❌

Normal view

  • ✇36氪
  • ProtonBase王绍翾:PostgreSQL正成为AI时代的数据接口标准
    36氪获悉,近日,ProtonBase创始人王绍翾表示,PostgreSQL正成为AI时代的数据接口标准,未来企业只需对接两类API——Data API与AI API,即可完成从数据到智能的系统闭环。同时他表示,Data Warebase以PostgreSQL为统一生态基础,融合行列混存、多模索引、存算分离等核心技术,配合实时增量物化视图,彻底终结流批分离时代,构建面向AI的原生数据引擎。
     

ProtonBase王绍翾:PostgreSQL正成为AI时代的数据接口标准

30 June 2025 at 15:05
36氪获悉,近日,ProtonBase创始人王绍翾表示,PostgreSQL正成为AI时代的数据接口标准,未来企业只需对接两类API——Data API与AI API,即可完成从数据到智能的系统闭环。同时他表示,Data Warebase以PostgreSQL为统一生态基础,融合行列混存、多模索引、存算分离等核心技术,配合实时增量物化视图,彻底终结流批分离时代,构建面向AI的原生数据引擎。

OWASP Launches AI Testing Guide to Address Security, Bias, and Risk in AI Systems

28 June 2025 at 13:23

The OWASP Foundation has officially introduced the AI Testing Guide (AITG), a new open-source initiative aimed at assisting organizations in the systematic testing and security of artificial intelligence systems. This guide serves as a fundamental resource for developers, testers, risk officers, and cybersecurity professionals, promoting best practices in AI system security.

By Robert Krzaczyński

Obesity influences the biological response to injury: a multi-omics analysis

Eur J Trauma Emerg Surg. 2025 Jun 27;51(1):238. doi: 10.1007/s00068-025-02922-7.

ABSTRACT

PURPOSE: Obesity is a prevalent disease, but its influence on post-injury biology remains unclear. In this study, we aimed to characterize the independent effect of obesity on the proteomic and metabolomic signatures of trauma.

METHODS: Plasma was obtained on arrival from injured patients at a Level 1 Trauma Center and analyzed with modern mass spectrometry-based proteomics and metabolomics. Samples obtained after start of transfusion were excluded. Patients were stratified by "obesity" (body mass index [BMI]≥30 kg/m2) vs. "no obesity" (BMI < 30 kg/m2). In sub-group analyses, patients were sub-stratified by Low Injury/Low Shock (ISS < 15, base excess [BE]≥-6mEq/L) and High Injury/High Shock (ISS≥15, BE<-6). Multiple regression was used to adjust the omics data for significant covariates prior to performing ome-wide analyses.

RESULTS: There were 183 patients included (48 [26%] with obesity and 135 [74%] without). After covariate-adjustment, multiple proteins and metabolites were correlated with ISS and/or BE and were significantly different from Low Injury/Low Shock to High Injury/High Shock only in patients with obesity. This obesity-specific omics response to injury was characterized by increased inflammation, hypercoagulability, altered nitrogen metabolism, and mitochondrial dysfunction. Patients with obesity also exhibited excessive injury-provoked tissue destruction and organ damage compared to patients without obesity. In injury severity-adjusted analyses, the obesity signature consistently displayed markers of hemolysis, likely reflecting a pre-injury hemolytic propensity.

CONCLUSION: Obesity is independently associated with altered post-injury biology, which likely underlies unique pathology in trauma patients with obesity. Identifying this aberrant response to injury is the first step in developing personalized therapies for this patient population.

PMID:40576654 | DOI:10.1007/s00068-025-02922-7

This AI-powered startup studio plans to launch 100,000 companies a year — really

27 June 2025 at 09:59
Henrik Werdelin has spent the last 15 years helping entrepreneurs build big brands like Barkbox through his startup studio Prehype. Now, with his new, New York-based venture Audos, he’s betting that AI can help him scale that process from “tens” of startups a year to “hundreds of thousands” of aspiring business owners. The timing certainly […]

Cloudflare Expands AI Capabilities with Launch of Thirteen New MCP Servers

26 June 2025 at 20:00

Cloudflare has unveiled thirteen new Model Context Protocol (MCP) servers, enhancing the integration of AI agents with its platform. These servers allow AI clients to interact with Cloudflare's services through natural language, streamlining tasks such as debugging, data analysis, and security monitoring.

