Post-Polio News RSS Feed Daily Digest for 09/24/2022

[UK] [England] [NHS] The mess we're in... | News and comment from Roy Lilley.

[ppn skeleton service] [23rd September 2022]

Variation… the enemy of quality…

That’s our old friend, Edwards Deming talking…

… he’s right. Variation always tries to tell us something. We just have to figure out what it is.

There five types:

Controlled… when we want things to be different
Random… when things are unexpectedly different
Predictable… when we can expect things to be different 
Common cause… when something happens to make all things different
System… when the process causes variation

So, why is there a variation in waiting times for a GP appointment and ambulance handovers… and there is… and it’s big.

For example; in winter 2021, 45% of ambulance handover delays occurred in 15 Trusts.

Yesterday, when No21 presented ‘Our Plan for Patients’, to the House, not unreasonably, she asked; why are there variations?

The DH+ are collecting data and that is very good!

If the data gives us a random pattern, it’ll be a failure from within the system but I’d be looking for indicators in the three ‘C’s;

communities,
capacity
competence.

How does it work;

Communities; their demography, a higher incidence of the elderly or deprivation, for example.

Capacity; the practices are using all their available appointments and can’t expand for reasons of resource, staffing or constraints on planning.

Competence? Face it, some practices just aren’t run very well and can probably learn from places that are.

In the meantime, this;

‘…We expect that patients, who need an appointment with their GP practice within 2 weeks, should get one and that patients with urgent needs should be seen on the same day.’

It’s worth pointing out there were 26m GP appointments in July and 44% were seen on the day they were booked.

And…

‘… [we will] open-up time for more than a million extra appointments over winter.’

Last year GPs delivered over 300m appointments. An extra million is less than one percent.

To be frank… this is not much of a plan. It's largely the response to Covid, rebadged.

A chunk of it is stuff already being done; more call handlers, falls prevention, volunteers, making return to practice easier, treatment-hubs, fixing the pension rules.

There’s a promise of 7,000 more beds but...

... without more people to look after the seven thousand people in the beds, nurse-to-patient ratios will fall, risks will go up and more good people will get fed up and go to work for Marks and Sparks.

Four hundred people a week are leaving, now.

There's a promise of £500m, for an Adult Social Care Discharge Fund:

‘… [this ] first step will inform our further action from next year to rebalance funding across health and care, to establish a strong and sustainable social care sector, with greater accountability for use of taxpayers’ money.’

What does this mean? Dunno...

I do know, it's partially funded from the NHS reserve for the employers NI increase, no longer being paid. Described as a 'downpayment'.

Where is more likely to come from? Dunno...

I do know, without an allocations model...

... and a handle on using the money to improve the wages and training for front-line care staff, I can see it used for paying off the over-draft of some nearly-broke domiciliary-care companies and create care-package cost-inflation.

This report is pretty thin, just over 3,500 words.

But, here’s the point. What else is there? In all honesty, what is there that this or any government can do, right now, that is going to change anything, right now.

Health and Social Care are suffering the effects of twelve years of neglect. Twelve years of inattention and most of it in a period of austerity funding.

We didn’t;

train enough people,
keep enough people,
build enough,
repair enough,
innovate enough,
do enough...

... and when Covid caught us out there were already signs of trouble. Tens of thousands of vacancies and 4.5 million waiting for care.

Now, vacancies are in the hundred thousands and 7million are waiting.

No matter how much money you have, it can't buy time...

... and it is time that we need to train and re-build, innovate and make an ambulance arrive at your house, instead of queuing outside the hospital.

This report describes what we can do with what we've got.

The final paragraph says:

‘We will design and deliver our long-term workforce plan.

We will review our education and training requirements and...

... will come forward with proposals to meet the changing needs and expectations of patients in the future.’

When? Dunno… but note the word, ‘deliver’…

… and it’s about the only thing that will solve the longterm mess we are in.

Have the best weekend you can.

Original Source Article »

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Effects and mechanism of Aβ1−42 on EV-A71 replication | Virology Journal.

[ppn skeleton service] [Open Access] [Received 30 June 2022; Accepted 16 September 2022; Published 20 September 2022]

Abstract.

Background.

β-Amyloid (Aβ) protein is a pivotal pathogenetic factor in Alzheimer’s disease (AD). However, increasing evidence suggests that the brain has to continuously produce excessive Aβ to efficaciously prevent pathogenic micro-organism infections, which induces and accelerates the disease process of AD. Meanwhile, Aβ exhibits activity against herpes simplex virus type 1 (HSV-1) and influenza A virus (IAV) replication, but not against other neurotropic viruses. Enterovirus A71 (EV-A71) is the most important neurotropic enterovirus in the post-polio era. Given the limitation of existing research on the relationship between Aβ and other virus infections, this study aimed to investigate the potent activity of Aβ on EV-A71 infection and extended the potential function of Aβ in other unenveloped viruses may be linked to Alzheimer's disease or infectious neurological diseases.

Methods.

Aβ peptides 1–42 are a major pathological factor of senile plaques in Alzheimer’s disease (AD). Thus, we utilized Aβ_1–42 as a test subject to perform our study. The production of monomer Aβ_1–42 and their high-molecular oligomer accumulations in neural cells were detected by immunofluorescence assay, ELISA, or Western blot assay. The inhibitory activity of Aβ_1–42 peptides against EV-A71 in vitro was detected by Western blot analysis or qRT-PCR. The mechanism of Aβ_1–42 against EV-A71 replication was analyzed by time-of-addition assay, attachment inhibition assay, pre-attachment inhibition analysis, viral-penetration inhibition assay, TEM analysis of virus agglutination, and pull-down assay.

Results.

We found that EV-A71 infection induced Aβ production and accumulation in SH-SY5Y cells. We also revealed for the first time that Aβ_1–42 efficiently inhibited the RNA level of EV-A71 VP1, and the protein levels of VP1, VP2, and nonstructural protein 3AB in SH-SY5Y, Vero, and human rhabdomyosarcoma (RD) cells. Mechanistically, we demonstrated that Aβ_1–42 primarily targeted the early stage of EV-A71 entry to inhibit virus replication by binding virus capsid protein VP1 or scavenger receptor class B member 2. Moreover, Aβ_1–42 formed non-enveloped EV-A71 particle aggregates within a certain period and bound to the capsid protein VP1, which partially caused Aβ_1–42 to prevent viruses from infecting cells.

Conclusions.

Our findings unveiled that Aβ_1–42 effectively inhibited nonenveloped EV-A71 by targeting the early phase of an EV-A71 life cycle, thereby extending the potential function of Aβ in other non-envelope viruses linked to infectious neurological diseases.