over a dozen human brains and ask questions about how the brain changes during development, over people’s lifespans, and with disease. That more detailed work on a larger number of brains, Ecker says, will pave the way toward a better understanding of how certain brain cell types go awry in brain disorders and diseases. “We want to have a full understanding of the brain across the lifespan so that we can pinpoint exactly when, how, and in which cell types things go wrong with disease—and potentially prevent or reverse those harmful changes,” says Ecker. Reference: “Single-cell DNA methylation and 3D genome architecture in the human brain” by Wei Tian, Jingtian Zhou, Anna Bartlett, Qiurui Zeng, Hanqing Liu, Rosa G. Castanon, Mia Kenworthy, Jordan Altshul, Cynthia Valadon, Andrew Aldridge, Joseph R. Nery, Huaming Chen, Jiaying Xu, Nicholas D. Johnson, Jacinta Lucero, Julia K. Osteen, Nora Emerson, Jon Rink, Jasper Lee, Yang E. Li, Kimberly Siletti, Michelle Liem, Naomi Claffey, Carolyn O’Connor, Anna Marie Yanny, Julie Nyhus, Nick Dee, Tamara Casper, Nadiya Shapovalova, Daniel Hirschstein, Song-Lin Ding, Rebecca Hodge, Boaz P. Levi, C. Dirk Keene, Sten Linnarsson, Ed Lein, Bing Ren, M. Margarita Behrens and Joseph R. Ecker, 13 October 2023, Science. DOI: 10.1126/science.adf5357 Other authors of the paper are Anna Bartlett, Qiurui Zeng, Hanqing Liu, Rosa G. Castanon, Mia Kenworthy, Jordan Altshul, Cynthia Valadon, Andrew Aldridge, Joseph R. Nery, Huaming Chen, Jiaying Xu, Nicholas D. Johnson, Jacinta Lucero, Julia K. Osteen, Nora Emerson, Jon Rink, Jasper Lee, Michelle Liem, Naomi Claffey and Caz O’Connor of Salk; Yang Li and Bing Ren of the Ludwig Institute for Cancer Research at UC San Diego; Kimberly Siletti and Sten Linnarsson of the Karolinska Institutet; Anna Marie Yanny, Julie Nyhus, Nick Dee, Tamara Casper, Nadiya Shapovalova, Daniel Hirschstein, Rebecca Hodge, Boaz P. Levi and Ed Lein of the Allen Institute for Brain Science; and C. Dirk Keene of the University of Washington. The work was supported by grants from the National Institute of Mental Health (U01MH121282, UM1 MH130994, NIMH U01MH114812), the National Institutes of Health BRAIN Initiative (NCI CCSG: P30 014195), the Nancy and Buster Alvord Endowment, and the Howard Hughes Medical Institute. RRG455KLJIEVEWWF |
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| 最新創作 |
|
||||
|
||||
|
||||
|
||||
|
||||



























