陳紋珮的購物守則

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。

評分項目	滿分5分	評比重點
環境氛圍	⭐⭐⭐⭐⭐	用餐空間是否舒適、有設計感、適合聚會或約會
口味表現	⭐⭐⭐⭐⭐	餐點是否新鮮、調味平衡、有無記憶點
CP值	⭐⭐⭐⭐⭐	價位與份量是否合理，是否值得回訪
再訪意願	⭐⭐⭐⭐⭐	整體體驗是否令人想再來、服務是否加分

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。

餐廳名稱	料理類型	價位範圍（每人）	推薦菜色	適合族群	我的評價摘要
1️⃣ 一頭牛日式燒肉	和牛燒肉	$1200~$1400	A5和牛拼盤、 旬味野炊飯	情侶慶祝、燒肉愛好者	肉質頂級、陶瓷烤爐，沒有用木炭
2️⃣ TANG Zhan 湯棧	火鍋 / 麻香鍋	$500–$800	麻香鍋、麻油雞鍋	情侶、朋友、文青聚會	文青風火鍋代表，湯底濃郁卻不膩、環境質感佳
3️⃣ NINI 尼尼臺中店	義式料理 / 早午餐	$400–$700	松露燉飯、薄餅披薩	姊妹聚會、家庭聚餐	採光好、氣氛輕鬆，餐點份量實在
4️⃣ 加分100%浜中特選昆布鍋物	北海道鍋物	$400–$700	牛奶昆布鍋、海鮮拼盤	家庭聚餐、親子用餐	湯底細緻清爽、CP值高、服務親切
5️⃣ 印月餐廳	中式創意料理 / 宴會餐廳	$800–$1500	松露雞湯、蒜香牛肋條	商務宴客、家庭聚餐	菜色融合創意與傳統，氣氛高雅
6️⃣ KoDō 和牛燒肉	高檔日式燒肉	$1200–$2000	冷藏肋眼、壽喜燒套餐	節慶慶祝、燒肉控	儀式感十足、肉質極佳、服務細膩
7️⃣ 永心鳳茶	臺式茶館 / 早午餐	$300–$500	炸雞腿飯、鳳茶甜點	姊妹下午茶、親子餐聚	茶香融入料理，氛圍優雅放鬆
8️⃣ 三希樓	江浙菜 / 港點	$600–$900	小籠包、東坡肉	家庭聚餐、長輩慶生	火候精準、味道穩定，傳統中菜代表
9️⃣ 一笈壽司	日式壽司 / 無菜單料理	$1000–$1500	握壽司套餐、生魚片	日料控、紀念日用餐	食材新鮮、主廚手藝細膩，私密高雅
🔟 茶六燒肉堂	和牛燒肉 / 精緻套餐	$700–$1000	厚切牛舌、和牛拼盤	家庭、情侶、朋友聚餐	品質穩定、氣氛熱絡，年輕族群最愛

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」。
嚴選的和牛部位，共八個部位、十樣餐點，讓人能從牛頭一路品嘗到牛尾。
油花分布均勻、切片厚薄恰好，經過炭火烤炙後香氣四溢，焦香與油脂在口中交融，入口即化的滑順感令人難忘。
值得一提的是，一頭牛的菜單設計十分彈性
想要一次體驗完整套餐也可以，偏好客製口味則能自由單點組合，不受套餐限制，想吃什麼就點什麼。
而且每桌都能選擇「自行燒烤」或「專人代烤」服務，代烤師的火侯掌握與節奏讓整體體驗更輕鬆愉快。
除了主角和牛，旬味野炊飯 與 主廚冰淇淋 也是隱藏版亮點，前者粒粒分明、香氣撲鼻；後者以香草與焙茶為基底，隨季節更換口味，完美收尾。整體服務親切熱情，特別是壽星還能享有 生日畫盤驚喜，讓慶祝時刻更添儀式感。

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。
如果是第一次約會或慶祝特別節日，這裡的氛圍既不尷尬又不吵鬧，是營造氣氛的理想選擇。

綜合評分

評分項目	分數（滿分5分）	評語
環境氛圍	⭐⭐⭐⭐⭐	光線柔和、氣氛沉穩，極具日式質感
口味表現	⭐⭐⭐⭐⭐	A5和牛入口即化、炭香迷人
CP值	⭐⭐⭐⭐	價格略高但品質與服務對得起價位
再訪意願	⭐⭐⭐⭐⭐	適合慶祝、約會，一吃就難忘的燒肉店

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。
若要在公益路找一間能讓人「邊吃邊微笑」的燒肉店，一頭牛 絕對值得列入你的必訪清單。

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。
黑灰調的現代外觀、搭配微霧玻璃與招牌的「湯棧」燈字，呈現出一種低調的時尚感。
店內設計延續品牌主題，以「湯」為靈魂打造整體體驗，從裝潢到香氣，都有濃厚的溫潤氣息。

