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Human Immunodeficiency Virus type 1 (HIV-1) latency represents a significant hurdle in finding a cure for HIV-1 infections, despite tireless research efforts. This challenge is partly attributed to the intricate nature of HIV-1 latency, wherein various host and viral factors participate in multiple physiological processes. While substantial progress has been made in discovering therapeutic targets for HIV-1 transcription, targets for the post-transcriptional regulation of HIV-1 infections have received less attention. However, cumulative evidence now suggests the pivotal contribution of post-transcriptional regulation to the viral latency in both in vitro models and infected individuals.

“Surgery means extensive recovery time and can significantly impact patient health. Our system doesn’t require surgery because we use a conventional stent, the catheter, as a delivery vehicle,” said W. Hong Yeo, the Harris Saunders Jr. Endowed Professor and an associate professor in the George W. Woodruff School of Mechanical Engineering.

Made from ultra-thin, flexible silicone, these nanosensors can be embedded in almost anything, from pacifiers to catheters. But size was just one element the researchers needed to consider when developing this device; accuracy was just as important.


Hong Yeo holds an in-stent nanomembrane sensor that can detect intracranial pressure.

A car accident, football game, or even a bad fall can lead to a serious or fatal head injury. Annually, traumatic brain injuries (TBI) cause half a million permanent disabilities and 50,000 deaths. Monitoring pressure inside the skull is key to treating TBI and preventing long-lasting complications.

Most of these monitoring devices are large and invasive, requiring surgical emplacement. But Georgia Tech researchers have recently created a sensor smaller than a dime. The miniature size offers huge benefits.

The immune system fights germs on the skin, in the tissues of the body, and in bodily fluids such as blood. It is made up of the innate (general) immune system and the adaptive (specialized) immune system. These two systems work closely together and take on different tasks.

The innate immune system is the body’s first line of defense against intruders. It responds in the same way to all germs and foreign substances, which is why it is sometimes referred to as the “non-specific” immune system. It acts very quickly – for instance, it makes sure that bacteria that have entered the skin through a small wound are detected and destroyed on the spot within a few hours. But the innate immune system can’t always stop germs from spreading.

This Review explores how experimental models of metastasis, such as mouse models and cell cultures, can complement the (multi)omics analysis of human metastasis samples, thereby filling knowledge gaps left by model studies and validating the findings from human sequencing data.

Aging is a complex, progressive, and irreversible biological process that entails numerous structural and functional changes in the organism. These changes affect all bodily systems, reducing their ability to respond and adapt to the environment. Chronic inflammation is one of the key factors driving the development of age-related diseases, ultimately causing a substantial decline in the functional abilities of older individuals. This persistent inflammatory state (commonly known as “inflammaging”) is characterized by elevated levels of pro-inflammatory cytokines, an increase in oxidative stress, and a perturbation of immune homeostasis. Several factors, including cellular senescence, contribute to this inflammatory milieu, thereby amplifying conditions such as cardiovascular disease, neurodegeneration, and metabolic disorders.

To grow, cancer tumors must hijack the immune system for their needs. One of the main tricks that most tumors use is to manipulate a type of immune cell called a macrophage, causing it to protect the tumor from the rest of the immune system, recruit blood vessels and help the cancer spread to other tissues.

Now researchers in Prof. Ido Amit’s lab at the Weizmann Institute of Science have used state-of-the-art gene editing and single-cell and AI technologies to identify a master switch that turns macrophages into cancer helpers.

Based on this discovery, the team developed a new therapy that was shown to be effective in mice with bladder tumors, one of the most common types of cancer in humans and one for which only limited therapeutic innovations are currently available. The discovery is presented in a paper published in the journal Cancer Cell.

A revolutionary blueprint is emerging from a fragment of brain tissue, promising new insights into the mysteries of the human mind. At the heart of this innovation is NEURD—short for “NEURal Decomposition”—a groundbreaking software package developed by researchers at Baylor College of Medicine.

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With NEURD, the time-consuming process of mapping the intricate “street map” of brain connections is being transformed, enabling faster error detection and data corrections that pave the way for discovery.