Toggle light / dark theme

Revealing the epigenetic modulator lysine-specific histone demethylase 1a as a new target for kidney diseases

https://doi.org/10.1172/jci.insight.

Here, Tobias B. Huber & team use a state-of-the-art, tour de force experimental design to show LSD1 regulates kidney development, and its dysfunction disrupts key kidney cells, leading to cyst formation in mouse and organoid models.

The image shows severe structural changes in the adult mouse kidney with loss of KDM1a. Nephrology.


4Faculty of Biology, Albert Ludwigs University of Freiburg, Freiburg, Germany.

5Institute of Medical Bioinformatics and Systems Medicine and.

6Institute of Surgical Pathology, Faculty of Medicine, Medical Center — University of Freiburg, Freiburg, Germany.

Diagnostic Performance of Anti–Epstein-Barr Virus BNLF2b in Suspected Nasopharyngeal Carcinoma

In a multicenter prospective cohort study of 3,777 participants with suspected nasopharyngeal carcinoma (NPC), anti–Epstein-Barr virus (EBV) BNLF2b total antibody (P85-Ab) demonstrated superior diagnostic performance compared to EBV viral capsid antigen (VCA)-immunoglobulin A, EBV early antigen-IgA, and EBV nuclear antigen 1-IgA.

P85-Ab showed high sensitivity and specificity across outpatient populations, particularly among asymptomatic individuals and those with NPC-nonspecific symptoms.

For patients with NPC-specific symptoms, a triplet-antibody strategy combining P85-Ab, VCA-IgA, and EBNA1-IgA further improved sensitivity, supporting distinct diagnostic approaches based on clinical presentation.


This multicenter, observational cohort study with prospective sample collection was conducted at 5 medical centers across 4 provinces in China. Participants were consecutively recruited from the ENT or oncology outpatient clinics of the following institutions: Sun Yat-sen University Cancer Centre (SYSUCC), Zhongshan City People’s Hospital (ZSCPH), Tongji Hospital affiliated with Tongji Medical College of Huazhong University of Science and Technology (TJH-HUST), Wuzhou Red Cross Hospital (WZRCH), and Fujian Cancer Hospital (FJCH).

Key inclusion criteria included participants with symptoms or signs suggestive of possible NPC, non-NPC head and neck diseases, EBV-associated diseases, and positive results from commercially available EBV-based tests without signs or symptoms in medical examination centers or screening initiatives and subsequently seeking further differential diagnosis of NPC. Key exclusion criteria included previous radiotherapy or systemic chemotherapy (detailed in eMethods 1 in Supplement 2).

The Effect of Physical Activity on the Gut Microbiome in Prediabetes: Results From a Randomized Controlled Trial

Adults with prediabetes randomized to 8-weeks of walking realized gut microbiome changes suggestive of more resilience, growth, and enhanced metabolic activity. DOCM

Read here ➡️ doi.org/10.2337/doc25-0067

American Diabetes Association American Diabetes Association – DiabetesPro


OBJECTIVE. To test the effect of physical activity on the gut microbiome and circulating short-chain fatty acids (SCFAs) among sedentary adults with prediabetes and overweight or obesity.

Scientists Find ‘Kill Switch’ That Activates Cancer Cell Death in The Lab

Year 2023 face_with_colon_three


Scientists have figured out a way to detonate the ‘doors’ that lead to the heart of cancerous tumors, blowing them wide open for drug treatments.

The strategy works by triggering a ‘timer bomb’ on the cells that line a tumor’s associated blood vessels.

These vessels control access to the tumor tissue, and until they are opened, engineered immune cells can’t easily gain entry to the cancer to fight it off.

Scientists discover on/off gene switches that could revolutionize personalized medicine

Year 2025 This could essentially end disease where the diseases would be edited off and the host repaired internally.


Scientists identified 473 human genes that act as genetic “on/off switches,” shaping disease risk through tissue-specific or universal patterns regulated by DNA changes and hormones.

Study: Switch-like gene expression modulates disease risk. Image Credit: gopixa / Shutterstock.

In a recent article published in Nature Communications, researchers analyzed methylomes, transcriptomes, and genomes from 943 individuals to characterize and identify genes that exhibit distinct on-off switches and explore their epigenetic and genetic regulation.

