There are two activities in medical science in which both the academic research community and clinical development industry are truly terrible at achieving results, or indeed even at getting started at all. The first is transfer of programs from academia to industry. The renowned valley of death in the development of new medical biotechnologies is very real; so very many programs languish undeveloped simply because neither side can effectively coordinate with the other. The second is the testing of synergies between multiple therapies that are applied at the same time to the same patient for the treatment of the same condition. We live in a world in which age-related conditions are the result of multiple distinct contributing mechanisms, so why is it that the exploration and application of combined therapies targeting separate mechanisms is such a rare occurrence?
Firstly, different therapies tend to be owned by different groups (companies or universities) who have only limited incentives to collaborate with one another. Because the biotech field is governed in a very heavy-handed way by intellectual property and other forms of government regulation, setting up a collaboration is a costly matter. Thus in a world in which the expectation is that few efforts will be successful, as is the case for most initiatives in medical science, there is an unwillingness to explore. Secondly, the regulatory process for approval is very, very costly. Taking a candidate drug through to phase III trial success is at least a $150M proposition, and usually more. Companies do all they can to make clinical trials as simple as possible, and there is no incentive to roll the dice on a collaborative trial that depends on another drug outside the control of the company in question.
And yet, aging and all age-related diseases are the consequence of multiple underlying forms of molecular damage. They will require multiple very different therapies to achieve complete reversal or prevention. The perverse incentives in medical regulation and intellectual property are acting to close off the most promising strategy for the treatment of aging, which is to tackle all of its varied causes concurrently. Something must change here. As Aubrey de Grey points out in the short interview below, this is the next frontier for patient advocacy. Now that the first rejuvenation therapies are being actively developed, using them together is a logical next step.
Aubrey is a plain-speaking biomedical gerontologist who is committed to combating the aging process. We started by asking him about what he was up to at the moment.
SENS Research Foundation suffered a fair amount of slowdown as a result of the pandemic, but we’re picking up now. I think the most exciting thing we’re doing is continuing to strengthen the pipeline between the really early-stage translational work we do at SENS and the “just investable” stage work pursued by startups in our space, including our own spinouts. Basically, the appetite of some investors is increasingly emphasising projects that are so early that they would historically be viewed as pre-competitive; that boundary is now becoming very blurred.
What isn’t getting sufficient exposure?
I would say that the single biggest elephant in the room is the simultaneous administration of multiple therapies. It is subliminally understood that damage repair is the future of longevity medicine, and also that the damage repair paradigm is inescapably a divide-and-conquer one that will entail combination therapies, but the medical industry is really not set up to develop and promote that way of working. At some point that has to change, and I’m hopeful that investors at the more courageous end of the spectrum will soon find ways to start that process in earnest.
Our survey found that most investors appear to prefer seed-to-early-stage investing, have you found this to be case in your networks?
Absolutely. At this point I don’t see how things could be otherwise, actually, because the investment opportunities consist almost entirely of startups, which in turn is because the underlying technologies are so new.
We also saw that senolytics are a very popular category for investors – are you seeing an increased appetite from investors?
I do see that tendency too, and it’s not surprising to me, because senolytics have two huge things going for them: they are bona fide rejuvenators (i.e. they repair a type of aging damage rather than just slowing down its accumulation), which is much more exciting to people old enough to have money to invest, and they are only just now going into clinical trials and showing impressive results, so they are opportunities for first movers.
Source: Fight Aging!
Realme Q Series Phone Allegedly Spotted on TENAA, Key Specifications Tipped
Realme Q series seem to be getting a new smartphone and it allegedly been spotted on TENAA, offering a glimpse of the possible specifications. A Realme smartphone with model number RMX2117 was spotted on the regulator’s website and it is being speculated that the phone could be a part of the company’s Q series that already includes one phone. The TENAA listing shows the phone sporting a 6.5-inch display and powered by an octa-core SoC clocked at 2.4GHz. The listing also hints that the phone may carry up to 8GB of RAM and up to 256GB of onboard storage. Realme hasn’t officially confirmed any of the specifications.