餐點特色

湯棧最有名的當然是它的「麻香鍋」。
湯底以雞骨與多種辛香料慢熬，香氣濃郁卻不嗆辣，入口後會在喉間留下柔和的花椒香。
「招牌麻油雞鍋」與「黃金牛奶鍋」也是人氣選項，特別是在冬天，溫潤的湯底配上滑嫩肉片，讓人每一口都覺得暖心。
他們的「滷肉飯」和「香蔥豆腐皮」更是許多老客人必點的靈魂配角，簡單卻有記憶點。

用餐體驗

整體氛圍比一般火鍋店更有質感。
桌距寬敞、燈光柔和，店員動作俐落又親切。即使客滿，也不會感覺吵雜或壓迫。
不論是一個人想靜靜吃鍋、或是朋友聚餐，湯棧都能給你剛剛好的距離與溫度。
值得一提的是，上菜速度快、湯底續湯毫不手軟，細節服務到位。

綜合評分

評分項目	分數（滿分5分）	評語
環境氛圍	⭐⭐⭐⭐⭐	文青感強、光線柔和，是拍照好選擇
口味表現	⭐⭐⭐⭐☆	麻香濃郁、湯頭層次豐富、不油不膩
CP值	⭐⭐⭐⭐	份量足、價格中等偏上
再訪意願	⭐⭐⭐⭐⭐	冬天或雨天時會特別想再訪的火鍋店

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。
此外，他們的薄餅披薩相當受歡迎，餅皮薄脆、餡料新鮮，是三五好友共享的好選擇。

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

評分項目	分數（滿分5分）	評語
環境氛圍	⭐⭐⭐⭐⭐	採光好、座位寬敞，氛圍悠閒舒適
口味表現	⭐⭐⭐⭐	義式風味穩定，燉飯與披薩表現亮眼
CP值	⭐⭐⭐⭐	價位合理、份量實在
再訪意願	⭐⭐⭐⭐	適合假日早午餐或輕鬆聚會再訪

地址：40861臺中市南屯區公益路二段18號

電話：04-23288498

官網：https://nini.com.tw/

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。
我這次點的是「牛奶昆布鍋」，入口時奶香與昆布香完美融合，搭配新鮮的牛五花肉片，滑順又不膩。
菜盤走健康取向，蔬菜比例高，連玉米、南瓜、豆皮都能吃出甜味；附餐的烏龍麵Q彈有嚼勁，吃完十分有飽足感。

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。
最難得的是，即使價位不高，食材新鮮度仍維持得很好，能感受到店家對品質的堅持。

綜合評分

評分項目	分數（滿分5分）	評語
環境氛圍	⭐⭐⭐⭐	簡約乾淨、座位舒適，適合家庭聚餐
口味表現	⭐⭐⭐⭐☆	湯頭清爽細緻、奶香與昆布香交融自然
CP值	⭐⭐⭐⭐⭐	份量足、價位親民，整體表現超值
再訪意願	⭐⭐⭐⭐☆	想吃鍋又不想花太多時的首選

地址：403臺中市西區公益路288號

電話：0910855180

官網：https://giafine100.com/

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。
如果你想在公益路找一間可以放心帶家人一起吃的鍋物店，這裡絕對會讓人感到「加分」不少。

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。
走進印月，挑高的空間、柔和的燈光與木質桌椅構成沉穩的氛圍。
不論是家庭聚餐、商務宴客，還是節日慶祝，都能找到恰到好處的格調。

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。
這次我品嚐的「松露雞湯」香氣濃郁、層次分明，一口下去既有中式的溫潤感，又帶出西式松露的奢華香氣。
「蒜香牛肋條」則是另一道招牌菜，外酥內嫩、油香十足，咬下去肉汁在口中散開，搭配特調醬汁非常過癮。
此外，他們的創意港點如「麻辣小籠包」與「金沙流沙包」也深受年輕客群喜愛，既保留經典又玩出新意。

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。
雖然價位偏中高，但在這樣的氛圍與品質下，物有所值。

綜合評分

評分項目	分數（滿分5分）	評語
環境氛圍	⭐⭐⭐⭐⭐	典雅寬敞、氣氛沈穩，宴客首選
口味表現	⭐⭐⭐⭐⭐	每道菜都有層次與記憶點，融合創意與傳統
CP值	⭐⭐⭐⭐	價位偏高但品質穩定
再訪意願	⭐⭐⭐⭐☆	節慶或招待長輩時會再次選擇

地址：408臺中市南屯區公益路二段818號

電話：0422511155

官網：https://wein818.com/

小結語

印月餐廳是一間「不只吃飯，更像品味生活」的地方。
它成功地讓中式料理不再只是圓桌菜，而是能展現質感、講究細節的美食體驗。
若你在找一間能同時滿足味蕾與體面的餐廳，印月 絕對是公益路上的不敗經典。

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」。
隱身在公益路一隅，KoDō 的外觀低調典雅，店內以深色木質調與間接照明營造出沉穩氛圍。
從踏入店門那一刻開始，服務人員的態度、動線、聲音控制，全都精準到位，讓人彷彿走進日式劇場。

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。
我點的「壽喜燒風和牛套餐」是本日最驚艷的一道——服務人員現場以鐵鍋輕煎，再淋上特製壽喜燒醬汁，香氣瞬間瀰漫整桌。
肉片油花細緻、入口即化，搭配生蛋液後更添柔滑口感。
另一道「冷藏肋眼心」則保留了和牛的彈性與甜度，每一口都能感受到油脂與炭火交織出的層次。
即使是配角如「季節小菜」與「日式和風飯」也毫不馬虎，整體呈現出高級卻不造作的平衡。