By Craig Risi
  • ✇36氪
  • 中信证券:Web3监管生态完善加速,有望提升香港在全球数字资产生态中的竞争力
    36氪获悉,中信证券指出,6月26日中国香港政府发表的《香港数字资产发展政策宣言2.0》延续了2022年1.0的政策导向,代表了香港成为全球数字资产领域领导者的决心。展望未来,港府正为进一步创新及市场发展奠定基础,我们认为凭借监管机构、业界及社会的共同努力,香港数字资产监管架构及生态正在加速完善,对全球Web3人才、资金及项目吸引力有望大幅提升,有望引领香港从传统国际金融中心,迈向全球领先数字资产创新中心,巩固其作为国际金融中心、人民币国际化桥头堡和超级联系人的战略地位。
     

中信证券:Web3监管生态完善加速,有望提升香港在全球数字资产生态中的竞争力

27 June 2025 at 08:35
36氪获悉,中信证券指出,6月26日中国香港政府发表的《香港数字资产发展政策宣言2.0》延续了2022年1.0的政策导向,代表了香港成为全球数字资产领域领导者的决心。展望未来,港府正为进一步创新及市场发展奠定基础,我们认为凭借监管机构、业界及社会的共同努力,香港数字资产监管架构及生态正在加速完善,对全球Web3人才、资金及项目吸引力有望大幅提升,有望引领香港从传统国际金融中心,迈向全球领先数字资产创新中心,巩固其作为国际金融中心、人民币国际化桥头堡和超级联系人的战略地位。

Gene Expression Analysis and Validation of a Novel Biomarker Signature for Early-Stage Lung Adenocarcinoma

Biomolecules. 2025 May 31;15(6):803. doi: 10.3390/biom15060803.

ABSTRACT

Lung cancer is responsible for 2.21 million annual cancer cases and is the leading worldwide cause of cancer-related deaths. Specifically, lung adenocarcinoma (LUAD) is the most prevalent lung cancer subtype resulting from genetic causes; LUAD has a 15% patient survival rate due to it commonly being detected in its advanced stages. This study aimed to identify a novel biomarker signature of early-stage LUAD utilizing gene expression analysis of human lung tissue samples. Using 22 pairs of LUAD and matched normal lung microarrays, 229 differentially expressed genes were identified. These genes were networked for their protein-protein interactions, and 44 hub genes were determined from protein essentiality. Survival analysis of 478 LUAD patient samples identified four statistically significant candidates. These candidate genes' expression profiles were validated from GTEx and TCGA (347 normal, 483 LUAD samples); immunohistochemistry validated the subsequent protein presence. Through intensive bioinformatic identification and multiple validations of the four-biomarker gene signature, AGER, MGP, and PECAM1 were identified as downregulated in LUAD; SLC2A1 was identified as upregulated in LUAD. These four biologically significant genes are involved in tumorigenesis and poor LUAD prognosis, meriting their use as a clinical biomarker signature and therapeutic targets for early-stage LUAD.

PMID:40563443 | PMC:PMC12191159 | DOI:10.3390/biom15060803

  • ✇36氪
  • 创新药激战,资金借道ETF“越跌越买”
    近一周多以来,国内创新药板块结束此前单边上涨行情,转而进入震荡。然而,场内资金却呈现出“越跌越买”的迹象。业内人士认为,创新药研发本身具有高度不确定性,尤其在当前部分个股估值已较高的情况下,任何瑕疵都可能被放大并导致股价回调。具有更高置信度、更优竞争格局、更完备商业逻辑的创新药企业才是具备更好投资逻辑的标的。(中证网)
     

创新药激战,资金借道ETF“越跌越买”

