https://doi.org/10.1172/jci.insight.199232 Here, Savita G. Pahwa & team demonstrate high-dose vaccination for influenza strengthens immunity in older adults with HIV after prior standard dosing, but not all strain-specific weaknesses were overcome.
1Department of Microbiology and Immunology.
2Division of Biostatistics, Department of Public Health Sciences; and.
3Division of Infectious Diseases, Department of Medicine, University of Miami Miller School of Medicine, Miami, Florida, USA.
Mark Zuckerberg is following a path paved by fellow billionaires Bill Gates and Warren Buffet: laundering his untold billions through a health research prestige project.
Called the Chan Zuckerberg Biohub — his wife Priscilla Chan, a pediatrician, is also involved — the foundation’s stated long-term mission is to “cure and prevent all disease through AI-powered biology, frontier research, and state-of-the-art technology.”
True to those enormous goals, the Biohub recently announced a $500 million investment into AI models of human cells, specifically, in order to “accelerate the cure and prevention of all diseases,” Euronews reported.
We already know that moving your body is important for brain health, but a new study reveals a possible reason why: It could be triggering a kind of hydraulic pump that flushes out fluid in the brain.
By studying mice and conducting simulations, researchers at the Pennsylvania State University (Penn State) have found that movements in the abdominal muscles can ripple all the way up to the brain, potentially cleaning out waste materials that build up during the day.
It’s tangible evidence that what goes on in our brains and our bodies isn’t so separate after all, and a good reminder to get that body moving, in whatever way works for you, throughout the day.
In a world where technology and biology converge at an accelerating pace, a new era of self-improvement is emerging — biohacking. This once-niche movement has transformed into a global phenomenon, attracting everyone from Silicon Valley executives to amateur enthusiasts. The promise? To optimize the human mind and body beyond natural limits using a blend of science, lifestyle adjustments, and cutting-edge technology.
But what exactly is biohacking? Is it the future of personal health and evolution, or a slippery slope into risky experimentation? In this article, we’ll delve deep into the world of biohacking — its origins, principles, popular techniques, controversies, and future potential. Whether you’re a skeptic, a curious observer, or a self-improvement junkie, the world of biohacking has something provocative for everyone.
Over the past few decades, neuroscientists and medical researchers worldwide have been trying to leverage available health records, brain scans and other medical data to uncover biological markers associated with the onset of specific diseases or neuropsychiatric disorders. The identification of these biomarkers could help to devise new tools to predict the risk that individual patients will develop a specific condition, allowing doctors to intervene early, preventing or delaying its emergence or slowing down its progression.
Researchers at the University of Texas Health Science Center, UTHealth Houston School of Behavioral Health Sciences, Keck School of Medicine of USC, and University of Maryland School of Medicine recently devised a new brain-based index that could be used to track early risk factors that, in specific people, may lead to the development of Alzheimer’s disease (AD). AD is a progressive neurodegenerative condition that prompts the deterioration and death of brain cells, leading to progressive memory loss and a decline in mental functions. AD has very limited treatment options after the diagnosis but the brain changes that culminate in AD take decades, thus suggesting that public effort should be focused on prevention.
The researchers devised an index that could be used to quantify patterns in a person’s brain that measure the similarity to those observed in individuals diagnosed with AD and followed as a part of the research studies such as Alzheimer’s Disease Neuroimaging Initiative (ADNI). This index, introduced in a paper published in Molecular Psychiatry, was derived by performing a mega-analysis of publicly available brain imaging data collected from people with and without AD.
Photodetectors remain a critical component in the development of advanced electronics and photonics, particularly in the role of signal readout through the conversion of photons into electrons. These digital imaging components are ubiquitous in sensors, cameras, adaptive displays, telecommunications, LiDAR systems, health monitoring wearables, and oximeters.
In the quest toward the next generation of optoelectronic devices, the spotlight lands upon ultrathin 2D materials with improved performance for integrated circuits and wearable electronics. In a recent study published in ACS Applied Electronic Materials, a team of researchers led by Haizhao Zhi and Eng Tuan Poh introduced a series of wide bandgap 2D materials—transition metal thio(seleno)phosphates into the light.