用餐體驗

KoDō 的最大特色是「儀式感」。
每位店員的動作都有節奏，從擺盤、火候、換網到講解，都像排練過無數次的演出。
在這裡用餐，會自然地放慢速度，專注於每一口肉帶來的細膩變化。
特別推薦搭配店內的紅酒或日本威士忌，風味更加圓潤。

綜合評分

評分項目	分數（滿分5分）	評語
環境氛圍	⭐⭐⭐⭐⭐	私密高雅、光線柔和，極具儀式感
口味表現	⭐⭐⭐⭐⭐	和牛品質極高、火候掌控完美
CP值	⭐⭐⭐☆	價位高，但每一口都吃得出誠意
再訪意願	⭐⭐⭐⭐☆	節慶、紀念日值得再次造訪

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。
從環境、服務到食材，每個細節都讓人感受到對「完美」的執著。
若你想在公益路找一間能讓人留下深刻印象、適合紀念日慶祝的餐廳，KoDō 絕對是值得收藏的一次「味覺儀式」。

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。
柔和的燈光灑在復古綠牆上，搭配大理石桌面與金色餐具，整體氛圍既典雅又帶有一絲文青氣息。
這裡不只是喝茶的地方，更像是把「臺灣味」以早午餐的形式重新演繹。

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。
炸雞腿外酥內嫩，搭配自製酸菜與溏心蛋，鹹香中帶著層次感。
「鳳茶甜點拼盤」則以茶為靈魂——伯爵茶蛋糕、烏龍茶奶酪、紅茶雪酥，每一口都有細緻的香氣變化。
最特別的是他們的茶飲，從臺灣高山紅茶到金萱冷泡茶，每一壺都現泡現倒，香氣清雅。
對我而言，這不只是一頓飯，更是一段放鬆的午後儀式。

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。
整體氛圍很「耐坐」，許多客人吃完正餐後仍會續點一壺茶聊天。
音樂輕柔、光線柔和，是那種可以靜靜待上兩小時的地方。

綜合評分

評分項目	分數（滿分5分）	評語
環境氛圍	⭐⭐⭐⭐⭐	優雅放鬆、裝潢細緻，是拍照與休憩首選
口味表現	⭐⭐⭐⭐⭐	茶香融入料理，整體風味溫潤平衡
CP值	⭐⭐⭐⭐	餐點份量適中、價位合理
再訪意願	⭐⭐⭐⭐⭐	想放鬆、聊天、喝好茶時會立刻想到這裡

地址：40360臺中市西區公益路68號三樓(勤美誠品)

電話：0423221118

官網：https://linktr.ee/yonshin

小結語

永心鳳茶讓人重新定義「臺味」。
它不走傳統路線，而是把熟悉的元素以更細緻、更現代的方式呈現。
無論是姊妹下午茶、親子餐聚，或是想一個人沉澱片刻，永心鳳茶 都是一處能讓人慢下來、品味生活的好地方。

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。
它沒有浮誇的裝潢，卻有一種低調的自信。從大門進入，就能聞到淡淡的醬香與蒸氣味，那是正宗江浙菜的靈魂。
整體裝潢以深木色為主，搭配圓桌與包廂設計，非常適合家庭聚餐或請客宴會。

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。
我這次點了「東坡肉」與「蝦仁炒飯」，兩道都展現了主廚深厚的火候功力。
東坡肉油亮卻不膩，入口即化、鹹甜交織；蝦仁炒飯粒粒分明、香氣十足，每一口都吃得到鑊氣。
此外，「小籠包」皮薄多汁，是幾乎每桌必點的招牌；港點類如「金牌流沙包」與「干貝燒賣」也都表現穩定。

用餐體驗

三希樓的服務給人一種老派但貼心的感覺。
店員上菜節奏掌握得很好，會主動幫忙分菜、收盤，態度沉穩而不打擾。
最讓我印象深刻的是，這裡的客群非常多元——有帶長輩的家庭、公司聚餐，也有情侶共度節日，卻都能在同一空間裡感到自在。

綜合評分

評分項目	分數（滿分5分）	評語
環境氛圍	⭐⭐⭐⭐	傳統圓桌設計、氛圍穩重舒適
口味表現	⭐⭐⭐⭐⭐	火候精準、味道濃郁，經典不失真
CP值	⭐⭐⭐⭐	價格合理、份量足，適合多人共享
再訪意願	⭐⭐⭐⭐	家庭聚餐與宴客的安心首選

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。
它不追求創新，而是用穩定的味道與真材實料，抓住每一位饕客的胃。
如果你想在公益路上找一間能兼顧長輩口味、氣氛又不拘謹的中餐廳，三希樓 絕對是最穩妥的選擇。

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。
外觀簡約，沒有華麗招牌，只有小小的木質門面與柔黃燈光。
一推開門，迎面而來的是日式杉木香氣與寧靜的氛圍，吧檯座位整齊排列，主廚站在中間，彷彿舞臺上的演出者。

