Lifeboat Foundation

Huge libraries of drug compounds may hold potential treatments for a variety of diseases, such as cancer or heart disease. Ideally, scientists would like to experimentally test each of these compounds against all possible targets, but doing that kind of screen is prohibitively time-consuming.

In recent years, researchers have begun using computational methods to screen those libraries in hopes of speeding up drug discovery. However, many of those methods also take a long time, as most of them calculate each target protein’s three-dimensional structure from its amino-acid.

Recent advances in cancer diagnosis, treatment, and management have resulted in a growing number of cancer survivors. Researchers constantly strive to understand new ways to support cancer survivors and help them lead a healthy and happy life post-treatment. This has led to our understanding that cancer survivors have different healthcare needs than their counterparts with no history of cancer.

One concern facing cancer survivors involves cardiovascular disease (CVD), a general term including conditions that inflict the heart or blood vessels. Many cancer survivors face a higher risk of dying from cardiovascular disease (CVD) than from cancer itself.

Despite the well-known adverse effects of tobacco use associated with both cancer and CVD, about 20% of cancer survivors continue smoking after diagnosis. How smoking cessation impacts CVD risk after cancer diagnosis remains poorly understood. To address this, a team of researchers recently published their study investigating the cardiovascular consequences of quitting smoking after a cancer diagnosis in the European Heart Journal.

During the experiment, pluripotent stem cells – a special kind of stem cells that have the potential to grow into all major human cells – were brought into the Wentian lab module on the space station, where some of them successfully grew into hematopoietic stem cells – another kind of stem cells that produce blood cells.

Dozens of other science experiments were also conducted by the Shenzhou-15 crew during their stay at the China Space Station.

Here we address the important question of cross-talk between the mitochondria and cytosol. We show that the inner mitochondrial protein, MiNT, interacts with a protein on the outer mitochondrial membrane (mNT). This interaction occurs within the major outer membrane protein VDAC1. Inside the inner space of VDAC1, MiNT transfers its [2Fe-2S] clusters to mNT, which was shown to be a [2Fe-2S] cluster donor protein that donates its cluster(s) to apo-acceptor proteins residing in the cytosol. Hence, we suggest a pathway for transferring [2Fe-2S] clusters from inside the mitochondria to the cytosol.

Mitochondrial inner NEET (MiNT) and the outer mitochondrial membrane (OMM) mitoNEET (mNT) proteins belong to the NEET protein family. This family plays a key role in mitochondrial labile iron and reactive oxygen species (ROS) homeostasis. NEET proteins contain labile [2Fe-2S] clusters which can be transferred to apo-acceptor proteins. In eukaryotes, the biogenesis of [2Fe-2S] clusters occurs within the mitochondria by the iron–sulfur cluster (ISC) system; the clusters are then transferred to [2Fe-2S] proteins within the mitochondria or exported to cytosolic proteins and the cytosolic iron–sulfur cluster assembly (CIA) system. The last step of export of the [2Fe-2S] is not yet fully characterized. Here we show that MiNT interacts with voltage-dependent anion channel 1 (VDAC1), a major OMM protein that connects the intermembrane space with the cytosol and participates in regulating the levels of different ions including mitochondrial labile iron (mLI). We further show that VDAC1 is mediating the interaction between MiNT and mNT, in which MiNT transfers its [2Fe-2S] clusters from inside the mitochondria to mNT that is facing the cytosol. This MiNT–VDAC1–mNT interaction is shown both experimentally and by computational calculations. Additionally, we show that modifying MiNT expression in breast cancer cells affects the dynamics of mitochondrial structure and morphology, mitochondrial function, and breast cancer tumor growth. Our findings reveal a pathway for the transfer of [2Fe-2S] clusters, which are assembled inside the mitochondria, to the cytosol.

Malaria, a mosquito-borne infectious disease mostly found in tropical climates, is now on American shores. Late Monday, the Centers for Disease Control and Prevention announced a spat of cases — one in Texas and four in Florida — discovered in May and June that were locally acquired versus acquired while traveling abroad. This is the first time this has happened since 2003.

The CDC said that all five patients received treatment and are recovering, but the agency remains on alert for any new cases. While malaria was once a public health threat in the US, its presence was eradicated in the early 1950s. The last major outbreak was in 2003 with eight patients in Palm Beach County, Florida, all of whom had significant outdoor exposure.

For now, the CDC says the risk of catching malaria in the US “remains extremely low.” However, the instance shouldn’t be taken lightly, especially as many of us will be spending more time outdoors and traveling during the summer. Here’s what you need to know.

In an organism, different kinds of cells carry out specific, specialized functions. Scientists can grow and study various types of cells in the lab. For a long time, a source of many of those cell lines were cancer samples that could be easily cultured over many generations. But those cells were not always representative of a particular cell type. Now, following huge breakthroughs, scientists learned how to create stem cells from adult skin cells. This has allowed scientists to utilize adult cells like those from the skin to create induced pluripotent cells (iPSCs), which can then be made into virtually any cell type.

The creation of so-called iPSCs was made possible through changing gene expression in cells, often with certain molecules or specialized proteins. Cells can also now be directly reprogrammed in some ways, without needing to bring them to a pluripotent state. The number of cell types that can be generated in this way is also expanding, bringing new insights into how specialized cells function.

It sucks that the primary reason this has not gone forward is because it is off patent.

This video is reproduced from a presentation I gave to the Euro-Geroscience Task Force “Challenges in Developing Geroscience Drug Trials” held March 23, 2022 in Toulouse, France. It gives an introduction to the state of research on rapamycin as a potential longevity and healthspan drug and some of the challenges and opportunities for clinical development.

Year 2022 😗😁

Summary: A rare genetic mutation that causes blindness also appears to be associated with above-average intelligence, a new study reports.

Source: University of Leipzig

Continue reading “How a Gene Mutation Causes Higher Intelligence” »

The 2023 edition of the exclusive Longevity Investors Conference is fast approaching, bringing together investors, companies and researchers in Gstaad, Switzerland in September. One of the speakers at this year’s conference is scientist, writer and presenter Dr Andrew Steele, the author of the best-selling book Ageless: The new science of getting older without getting old. When it comes to his views on longevity, Steele sits firmly in the camp that aging, like cancer, is something that humanity should be focused on curing.

Longevity. Technology: Last year, Steele told us he was “absolutely convinced” curing aging is possible, but that significant questions remain around how quickly we can get there. As he prepares to speak to more than 100 investors at LIC, we caught up with Steele to see how his views on longevity have evolved, and what he would say to those considering investing in the field.

First and foremost, Steele, who recently published a new, free chapter of Ageless on the moral, ethical and social consequences of treating aging, believes that longevity represents a huge “human opportunity” for investors.