Sunday, 27 February 2022

The Origins of the Anglo-Saxons

The origins of the Anglo-Saxons by Jean Manco (Thames & Hudson Ltd, 2019)

This is a very detailed and fascinating book, which includes the following information.

  • Population
  • In 1066 England was conquered by the Normans, who replaced the English aristocracy. In the medieval period there was immigration into England from continental Europe, as well as from Scotland, Wales and Ireland.
  • The DNA of the modern English population cannot be modeled as a simple mixture of Anglo-Saxon and Celtic. Migration from 1066 onwards has left its mark.
  • Language
  • Old English, the language of the Anglo-Saxons, developed into Middle English (1100-1500), followed by Early Modern English (1500-1800) and Modern English.
  • Although Modern English is a Germanic language, 70% of its vocabulary is non-Germanic, borrowed from many other languages, notably Latin and French. This polyglot vocabulary makes English the richest language in the world.
  • English today is a global lingua franca, partly as a legacy of the British Empire, but mainly due to the super-power status of the US.
  • History
  • In the Middle Ages, a pseudo-history of Britain was far more popular than the genuine article.
  • Interest in the Anglo-Saxons began to revive in the Tudor period and greatly increased in the Victorian period.
  • The surge of national pride in the 19th century encouraged racism and an inflated concept of the Anglo-Saxon achievement, which produced a backlash after the Second World War.
  • JRR Tolkein was a scholar of the Anglo-Saxon language, who changed the scholarly view of Beowulf but left a greater legacy in his popular fiction (The Hobbit and Lord of the Rings), which have now been produced as films.
  • Who were the Anglo-Saxons?
  • Archaeology can reveal those details of contemporary life in Anglo-Saxon times that documentary sources omit.
  • The Romano-British population was overwhelmingly Celtic but included individuals from many parts of the Roman Empire, including some Germani (this is the correct spelling) within the Roman army.
  • The Anglo-Saxon ingress was almost the opposite of the Roman conquest.
  • Ancient DNA indicates that the Anglo-Saxons were incomers.
  • There was no reason for the Roman British population on the whole to imitate the Germanic way of life, but individuals could adopt it by marriage or other assimilation.
END

Sunday, 20 February 2022

Should We Reform the UK School External Exam System?

 The external school exam system in the UK has been unchanged for some years. In school year 11, students usually sit their GCSE exams. [These were previously known as O (Ordinary) Levels] In year 13 (Upper Sixth form) students sit A Levels (Advanced). Both are set by a number of national exam boards.The exams consist of written papers, with some subjects requiring one or more elements of course work, practical work and oral examinations for languages. The marking is done by external examiners and moderated. Marks are allocated to a range of grades. Based on mock (practice) exams, teachers typically give students a predicted grade, but this is only an indication of their likely actual grade.

No exams took place in summer 2020 due to the coronavirus (Covid-19) outbreak. To enabled students to receive qualifications, it was announced  that students who were due to sit A level, AS level or GCSE exams this summer would receive a calculated grade. For each student, schools and colleges provided a centre assessment grade for each subject; this is the grade their school or college believed they would be most likely to have achieved had external exams gone ahead, taking into account a range of evidence including, for example, non-exam assessment and mock exam results. This grade was intended to be put through a process of standardisation, using a model developed with Ofqual, to arrive at the final calculated grade.

However the moderation process was flawed and downgraded (sometimes heavily) the marks for many students. The biggest effect was on A level students, many of whom were unable to take up university places, and these were allocated to other students. On Monday 17th August, Ofqual confirmed that there would no longer be a standardisation process for A level, AS level or GCSE exams and instead all students would be awarded the centre assessment grade submitted by their school or college, unless it was lower than their calculated grade, in which case the calculated grade would stand. Unless there was evidence that a processing error had been made, these grades would be final. This U-turn meant that students who had been refused a university place on the basis of the flawed grades, now had no places and universities had to try and sort out the mess.

Tom Brighouse has written about the system of examinations in the UK, indicating that he feels our children are possibly the most tested. He notes that in other countries the system is less stratified, and the English system is unusual in having decisive exams at age 18.

TB has suggested that we need to move to a broader qualification at 18, which is part exam, part record of achievement and part long-term project. Some students might excel in one type of assessment (e.g. open-ended essay, multiple choice questions or oral examination) and do less well at others. Universities use the same methods but add in observation of work by staff, collaborative work and vivas (where the student is questioned individually in an interview).