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。
我這次選擇中價位套餐（約 $1200），共十多道料理，從前菜、小鉢、刺身、握壽司到甜點一氣呵成。
「比目魚鰭邊握」是整場最驚豔的瞬間——主廚以火槍輕炙，油脂瞬間釋放，入口後化成柔滑香氣。
「甜蝦海膽軍艦」則完美展現鮮度與層次感，海膽甘甜、甜蝦緊實。
搭配主廚親自調配的醬汁，每一口都像在品嚐季節的節奏。

用餐體驗

整場用餐約90分鐘，節奏緩慢但沉穩。
主廚會邊料理邊與客人互動，介紹魚種產地與食材處理方式。
雖然整體空間不大，但氣氛極佳——柔和的音樂、清酒的香氣、刀刃切魚時的聲音，讓人完全沉浸其中。
特別喜歡他們最後的甜點「焙茶奶酪」，收尾清爽優雅，為整場體驗畫下完美句點。

綜合評分

評分項目	分數（滿分5分）	評語
環境氛圍	⭐⭐⭐⭐⭐	私密安靜、燈光柔和，儀式感十足
口味表現	⭐⭐⭐⭐⭐	食材新鮮、刀工精準、層次分明
CP值	⭐⭐⭐⭐	以品質與體驗來說，價位合理
再訪意願	⭐⭐⭐⭐⭐	適合紀念日或想犒賞自己時再訪

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。
這裡沒有多餘擺盤，也不靠噱頭，而是以主廚對食材的尊重與技術堆疊出一場味覺饗宴。
若你想在公益路體驗日本料理最純粹的精神，一笈壽司 絕對值得你預約、靜靜期待。

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。
不管平日或假日，用餐時段幾乎一位難求。外觀以木質格柵搭配大面玻璃設計，呈現出年輕又有質感的風格。店內空間明亮、桌距適中，播放著輕快的音樂，整體氛圍熱鬧中帶點高級感，是許多年輕人聚餐、慶生的首選地。

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。
我這次點的是「厚切牛舌套餐」，肉片厚實彈牙，略帶脆感，搭配鹽蔥提味剛剛好。
另一道「和牛拼盤」也相當受歡迎，油花分布均勻、香氣濃郁，輕烤幾秒即可入口即化。
套餐附餐部分也相當用心：沙拉新鮮、味噌湯濃郁，最後還有一份「茶香冰淇淋」作結尾，香氣清爽，完美收尾。

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。
雖然客人很多，但環境維持得乾淨整潔，動線規劃良好。
最令人印象深刻的是他們的 整體節奏拿捏得剛剛好 ——餐點上桌快、氣氛熱絡，卻不會讓人覺得匆忙。
不論是朋友聚會、家庭聚餐，甚至是情侶約會，都能找到各自的樂趣。

綜合評分

評分項目	分數（滿分5分）	評語
環境氛圍	⭐⭐⭐⭐	明亮活潑、氣氛熱絡但不嘈雜
口味表現	⭐⭐⭐⭐⭐	肉質穩定、調味自然、甜點有記憶點
CP值	⭐⭐⭐⭐⭐	價格實在、份量足，是高回訪率代表
再訪意願	⭐⭐⭐⭐⭐	聚會、慶生都會再次選擇的燒肉店

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。
不論是第一次約會還是老朋友重聚，都能在這裡找到屬於燒肉的快樂節奏。
若你在公益路只想挑一家「保證不踩雷」的燒肉店，茶六燒肉堂 絕對是首選。

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？
 最熱鬧的區段大約在「公益路與黎明路口」一帶，這裡聚集了許多知名餐廳，從高級燒肉到早午餐通通有。
像 一頭牛日式燒肉、TANG Zhan 湯棧、茶六燒肉堂 都在這附近，交通方便、停車也相對容易。

Q2：需要提前訂位嗎？
 公益路的熱門餐廳幾乎都建議 提早3～5天訂位，尤其是假日或節慶期間。
特別是 一頭牛日式燒肉、KoDō 和牛燒肉、一笈壽司 這幾家，若臨時前往幾乎很難有位。

最後的話

若要用一句話形容這趟美食之旅，我會說：
「在公益路，吃飯不是選擇，而是一種享受。」
這條路上的每一次用餐，都像一段城市裡的小旅行。
下次當你不確定想吃什麼時，不妨沿著公益路走一圈，或許下一家，正好就是你新的最愛。

