IELTS Academic Reading Practice Test 319

Mary Seacole was born Mary Jane Grant in Kingston, Jamaica, in 1805. Her father was a Scottish officer in the British army; her mother kept a boarding house in the town and was known locally as a doctress. The boarding house took in officers' families and visitors from abroad. Using herbal remedies and a good deal of practical nursing, the older woman treated neighbours and travellers alike. The young Mary learned to mix medicines, dress wounds and judge when a fever was dangerous by watching her mother at work.

In 1836 she married Edwin Horatio Hamilton Seacole, an Englishman who had settled in Jamaica. The couple opened a small store, but trade was poor and Edwin's health was worse. He died in 1844, in the same period in which Mary lost her mother. A fire destroyed the family's boarding house in Kingston not long afterwards, and she rebuilt it on a larger scale, running it successfully for several years. She acquired a reputation for energy and competence that she would draw on for the rest of her life.

Her own health was never robust, and she travelled partly in search of a climate that suited her. She had spent time in England as a young woman. In the early 1850s she went to Panama, where her brother kept a hotel in the town of Cruces, on the route across the isthmus. She arrived as thousands of travellers were crossing on their way to California, and stayed to run a small business of her own.

When cholera reached Cruces, the town had no doctor and no hospital. Seacole treated patients with the remedies she had learned in Jamaica, and her efforts were noticed by local newspapers. Her services were in demand from rich and poor alike, and she later described the epidemic as one of the hardest tests of her life. The months in Panama gave her a practical confidence in dealing with infectious disease.

News of the Crimean War reached Jamaica in 1854, and Seacole decided to offer herself as a nurse. She sailed to London. There the War Office was recruiting nurses for the military hospital at Scutari and for Florence Nightingale's separate nursing expedition, and she applied to both. Her applications were not successful: she was not interviewed, and her offers were declined. She believed for the rest of her life that her colour had been held against her, although other explanations have also been suggested, including her age and her lack of formal training. None of this is documented in a way that settles the question.

Rather than go home, she went to the Crimea on her own terms. With a relative named Thomas Day, and with money raised from her business interests, she bought a large stock of goods and sailed in early 1855. Near the port of Balaklava she opened a shop and refreshment house that she called the British Hotel, and sold food, drink and supplies to officers and men alike. It served as a store, a canteen and an informal surgery at once.

Seacole did not stay behind her counter. She rode out to the battlefields, sometimes while the fighting was still going on, to tend men who had not yet been carried to the hospitals. She also went aboard ships in Balaklava harbour to nurse the sick. The soldiers gave her the name Mother Seacole, and officers later wrote of her courage. Her treatments were those she had learned in Jamaica rather than the methods favoured in the military hospitals, and she made no secret of her impatience with official rules.

When the war ended in 1856 she was left with unsold stock and unpaid debts, and she returned to London almost penniless and in poor health. Friends and former officers came to her aid, and a public appeal was supported by William Howard Russell, the correspondent whose reports from the Crimea had shaped British opinion of the war. A fund-raising gala at the Royal Surrey Gardens in July 1857 drew a crowd of thousands.

In the same year she published her autobiography, Wonderful Adventures of Mrs Seacole in Many Lands. It is a lively book, frank about her commercial instincts and about the humiliations she had suffered, and it remains the main source for much of what is known about her life. She spent her remaining years in London, where she died in 1881 and was buried at Kensal Green.

For more than a century her story was largely forgotten. It was recovered from the 1980s onwards, as historians began to ask why a woman celebrated in her own lifetime had vanished from the record. In 2004 a public vote placed her first in a list of great Black Britons. In 2016 a statue of her was unveiled at St Thomas' Hospital in London, close to the site of the nursing school that Nightingale had founded.

Historians now read her book with the caution that any autobiography deserves. It was written to entertain and to vindicate its author, and some of its episodes cannot be checked against other evidence. Her knowledge was that of an experienced practitioner of her period rather than that of a trained nurse, and the case for her skill rests largely on her own account. What is not in doubt is that she went where she was not wanted and worked where she was not paid.

