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 茶六燒肉堂飲料值得加點嗎？》公益路餐廳怎麼挑？10家人氣店幫你選 |
| 在地生活｜大台北 2026/04/22 11:33:57 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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%浜中特選昆布鍋物平日好排隊嗎？ 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。加分100%浜中特選昆布鍋物甜點好吃嗎？ 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。印月餐廳春酒場面夠體面嗎？ 下一餐，不妨從這10家開始。加分100%浜中特選昆布鍋物尾牙氣氛熱鬧嗎？ 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。NINI 尼尼臺中店慶生氛圍夠嗎？ 如果你有私心愛店，也歡迎留言分享，一笈壽司需要訂位嗎？ 你的推薦，可能讓我下一趟美食旅程變得更精彩。一頭牛日式燒肉清淡口味適合嗎？ Lifelong production of sperm is made possible by a newly discovered stem cell regulator. According to research conducted by the University of Pennsylvania, the enzyme DOT1L, a stem cell self-renewal factor, is necessary for mice to continue producing sperm throughout adulthood. Men may continue to generate sperm throughout their adult life, in contrast to women who are born with all the eggs they will ever have. To do so, they must constantly renew the spermatogonial stem cells that give birth to sperm. According to research by Jeremy Wang of the University of Pennsylvania School of Veterinary Medicine and colleagues, this stem cell renewal is dependent on a recently identified stem cell self-renewal factor known as DOT1L. The scientists demonstrated that animals lacking DOT1L are unable to retain spermatogonial stem cells, which affects their ability to constantly make sperm. The finding, which was reported in the journal Genes and Development, adds another entity to the handful of stem cell renewal factors that have already been identified by scientists. “This novel factor was only able to be identified by finding this unusual phenotype: the fact that mice lacking DOT1L were not able to continue to produce sperm,” says Wang, the Ralph L. Brinster President’s Distinguished Professor at Penn Vet and a corresponding author on the paper. “Identifying this essential factor not only helps us understand the biology of adult germline stem cells but could also allow us to one day reprogram somatic cells, like a type of skin cell called fibroblasts, to become germline stem cells, essentially creating a gamete in a petri dish. That is the next frontier for fertility treatment.” When the enzyme DOT1L is not functional, spermatogonial stem cells become exhausted, leading to a failure of sperm cell development. This crucial role for DOT1L places it in rarefied company as one of just a handful of known stem cell self-renewal factors, a Penn Vet team found. Credit: Jeremy Wang The Role of DOT1L in Sperm Production The function of DOT1L in stem cell self-renewal was accidentally discovered by the researchers. The gene is widely expressed; mice with a mutant form of DOT1L in every cell do not survive beyond the embryonic stage. However, Wang and colleagues hypothesized that DOT1L could be involved in meiosis, the process of cell division that results in sperm and eggs, based on the genetic expression patterns of DOT1L. So they made the decision to investigate what would happen if they mutated the gene only in these germ cells. “When we did this, the animals lived and appeared healthy,” Wang says. “When we looked closer, however, we found that the mice with the mutant DOT1L in their germ cells could complete an initial round of sperm production, but then the stem cells became exhausted and the mice lost all germ cells.” This drop-off in sperm production could arise due to other problems. But various lines of evidence supported the link between DOT1L and a failure of stem cell self-renewal. In particular, the researchers found that the mice experienced a sequential loss of the various stages of sperm development, first failing to make spermatogonia and then spermatocytes, followed by round spermatids, and then elongated spermatids. In a further experiment, the researchers observed what happened when DOT1L was inactivated in germ cells not from birth, but during adulthood. As soon as Wang and colleagues triggered the DOT1L loss, they observed the same sequential loss of sperm development they had seen in the mice born without DOT1L in their germ cells. Previously, other scientific groups have studied DOT1L in the context of leukemia. Overexpression of the gene in the progenitors of blood cells can lead to malignancy. From that line of investigation, it was known that DOT1L acts as a histone methyltransferase, an enzyme that adds a methyl group to histones to influence gene expression. DOT1L’s Mechanism: Histone Methylation and Gene Regulation To see whether the same mechanism was responsible for the results Wang and his team had observed in sperm development, the researchers treated spermatogonial stem cells with a chemical that blocks the methyltransferase activity of DOT1L. When they did so, the stem cells’ ability to give rise to spermatogonia was significantly reduced. The treatment also impaired the ability of stem cells to tag histones with a methyl group. And when these treated stem cells were transplanted into otherwise healthy mice, the