一頭牛日式燒肉年末聚餐推薦嗎？

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。NINI 尼尼臺中店慶生氛圍夠嗎？

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。永心鳳茶年末聚餐推薦嗎？

下一餐，不妨從這10家開始。NINI 尼尼臺中店大型聚餐空間夠不夠？

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 尼尼臺中店過年期間會開門嗎？

如果你有私心愛店，也歡迎留言分享，永心鳳茶必點有哪些？

你的推薦，可能讓我下一趟美食旅程變得更精彩。三希樓長輩會喜歡嗎？

Harvard Medical School researchers have discovered that Staphylococcus aureus directly causes itch by activating nerve cells. This finding, based on mouse and human cell studies, challenges the traditional view that itch in skin conditions arises from inflammation. It opens new possibilities for treating chronic itch and understanding its evolutionary significance. Researchers discover that a common microbe is an unrecognized cause of itching. Researchers at Harvard Medical School have discovered that the bacterium Staphylococcus aureus, commonly found on the skin, can directly trigger itching by interacting with nerve cells. The findings, based on research in mice and in human cells, was recently published in the journal Cell. This study provides a significant insight into the longstanding mystery of itching and sheds light on why skin disorders such as eczema and atopic dermatitis are often accompanied by persistent itch. In such conditions, the equilibrium of microorganisms that keep our skin healthy is often thrown off balance, allowing S. aureus to flourish, the researchers said. Up until now, the itch that occurs with eczema and atopic dermatitis was believed to arise from the accompanying inflammation of the skin. But the new findings show that S. aureus single-handedly causes itch by instigating a molecular chain reaction that culminates in the urge to scratch. “We’ve identified an entirely novel mechanism behind itch — the bacterium Staph aureus, which is found on almost every patient with the chronic condition atopic dermatitis. We show that itch can be caused by the microbe itself,” said senior author Isaac Chiu, associate professor of immunology in the Blavatnik Institute at HMS. The study experiments showed that S. aureus releases a chemical that activates a protein on the nerve fibers that transmit signals from the skin to the brain. Treating animals with an FDA-approved anti-clotting medicine successfully blocked the activation of the protein to interrupt this key step in the itch-scratch cycle. The treatment relieved symptoms and minimized skin damage. Credit: Harvard Medical School The findings can inform the design of oral medicines and topical creams to treat persistent itch that occurs with various conditions linked to an imbalance in the skin microbiome, such as atopic dermatitis, prurigo nodularis, and psoriasis. The repeated scratching that is a hallmark of these conditions can cause skin damage and amplify inflammation. “Itch can be quite debilitating in patients who suffer from chronic skin conditions. Many of these patients carry on their skin the very microbe we’ve now shown for the first time can induce itch,” said study first author Liwen Deng, a postdoctoral research fellow in the Chiu Lab. Identifying the molecular spark plug that ignites itch  Researchers exposed the skin of mice to S. aureus. The animals developed an intensifying itch over several days, and the repeated scratching caused worsening skin damage that spread beyond the original site of exposure. Moreover, mice exposed to S. aureus became hypersensitive to innocuous stimuli that would not typically cause itch. The exposed mice were more likely than unexposed mice to develop abnormal itching in response to a light touch. This hyperactive response, a condition called alloknesis, is common in patients with chronic conditions of the skin characterized by persistent itch. But it can also happen in people without any underlying conditions — think of that scratchy feeling you might get from a wool sweater. To determine how the bacterium triggered itch, the researchers tested multiple modified versions of the S. aureus microbe that were engineered to lack specific pieces of the bug’s molecular makeup. The team focused on 10 enzymes known to be released by this microbe upon skin contact. One after another, the researchers eliminated nine suspects — showing that a bacterial enzyme called protease V8 was single-handedly responsible for initiating itch in mice. Human skin samples from patients with atopic dermatitis also had more S. aureus and higher V8 levels than healthy skin