The skin is the largest organ of the human body, covering an area of roughly two square metres in an adult and accounting for about one-seventh of body weight. It is often imagined as a passive wrapping, but it is a living system that manufactures vitamin D, regulates temperature, senses touch and repairs itself after injury. It is also the first line of defence against a world of microbes, chemicals and physical damage.

The skin has three principal layers. The outermost, the epidermis, is thin and has no blood vessels of its own. Its cells, called keratinocytes, are produced in a basal layer at the bottom and are pushed steadily upwards as new cells form beneath them. By the time they reach the surface they are flattened, dead and packed with keratin, a tough protein that resists water and abrasion. Keratinocytes also manufacture lipids that help to seal the spaces between them. The whole epidermis renews itself roughly every four weeks, and its outer cells flake away in their millions every day.

Beneath it lies the dermis, a much thicker layer in which collagen gives strength and elastin gives elasticity. This is where most of the skin's blood vessels and nerve endings are found, together with hair follicles. The dermis also contains sebaceous glands, which release an oily substance called sebum. Coiled sweat glands in the same layer cool the body by evaporation. Below the dermis is the hypodermis, a layer of fat that insulates the body, cushions it against impact and stores energy.

The barrier itself is often compared to a brick wall, with the keratin-filled cells as the bricks and a mixture of lipids, including ceramides, as the mortar. This structure is remarkably effective: it keeps water inside the body and keeps most harmful substances out. The surface is also slightly acidic, with a pH of about five, which discourages many bacteria and fungi from settling. Sweat, sebum and the products of the skin's own metabolism combine to maintain this acid mantle. Even so, the barrier is not impermeable: some chemicals, including certain medicines, pass through it, which is why drugs can be delivered in patches.

Healthy skin is not sterile. It supports a varied community of bacteria, fungi and viruses, collectively known as the skin microbiome. Some of these residents are useful: bacteria such as Staphylococcus epidermidis occupy space and consume nutrients that harmful species would otherwise use, and they produce substances that inhibit their competitors. The composition of this community varies between individuals and between sites on the body, and it changes with age, hygiene and the use of antibiotics. Infection occurs when this balance breaks down, for example after a scrape or when the skin becomes unusually dry.

Immunology in the skin is active rather than passive. Langerhans cells, which sit among the keratinocytes, capture material from microbes and carry it to the lymph nodes, where the immune system learns to recognise it. Keratinocytes themselves release signalling molecules that summon immune cells and produce antimicrobial peptides - short proteins that puncture bacterial membranes. When the barrier is broken, these responses produce the redness and warmth of inflammation and begin the sequence of clotting, cell division and remodelling that closes a wound.

One of the skin's least obvious roles is the manufacture of vitamin D. Ultraviolet B radiation from sunlight converts a form of cholesterol in the epidermis into a precursor of vitamin D3, which the body needs in order to absorb calcium and keep its bones strong. Some exposure to sunlight is therefore necessary, and skin containing more of the pigment melanin requires longer exposure to make the same amount. This is one reason why vitamin D deficiency is common among people with darker skin living in high latitudes.

Melanin does more than determine colour. Produced by cells called melanocytes and passed to surrounding keratinocytes, it absorbs ultraviolet radiation and protects the genetic material of skin cells from damage. How much protection it gives varies: individuals differ widely in the number and activity of their melanocytes, and the skin's response to sun exposure - tanning, burning or neither - depends on that variation and on the intensity of the radiation.

Much remains uncertain. The reasons why some people's skin barrier is more permeable than others, and why that tendency runs in families, are only partly understood. Research on atopic dermatitis, the common form of eczema, has shown a strong association with changes in a structural protein called filaggrin, but why the condition flares and settles at different times is still unexplained. The role of the microbiome in health and disease is under intense study, and engineered skin substitutes, already used to cover severe burns, cannot yet reproduce every function of the tissue they replace.