27 June 2025 at 08:15
近一周多以来,国内创新药板块结束此前单边上涨行情,转而进入震荡。然而,场内资金却呈现出“越跌越买”的迹象。业内人士认为,创新药研发本身具有高度不确定性,尤其在当前部分个股估值已较高的情况下,任何瑕疵都可能被放大并导致股价回调。具有更高置信度、更优竞争格局、更完备商业逻辑的创新药企业才是具备更好投资逻辑的标的。(中证网)

Spatial Proteomics and Transcriptomics Reveal Early Immune Cell Organization in Pancreatic Intraepithelial Neoplasia

JCI Insight. 2025 Jun 26:e191595. doi: 10.1172/jci.insight.191595. Online ahead of print.

ABSTRACT

Pancreatic ductal adenocarcinoma (PDAC) has a poor survival rate due to late detection. PDAC arises from precursor microscopic lesions, termed pancreatic intraepithelial neoplasia (PanIN), that develop at least a decade before overt disease--this provides an opportunity to intercept PanIN-to-PDAC progression. However, immune interception strategies require full understanding of PanIN and PDAC cellular architecture. Surgical specimens containing PanIN and PDAC lesions from a unique cohort of five treatment-naïve patients with PDAC were surveyed using spatial-omics (proteomic and transcriptomic). Findings were corroborated by spatial proteomics of PanIN and PDAC from tamoxifen-inducible KPC (tiKPC) mice. We uncovered the organization of lymphoid cells into tertiary lymphoid structures (TLSs) adjacent to PanIN lesions. These TLSs lacked CD21+CD23+ B cells compared to more mature TLSs near the PDAC border. PanINs harbored mostly CD4+ T cells with fewer Tregs and exhausted T cells than PDAC. Peri-tumoral space was enriched with naïve CD4+ and central memory T cells. These observations highlight the opportunity to modulate the immune microenvironment in PanINs before immune exclusion and immunosuppression emerge during progression into PDAC.

PMID:40569674 | DOI:10.1172/jci.insight.191595

Extrachromosomal DNA replication and maintenance couple with DNA damage pathway in tumors

This study demonstrates that extrachromosomal DNA (ecDNA) replication induces DNA double-strand breaks and activates the DNA damage response (DDR). The DDR pathways, such as alt-NHEJ, are critical for ecDNA maintenance in tumor cells. Mechanistic insights into ecDNA replication and maintenance unveil a therapeutic approach for treating tumors harboring ecDNA.
  • ✇MIT Technology Review
  • The Download: Google DeepMind’s DNA AI, and heatwaves’ impact on the grid Rhiannon Williams
    This is today’s edition of The Download, our weekday newsletter that provides a daily dose of what’s going on in the world of technology. Google’s new AI will help researchers understand how our genes work When scientists first sequenced the human genome in 2003, they revealed the full set of DNA instructions that make a person. But we still didn’t know what all those 3 billion genetic letters actually do.Now Google’s DeepMind division says it’s made a leap in trying to understand the code
     

The Download: Google DeepMind’s DNA AI, and heatwaves’ impact on the grid

26 June 2025 at 20:10

This is today’s edition of The Download, our weekday newsletter that provides a daily dose of what’s going on in the world of technology.

Google’s new AI will help researchers understand how our genes work

When scientists first sequenced the human genome in 2003, they revealed the full set of DNA instructions that make a person. But we still didn’t know what all those 3 billion genetic letters actually do.

Now Google’s DeepMind division says it’s made a leap in trying to understand the code with AlphaGenome, an AI model that predicts what effects small changes in DNA will have on an array of molecular processes, such as whether a gene’s activity will go up or down.

It’s just the sort of question biologists regularly assess in lab experiments, and is an attempt to further smooth biologists’ work by answering basic questions about how changing DNA letters alters gene activity and, eventually, how genetic mutations affect our health. Read the full story.

—Antonio Regalado

It’s officially summer, and the grid is stressed

It’s crunch time for the grid this week. Large swaths of the US have reached or exceeded record-breaking temperatures. Spain recently went through a dramatic heat wave too, as did the UK, which is bracing for another one soon.