animals’ spermatogonial stem cell activity was cut in half. The team found that DOT1L appeared to be regulating a gene family known as Hoxc, transcription factors that play significant roles in regulating the expression of a host of other genes. “We think that DOT1L promotes the expression of these Hoxc genes by methylating them,” says Wang. “These transcription factors probably contribute to the stem cell self-renewal process. Finding out the details of that is a future direction for our work.” A longer-term goal is to use factors like DOT1L and others involved in germline stem cell self-renewal to help people who have fertility challenges. The concept is to create germ cells from the ground up. “That’s the future of this field: in vitro gametogenesis,” Wang says. “Reprogramming somatic cells to become spermatogonial stem cells is one of the steps. And then we’d have to figure out how to have those cells undergo meiosis. We’re in the early stages of envisioning how to accomplish this multi-step process, but identifying this self-renewal factor brings us one step closer.” Reference: “Histone methyltransferase DOT1L is essential for self-renewal of germline stem cells” by Huijuan Lin, Keren Cheng, Hiroshi Kubota, Yemin Lan, Simone S. Riedel, Kazue Kakiuchi, Kotaro Sasaki, Kathrin M. Bernt, Marisa S. Bartolomei, Mengcheng Luo and P. Jeremy Wang, 23 June 2022, Genes & Development. DOI: 10.1101/gad.349550.122 The study was funded by the Eunice Kennedy Shriver National Institute of Child Health and Human Development, the National Natural Science Foundation of China, the China Scholarship Council, and the Japan Society for the Promotion of Science. A study led by Harvard Medical School researchers has discovered how bacteria break through the brain’s protective layers to cause meningitis, a highly fatal disease. The researchers found that bacteria exploit nerve cells in the meninges to suppress the immune response, allowing the infection to spread. The study identified a chemical released by nerve cells and an immune cell receptor that, when blocked, can interrupt the cascade and prevent bacterial invasion. If replicated through further research, these findings could lead to therapies for this hard-to-treat condition. The treatments would target the early stages of infection before bacteria can spread deep into the brain. Study shows bacteria hijack crosstalk between nerve and immune cells to cause meningitis. A new study led by researchers at Harvard Medical School details the step-by-step cascade that allows bacteria to break through the brain’s protective layers — the meninges — and cause brain infection, or meningitis, a highly fatal disease. The research, conducted in mice and published recently in the journal Nature, shows that bacteria exploit nerve cells in the meninges to suppress the immune response and allow the infection to spread into the brain. “We’ve identified a neuroimmune axis at the protective borders of the brain that is hijacked by bacteria to cause infection — a clever maneuver that ensures bacterial survival and leads to widespread disease,” said study senior author Isaac Chiu, associate professor of immunology in the Blavatnik Institute at HMS. Scientists have identified the maneuvers bacteria use to invade the brain and cause meningitis. Shown here are pain receptors (in red) in the brain’s protective layers, known as meninges. When activated by bacteria, pain receptors release a chemical that disables the normal protective functions of immune cells known as macrophages (in blue), weakening the brain’s defenses. Credit: Chiu Lab/Harvard Medical School The study identifies two central players in this molecular chain of events that leads to infection — a chemical released by nerve cells and an immune cell receptor blocked by the chemical. The study experiments show that blocking either one can interrupt the cascade and thwart the bacterial invasion. If replicated through further research, the new findings could lead to much-needed therapies for this hard-to-treat condition that often leaves those who survive with serious neurologic damage. Such treatments would target the critical early steps of infection before bacteria can spread deep into the brain. “The meninges are the final tissue barrier before pathogens enter the brain, so we have to focus our treatment efforts on what happens at this border tissue,” said study first author Felipe Pinho-Ribeiro, a former post-doctoral researcher in the Chiu lab, now an assistant professor at Washington University in St. Louis. A Recalcitrant Disease in Need of New Treatments More than 1.2 million cases of bacterial meningitis occur globally each year, according to the U.S. Centers for Disease Control and Prevention. Untreated, it kills seven out of 10 people who contract it. Treatment can reduce mortality to three in 10. However, among those who survive, one in five experience serious consequences, including hearing or vision loss, seizures, chronic headache, and other neurological problems. Current therapies — antibiotics