samples. The analyses showed that V8 triggers itch by activating a protein called PAR1, which is found on skin neurons that originate in the spinal cord and carry various signals —touch, heat, pain, itch — from the skin to the brain. Normally, PAR1 lies dormant but upon contact with certain enzymes, including V8, it gets activated. The research showed that V8 snips one end of the PAR1 protein and awakens it. Experiments in mice showed that once activated, PAR1 initiates a signal that the brain eventually perceives as an itch. When researchers repeated the experiments in lab dishes containing human neurons, they also responded to V8. Interestingly, various immune cells implicated in skin allergies and classically known to cause itch — mast cells and basophils — did not drive itch after bacterial exposure, the experiments showed. Nor did inflammatory chemicals called interleukins, or white cells, which are activated during allergic reactions and are also known to be elevated in skin diseases and even in certain neurologic disorders. “When we started the study, it was unclear whether the itch was a result of inflammation or not,” Deng said. “We show that these things can be decoupled, that you don’t necessarily have to have inflammation for the microbe to cause itch, but that the itch exacerbates inflammation on the skin.” Interrupting the itch-scratch cycle Because PAR1 — the protein activated by S. aureus — is involved in blood clotting, researchers wanted to see whether an already approved anticlotting drug that blocks PAR1 would stop itch. It did. The itchy mice whose skin was exposed to S. aureus experienced rapid improvement when treated with the drug. Their desire to scratch diminished dramatically, as did the skin damage caused by scratching. Moreover, once treated with PAR1 blockers, the mice no longer experienced abnormal itch in response to innocuous stimuli. The PAR1 blocker is already used in humans to prevent blood clots and could be repurposed as anti-itch medication. For example, the researchers noted, the active ingredient in the medicine could become the basis for anti-itch topical creams. One immediate question that the researchers plan to explore in future work is whether other microbes besides S. aureus can trigger itch. “We know that many microbes, including fungi, viruses, and bacteria, are accompanied by itch but how they cause itch is not clear,” Chiu said. Beyond that, the findings raise a broader question: Why would a microbe cause itch? Evolutionarily speaking, what’s in it for the bacterium? One possibility, the researchers said, is that pathogens may hijack itch and other neural reflexes to their advantage. For example, previous research has shown that the TB bacterium directly activates vagal neurons to cause cough, which might enable it to spread more easily from one host to another.  “It’s a speculation at this point, but the itch-scratch cycle could benefit the microbes and enable their spread to distant body sites and to uninfected hosts,” Deng said. “Why do we itch and scratch? Does it help us, or does it help the microbe? That’s something that we could follow up on in the future.” Reference: “S. aureus drives itch and scratch-induced skin damage through a V8 protease-PAR1 axis” by Liwen Deng, Flavia Costa, Kimbria J. Blake, Samantha Choi, Arundhasa Chandrabalan, Muhammad Saad Yousuf, Stephanie Shiers, Daniel Dubreuil, Daniela Vega-Mendoza, Corinne Rolland, Celine Deraison, Tiphaine Voisin, Michelle D. Bagood, Lucia Wesemann, Abigail M Frey, Joseph S. Palumbo, Brian J. Wainger, Richard L. Gallo, Juan-Manuel Leyva-Castillo, Nathalie Vergnolle, Theodore J. Price, Rithwik Ramachandran, Alexander R. Horswill and Isaac M. Chiu, 22 November 2023, Cell. DOI: 10.1016/j.cell.2023.10.019 The work was funded by the National Institutes of Health (grants R01AI168005, R01AI153185, R01NS065926, R01NS102161, R01NS111929, R37AI052453, R01AR076082, U01AI152038, UM1AI151958, R01AI153185, R01JL160582, F32AI172080, T32AI049928, 1R21AG075419), Food Allergy Science Initiative (FASI), Burroughs Wellcome Fund, Drako Family Fund, Jackson-Wijaya Research Fund, Canadian Institutes of Health Research (CIHR) (grants 376560 and 469411), and ANR-PARCURE (PRCE-CE18, 2020). Chiu serves on the scientific advisory board of GSK Pharmaceuticals. Provisional patent application Serial No. 63/438,668, in which some coauthors are listed as inventors, was filed based on these findings.