We rely on electricity to keep ourselves comfortable, and more to the point, safe. These are the moments we design the grid for: when need is at its very highest. The key to keeping everything running smoothly during these times might be just a little bit of flexibility. But demand for electricity from major grids is already peaking, and that’s a good reason to be a little nervous. Read the full story.

—Casey Crownhart

This article is from The Spark, MIT Technology Review’s weekly climate newsletter. To receive it in your inbox every Wednesday, sign up here.

MIT Technology Review Narrated: How did China come to dominate the world of electric cars?

From generous government subsidies to support for lithium batteries, here are the keys to understanding how China managed to build a world-leading industry in electric vehicles.

This is our latest story to be turned into a MIT Technology Review Narrated podcast, which we’re publishing each week on Spotify and Apple Podcasts. Just navigate to MIT Technology Review Narrated on either platform, and follow us to get all our new content as it’s released.

Inside OpenAI’s empire with Karen Hao

Journalist Karen Hao’s newly released book, Empire of AI: Dreams and Nightmares in Sam Altman’s OpenAI, tells the story of OpenAI’s rise to power and its far-reaching impact all over the world.

Hao, a former MIT Technology Review senior editor, will join our executive editor Niall Firth in an intimate subscriber-exclusive Roundtable conversation exploring the AI arms race, what it means for all of us, and where it’s headed. Register here to join us at 9am ET on Monday June 30th June.

Special giveaway: Attendees will have the chance to receive a free copy of Hao’s book. See registration form for details.

The must-reads

I’ve combed the internet to find you today’s most fun/important/scary/fascinating stories about technology.

1 Meta has won an AI copyright case against authors
The judge said the authors hadn’t presented enough evidence to back up their case. (TechCrunch)
+ It’s not an entirely decisive victory for Meta, though. (Wired $)
+ It’s the second lawsuit in favor of AI giants this week. (Insider $)

2 The US will stop contributing towards a global vaccine alliance
RFK Jr made unsubstantiated claims about Gavi’s safety record. (WP $)
+ Kennedy’s newly-assembled vaccine panel is reviewing its guidelines for children. (Vox)
+ Experts are worried the once-influential panel will cause irreparable harm. (Ars Technica)
+ How measuring vaccine hesitancy could help health professionals tackle it. (MIT Technology Review)

3 Jeff Bezos is cozying up to Donald Trump
If the Trump administration happens to need a new space company, he’s ready and willing to supply it. (WSJ $)
+ Meanwhile, a private astronaut mission is on its way to the ISS. (CNN)

4 Taiwan is working on suicide drones to defend itself from China
The country is taking a leaf out of Ukraine’s defense book. (FT $)
+ This giant microwave may change the future of war. (MIT Technology Review)

5 Biohackers are feeling emboldened by the Trump administration
They welcome lower barriers to entry for their unorthodox treatments. (Wired $)
+ The first US hub for experimental medical treatments is coming. (MIT Technology Review)

6 A UK cyberattack on a health firm contributed to a patient’s death
The ransomware attack disrupted blood services at London hospitals. (BBC)
+ A Russian hacking gang is to blame for the incident. (Bloomberg $)

7 Take a look inside Amazon’s colossal new data center
Four construction teams are working around the clock to finish it. (NYT $)
+ Generating video is the most energy-intensive AI prompt. (WSJ $)
+ We did the math on AI’s energy footprint. Here’s the story you haven’t heard. (MIT Technology Review)

8 The debate around dark energy is intensifying
New research suggests it evolves over time. But not everyone agrees. (Undark)

9 Trump Mobile is no longer claiming to be ‘made in the USA’
It’s now “designed with American values in mind” instead. (Ars Technica)

10 It’s official: The Social Network is getting a sequel
Zuck goes MAGA? (Deadline $)

Quote of the day

“By training generative AI models with copyrighted works, companies are creating something that often will dramatically undermine the market for those works, and thus dramatically undermine the incentive for human beings to create things the old-fashioned way.”