that kill bacteria and steroids that tame infection-related inflammation — can fail to ward off the worst consequences of the disease, particularly if therapy is initiated late due to delays in diagnosis. Inflammation-reducing steroids tend to suppress immunity, weakening protection further and fueling infection spread. Thus, physicians must strike a precarious balance: They must rein in brain-damaging inflammation with steroids, while also ensuring that these immunosuppressive drugs do not further disable the body’s defenses. The need for new treatments is magnified by the lack of a universal meningitis vaccine. Many types of bacteria can cause meningitis, and designing a vaccine for all possible pathogens is impractical. Current vaccines are formulated to protect against only some of the more common bacteria known to cause meningitis. Vaccination is recommended only for certain populations deemed at high risk for bacterial meningitis. Additionally, vaccine protection wanes after several years. Chiu and colleagues have long been fascinated by the interplay between bacteria and the nervous and immune systems and by how the crosstalk between nerve cells and immune cells may either precipitate or ward off disease. Previous research led by Chiu has shown that the interaction between neurons and immune cells plays a role in certain types of pneumonia and in flesh-destroying bacterial infections. This time around, Chiu and Pinho-Ribeiro turned their attention to meningitis — another condition in which they suspected the relationship between nervous and immune systems plays a role. The meninges are three membranes that lie atop one another, wrapping the brain and spinal cord to shield the central nervous system from injury, damage, and infection. The outermost of the three layers — called dura mater — contains pain neurons that detect signals. Such signals could come in the form of mechanical pressure — blunt force from impact or toxins that make their way into the central nervous system through the bloodstream. The researchers focused precisely on this outermost layer as the site of initial interaction between bacteria and protective border tissue. Recent research has revealed that the dura mater also harbors a wealth of immune cells, and that immune cells and nerve cells reside right next to each other — a clue that captured Chiu’s and Pinho-Ribeiro’s attention. “When it comes to meningitis, most of the research so far has focused on analyzing brain responses, but responses in the meninges — the barrier tissue where infection begins — have remained understudied,” Ribeiro said. What exactly happens in the meninges when bacteria invade? How do they interact with the immune cells residing there? These questions remain poorly understood, the researchers said. How Bacteria Break Through the Brain’s Protective Layers In this particular study, the researchers focused on two pathogens —Streptococcus pneumoniae and Streptococcus agalactiae, leading causes of bacterial meningitis in humans. In a series of experiments, the team found that when bacteria reach the meninges, the pathogens trigger a chain of events that culminates in disseminated infection. First, researchers found that bacteria release a toxin that activates pain neurons in the meninges. The activation of pain neurons by bacterial toxins, the researchers noted, could explain the severe, intense headache that is a hallmark of meningitis. Next, the activated neurons release a signaling chemical called CGRP. CGRP attaches to an immune-cell receptor called RAMP1. RAMP1 is particularly abundant on the surface of immune cells called macrophages. Once the chemical engages the receptor, the immune cell is effectively disabled. Under normal conditions, as soon as macrophages detect the presence of bacteria, they spring into action to attack, destroy, and engulf them. Macrophages also send distress signals to other immune cells to provide a second line of defense. The team’s experiments showed that when CGRP gets released and attaches to the RAMP1 receptor on macrophages, it prevented these immune cells from recruiting help from fellow immune cells. As a result, the bacteria proliferated and caused widespread infection. To confirm that the bacterially induced activation of pain neurons was the critical first step in disabling the brain’s defenses, the researchers checked what would happen to infected mice lacking pain neurons. Mice without pain neurons developed less severe brain infections when infected with two types of bacteria known to cause meningitis. The meninges of these mice, the experiments showed, had high levels of immune cells to combat the bacteria. By contrast, the meninges of mice with intact pain neurons showed meager immune responses and far fewer activated immune cells, demonstrating that neurons get hijacked by bacteria to subvert immune protection. To confirm that CGRP was, indeed, the activating signal, researchers compared the levels of CGRP in meningeal tissue from infected mice with intact pain neurons and meningeal