The team focused on manganese thiophosphate (MnPS3), a wide-bandgap semiconductor that is naturally “solar-blind,” meaning it is highly sensitive to UV light while remaining transparent to much of the visible spectrum. While MnPS3 is an excellent candidate for UV sensing, its performance as a standalone material is often limited by low carrier mobility—it acts almost like a “near-perfect insulator.”
FNDC5/irisin detection was performed by a sandwich ELISA reaction using DuoSet® ELISA Development Systems kit (R&D Systems), according to manufacturer’s instructions. Blood samples were collected at 10 or 40 dpi, allowed to sit for at least 1 h, and then centrifuged for 10 min at 224 g in a refrigerated centrifuge (4 °C) to isolate the serum. Samples were stored at −80 °C until irisin detection.
Serum samples were assayed for TNF-α, INF-γ, IL-2, IL-4, IL-6, IL-10, and IL-17a using a Cytometric Bead Array (CBA) Th1/ Th2/ Th17 kit (BD Biosciences), according to the manufacturer’s instructions. Data were acquired using a Cytoflex S (Beckman Coulter) flow cytometer. After data acquisition, dedicated software (FCAP Array, BD Biosciences) was used to analyze the results by gating bead populations, calculating MFI values, generating standard curves, and determining analyte concentrations. These analyses were performed at the Flow Cytometry Facility of the Instituto Oswaldo Cruz (Fiocruz).
T. gondii infection was quantified using RT-qPCR with bag1 and enolase2 primers to detect bradyzoite and tachyzoite forms, respectively, according to49. Ct values were compared to a standard curve amplification, derived from known T. gondii RNA concentrations. The standard curve was constructed with six 10-fold dilutions, starting with 6.0 × 106 parasites for either bradyzoites or tachyzoites. Primer sequences are available in Table 2.
The chikungunya virus (ChikV) was first isolated during an arthritic disease outbreak in Tanzania in 1952 [1, 2]. ChikV is a mosquito-borne virus that belongs to the Alphavirus genus of the Togaviridae family. ChikV infections have emerged as a global health risk with approximately 16.9 million cases per year [3]. Major symptoms of ChikV infection include severe fever, rashes, and joint pain. Chronic arthritis-like symptoms may persist and can be debilitating [4, 5]. ChikV, a positive-sense RNA virus, encodes 5 structural proteins and 4 nonstructural proteins (NSP1 to NSP4) [6]. Nonstructural protein 3 (NSP3) consists of a conserved macrodomain (Mac1) at the N-terminus, a poorly conserved hypervariable domain, and a central zinc-binding domain known as the alphavirus unique domain [7]. The macrodomain fold is highly conserved across evolution, having been identified in bacteria, algae, and eukaryotes [8, 9]. It has been suggested that ChikV Mac1 suppresses the host immune response through its adenosine diphosphate ribosyl (ADP-ribosyl) hydrolase activity [10], which removes ADP-ribose posttranslational modifications from target host proteins by hydrolyzing mono-ADP-ribosylated aspartate and glutamate residues. Mac1 has therefore emerged as a promising antiviral drug target [10], supported by evidence suggesting that it is a key determinant of ChikV virulence in mice. Despite their therapeutic potential, efforts to identify ChikV inhibitors have had limited success. A fragment screen of ~14,000 compounds identified only weak inhibitors (e.g., 2-pyrimidone-4-carboxylic acid scaffold, with one of the compounds showing IC50 of 23 μM) [11]. Another computational docking and simulation study screened 820 compounds and predicted that natural compounds from plants, including apigetrin, baicalin, baloxavir, luteoloside, rutaecarpine, and amentoflavone [12], are Mac1 inhibitors. The predicted binding affinity of baicalin was −10.8 kcal/mol against ChikV Mac1. Another study identified N-[2-(5-methoxy-1 H-indol-3-yl) ethyl]-2-oxo-1,2-dihydroquinoline-4-carboxamide through virtual screening of 245,532 natural compounds, followed by in vitro validation using a microscale thermophoresis binding assay (binding constant [Kd] of 1.066 × 10−6 ± 0.95 μM) and in vivo inhibition of ChikV replication [13].