Scientists have found a new way cells degrade unneeded proteins, which influence vital neural, immune, and developmental genes. This discovery may lead to treatments for conditions caused by protein imbalances in cells. The Mechanism Degrades Short-Lived Proteins That Support Brain and Immune Functions Short-lived proteins control gene expression in cells and execute critical roles ranging from assisting brain connectivity to fortifying the body’s immune response. Originating in the nucleus, these proteins are swiftly degraded after fulfilling their purpose. For decades, the mechanism behind the degradation and removal of these essential proteins from cells remained a mystery to researchers — until now. In a cross-departmental collaboration, researchers from Harvard Medical School identified a protein called midnolin that plays a key role in degrading many short-lived nuclear proteins. The study shows that midnolin does so by directly grabbing the proteins and pulling them into the cellular waste-disposal system, called the proteasome, where they are destroyed. The findings were recently published in the journal Science. “These particular short-lived proteins have been known for over 40 years, but no one has established how they are actually degraded,” said co-lead author Xin Gu, a research fellow in neurobiology at HMS. Because the proteins broken down by this process modulate genes with important functions related to the brain, the immune system, and development, scientists may eventually be able to target the process as a way of controlling protein levels to alter these functions and correct any dysfunction. “The mechanism we found is very simple and quite elegant,” added co-lead author Christopher Nardone, a PhD candidate in genetics at HMS. “It is a basic science discovery, but there are many implications for the future.” A Molecular Mystery It is well-established that cells can break down proteins by tagging them with a small molecule called ubiquitin. The tag tells the proteasome that the proteins are no longer needed, and it destroys them. Much of the pioneering research on this process was done by the late Fred Goldberg at HMS. However, sometimes the proteasome breaks down proteins without the help of ubiquitin tags, leading researchers to suspect that there was another, ubiquitin-independent mechanism of protein degradation. “There has been sporadic evidence in the literature that somehow the proteasome can directly degrade unmarked proteins, but no one understood how that can happen,” Nardone said. One group of proteins that seemed to be degraded by an alternative mechanism are stimuli-induced transcription factors: Proteins rapidly made in response to cellular stimuli that travel to the nucleus of a cell to turn on genes, after which they are rapidly destroyed. “What struck me, in the beginning, is that these proteins are extremely unstable and they have a very short half-life — once they are produced, they carry out their function, and they are quickly degraded afterward,” Gu said. These transcription factors support a range of important biological processes in the body, yet even after decades of research, “the mechanism of their turnover was largely unknown,” said Michael Greenberg, the Nathan Marsh Pusey Professor of Neurobiology in the Blavatnik Institute at HMS and a co-senior author on the paper with Stephen Elledge, the Gregor Mendel Professor of Genetics and of Medicine at HMS and Brigham and Women’s Hospital. From a Handful to Hundreds To investigate this mechanism, the team began with two familiar transcription factors: Fos, studied extensively by the Greenberg lab for its role in learning and memory, and EGR1, which is involved in cell division and survival. Using sophisticated protein and genetic analyses developed in the Elledge lab, the researchers homed in on midnolin as a protein that helps break down both transcription factors. Follow-up experiments revealed that in addition to Fos and EGR1, midnolin may also be involved in breaking down hundreds of other transcription factors in the nucleus. Gu and Nardone recall being shocked and skeptical about their results. To confirm their findings, they decided they needed to figure out exactly how midnolin targets and degrades so many different proteins. “Once we identified all these proteins, there were many puzzling questions about how the midnolin mechanism actually works,” Nardone said. With the aid of a machine learning tool called AlphaFold that predicts protein structures, plus results from a series of lab experiments, the team was able to flesh out the details of the mechanism. They established that midnolin has a “Catch domain” — a region of the protein that grabs other proteins and feeds them directly into the proteasome, where they are broken down. This Catch domain is composed of two separate regions linked by amino acids (think mittens on a string) that grab a relatively unstructured region of a protein, thus allowing midnolin to capture many different types of proteins. Of note are proteins like Fos that are responsible for turning on genes that prompt neurons in the brain to wire and rewire themselves in response to stimuli. Other proteins like IRF4 activate genes that support the immune system by ensuring that cells can make functional B and T cells. “The most exciting aspect of this study is that we now understand a new general, ubiquitination-independent mechanism that degrades proteins,” Elledge said. Tantalizing Translational Potential In the short term, the researchers want to delve deeper into the mechanism they discovered. They are planning structural studies to better understand the fine-scale details of how midnolin captures and degrades proteins. They are also making mice that lack midnolin to understand the protein’s role in different cells and stages of development. The scientists say their finding has tantalizing translational potential. It may offer a pathway that researchers can harness to control levels of transcription factors, thus modulating gene expression, and in turn, associated processes in the body. “Protein degradation is a critical process and its deregulation underlies many disorders and diseases,” including certain neurological and psychiatric conditions, as well as some cancers, Greenberg said. For example, when cells have too much or too little of transcription factors such as Fos, problems with learning and memory may arise. In multiple myeloma, cancer cells become addicted to the immune protein IRF4, so its presence can fuel the disease. The researchers are especially interested in identifying diseases that may be good candidates for the development of therapies that work through the mindolin-proteasome pathway. “One of the areas we are actively exploring is how to tune the specificity of the mechanism so it can specifically degrade proteins of interest,” Gu said. Reference: “The midnolin-proteasome pathway catches proteins for ubiquitination-independent degradation” by Xin Gu, Christopher Nardone, Nolan Kamitaki, Aoyue Mao, Stephen J. Elledge and Michael E. Greenberg, 25 August 2023, Science. DOI: 10.1126/science.adh5021 Funding was provided by a National Mah Jongg League Fellowship from the Damon Runyon Cancer Research Foundation, a National Science Foundation Graduate Research Fellowship, and the National Institutes of Health (T32 HG002295; R01 NS115965; AG11085).