Blood-brain barrier disruption, traumatic encephalopathy, and cognitive decline in retired athletes

Traumatic head injuries from collision and combat sports disrupt the blood-brain barrier and trigger inflammation for years after retirement, shows a new MRI and transcriptomic analysis of retired athletes.

Find out more in Science TranslationalMedicine.


Sci. Transl. Med. 18, eadu6037 (2026). DOI:10.1126/scitranslmed.adu6037

Select the format you want to export the citation of this publication.

The role of nutrient stress in DNA damage

Nutrient stress in DNA damage.

The dynamic interplay between nutrient stress and DNA damage governs cellular survival through coordinated regulation of genomic integrity and metabolic adaptation. Nutrient deprivation, such as glucose or amino acid limitation, engages nutrient sensors, including AMPK and mTORC1, to rewire energy homeostasis while directly influencing DNA repair via regulating PARP1, BRCA1, and other core repair machinery.

DNA damage-activated kinases (ATM/ ATR) orchestrate metabolic reprogramming to fuel repair processes, enforcing context-dependent cell fate decisions via cell cycle arrest or apoptosis regulation.

Nutrient stress exacerbates genomic instability through depleting antioxidants, such as NADPH or glutathione (GSH), promoting oxidative DNA lesions that overwhelm repair capacity, while defective DNA repair conversely drives metabolic dysregulation in tumors.

In the future, more efficacious tumor therapeutic strategies propose combining targeted nutrient stress with DNA damage repair inhibitors to exploit synthetic lethality. However, clinical translation requires resolving key challenges including tumor heterogeneity in nutrient stress-response pathways and adaptive metabolic plasticity during therapy sciencenewshighlights ScienceMission https://sciencemission.com/nutrient-stress–and-DNA-damage


Cells are constantly exposed to various stresses, including nutrient deprivation and genotoxic stress, which dynamically interact with cellular sensing pathways to influence metabolism, gene expression, and homeostasis. The integration of nutrient-sensing mechanisms and DNA damage response pathways is critical in cancer progression. While individual processes are well-characterized, their cross-regulatory mechanisms are just beginning to emerge. Deciphering the interplay between nutrient stress and DNA damage is crucial for elucidating the mechanisms underlying cellular responses to stress and developing therapeutic strategies for various diseases, including cancer. This review highlights the relationship between nutrient stress and DNA damage, especially its underlying sensing pathway and cell fate determination.

Assembly and annotation of hexaploid Sesuvium portulacastrum genome reveals insights into ion transport-mediated high-salinity adaptation

Yuan et al. report a high-quality chromosome-scale genome of the hexaploid halophyte Sesuvium portulacastrum. Comparative genomics and transcriptomics provide insights into its salt-adaptation evolution and identify the key salt-tolerant gene SpHAK3, offering genetic resources for improving crop tolerance.

How deadly Marburg virus enters human cells

The researchers also discovered a tiny antibody, called a nanobody, which mimics NPC1 at the receptor-binding site and can slip past a protective cap on Marburg’s entry protein, bind to it and block its attachment to the receptor. In lab tests, this nanobody prevented Marburg virus from entering cells. ScienceMission sciencenewshighlights.


In a new study published in Nature the researchers found that the Marburg virus (MBV), one of the world’s deadliest pathogens with an average 73% fatality rate, is unusually efficient at getting inside human cells. They also showed that the virus’s entry protein contains structural features that explain this efficiency and point to a strategy for blocking infection.

The researchers designed a tightly controlled system that enables a fair comparison of the entry proteins of Marburg and its relative Ebola. The team further found that the two viruses share the same human receptor. The authors determined structures of MBV glycoprotein (GP) in three states: unbound; bound to its endosomal receptor NPC1; and complexed with a neutralizing nanobody.

Marburg’s entry protein binds this receptor in a distinct orientation and with higher affinity, then changes shape in ways that help the virus enter cells. The authors show that the glycan cap shields the receptor-binding site from NPC1 but only partially from the nanobody, enabling limited immune evasion. After glycan cap cleavage, NPC1 binds to MBV GP in a distinct orientation compared with EBOV GP, providing an additional anchor and enhancing receptor affinity. NPC1 engagement also induces substantial conformational changes in MBV GP, probably facilitating membrane fusion. Using this approach, they showed that Marburg’s entry protein can drive viral entry into human cells up to 300 times more efficiently than Ebola’s.

/* */