tissue from mice lacking pain neurons. The brain cells of mice lacking pain neurons had barely detectable levels of CGRP and few signs of bacterial presence. By contrast, meningeal cells of infected mice with intact pain neurons showed markedly elevated levels of both CGRP and more bacteria. In another experiment, the researchers used a chemical to block the RAMP1 receptor, preventing it from communicating with CGRP, the chemical released by activated pain neurons. The RAMP1 blocker worked both as preventive treatment before infection and as a treatment once infection had occurred. Mice pretreated with RAMP1 blockers showed reduced bacterial presence in the meninges. Likewise, mice that received RAMP1 blockers several hours after infection and regularly thereafter had milder symptoms and were more capable of clearing bacteria, compared with untreated animals. A Path to New Treatments The experiments suggest drugs that block either CGRP or RAMP1 could allow immune cells to do their job properly and increase the brain’s border defenses. Compounds that block CGRP and RAMP1 are found in widely used drugs to treat migraine, a condition believed to originate in the top meningeal layer, the dura mater. Could these compounds become the basis for new medicines to treat meningitis? It’s a question the researchers say merits further investigation. One line of future research could examine whether CGRP and RAMP1 blockers could be used in conjunction with antibiotics to treat meningitis and augment protection. “Anything we find that could impact treatment of meningitis during the earliest stages of infection before the disease escalates and spreads could be helpful either to decrease mortality or minimize the subsequent damage,” Pinho-Ribeiro said. More broadly, the direct physical contact between immune cells and nerve cells in the meninges offers tantalizing new avenues for research. “There has to be an evolutionary reason why macrophages and pain neurons reside so closely together,” Chiu said. “With our study, we’ve gleaned what happens in the setting of bacterial infection, but beyond that, how do they interact during viral infection, in the presence of tumor cells, or the setting of brain injury? These are all important and fascinating future questions.” Reference: “Bacteria hijack a meningeal neuroimmune axis to facilitate brain invasion” by Felipe A. Pinho-Ribeiro, Liwen Deng, Dylan V. Neel, Ozge Erdogan, Himanish Basu, Daping Yang, Samantha Choi, Alec J. Walker, Simone Carneiro-Nascimento, Kathleen He, Glendon Wu, Beth Stevens, Kelly S. Doran, Dan Levy and Isaac M. Chiu, 1 March 2023, Nature. DOI: 10.1038/s41586-023-05753-x Co-authors included Liwen Deng, Dylan Neel, Himanish Basu, Daping Yang, Samantha Choi, Kathleen He, Alec Walker, Glendon Wu, and Beth Stevens of Harvard Medical School; Ozge Erdogan, of the Harvard School of Dental Medicine; Kelly Doran of the University of Colorado; Dan Levy and Simone Carneiro-Nascimento of Beth Israel Deaconess Medical Center. This work was supported by National Institutes of Health (NIH) grants R01AI130019, R01DK127257, 2R01NS078263, 5R01NS115972, P50MH112491, R01NS116716, T32GM007753; by the Burroughs Wellcome Fund, the Kenneth Rainin Foundation, the Food Allergy Science Initiative, the Fairbairn Lyme Initiative; with additional support from the Harvard Medical School Immunology Undergraduate Summer Program. Chiu and Ribeiro are inventors on U.S. patent application 2021/0145937A1, “Methods and Compositions for Treating a Microbial Infection,” which includes targeting CGRP and its receptors to treat infections. The Chiu lab receives research support from Abbvie/Allergan and Moderna, Inc. Oil painting by Victor Eustaphieff of Darwin in his study at Down House with one of his bookcases that made up his extensive personal library reflected in the mirror. Credit: Reproduced with kind permission by State Darwin Museum, Moscow. Charles Darwin – arguably the most influential man of science in history, accumulated a vast personal library throughout his working life. Until now, 85 percent of its contents were unknown or unpublished. This year, coinciding with Darwin’s 215th birthday, The Complete Work of Charles Darwin Online, the scholarly project helmed by Dr. John van Wyhe at the National University of Singapore (NUS) Department of Biological Sciences, has released an online 300-page catalog detailing Darwin’s complete personal library, with 7,400 titles across 13,000 volumes and items including books, pamphlets, and journals. Previous lists only had 15 percent of his whole collection. Darwin’s library has also been virtually re-assembled with 9,300 links to copies of the works freely available online. “This unprecedentedly detailed view of Darwin’s complete library allows one to appreciate more than ever that he was not an isolated figure working alone but an expert of his time building on the sophisticated science and studies and other knowledge of thousands of people. Indeed, the size and range of works in the library makes manifest the