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What would happen if a cell is poked by a fine needle?

What would happen if a cell is poked by a fine needle?



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I had seen this question in an exam:

A living cell has a protoplasm which is water based and demarcated by a lipid bilayer membrane. If a cell is pierced to 1/5th of its diameter with a very sharp needle, after taking the needle out (a) no effect will be observed. (b) protoplasm will leak out from the hole made by the needle for a few minutes until the cell heals the wound. (c) protoplasm will keep on leaking out till the cell is dead (d) the cell will burst like a balloon.

I understand that the answer is option (a) as the cell membrane will reseal itself after getting pierced. But my doubt is that if in the question 1/5th was replaced by 1/2 or by any number greater than 1/2, will the answer be different. Or in other words, I want to know whether the number 1/5 significant in this question.


Generally speaking, there is no effect in microinjections.

This is relevant in the real world example of micro-injections. A video of a pronucleus injection can be seen here, or here is a more thoroughly explained procedure involving cloning. As you can see in the video the membrane, almost no effect will be observed - molecular dynamic simulations show that the membrane can spontaneously reform from fragments in the tens-of-nanoseconds timescale.

1/5 refers to the question "is the needle small enough?"

The question does include the term "1/5", which is a bit unusual. I guess they want you to recall a specific piece of information about the correct ratio size of needle should be. Here is a video of a microinjection at approximately that ratio. However the exit hole is unintentionally filled with the inserted material and cannot close immediately. The cell disappears out of frame before we can confirm the hole is closed.

Cell diameters are very variable

Cell sizes vary greatly.

From using these values, assuming a cell is a sphere an oocyte has a diameter of approximately 196µm, whereas a neutrophil has a diameter of 8µm. It's a bizarre question given this range because usually micro-needles are between 0.5 and 5 µm diameter in length, except in the case of oocytes where larger needles are used (according to wikipedia). I don't think this is relevant, and it is just arbitrarily picking a needle size that wouldn't completely maul the cell!


Bone Metasis

I've undergone a total thyrodectomy due to multiple goiters and my fine needle was negative for cancer, however post surgery found out that I do have thyroid cancer, and have under gone radioactive iodine treatment a couple of time. After my 1st treatment the cells in the region of the neck were cleared but we found a "hot spot" in the left paretial bone in the skull. have gone through 2 stronger iodine treatments and this "hot spot" hasn't cleared - neither spread. Else where all is clear - and have been asked to go through the treatment again - which at this point in time I don't want to. Was wondering if there are other treatments available, and also if I do refuse iodine treatment, what could possibly happen?


Fine Needle Aspiration Biopsy (FNA)

A Fine Needle Aspiration (FNA) Biopsy is a simple procedure that involves passing a thin needle through the skin to sample fluid or tissue from a cyst or solid mass, as can be seen in the picture below. The sample of cellular material taken during an FNA is then sent to a pathology laboratory for analysis. Fine needle aspiration biopsies are often performed when a suspicious lump is found, for example a breast lump or enlarged lymph node, or if an abnormality is detected on an imaging test such as x-ray, ultrasound or mammography. Fine needle aspiration is a relatively non-invasive, less painful and quicker method when compared to other methods of tissue sampling such as surgical biopsy. A cyst aspiration can also be achieved with a FNA, where the fluid is drained from a cyst with no need for analysis.

Performing a Fine Needle Aspiration Biopsy (FNA)

A fine needle aspiration biopsy is a simple and quick procedure. It is performed to collect a sample of cells or fluid from a cyst or solid mass, to allow the cells to be examined under a microscope. Local anaesthetic is not usually required for a fine needle aspiration, as the procedure should not be painful. Fine needle aspirations may be performed on palpable lumps (lumps which can be felt), or impalpable lumps which have been detected on ultrasound or x-ray. Once the skin has been cleaned at the needle entry point, the lump is then examined. If the lump can be felt, your doctor or surgeon will palpate the lump to position it for the needle. If the lump cannot be felt, imaging may be required to find the exact location. This can be done with ultrasound, where the surgeon will watch the needle on the ultrasound monitor and guide it to the area, or with a stereotactic mammogram (for the breast) which uses two mammograms at different angles and a computer to create exact coordinates. The type of needle used for fine needle aspiration biopsy has a hollow interior and is much finer than a regular needle used to draw blood. You can see an example of what the needle may look like in the image to the right. The insertion of the needle is said to be similar to the sensation of a blood test. A vacuum or negative pressure is created in the needle and with an in and out motion of the needle, the sample is taken. Several needle insertions may be required to ensure that the sample is adequate. Once the test is completed, a small bandage will be placed over the site and you can continue your normal activities. There are generally no complications with this procedure, though you may experience some tenderness or bruising over the needle insertion site. If you experience any bleeding, swelling, fever or pain that is not relieved with paracetamol, contact your doctor immediately. It is not recommended that you use aspirin to relive pain as it may worsen any bruising.