—US district judge Vince Chhabria, who presided over a copyright lawsuit brought against Meta by a group of authors, warns of the implications of the company’s actions, the Guardian reports.

One more thing

Beyond gene-edited babies: the possible paths for tinkering with human evolution

Editing human embryos is restricted in much of the world—and making an edited baby is fully illegal in most countries surveyed by legal scholars. But advancing technology could render the embryo issue moot.

New ways of adding CRISPR, the revolutionary gene editing tool, to the bodies of people already born could let them easily receive changes as well. It’s possible that in 125 years, many people will be the beneficiaries of multiple rare, but useful, gene mutations currently found in only small segments of the population. 

These could protect us against common diseases and infections, but eventually they could also yield improvements in other traits, such as height, metabolism, or even cognition. But humanity won’t necessarily do things the right way. Read the full story.

—Antonio Regalado

We can still have nice things

A place for comfort, fun and distraction to brighten up your day. (Got any ideas? Drop me a line or skeet ’em at me.)

+ Amazing things are happening in New York’s Central Park.
+ A newly-discovered species of dinosaur has gone on display in London, and it’s small but perfectly formed.
+ Cool—Bob Dylan is releasing a new art book, this time of his drawings.
+ Iron Maiden bassist Steve Harris has a secret second career—as a footballer ⚽

  • ✇MIT Technology Review
  • Google’s new AI will help researchers understand how our genes work Antonio Regalado
    When scientists first sequenced the human genome in 2003, they revealed the full set of DNA instructions that make a person. But we still didn’t know what all those 3 billion genetic letters actually do.  Now Google’s DeepMind division says it’s made a leap in trying to understand the code with AlphaGenome, an AI model that predicts what effects small changes in DNA will have on an array of molecular processes, such as whether a gene’s activity will go up or down. It’s just the sort of questi
     

Google’s new AI will help researchers understand how our genes work

25 June 2025 at 22:00

When scientists first sequenced the human genome in 2003, they revealed the full set of DNA instructions that make a person. But we still didn’t know what all those 3 billion genetic letters actually do. 

Now Google’s DeepMind division says it’s made a leap in trying to understand the code with AlphaGenome, an AI model that predicts what effects small changes in DNA will have on an array of molecular processes, such as whether a gene’s activity will go up or down. It’s just the sort of question biologists regularly assess in lab experiments.

“We have, for the first time, created a single model that unifies many different challenges that come with understanding the genome,” says Pushmeet Kohli, a vice president for research at DeepMind.

Five years ago, the Google AI division released AlphaFold, a technology for predicting the 3D shape of proteins. That work was honored with a Nobel Prize last year and spawned a drug-discovery spinout, Isomorphic Labs, and a boom of companies that hope AI will be able to propose new drugs.

AlphaGenome is an attempt to further smooth biologists’ work by answering basic questions about how changing DNA letters alters gene activity and, eventually, how genetic mutations affect our health. 

“We have these 3 billion letters of DNA that make up a human genome, but every person is slightly different, and we don’t fully understand what those differences do,” says Caleb Lareau, a computational biologist at Memorial Sloan Kettering Cancer Center who has had early access to AlphaGenome. “This is the most powerful tool to date to model that.”

Google says AlphaGenome will be free for noncommercial users and plans to release full details of the model in the future. According to Kohli, the company is exploring ways to “enable use of this model by commercial entities” such as biotech companies. 

Lareau says AlphaGenome will allow certain types of experiments now done in the lab to be carried out virtually, on a computer. For instance, studies of people who’ve donated their DNA for research often turn up thousands of genetic differences, each slightly raising or lowering the chance a person gets a disease such as Alzheimer’s.

Lareau says DeepMind’s software could be used to quickly make predictions about how each of those variants works at a molecular level, something that would otherwise require time-consuming lab experiments. “You’ll get this list of gene variants, but then I want to understand which of those are actually doing something, and where can I intervene,” he says. “This system pushes us closer to a good first guess about what any variant will be doing when we observe it in a human.”