TB further notes that (a) teachers are not taught how to assess, and want their students to do well, (b) teachers are not immune to unconscious bias and (c) exams are a single day snapshot. Companies who want problem solvers, collaborators and good communicators, are therefore devising their own skills based assessments as part of their recruitment process.

Digitisation may offer ways to track progress, using results over time from different 'tests'. The bigger the variety of assessment methods, the more chance it will be fair.

END

Friday, 28 January 2022

Alzheimer Dementia Causes and Treatments

 Alzheimer's is typically thought of a disease that affects the elderly, but ten per cent of people with Alzheimer's have the early-onset form and are under the age of sixty-five. While about 50% of early-onset Alzheimer's cases do not show specific mutations, there is a strong genetic linkage. Mutation positive for genes APP, PS1 or PS2 is a solid confirmation of the diagnosis. It is possible that those without these mutated genes may have other mutated genes that also cause the disease. Sadly, the genetic element means that any offspring may have inherited the mutated form of a gene. This can only be diagnosed by genetic screening.

2012: Current drugs for treating Alzheimer's dementia can slow its progression for a significant period of time but are not a cure. The sooner someone is diagnosed and put on medication the more likely they will be able to benefit if better treatments become available. Examples are Aricept (boosts cholinergic functioning) and Namenda.

Diagnosis: finding amyloid plaques and/or neurofibrillary tangles in the brain.

The cognitive deficits - the symptoms of dementia - occur before the plaques form and neurons die. 

In the brain of someone with Alzheimer's, there is too much of a soluble protein called amyloid-beta 42. Either too much is made or not enough is cleared away. When too much is present, these individual little peptides stick together and form small oligomers. These gluey oligomers of amyloid-beta 42 lodge in synapses - the spaces between neurons - and interfere with synaptic transmission, the ability of neuron number one to 'talk' to neuron number two. And when this happens, new information isn't learned. Or old information can't be accessed. Synaptic plasticity suffers. Over time because this synapse isn't working properly and because of inflammation and other problems, that nerve axon terminal will retract. Eventually, unable to function, the neuron will die, leaving behind empty space (the atrophy seen on MRI scans) and possibly a heap of amyloid-beta 42 in an amyloid plaque.

The degree of dementia correlates only with  synapse dysfunction, not with neuronal loss, not with number of plaques, not with atrophy on an MRI scan.

The cure (disease altering) treatments will need to:

  • impede production of amyloid-beta 42,
  • increase clearance of already produced amyloid-beta 42,
  • prevent amyloid-beta 42 from sticking to itself so it can't form oligomers, or
  • rip these already formed oligomers apart.

If such treatments are found, the hope is that people suffering from symptoms of dementia can be treated before they've experienced any neuron death. If the synapses are fixed, neurotransmission can work again.

Source: Still Alice by Lisa Genova (Simon & Schuster, 20012)

Sunday, 10 October 2021

Cataracts

What are cataracts?

Cataracts are cloudy patches on the lens in the eye, which cause blurred vision and eventual blindness if left untreated. It is estimated that in the UK one in three people aged 65 has a cataract in one or both eyes.

Most develop due to age-related changes in the lens

  • An imbalance between free radicals (unstable atoms that damage cells) and antioxidants (which keep free radicals in check). Cells in the body produce both, but smoking, drinking too much alcohol and exposure to chemicals can speed up production of the damaging free radicals.
  • As we age, fewer antioxidants are produced, resulting in oxidative stress, leading to tissue damage; proteins and fibres in the lens start to break down and calcium builds up in the lens.
  • Cataracts are also linked to conditions such as diabetes and to medications, includinglong-term use of steroids.
Current treatment
The current treatment is to replace the cloudy lens in a 30-minute operation under local anaesthetic. The cloudy lens is removed through a small cut in the eye, and replaced with a plastic one. About 350,000 cataract operations are performed in the UK each year.

New treatment developed
Scientists at US-based Nacuity Pharmaceuticals have developed a 'pellet' implant (NPI-002) that is injected into the eye to prevent cataracts forming, and might even reverse the growth of existing cataracts without surgery. This is now being tested in the first clinical trial.
  • The implant is thought to work by lowering calcium levels in the eye.
  • The implant is loaded with antioxidants and injected into the vitreous, the gel-like fluid between the lens and the retina (the light-sensitive area in the eye). The solution includes N-acetylcysteine amide (NACA), an effective antioxidant.
  • The implant slowly releases its contents into the vitreous, which carries them to the lens where it acts on the cataract. 
First clinical trial
An animal study by ophthalmologists at Washington University, US, and other centres, reported in the journal BMC Ophthalmology in 2018, showed that the implant prevented and reduced the severity of cataracts. It also led to an increase in protective antioxidants, and reduced calcium levels to 2.5 times lower than a control group.