The skin is also a sensory organ and a thermostat. Different nerve endings in the dermis register pressure, vibration, temperature and pain, while the flow of blood through the dermis and the production of sweat allow the body to lose heat quickly when it is too warm. These functions are easily taken for granted until they fail: a serious burn destroys them along with the barrier.

Preimplantation genetic testing has been used in fertility clinics for three decades. In its standard form, embryos created by in vitro fertilisation are examined after a few days, and those carrying a known mutation for a severe inherited disorder - cystic fibrosis, for example, or Huntington's disease - are not transferred. To many people this is uncontroversial: a couple at risk of passing on a fatal illness are spared a tragedy, and no existing person is harmed. Few people object to this use of the technology. The technology, however, is changing, and with it the questions it raises.

Two developments have pushed the debate forward. The first is the falling cost and rising power of genetic analysis, which allows hundreds of thousands of variants to be read from a single cell. The second is the growth of polygenic scores, in which many small genetic effects are added together to estimate a person's statistical chance of developing a common condition such as heart disease or diabetes. Companies have begun to market embryo screening based on such scores. Regulators in most countries have not decided how to treat it, and the science behind it is far from settled.

The case for allowing parents to choose is usually built on reproductive autonomy. Parents already make countless decisions that shape their children - where they live, what they eat, which school they attend - and it is not obvious why choices made before birth should be treated differently. Nor does anyone else seem to be harmed when a couple avoid a disease that runs in the family. On this view, the state should ensure that the tests are accurate and the counselling honest, and otherwise leave the decision to those who will raise the child.

Against this, critics argue that selection carries a message. If a society systematically chooses against embryos that would develop a particular condition, it is hard to avoid the implication that lives lived with that condition are less worth living. Disability scholars call this the expressivist objection, and it matters because many disabled people report good lives and describe discrimination, not their impairment, as their main difficulty. What is at stake is not only which children are born but how those already living are regarded.

A second objection concerns where the line would fall. Selection against a condition that kills in infancy is one thing; selection against a condition that causes discomfort or short stature is another; selection for height, or for a statistical tendency towards a particular temperament, is another again. In practice the boundary is drawn by regulators who must define 'serious', a word that hides a mass of judgement. Once the principle of choosing is accepted, the argument runs, the limits will be set by social fashion rather than by medicine.

The evidence for the newer tests is also weaker than the advertising suggests. A polygenic score describes the average effect of many variants in the population that was studied, and its power to predict an individual's future is usually modest. Because the studies have mostly been carried out on people of European ancestry, the scores transfer poorly to other groups. Selecting embryos on this basis would, at best, slightly shift the odds; at worst, it would sell parents a certainty that does not exist.

Editing genes is a different matter from choosing among embryos. In 2018 a Chinese scientist announced that he had edited the embryos of twin girls to make them resistant to HIV, and he was later imprisoned for his actions. The experiment was condemned worldwide, less for its aim than for its recklessness: editing carries risks of unintended changes to the genome, and the children could not consent. Most scientists regard heritable editing as premature, whatever they think about selection.

How, then, should the law respond? A total ban sounds decisive but has drawbacks: it drives the work to places with no rules, and it prevents legitimate research on miscarriage and early development. It is more defensible to license clinics, to require evidence of accuracy, to restrict the traits for which testing is offered, and to insist that counselling sets out what the tests cannot tell. Above all, licensing keeps open the possibility of revising the rules as the evidence changes. Regulation of this kind is slow and unglamorous, but it keeps the decisions in public hands.

The question of access cuts across all of these arguments. Tests that are not paid for by public health systems will be bought by those who can afford them. If selection works, it will benefit the children of the wealthy first; if it does not, the wealthy will have paid for nothing. Either way, a new inequality is created at the moment of conception, and no later policy can undo it.

My own position is that selection for serious disease is acceptable and selection for enhancement is not, and that the distinction, though blurred at the edges, is real enough for regulators to work with. But I would add a condition. A society that allows parents to choose which illnesses their children will avoid must be generous to those who are born with them. If the same government that licenses the tests is cutting support for disabled people, the expressivist objection becomes not a philosophical puzzle but a description of what is actually happening.