Toggle light / dark theme

❀ Check out the Gradient Dissent podcast by Weights & Biases: http://wandb.me/gd.

📝 The paper “Endless Loops: Detecting and Animating Periodic Patterns in Still Images” and the app are available here:
https://pub.res.lightricks.com/endless-loops/

🙏 We would like to thank our generous Patreon supporters who make Two Minute Papers possible:
Aleksandr Mashrabov, Alex Haro, Andrew Melnychuk, Angelos Evripiotis, Benji Rabhan, Bryan Learn, Christian Ahlin, Eric Haddad, Eric Martel, Gordon Child, Ivo Galic, Jace O’Brien, Javier Bustamante, John Le, Jonas, Kenneth Davis, Klaus Busse, Lorin Atzberger, Lukas Biewald, Matthew Allen Fisher, Mark Oates, Michael Albrecht, Nikhil Velpanur, Owen Campbell-Moore, Owen Skarpness, Ramsey Elbasheer, Steef, Taras Bobrovytsky, Thomas Krcmar, Torsten Reil, Tybie Fitzhugh, Ueli Gallizzi.
If you wish to appear here or pick up other perks, click here: https://www.patreon.com/TwoMinutePapers.

Meet and discuss your ideas with other Fellow Scholars on the Two Minute Papers Discord: https://discordapp.com/invite/hbcTJu2

Infinity Cache is one of the headline features found in AMD’s RDNA 2 – the GPU architecture behind the next generation of gaming graphics, including the PS5, the Xbox Series X and, of course, AMD’s own Radeon RX 6000 graphics cards. But, what is Infinity Cache?

Read on to learn more about Infinity Cache, how it works and where you can find it.

Infinity Cache is an all-new cache level AMD says will improve the efficiency and performance of its RDNA 2 architecture during 4K and 1440p gaming.

Circa 2010


In this review, we consider the evidence that a reduction in neurogenesis underlies aging-related cognitive deficits, and impairments in disorders such as Alzheimer’s disease (AD). The molecular and cellular alterations associated with impaired neurogenesis in the aging brain are discussed. Dysfunction of presenilin-1, misprocessing of amyloid precursor protein and toxic effects of hyperphosphorylated tau and ÎČ-amyloid likely contribute to impaired neurogenesis in AD. Since factors such as exercise, enrichment and dietary energy restriction enhance neurogenesis, and protect against age-related cognitive decline and AD, knowledge of the underlying neurogenic signaling pathways could lead to novel therapeutic strategies for preserving brain function. In addition, manipulation of endogenous neural stem cells and stem cell transplantation, as stand-alone or adjunct treatments, seem promising.

There is a progressive decline in the regenerative capacity of most organs with increasing age, resulting in functional decline and poor repair from injury and disease. Once thought to exist only in high turnover tissues, such as the intestinal lining or bone marrow, it now appears that most tissues harbor stem cells that contribute to tissue integrity throughout life. In many cases, stem cell numbers decrease with age, suggesting stem cell aging may be of fundamental importance to the biology of aging (for review, see Ref. [1]). Therefore, understanding the regulation of stem cell maintenance and/or activation is of considerable relevance to understanding the age-related decline in maintaining tissue integrity, function, and regenerative response.

The adult brain contains neural stem cells (NSCs) that self-renew, proliferate and give rise to neural progenitor cells (NPC) that exhibit partial lineage-commitment. Following several cycles of proliferation, NPC differentiate into new neurons and glia. NSCs are increasingly acknowledged to be of functional significance and harbor potential for repair of the diseased or injured brain. The dramatic decline in neurogenesis with age is thought to underlie impairments in learning and memory, at least in part. Aging is also the greatest risk factor for Alzheimer’s disease (AD), a neurodegenerative disease characterized by progressive loss of memory and cognitive decline. Alterations in neurogenesis have been described extensively in animal models of AD, and key proteins involved in AD pathogenesis are shown to regulate neurogenesis.

Breast cancer is the leading cause of cancer death in women around the world, responsible for 1700 deaths every day. Although the vast majority of breast cancers are treatable, the most aggressive subtype—triple negative breast cancer (TNBC) – has a high recurrence rate, a high potential for metastasis and shows resistance to conventional treatments, leading to very poor prognosis and survival outcomes. A team of researchers at the Research Institute of the McGill University Health Center (RI-MUHC) conducted a preclinical study and discovered a novel targeted combination therapy that efficiently reduced tumor growth in metastatic breast cancer. Published in Nature Communications, their findings could lead to the development of a novel first line targeted therapy for the treatment of TNBC, with the prospect of rapidly transitioning to clinical trials in humans.

“There is no targeted therapy for TNBC. Chemotherapy treatment can even enrich these tumors in and be detrimental to the patient, as we have shown in a previous study,” says Dr. Jean-Jacques Lebrun, senior scientist in the Cancer Research Program at the RI-MUHC and principal investigator of the study. “Filling that huge medical gap was our motivation in conducting this study.”

While most breast cancers have one of three main receptors that are like entrance gates for treatments—estrogen, progesterone and a protein called human epidermal growth factor (HER2) – TNBC has none, thus the name triple negative . Using state-of-the-art technologies such as and genome-wide molecular approaches, the team identified two pathways which could be targeted in a therapeutic strategy.