As per the listing on TENAA, the smartphone with model number RMX2117 sports a 6.5-inch full-HD+ (1,080×2,400 pixels) display with a 20:9 aspect ratio. Allegedly belonging to the rumoured Realme Q series, the smartphone supports 5G and is powered by an octa-core SoC clocked at 2.4GHz.
The Realme Q series phone may be launched in China in three RAM options – 4GB, 6GB, and 8GB, that may be coupled with three inbuilt storage configurations – 64GB, 128GB, and 256GB. The listing also shows a microSD card slot for storage expansion. It may be launched in four colour options – Black, Blue, Gray, and Silver.
The phone is seen featuring a rectangular camera module that includes a 48-megapixel primary sensor, an 8-megapixel snapper, and a 2-megapixel shooter. For selfies and video calls, the phone features a 16-megapixel camera at the front. The Realme RMX2117 smartphone packs a 4,900mAh battery. The handset runs on Android 10 and features a side-mounted fingerprint scanner. The smartphone measures 162.2 x 75.1 x 9.1mm and weighs 194 grams.
The development comes a week after Realme vice president Xu Qi Chase teased the arrival of a new series, including the Q series, V series, and X series, with in a poster. Chase noted that the upcoming phone will be powered by a 5nm flagship chipset.
Redmi Note 8 or Realme 5s: Which is the best phone under Rs. 10,000 in India right now? We discussed this on Orbital, our weekly technology podcast, which you can subscribe to via Apple Podcasts or RSS, download the episode, or just hit the play button below.
How to remove the 3D Objects folder from File Explorer in Windows 10
The 3D Objects folder is not useful for many users but removing it from File Explorer in Windows 10 requires a tweak of the Registry File. We show you how.
In addition to the traditional Paint application, which has been a part of Windows since its beginning, Microsoft has also added Paint 3D to its list of standard Windows 10 applications. When combined with a touch display and a stylus or pen, Paint 3D can be a powerful tool for creating three-dimensional objects, a feature many artists and designers find useful.
SEE: 30 Excel tips you need to know (TechRepublic Premium)
However, if you are not inclined to use Paint 3D, you may find the prominence of a 3D Objects folder, and possibly several other folders, on the This PC screen of File Explorer obtrusive and unnecessary. Unfortunately, you cannot remove those folders from File Explorer with a simple change to default settings. That procedure requires an edit of the Windows 10 Registry File.
This how-to tutorial shows you how to remove the 3D Objects folder, and other folders, from the This PC screen of the Windows 10 File Explorer.
How to remove 3D Objects folder from File Explorer
Disclaimer: Editing the Windows Registry file is a serious undertaking. A corrupted Windows Registry file could render your computer inoperable, requiring a reinstallation of the Windows 10 operating system and potential loss of data. Back up the Windows 10 Registry file and create a valid restore point before you proceed.
To get a better idea of what we are talking about, open File Explorer in Windows 10 and then navigate to the This PC screen, as shown in Figure A. Take note of the default listing of folders in the right-hand window.
We are going to concentrate our efforts on the 3D Objects folder, but this technique will work for any of the default folders listed in that section of File Explorer, if you know the code. Further, if you are running the 64-bit version of Windows 10, you will have to perform two edits.
Type “regedit” into the search box on the Windows 10 desktop and select the appropriate result to start the Registry Editor application. As shown in Figure B, navigate to this key (it’s a deep dive):
To complicate matters, the subkeys in the NameSpace section are coded, so you have to carefully choose the key with this code (on my computer, it was in the second position, see Figure C):
Right-click the key and select “Delete” from the context menu and confirm your action.
If you are running the 32-bit version of Windows 10, you have completed the procedure, however, if you are running the 64-bit version, you will have to perform a second edit. As shown in Figure D, navigate to this key:
As before, locate this coded key in the NameSpace folder, as shown in Figure E:
Right-click the key and select “Delete” from the context menu and then confirm your selection to complete the process. Exit out of the Registry File editor. The change should take effect the next time you open File Explorer.
