Core Viewpoint - The interaction between the brain and tumors is a critical yet underexplored aspect of cancer biology, with evidence suggesting that psychological stress significantly influences tumor development and treatment response [2][4]. Group 1 - A large meta-analysis involving 2,611,907 participants found a strong correlation between depression and anxiety with increased cancer incidence, cancer-specific mortality, and all-cause mortality [2]. - The brain regulates tumor occurrence and development through various neuroendocrine and neural pathways, including the hypothalamic-pituitary-adrenal (HPA) axis and the autonomic nervous system, although the exact mechanisms remain largely unclear [2][4]. Group 2 - A recent study published in Nature Cancer revealed that colorectal cancer cells hijack a brain-gut polysynaptic circuit from the lateral septum to enteric neurons to sustain tumor growth [3][4]. - The study identified that GABAergic neurons in the lateral septum connect with cholinergic neurons in the gut, which extend to the tumor microenvironment (TME), and these neurons are exploited by colorectal cancer cells to promote tumor growth [7]. - Chronic stress in a mouse model enhances the activity of this circuit, exacerbating tumor progression, and clinical observations indicate that increased neuronal activity in the lateral septum correlates with larger primary tumors in colorectal cancer patients [7][9].

Core Viewpoint - The article discusses the career trajectory of David Sabatini, highlighting his significant contributions to mTOR research and the subsequent controversies that led to his professional downfall and relocation to the Czech Academy of Sciences for continued research [3][4][5]. Group 1: David Sabatini's Career Achievements - David Sabatini, born in 1968, is renowned for his discovery of the mTOR protein and its role as a direct target of rapamycin [3]. - He published over 200 papers, with more than 70 in top journals like Cell, Nature, and Science, accumulating over 190,000 citations and an H-index of 160 [3]. Group 2: Controversy and Professional Downfall - In October 2020, Sabatini faced allegations of sexual harassment from a female researcher, leading to his resignation from the Whitehead Institute in August 2021 and termination from HHMI [4]. - He filed a lawsuit claiming he was a victim of false accusations, which he argued destroyed his professional and personal reputation [4]. Group 3: Current Research and Future Directions - After unsuccessful attempts to secure a position at New York University due to protests, Sabatini accepted a position at the Czech Academy of Sciences in November 2023 [5]. - His team published a significant paper in Nature in August 2025, detailing the structural basis for the dynamic regulation of mTORC1 by amino acids [5]. - The research revealed the complex interactions within the mTORC1 signaling pathway, emphasizing the role of amino acid sensors and their structural dynamics [7][9][10][12].

Core Viewpoint - The incidence of gallbladder diseases, such as gallstones and gallbladder polyps, is increasing globally due to changes in dietary structure. Gallbladder removal surgery is the most common procedure in biliary surgery and is considered a standard treatment for patients with gallbladder diseases. However, emerging evidence indicates that post-cholecystectomy syndrome and the incidence of diseases related to metabolic syndrome have significantly increased. Notably, previous clinical studies have linked gallbladder removal surgery to an elevated risk of colorectal cancer, although the underlying mechanisms remain unclear [3][7]. Group 1 - A recent study published by a team led by Professor Yang Shiming from the Army Medical University in Nature Communications indicates that gallbladder removal surgery is associated with gut microbiota dysbiosis and impaired bile acid metabolism, which exacerbates colorectal tumorigenesis through disrupted FXR/β-catenin interactions. The FXR agonist obeticholic acid (OCA) has been shown to prevent colorectal tumors associated with gallbladder removal surgery [4][10]. - The study utilized mouse models to confirm that gallbladder removal surgery increases the occurrence of colorectal tumors. Metagenomic sequencing and targeted metabolomics revealed a reduction in Bifidobacterium breve and an increase in Ruminococcus gnavus, along with elevated levels of glycochenodeoxycholic acid (GUDCA) and tauroursodeoxycholic acid (TUDCA) in the body [8][10]. - Experiments involving fecal microbiota transplantation, single strain colonization, and bile acid supplementation demonstrated that dysbiosis related to gallbladder removal surgery promotes the production of TUDCA, thereby facilitating colorectal tumor development. Impaired bile acid metabolism inhibits FXR signaling, which ultimately exacerbates colorectal tumorigenesis [8][10].

