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The number of people with pre-diabetes who go on to develop Type 2 Diabetes has been reducing over the past 2 decades, according to a study led by University of Manchester epidemiologists.

However, the changes, says lead author Dr Rathi Ravindrarajah, are likely to be attributed to changes in the definition of pre-diabetes and recording practices, but also preventative work by the NHS.

The study also seems to show that the conversion risk, from pre-diabetes (more recently formalised as non-diabetic hyperglycaemia or NDH) to Type 2 diabetes, for those aged over 85 is very low.

Conversion to Type 2 Diabetes declining

The NIHR funded study shows, based on data from the Clinical Practice Research Datalink of 148,363 participants with pre-diabetes/NDH from 2000 to 2015, how quickly these people go on to develop Type 2 Diabetes and what are their characteristics.

Between 2000 and 2015, before the introduction of the NHS Diabetes Prevention Programme, 1.6% of the sample converted to the illness after a month, 4.2% converted after 6 months and 20.4% converted after 4 years, according to the study published in BMJ Open.

The study found that a diagnosis pre-diabetes/NDH became much more common over time, rising from 0.07% in 2000 to 1.85% in 2015.

Although cases of pre-diabetes/NDH are rising, fewer of these people converted to Type 2 Diabetes, with the annual rate of conversion falling from 8% in 2000 to 4% in 2014.

NHS rightcare pathway estimates that around 5 million people have NDH, and Diabetes UK estimates that in January 2019, 3.9 million people had diabetes In the UK.

People with pre-diabetes/NDH are usually asymptomatic but will often be clinically obese. Many are diagnosed by chance- and are given dietary and lifestyle advice. Some are also prescribed the drug Metformin which is mainstream treatment for Type 2 diabetes.

This sample is large enough to give a good representation of what is going on across the UK. And intriguingly, our figures show that the number of these people with pre-diabetes/NDH who go on to develop Type 2 Diabetes is falling.

Dr Ravindrarajah from The University of Manchester said: “This sample is large enough to give a good representation of what is going on across the UK.

“And intriguingly, our figures show that the number of these people with pre-diabetes/NDH who go on to develop Type 2 Diabetes is falling.

“We are not certain why this is, but we suspect it’s a combination of good preventative work by the NHS and changing definitions of non-diabetic hyperglycaemia.

“The reduction in conversion rates reflects changes in the definition of pre-diabetes and to some extent NDH, at least in the UK, with people diagnosed with NDH more recently having lower conversion risks. This has implications for interventions, like the NHS Diabetes Prevention Programme.”

She added: “Non-diabetic hyperglycaemia refers to levels of blood glucose that are increased from the normal range but not yet high enough to be in the diabetic range.

“We hope this study will encourage policymakers to be consistent in their definition and recording of pre-diabetes, which has changed a few times in the last decade.

“Diabetic preventing programmes might need to target the individuals who are at higher risk of conversion to Type 2 diabetes, as identified in this study.

“Policymakers who aim to prevent conversion may wish to prioritise certain recipients who are at higher conversion risk, especially when resources might be limited.”

Source: University of Manchester




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How to install the FreeIPA identity and authorization solution on CentOS 8

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Jack Wallen walks you through the process of installing an identity and authorization platform on CentOS 8.

Image: CentOS

FreeIPA is an open source identity and authorization platform that provides centralized authorization for Linux, macOS, and Windows. This solution is based on the 389 Directory Server and uses Kerberos, SSSD, Dogtag, NTP, and DNS. The installation isn’t terribly challenging, and you’ll find a handy web-based interface that makes the platform easy to administer.

I’m going to walk you through the steps of getting FreeIPA up and running on CentOS 8. 

SEE: CentOS: A how-to guide (free PDF) (TechRepublic) 

What you’ll need

How to set your hostname

The first thing you must do is set your hostname. I’m going to be demonstrating with a LAN-only FQDN (which then must be mapped in /etc/hosts on any client machine that wants to access the server). 

Set your hostname with the command:

sudo hostnamectl set-hostname HOSTNAME

Where HOSTNAME is the FQDN of the server.

After you’ve set the hostname, you must add an entry in the server’s hosts file. Issue the command:

sudo nano /etc/hosts

Add a line at the bottom like this:

SERVER_IP HOSTNAME

Where SERVER_IP is the IP address of the server and HOSTNAME is the FQDN of the server.

Save and close the file.

How to install FreeIPA

The installation of FreeIPA starts with enabling the idm:DL1 repository with the command:

sudo module enable idm:DL1

When that command completes, sync the repository with the command:

sudo dnf distro-sync

Install FreeIPA with the command:

sudo dnf install ipa-server ipa-server-dns -y

How to set up FreeIPA Server

Next you have to run the configuration script for FreeIPA Server. To do that, issue the command:

sudo ipa-server-install

The first question you must answer is whether or not you want to install BIND for DNS. Accept the default (no) by pressing Enter on your keyboard. You must then confirm the domain and realm name, which will both be detected by the script. Once you’ve confirmed those entries, you’ll need to set a directory manager password, an IPA admin password for the web interface, and then accept the default (no) for the installation of chrony. 

After you’ve taken care of the above, you’ll be presented with the details of your installation (Figure A).

Figure A

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The details of my installation of FreeIPA Server.

Type y and hit Enter on your keyboard. The configuration will begin. This does take a bit of time, so either sit back and watch the text fly by or set about to take care of another task.

When the configuration completes, you’re ready to continue on.

How to access the web interface

Open a browser and point it to https://SERVER_IP (where SERVER IP is the IP address of the hosting server). You should be prompted for a username and password (Figure B). The username is admin and the password is the one you set for IPA admin during the configuration. 

Figure B

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The FreeIPA login screen.