The 3D Objects folder is located in the Users folder and will still be there after implementing this procedure, but it will no longer be displayed so prominently in the This PC section of File Explorer, as shown in Figure F.
To restore the 3D Objects folder to File Explorer, add the coded key back into the two NameSpace Folders using the Registry File Editor.
Twist on CRISPR Gene Editing Treats Adult-Onset Muscular Dystrophy in Mice
Myotonic dystrophy type I is the most common type of adult-onset muscular dystrophy. People with the condition inherit repeated DNA segments that lead to the toxic buildup of repetitive RNA, the messenger that carries a gene’s recipe to the cell’s protein-making machinery. As a result, people born with myotonic dystrophy experience progressive muscle wasting and weakness and a wide variety of other debilitating symptoms.
CRISPR-Cas9 is a technique increasingly used in efforts to correct the genetic (DNA) defects that cause a variety of diseases. A few years ago, University of California San Diego School of Medicine researchers redirected the technique to instead modify RNA in a method they call RNA-targeting Cas9 (RCas9).
In a new study published in Nature Biomedical Engineering, the team demonstrates that one dose of RCas9 gene therapy can chew up toxic RNA and almost completely reverse symptoms in a mouse model of myotonic dystrophy.
“Many other severe neuromuscular diseases, such as Huntington’s and ALS, are also caused by similar RNA buildup,” said senior author Gene Yeo, PhD, professor of cellular and molecular medicine at UC San Diego School of Medicine. “There are no cures for these diseases.” Yeo led the study with collaborators at Locanabio, Inc. and the University of Florida.
Normally, CRISPR-Cas9 works by directing an enzyme called Cas9 to cut a specific target gene (DNA), thereby allowing researchers to inactivate or replace the gene. RCas9 works similarly, but Cas9 is guided to an RNA molecule instead of DNA.
In a 2016 study, Yeo’s team demonstrated that RCas9 worked by using it to track RNA in live cells. In a 2017 study in lab models and patient-derived cells, the researchers used RCas9 to eliminate 95 percent of the aberrant RNA linked to myotonic dystrophy type 1 and type 2, one type of ALS and Huntington’s disease.
The current study advances RCas9 therapy further, reversing myotonic dystrophy type 1 in a living organism: a mouse model of the disease.
The approach is a type of gene therapy. The team packaged RCas9 in a non-infectious virus, which is needed to deliver the RNA-chewing enzyme inside cells. They gave the mice a single dose of the therapy or a mock treatment.
RCas9 reduced aberrant RNA repeats by more than 50 percent, varying a bit depending on the tissue, and the treated myotonic dystrophy mice became essentially indistinguishable from healthy mice.
Initially, the team was worried that the RCas9 proteins, which are derived from bacteria, might cause an immune reaction in the mice and be rapidly cleared away. So they tried suppressing the mice’s immune systems briefly during treatment. As a result, they were surprised and pleased to discover that they prevented immune reaction and clearance, leaving the viral vehicle and its RCas9 cargo to persist, and get the job done. What’s more, they did not see signs of muscle damage. In contrast, they saw an increase in the activity of genes involved in new muscle formation.
“This opens up the floodgates to start testing RNA-targeting CRISPR-Cas9 as a potential approach to treat other human genetic diseases — there are at least 20 caused by buildup of repetitive RNAs,” Yeo said.
It remains to be seen if RCas9-based therapies will work in humans, or if they might cause deleterious side effects, such as eliciting an undesired immune reaction. Preclinical studies such as this one will help the team work out potential toxicities and evaluate long-term exposure.
In 2017, Yeo co-founded a company called Locanabio to accelerate the development of RNA-targeting CRISPR-Cas9 through preclinical testing and into clinical trials for the treatment of myotonic dystrophy and potentially other diseases.
Source: UC San Diego
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