Researchers from the University of Copenhagen have discovered that Caribbean box jellyfish, previously believed to be simple creatures, possess advanced learning abilities despite their basic nervous system. Credit: Jan Bielecki Jellyfish are more advanced than once thought. A new study from the University of Copenhagen has demonstrated that Caribbean box jellyfish can learn at a much more complex level than ever imagined – despite only having one thousand nerve cells and no centralized brain. The finding changes our fundamental understanding of the brain and could enlighten us about our own mysterious brains. After more than 500 million years on Earth, the immense evolutionary success of jellyfish is undeniable. Still, we’ve always thought of them as simple creatures with very limited learning abilities. The prevailing opinion is that more advanced nervous systems equate with more advanced learning potential in animals. Jellyfish and their relatives, collectively known as cnidarians, are considered to be the earliest living animals to develop nervous systems and to have fairly simple nervous systems and no centralized brain. For more than a decade, neurobiologist Anders Garm has been researching box jellyfish, a group of jellyfish commonly known for being among the world’s most poisonous creatures. But these lethal jellies are interesting for another reason as well: it turns out that they are not quite as simple as once believed. And this shakes our entire understanding of what simple nervous systems are capable of. A Caribbean box jellyfish. Black dots embedded low on the bell are the animal’s visual sensory and learning center called rhopalia. Credit: Jan Bielecki “It was once presumed that jellyfish can only manage the simplest forms of learning, including habituation – i.e., the ability to get used to a certain stimulation, such as a constant sound or constant touch. Now, we see that jellyfish have a much more refined ability to learn, and that they can actually learn from their mistakes. And in doing so, modify their behavior,” says Anders Garm, an associate professor at the University of Copenhagen’s Department of Biology. One of the most advanced attributes of a nervous system is the ability to change behavior as a result of experience – to remember and learn. The research team, headed by Jan Bielecki of Kiel University and Anders Garm, set out to test this ability in box jellyfish. The findings have just been published in the journal Current Biology. About Tripedalia cystophora Box jellyfish are a class of jellyfish known for being among the most poisonous animals in the world. They use their venom to catch fish and large shrimp. Tripedalia cystophora has a somewhat milder venom and feeds on tiny copepods. Box jellyfish do not have a centralized brain like most animals. Instead, they have four parallel brain-like structures, with approximately holds a thousand nerve cells in each. A human brain has approximately 100 billion nerve cells. Box jellyfish have twenty four eyes distributed among their four brain-like structures. Some of these eyes are image forming, providing box jellyfish with more complex vision than other types of jellyfish. To find their way through murky mangroves, four of Tripedalia cystophora’s eyes look up through the surface of the water and navigate using the mangrove canopies. Tripedalia cystophora is one of the smallest box jellyfish species, with a body of only about one centimeter in diameter. It lives in the Caribbean Sea and Central Indo-Pacific. Unlike many jellyfish species, Tripedalia cystophora actually mates as the male captures the female with its tentacles. A female’s eggs are then fertilized in their gut system, where they also develop into larvae. A Thousand Nerve Cells Are More Capable Than Once Thought The scientists studied the Caribbean box jellyfish, Tripedalia cystophora, a fingernail-sized medusa that lives in Caribbean mangrove swamps. Here, they use their impressive visual system including 24 eyes to hunt for tiny copepods among mangrove roots. While making for a good hunting grounds, the web of roots is also a dangerous place for soft-bodied jellies. So, as the small box jellyfish approach the mangrove roots, they turn and swim away. Should they veer too soon, they won’t have enough time to catch any copepods. But if they turn too late, they risk bumping into the root and damaging their gelatinous bodies. Thus, assessing distances is crucial for them. And here, contrast is the key, as the researchers discovered: “Our experiments show that contrast, i.e., how dark the root is in relation to the water, is used by the jellyfish to assess distances to roots, which allows them to swim away at just the right moment. Even more interesting is that the relationship between distance and contrast changes on a daily basis due to rainwater, algae, and wave action,” says Anders Garm, who continues: “We can see that as each new day of hunting begins, box jellyfish learn from the current contrasts by combining visual impressions and sensations during evasive maneuvers that fail. So, despite having a mere one thousand nerve cells – our brains have roughly 100 billion – they can connect temporal convergences of various impressions and learn a connection – or what we call associative learning. And they actually learn about as quickly as advanced animals like fruit flies and mice.” The new research results break with previous scientific perceptions of what animals with simple nervous systems are capable of: “For fundamental neuroscience, this is pretty big news. It provides a new perspective on what can be done with a simple nervous system. This suggests that advanced learning may have been one of the most important evolutionary benefits of the nervous system from the very beginning,” says Anders Garm. Caribbean box jellyfish lives and feeds among underwater mangrove roots. Credit: Anders Gram How They Did It The researchers replicated mangrove swamp conditions in the laboratory, where box jellyfish were placed in a behavioral arena. Here, the researchers manipulated jellyfish behavior by changing the contrast conditions to see what effect this had on their behavior. They learned that jellyfish learning takes place through failed evasions. That is, they learn from misinterpreting contrast and bumping into roots. Here they combined the visual impression and mechanical shock they got whenever they bumped into a root – and in doing so, learned when to veer away. “Our behavioral experiments demonstrate that three to five failed evasive maneuvers are enough to change the jellyfish’s behavior so that they no longer hit the roots. It is interesting that this is roughly the same repetition rate that a fruit fly or mouse needs to learn,” says Anders Garm. The learning was further verified through electrophysiology and classical conditioning experiments, which also showed where in the jellyfish’s nervous system the learning takes place. Seeking the Brain Cells Where Memory Is Housed The scientists have also shown where the learning is happening in these box jellyfish. This has given them unique opportunities to now study the precise changes that occur in a nerve cell when it is involved in advanced learning. “We hope that this can become a supermodel system for looking at cellular processes in the advanced learning of all sorts of animals. We are now in the process of trying to pinpoint exactly which cells are involved in learning and memory formation. Upon doing so, we will be able to go in and look at what structural and physiological changes occur in the cells as learning takes place,” says Anders Garm. If the research team is able to pinpoint the exact mechanisms in jellyfish involved in learning, the next step will be to find out whether it applies specifically to jellies or if it can be found in all animals. “Eventually, we will look for the same mechanisms in other animals, to see if this is how memory works in general,” says the researcher. This kind of groundbreaking knowledge could be used for a wealth of purposes, according to Anders Garm: “Understanding something as enigmatic and immensely complex as the brain is in itself an absolutely amazing thing. But there are unimaginably many useful possibilities. One major problem in the future will undoubtedly be various forms of dementia. I don’t claim that we are finding the cure for dementia, but if we can gain a better understanding of what memory is, which is a central problem in dementia, we may be able to lay a building block to better understand the disease and perhaps counteract it,” concludes the researcher. The study will be published today (September 22) in the scientific journal Current Biology. Reference: “Associative learning in the box jellyfish Tripedalia Cystophora” by Jan Bielecki, Sofie Katrine Dam Nielsen, Gösta Nachman and Anders Garm, 22 September 2023, Current Biology. DOI: 10.1016/j.cub.2023.08.056 The study was conducted by Jan Bielecki from Kiel University and Anders Garm, Sofie Katrine Dam Nielsen, and Gösta Nachman from the Department of Biology, University of Copenhagen.

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