The first human trial, in the US, will start soon (late 2021) and will involve 30 patients aged 65 and over with cataracts.

Initial interest in the implant is tempered with caution. Gwyn Williams, a consultant ophthalmologist at Singleton Hospital in Swansea, said "It is a very interesting idea and I look forward to seeing the results. Cataracts are multi-factorial and I am sceptical that this one approach will be effective by itself, though this remains to be seen."

Source: Scientists develop 'pellet' that can be injected into patient's eye to prevent cataracts forming - and could even reverse existing traces. Daily Mail (5 Oct. 2021


Wednesday, 22 September 2021

Long Covid Facts

While many people recover from Covid-19 without further problems, some report having long-term health problems. A large range of symptoms are reported by these sufferers, for varying periods after the infection. Symptoms typically fall into four groups.

Types of Long Covid

Post intensive care syndrome (PICS)
Critically ill patients can suffer a range of health problems after a long time in hospital. This can include muscle weakness, and anxiety or another mental health problem. They may also have memory problems, which can affect whether they can return to work.

Post viral fatigue syndrome (PVFS)
Similar to problems following enteritis or rubella, fatigue and 'brain fog' may make it difficult to concentrate or remember things. 

Permanent organ damage (POD)
The lungs and heart, and also liver and pancreas, may have permanent damage.

Long-term Covid syndrome (LTCS)
This group report 'floating' symptoms which mean they do not fit into the other three groups. They suffer illness linked to one part of the body (e.g. respiratory system, brain, cardiovascular system and heart, kidneys, gut, liver or skin), which later abates, but then new symptoms arise in a different part of the body.

Why does this happen? 
Latest: A small study (at Stellenbosch University, South Africa) comparing blood collected from 11 people with long Covid and 13 healthy individuals found that those with long Covid have a large amount of tiny clots of inflammatory molecules trapped in their bloodstream. These blockages have the potential to disrupt the body's ability to distribute oxygen and vital nutrients, which could explain - or help to explain - the most common symptoms of fatigue, headaches and breathing difficulties. Some of the trapped molecules contain clotting proteins such as fibrinogen (helps the body to make clots to stop bleeding) and alpha(2)-antiplasmin (helps prevent blood clots from breaking down). Under normal conditions, the body maintains a balance of clotting and anti-clotting material to help the body reduce blood loss after injury, and preventing clots from growing too large and restricting oxygen flow. High amounts of alpha(2)-antiplasmin stuck in the blood mean the body's ability to break down clots is severely reduced. Other recent studies have also highlighted that the body's clotting system could be involved, while Covid itself has been linked to clotting disorders during the initial infection. More research with larger samples is needed to confirm these findings, and research to identify the type of treatment for the problem.

There are three possible reasons, and long covid may even be a combination of these.

  1. Direct damage by the virus. For example, the heart and lungs can be permanently damaged, which could explain prolonged shortness of breath and chest pains. 
  2. It is even possible that the virus could hide in some body tissues, and continually reactivate; some studies are looking into this possibility.
  3.  Inadvertent damage that the body can do when it responds to the virus.

Long Covid is less common than first feared.
Initially it was unclear how many people might be affected, nor how long symptoms might last and whether there might be permanent damage. It it is possible to have serious Covid-19 symptoms and not experience long-term syndromes, and for those with mild cases to develop one of the syndromes.

The UK Office for National Statistics (ONS) has been monitoring this, by testing people at random which ensures that the comparison between Covid sufferers and non-sufferers is good. Additionally they carry out long-term follow-ups of those with long covid. Their latest (September 2021), large and comprehensive analysis suggests that one in 40 (2.5%) people with coronavirus has symptoms lasting at least three months.

Those most likely to suffer long-term (at least 3 months after infection) health conditions are:

  • Women aged 35 to 69
  • Those aged 50 to 69
  • People with high levels of virus in their body when testing positive.
Long Covid in children: An Australian study indicates that long covid symptoms in children and teens resolve in four to twelve weeks.

Sources: BBC News 18 Sept. 2021 (link). Article in Daily Mail, (link) 15 Oct. 2020. Article in New Scientist, 31 Oct. 2020. Article in Daily Mail (link) 5 Oct. 2021.