Similar to ChikV, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) NSP3 contains 3 tandem macrodomains, with Mac1 serving as the catalytically active macrodomain that binds and hydrolyzes mono-ADP-ribose on posttranslationally modified target host proteins [14,15]. SARS-CoV-2 Mac1 is essential for viral pathogenesis and represents a promising drug target [16,17]. In contrast to ChikV Mac1, it has proven amenable to inhibitor development. An early crystallographic screen of approximately 2,600 compounds revealed 234 fragment structures bound to SARS-CoV-2 Mac1 [18]. Using these hits, several optimized inhibitors were designed, followed by another round of crystallographic screening [19]. Among the resulting top inhibitors was AVI-4206, a potent inhibitor with an IC50 of 20 nM that is effective in an animal model of SARS-CoV-2 infection [20]. Other studies have identified additional promising scaffolds, including 2-amide-3-methylester thiophene scaffold derivatives that bind SARS-CoV-2 Mac1 (IC50 = 1.5 μM) and inhibit viral replication [21], synthetic analogs of ADP-ribose that bind SARS-CoV-2 Mac1 with nanomolar affinity [22], and pyrrolo-pyrimidine-based compounds that inhibit viral replication in SARS-CoV-2 [23].
The structural similarity between ChikV Mac1 and SARS-CoV-2 Mac1 [24] has not translated into similar druggability. One strategy to improve ligand-binding affinity is to exploit the presence of water molecules in the binding site by designing inhibitors that effectively use them to form bridging interactions that strengthen binding to the protein [25]. This strategy is particularly relevant for Mac1 ADP-ribose-binding sites, which are large, solvent exposed, and known to maintain an extensive network of ordered water molecules upon ADP binding. In SARS-CoV-2 Mac1, ADP-ribose forms several water-mediated interactions, resulting in the water network in the ADP-ribose-binding site reorganizing upon ligand binding [18,26].
Scientists from A*STAR Infectious Diseases Labs (A*STAR IDL), Nanyang Technological University, Singapore’s Lee Kong Chian School of Medicine (LKCMedicine), the National University of Singapore (NUS), and international collaborators have uncovered how Mycobacterium abscessus—a bacterium that causes serious lung infections—can evade bacteriophage (phage) therapy, and demonstrated a combination strategy to overcome this resistance, offering a pathway toward more effective and durable treatments. The study was published in the Proceedings of the National Academy of Sciences.
Antimicrobial resistance (AMR) is an escalating health challenge that is expected to place growing strain on health care systems worldwide. As AMR continues to erode the effectiveness of existing antibiotics—with one in six bacterial infections worldwide now resistant to antibiotics—scientists are accelerating efforts to develop new countermeasures such as phage therapy, which uses viruses to target bacteria. These efforts are important for strengthening global health and infectious disease preparedness.
A simple nutrient from everyday vegetables could help supercharge the body’s fight against cancer. A common eye-health nutrient, zeaxanthin, may also help the body fight cancer more effectively. Scientists discovered it strengthens Tcells and enhances the impact of immunotherapy treatments. Found in everyday vegetables and supplements, it’s safe, accessible, and shows strong potential as a cancer therapy booster. Human trials are the next step.
Researchers at the University of Chicago have uncovered a surprising new role for zeaxanthin, a plant-based compound best known for supporting eye health. According to findings published in Cell Reports Medicine, this common carotenoid may also help the immune system fight cancer by enhancing the activity of key immune cells. The discovery points to zeaxanthin as a simple, widely available supplement that could improve how well cancer immunotherapies work.
“We were surprised to find that zeaxanthin, already known for its role in eye health, has a completely new function in boosting anti-tumor immunity,” said Jing Chen, PhD, Janet Davison Rowley Distinguished Service Professor of Medicine and senior author of the study. “Our study show that a simple dietary nutrient could complement and strengthen advanced cancer treatments like immunotherapy.”