Upon successful login, you’ll find yourself at the FreeIPA main window, where you can begin managing your centralized authentication server (Figure C).

Figure C

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The FreeIPA main window is ready to work.

And that’s all there is to getting FreeIPA installed on CentOS. You can now spend some time adding users and other bits to make your identity and authorization solution work for your business.

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Targeting Aging is the Way to Treat Diseases of Aging

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Near all work to date on the treatment of age-related disease has failed to consider or target underlying mechanisms of aging, the molecular damage that accumulates to cause pathology. It has instead involved one or another attempt to manipulate the complicated, disrrayed state of cellular metabolism in late stage disease, chasing proximate causes of pathology that are far downstream of the mechanisms of aging. This strategy has largely failed, and where it has succeeded has produced only modest benefits. Consider that statins, widely thought to be a major success in modern medicine, do no more than somewhat reduce and delay mortality due to atherosclerosis. They are not a cure. The mechanisms of aging are why age-related diseases such as atherosclerosis exist. They are the root cause of these diseases. Attempted therapies that continue to fail to target the mechanisms of aging will continue to fail to deliver meaningful benefits to patients. This must change.

Targeting Aging is the Way to Treat Diseases of Aging

Image credit: Pixabay (Free Pixabay license)

Aging doesn’t kill people – diseases kill people. Right? In today’s world, and in a country like the United States, most people die of diseases such as heart attack and stroke, cancer, and Alzheimer’s. These diseases tend to be complex, challenging, difficult, and extremely ugly to experience. And they are by nature chronic, caused by multifactorial triggers and predispositions and lifestyle choices. What we are only now beginning to understand is that the diseases that ultimately kill us are inseparable from the aging process itself. Aging is the root cause. This means that studying these diseases without taking aging into account could be dangerously misleading … and worst of all, impede real progress.

Take Alzheimer’s disease. To truly treat a disease like Alzheimer’s, we would need to identify and understand the biological targets and mechanisms that trigger the beginning of the disease, allowing us to intervene early – ideally, long before the onset of disease, to prevent any symptoms from happening. But in the case of diseases like Alzheimer’s, the huge problem is that we actually understand very little about those early targets and mechanisms. The biology underlying such diseases is incredibly complex. We aren’t sure what the cause is, we know for sure there isn’t only one target to hit, and all prior attempts to hit any targets at all have failed. When you start to think about how much of what we think we know about Alzheimer’s comes from very broken models – for example, mice, which don’t get Alzheimer’s naturally – it becomes totally obvious why we’re at a scientific stalemate in developing treatments for the disease, and that we’ve likely been coming at this from the wrong direction entirely.

The biggest risk factor for Alzheimer’s isn’t your APOE status; it’s your age. People in their twenties don’t get Alzheimer’s. But after you hit the age of 65, your risk of Alzheimer’s doubles every five years, with your risk reaching nearly one out of three by the time you’re 85. What if going after this one biggest risk factor is the best vector of attack? Maybe even the only way to truly address it? This isn’t about the vanity of staying younger, about holding on to your good looks or your ability to run an 8 minute mile. It’s about the only concrete possibility we have to cure these diseases. Instead of choosing targets for a single specific disease, i.e. a specific condition that arises in conjunction with aging, we can get out in front of disease by choosing targets that promote health. And we can identify these by looking at disease through the lens of the biology of aging.

Link: https://a16z.com/2020/10/07/aging-alzheimers-drug-discovery/

Source: Fight Aging!




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The Mandalorian Season 1 Recap Distills the Star Wars Series Into 89 Seconds

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Before The Mandalorian season 2 premieres Friday afternoon on Disney+ Hotstar (and Friday midnight on Disney+ in the US), Disney and Lucasfilm have given us an official 89-second recap of The Mandalorian season 1. That’s very brief, but it speaks to the fact that The Mandalorian wasn’t a narratively-heavy show on its debut last year.

Everything You Need to Know About The Mandalorian Season 2

The Mandalorian season 1 recap touches upon Mando’s (Pedro Pascal) profession (he’s a bounty hunter), his newest target (Baby Yoda), the people he meets along the way — Cara Dune (Gina Carano), Greef Karga (Carl Weathers), and Kuiil (voiced by Nick Nolte) — and the consequences of his decision to bring Baby Yoda under his wing.

“You have something I want. It means more to me than you will ever know,” the darksaber-wielding villain Moff Gideon (Giancarlo Esposito) says deep into The Mandalorian season 1 recap, as we are given a reminder of the Star Wars series’ action-heavy side. Gideon then declares: “It will be mine.”

The season 1 recap wraps by setting up The Mandalorian season 2, as tribe leader The Armorer (Emily Swallow) instructs Mando to reunite Baby Yoda “with its own kind”. Mando wonders: “You expect me to search the galaxy for the home of this creature?” Well, yes, otherwise what would we do in season 2, Mando.

In addition to Pascal, Carano, Weathers, and Esposito, The Mandalorian season 2 also stars Omid Abtahi as Dr. Pershing, Horatio Sanz as Mythrol, Rosario Dawson as Ahsoka Tano, Katee Sackhoff as Bo-Katan Kryze, Temuera Morrison as Boba Fett, Timothy Olyphant as former slave Cobb Vanth, Michael Biehn as a rival bounty hunter, and Sasha Banks in an undisclosed role.

Jon Favreau (The Lion King, Iron Man) created The Mandalorian and serves as showrunner and head writer on the Star Wars series. Favreau and Weathers are among the directors on season 2 alongside Dave Filoni, Rick Famuyiwa, Bryce Dallas Howard, Peyton Reed, and Robert Rodriguez.

The Mandalorian season 2 premieres October 30 on Disney+ Hotstar in India. Episodes will air weekly.

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