Core Insights - Researchers at Tulane University School of Medicine have discovered that the Schistosoma mansoni parasite has evolved a mechanism to shut down the body's pain and itch immune "alarms," allowing it to invade the skin unnoticed [1][2] - This "invisibility" strategy of the parasite may provide insights for the development of new pain relief medications [1] Group 1: Mechanism of Infection - Schistosoma mansoni can penetrate the skin without causing pain or itch, unlike other bacteria or parasites [1] - The research indicates that the parasite suppresses specific neuronal pathways in the skin, preventing the activation of pain or itch signals [1] Group 2: Implications for Pain Relief - The study highlights that Schistosoma mansoni reduces the activity of TRPV1+ protein, which is crucial for transmitting heat, pain, or itch signals to the brain [1] - Identifying and isolating the molecules produced by the parasite that block TRPV1+ activation could lead to new therapies for preventing schistosomiasis and developing alternative pain relief medications [2]

Core Viewpoint - The article discusses the importance of metabolism in maintaining homeostasis and its role in various diseases, while announcing the upcoming C2-MERIT conference focused on metabolic research, innovation, and translation [2][4]. Conference Overview - The C2-MERIT conference will be held from August 22 to August 25, 2025, at Wenzhou Junting Hotel, Zhejiang Province, China [5][6]. - The conference aims to share cutting-edge scientific insights and foster innovative ideas within the scientific community [3]. Conference Schedule - Key events include a face-to-face meeting with Cell Press editors on August 21, 2025, and various academic sessions from August 22 to August 25, 2025 [4][6]. - The schedule features a Young Scholar Forum, plenary lectures, and multiple sessions focusing on different aspects of metabolism [16][21]. Registration Details - Registration fees vary: 1700 RMB for regular representatives before July 1, 2025, and 1900 RMB thereafter; student representatives pay 1100 RMB [20]. - Payment methods include online payment, bank transfer, and on-site payment options [22]. Organizing Bodies - The conference is organized by the Chinese Biophysical Society Metabolism Biology Branch and Cell Press, with support from various academic institutions [8][9].

新华社耶路撒冷8月1日电（记者王卓伦 路一凡）以色列一项新研究显示，磁性材料表面的电子自旋方 向能显著影响阿尔茨海默病相关淀粉样蛋白的聚集过程。这一成果有望为神经退行性疾病的干预与治疗 开辟新路径。 "我们开始意识到，生物系统对电子自旋的敏感性可能远超此前认知。"参与这一研究的耶路撒冷希伯来 大学教授帕尔蒂尔说。研究团队表示，基于这项研究，未来有望开发出具备特定自旋极化特性的纳米颗 粒或功能材料，用于定向干预淀粉样蛋白的异常聚集过程，从而为阿尔茨海默病等疾病提供新的治疗思 路。 研究成果已发表在《美国化学学会·纳米》杂志上。（完） 耶路撒冷希伯来大学近日发布公报说，该校研究人员领衔的团队在这一研究中聚焦于一种短肽，它是淀 粉样β蛋白的重要变体，已知会在阿尔茨海默病患者大脑中形成黏性原纤维和斑块。研究人员借助具有 磁性的表面，探索这些肽在不同电子自旋方向影响下的聚集行为。结果显示，自旋方向的改变可显著影 响淀粉样蛋白形成的原纤维的数量、长度和结构。例如，当表面磁化方向为某一特定方向时，淀粉样蛋 白形成的原纤维数量几乎增加一倍，最长甚至可达对照组的20倍。 ...

Core Viewpoint - The article discusses the rising popularity of ketogenic diets and presents new research findings that reveal the mechanisms behind weight loss associated with this diet, particularly focusing on the role of specific bile acids and gut microbiota [5][15]. Group 1: Mechanisms of Ketogenic Diet - Ketogenic diets induce the production of ketone bodies, prompting the body to utilize fat as an energy source, but recent studies indicate that the weight loss mechanisms are more complex [5]. - Research from Fudan University shows that ketogenic diets alter gut microbiota composition, leading to decreased levels of bile salt hydrolase (BSH), which results in increased levels of taurodeoxycholic acid (TDCA) and taurocholic acid (TUDCA) in the bloodstream [5][6]. - TDCA and TUDCA inhibit the expression of intestinal carbonic anhydrase 1, directly blocking calorie absorption [5][12]. Group 2: Clinical Observations and Findings - A clinical study involving over 400 participants confirmed the findings, suggesting that TDCA and TUDCA could serve as potential drug targets for treating obesity and its complications [6]. - In a 7-week study on mice fed a high-fat ketogenic diet (75.1% fat), significant reductions in body weight and fasting blood glucose were observed, alongside an increase in 22 metabolites, including six bile acids [9]. - The study also indicated that the presence of certain bile acids, particularly TDCA and TUDCA, plays a crucial role in the weight loss effects of the ketogenic diet [9][14]. Group 3: Gut Microbiota and Weight Loss - Analysis of the gut environment in mice revealed that the levels of TDCA and TUDCA are closely related to gut microbiota changes, with specific strains like Lactobacillus murinus ASF361 significantly impacting body weight and blood glucose levels [11][12]. - The study found that L. murinus ASF361 reduces serum levels of TDCA and TUDCA by metabolizing them into other bile acids, which suggests a complex interaction between diet, gut bacteria, and metabolic outcomes [12]. Group 4: Human Study Correlation - Data from 416 healthy participants indicated a correlation between low plasma levels of TDCA and TUDCA with high BMI and fasting blood glucose levels [14]. - Participants in a 12-week ketogenic diet study lost an average of 5.27 kg, with significant increases in plasma TDCA and TUDCA levels, aligning with findings from mouse experiments [14].