extraordinary extent of Darwin’s research into the work of others,” said Dr van Wyhe. The frontispiece of the Principles of Geology, volume 1 by Charles Lyell, a book from which Darwin drew inspiration to explain how species change over time. Credit: NUS Discovering Darwin’s complete library After his death in 1882, much of Darwin’s library was preserved and cataloged, but many other items were dispersed or lost, and details of the vast majority of the contents have never been published until now. For many years, scholars have referred to Darwin’s library as containing 1,480 books, based on those that survive in the two main collections, the University of Cambridge and Down House. Over 18 years the Darwin Online project has identified thousands of Darwin’s obscure references in his own catalogs and lists of items such as pamphlets and journals that were originally in his library. Each reference required its own detective story to discover the publications that Darwin had hurriedly recorded. In addition, missing details such as author, date or the source of clippings in thousands of records from older catalogs have been identified for the first time. A major source of information that helped to reveal the original contents is the 426-page handwritten “Catalogue of the Library of Charles Darwin”, compiled from 1875. A painstaking comparison of its abbreviated entries revealed 440 unknown titles that were originally in the library. An inventory of his homemade after his death recorded 2,065 bound books and an unknown number of unbound volumes and pamphlets. In the drawing-room, 133 titles and 289 volumes of mostly unscientific literature were recorded. Amazingly, the legacy duty valuer estimated that the “Scientific Library that is books relating to Science” was worth only 30 pounds and 12 shillings [about £2,000 today] Indeed, all the books were valued at only 66 pounds and 10 shillings [about £4,400 today]. Today any book that belonged to Darwin is worth a great deal to collectors. Two historic images, a photograph (left) and an etching (right), are here combined to show the bookcases in his study. Credit: Reproduced with kind permission by Darwin Online Other sources of information that helped to build Darwin’s complete library were lists of pamphlets, Darwin’s reading notebooks, Emma Darwin’s diaries, the Catalogue of books given to the Cambridge Botany School in 1908 and the 30 volumes of the Darwin Correspondence. Items that still exist but were never included in the lists of Darwin’s library include his unbound materials at Cambridge University Library, books now in other institutional collections, private collections and books sold at auctions over the past 130 years. Combining these and many other sources of evidence allowed Darwin’s library to be reconstructed. For example, Darwin’s copy of an 1826 article by the ornithologist John James Audubon: ‘Account of the habits of the Turkey Buzzard (Vultura aura), particularly with the view of exploding the opinion generally entertained of its extraordinary power of smelling’ was sold in 1975. Darwin had investigated this point during the voyage of the Beagle and recorded reading a critic of Audubon in the lost Galapagos notebook. In 2019, a copy of Elizabeth Gaskell’s 1880 novel Wives and daughters appeared at auction. A note in it records: “This book was a great favourite of Charles Darwin’s and the last book to be read aloud to him.” An issue of a German scientific periodical was sent to Darwin in 1877 that contained the first published photographs of bacteria. Credit: NUS Understanding Darwin’s library Most of the works in Darwin’s library are, unsurprisingly, on scientific subjects, especially biology and geology. Yet, the library also included works on farming, animal breeding and behavior, geographical distribution, philosophy, psychology, religion, and other topics that interested Darwin, such as art, history, travel, and language. Most of the works are in English, but almost half are in other languages, especially German, French, and Italian as well as Dutch, Danish, Spanish, Swedish, and Latin. Some of the hundreds of books not previously known to be in Darwin’s library include Sun Pictures, a 1872 coffee table book showcasing photographs of artworks. Another book that the we did not know that the Darwins purchased was a copy of the popular science book on gorillas that was all the rage just after Origin of species was published: Paul Du Chaillu’s Explorations and adventures in equatorial Africa. Of the thousands of shorter items were also found in Darwin’s library, such as an issue of a German scientific periodical sent to him in 1877 that contained the first published photographs of bacteria and another article amusingly entitled The hateful or Colorado grasshopper. In his complete library, Darwin’s eclectic sources are there for all to see. Click to view The Complete Library of Charles Darwin Click to view Introduction to the Library by John van Wyhe RRG455KLJIEVEWWF |
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