Don’t expect AlphaGenome to predict very much about individual people, however. It offers clues to nitty-gritty molecular details of gene activity, not 23andMe-type revelations of a person’s traits or ancestry. 

“We haven’t designed or validated AlphaGenome for personal genome prediction, a known challenge for AI models,” Google said in a statement.

Underlying the AI system is the so-called transformer architecture invented at Google that also powers large language models like GPT-4. This one was trained on troves of experimental data produced by public scientific projects.

Lareau says the system will not broadly change how his lab works day to day but could permit new types of research. For instance, sometimes doctors encounter patients with ultra-rare cancers, bristling with unfamiliar mutations. AlphaGenome could suggest which of those mutations are really causing the root problem, possibly pointing to a treatment.

“A hallmark of cancer is that specific mutations in DNA make the wrong genes express in the wrong context,” says Julien Gagneur, a professor of computational medicine at the Technical University of Munich. “This type of tool is instrumental in narrowing down which ones mess up proper gene expression.” 

The same approach could apply to patients with rare genetic disease, many of whom never learn the source of their condition, even if their DNA has been decoded. “We can obtain their genomes, but we are clueless as to which genetic alterations cause the disease,” says Gagneur. He thinks AlphaGenome could give medical scientists a new way to diagnose such cases. 

Eventually, some researchers aspire to use AI to design entire genomes from the ground up and create new life forms. Others think the models will be used to create a fully virtual laboratory for drug studies. “My dream would be to simulate a virtual cell,” Demis Hassabis, CEO of Google DeepMind, said this year. 

Kohli calls AlphaGenome a “milestone” on the road to that kind of system. “AlphaGenome may not model the whole cell in its entirety … but it’s starting to sort of shed light on the broader semantics of DNA,” he says.

Rescuing dendritic cell interstitial motility sustains antitumour immunity

Nature, Published online: 25 June 2025; doi:10.1038/s41586-025-09202-9

Disruption of dendritic cell (DC) interstitial motility in the tumour microenvironment promotes immune evasion, and enhancement of DC interstitial motility offers a route for DC-centric immunotherapy.
  • ✇MRD
  • Clinical Utility of ctDNA Analysis in Lung Cancer-A Review Kamil Makar · Agata Wróbel · Adam Antczak · Damian Tworek
    Adv Respir Med. 2025 Jun 12;93(3):17. doi: 10.3390/arm93030017.ABSTRACTCirculating free DNA (cfDNA) is genetic material released from various cells into bodily fluids. Among its fractions, circulating tumor DNA (ctDNA) originates from tumor cells and reflects their genetic material, including mutations and epigenetic changes. Methods commonly employed for detecting ctDNA in blood include next-generation sequencing (NGS) and various types of PCR. The presence of ctDNA can be utilized in liquid bi
     

Clinical Utility of ctDNA Analysis in Lung Cancer-A Review

25 June 2025 at 18:00

Adv Respir Med. 2025 Jun 12;93(3):17. doi: 10.3390/arm93030017.

ABSTRACT

Circulating free DNA (cfDNA) is genetic material released from various cells into bodily fluids. Among its fractions, circulating tumor DNA (ctDNA) originates from tumor cells and reflects their genetic material, including mutations and epigenetic changes. Methods commonly employed for detecting ctDNA in blood include next-generation sequencing (NGS) and various types of PCR. The presence of ctDNA can be utilized in liquid biopsies for many diagnostic purposes related to various cancers. It is a minimally invasive method of sampling molecular compounds from tumor cells. In this paper, we focus on current knowledge regarding the liquid biopsy of blood ctDNA in the context of lung cancer, one of the leading causes of cancer-related mortality. Currently, as a clinically approved method, liquid biopsy serves as a complementary technique in NSCLC diagnostic and genetic profiling. Other applications of liquid biopsy that are still being investigated include the detection of minimal residual disease (MRD) after curative treatment and response monitoring to systemic treatment. This review discusses current and future potential directions for the development and implementation of ctDNA for patients with NSCLC.

PMID:40558116 | PMC:PMC12189613 | DOI:10.3390/arm93030017

❌