Core Viewpoint - The study reveals that hypoxia inhibits ferroptosis through a HIF-independent mechanism by suppressing KDM6A, a key player in lipid metabolism and ferroptosis resistance [2][5]. Group 1: Mechanism of Ferroptosis Regulation - Long-term hypoxia can inhibit ferroptosis in a HIF-independent manner [5]. - Hypoxia suppresses KDM6A, reshaping the lipid profile to confer resistance to ferroptosis [3][5]. - KDM6A acts as a non-classical oxygen sensor in the ferroptosis process, indicating a novel regulatory pathway [2][5]. Group 2: Implications for Cancer - The loss of KDM6A, a tumor suppressor, is commonly observed in bladder cancer, leading to resistance to ferroptosis [5]. - Pharmacological inhibition of EZH2, which opposes KDM6A activity, restores sensitivity to ferroptosis in bladder tumors carrying KDM6A mutations [4][5].

Core Viewpoint - The study reveals that lactylation of YTHDC1 at K82 enhances its phase separation, stabilizing oncogenic mRNA and promoting the progression of renal cell carcinoma (RCC) in a hypoxic environment [2][6][9]. Group 1: Research Findings - The research systematically mapped the lactylation profile of proteins under hypoxic conditions in RCC, focusing on the functional mechanism of YTHDC1 K82 lactylation [2][6]. - Elevated levels of global lysine lactylation (Kla) were found in human RCC tissues and cells, which promotes malignant development of RCC [6][7]. - YTHDC1 K82 lactylation, mediated by p300 under hypoxic conditions, promotes the malignancy of RCC both in vitro and in vivo [6][7]. Group 2: Mechanism of Action - YTHDC1 K82 lactylation enhances the phase separation of YTHDC1, leading to the expansion of nuclear condensates that protect oncogenic transcripts BCL2 and E2F2 from degradation by the PAXT-EXO complex [6][7][9]. - The study highlights that the increased lysine lactylation regulates the stability of YTHDC1 target genes, thereby facilitating the progression of RCC [9]. Group 3: Study Highlights - Quantitative lactylation proteomics analysis revealed high levels of lactylation modification proteins under hypoxic conditions [7]. - The study identifies a novel regulatory pathway involving YTHDC1 lactylation that opens new therapeutic targets in the intersection of tumor metabolism and RNA regulation [2][6].

Core Viewpoint - The proposed budget cut of $18 billion (40%) to the National Institutes of Health (NIH) by the Trump administration for 2026 is expected to significantly reduce the number of drugs entering the market, with long-term implications for biomedical research and innovation [1][2]. Group 1: Budget Cuts and Impacts - The NIH budget cut, if approved, will take effect on October 1, 2025, and is projected to lead to a reduction of at least 20 drugs entering development over the next 30 years, resulting in a decrease of approximately 4.5% in new drug approvals [1]. - A report from Grant Watch indicates that as of July 3, 2025, 4,473 NIH grant projects are affected, with over $10 billion at risk of funding freeze, primarily impacting research grants [1][2]. Group 2: Talent and Research Environment - The funding cuts may lead to a significant "brain drain," as young researchers may seek opportunities abroad, undermining the U.S.'s leadership in global research [2][3]. - The uncertainty in funding is expected to reduce the number of research institutions and laboratories in the U.S., potentially weakening collaborative capabilities and subsequent innovations [2][3]. Group 3: Regulatory Changes - In addition to budget cuts, the Trump administration has tightened drug approval regulations, including a significant layoff of 3,500 employees at the FDA, which is anticipated to increase the review time for new drug applications by nine months [3].