Results of a Fine Needle Aspiration Biopsy (FNA)

The samples taken are examined by a pathologist under a microscope. A detailed report will then be provided about the type of cells that were seen, including any suggestion that the cells might be cancer. It is important to remember that having a lump or mass does not necessarily mean that it is cancerous many fine needle aspiration biopsies reveal that suspicious lumps or masses are benign (non-cancerous) or cysts. Aspirate samples may be described as one of the following types:

  • Inadequate/insufficient: The sample taken was not adequate to exclude or confirm a diagnosis.
  • Benign: There are no cancerous cells present. The lump or growth is under control and has no spread to other areas of the body.
  • Atypical/indeterminate, or suspicious of malignancy: The results are unclear. Some cells appear abnormal but are not definitely cancerous. A surgical biopsy may be required to adequately sample the cells.
  • Malignant: The cells are cancerous, uncontrolled and have the potential or have spread to other areas of the body.

Effectiveiness of a Fine Needle Aspiration Biopsy

A fine needle biopsy is an effective tool in evaluating and diagnosing suspect lumps or masses. A quick diagnosis can mean that cancer is detected early, giving more options for treatment, or that benign lumps are diagnosed without the need for surgery. It is non-invasive and only slightly uncomfortable, compared to a surgical biopsy which requires a general anaesthetic, involves pain and the possibility of infection or scarring. Fine needle aspiration biopsies do require some expertise to perform and interpret. To ensure that an accurate result is achieved, it is important that the general practitioner, radiologist, surgeon, pathologist or oncologist who performs your procedure has experience in fine needle aspiration biopsy.

Benefits and Risks of a Fine Needle Aspiration Biopsy

A fine needle biopsy is a quick and effective test for determining the status of suspect tissue. Compared to a surgical biopsy, fine needle aspiration biopsy involves little possibility of scarring, infection or pain, and has a significantly shorter recovery time. It is also extremely useful in the diagnosis and treatment of cysts. The risks of fine needle aspiration biopsy include the possibility of cancer cells being trailed into unaffected tissue as the needle is removed, but this is rare when the test is performed by skilled practitioners. Because an FNA biopsy can only sample a small number of cells from a mass or lump, there is a risk that any abnormal cells may be missed and not detected. This may mean that a larger sample must be taken, for example by core needle biopsy.

Fine Needle Aspiration Biopsy or Core Biopsy?

Core Biopsy is another method of ’tissue diagnosis’ – that is, a way of sampling the cells in a suspicious lump or mass. It is sometimes used instead of fine needle aspiration biopsy, or vice versa. Core biopsy is a more invasive procedure than FNA, as it involves making a small incision (cut) in the skin. A large needle is then passed through this incision and several narrow samples of the tissue to be investigated (such as a lump) are taken. As with fine needle aspiration, ultrasound or mammographic guidance may be needed to locate the lump or area to be sampled. Core biopsy is done under local anaesthetic. The procedure usually takes between 30 minutes and 1 hour. After the procedure, the biopsy area will be covered with a simple dressing. A core biopsy may result in a small, very fine scar where the incision was made. The samples of tissue taken during a core biopsy differ from those taken during FNA. Because the cells from a fine needle aspiration biopsy are sucked up randomly into the needle, they are seen under the microscope as a disorganised jumble of cells (see the image at right). With a core biopsy sample, however, the larger needle allows the cells to be removed with their relationship to each other intact. This can sometimes help in diagnosis.


How is liposarcoma treated?

Surgery is the treatment for primary liposarcomas that have not yet spread to other organs. In most cases, a surgeon will remove the tumor, along with a wide margin of healthy tissue around the tumor, with the goal of leaving the area free of disease and preventing the tumor from returning. Most tumors of the arms and legs can be successfully removed while sparing the involved limb. Occasionally, in about 5% of cases, an amputation is the best way to completely remove the cancer and restore the patient to a functional life. Complete surgical removal of tumors within the abdomen is difficult, in part because of the difficulty in getting clear margins of normal tissue.

The combination of surgery and radiation therapy has been shown to prevent recurrence at the surgical site in about 85-90% of liposarcoma cases. These results vary depending on the subtype of sarcoma that is involved. Radiation therapy may be used before, during or after surgery to kill tumor cells and reduce the chance of the tumor returning in the same location. Radiation therapy that is given before surgery may be more beneficial, but it can also make it more difficult for surgical wounds to heal.

The role of chemotherapy in the treatment of liposarcoma is not clearly defined, but it may be recommended in certain situations where patients are at high risk of recurrence or already have widespread disease.


Cerebral Spinal Fluid Leakage

During nasal polyp surgery, a surgeon can accidentally damage the bone that provides a barrier between the nose and the brain. Damage to this bone can result in cerebral spinal fluid leakage. Approximately one percent of patients who undergo this surgical procedure experience cerebral spinal fluid leakage complications, according to Dr. Alberto D. Fernandez with the Baylor College of Medicine. Cerebral spinal fluid leakage increases a patient's risk of developing a severe brain and spinal cord infection called meningitis. Meningitis can be life-threatening and may cause severe headache, fever or stiff neck symptoms. Typically, leakage of cerebral spinal fluid is detected and repaired during nasal polyp surgery and does not cause additional complications. If the leak is not detected until after surgery is completed, affected patients may require additional surgery to repair the damaged bone.

  • During nasal polyp surgery, a surgeon can accidentally damage the bone that provides a barrier between the nose and the brain.

Needle Biopsy - lymph nodes in neck

Hello, I have a biopsy scheduled for Monday morning. The cat scan with contrast results state that I have 6, 3.5 cms lymph glands on the right side of my neck.

Should I be worried? I'm not the best with needles. Will I be able to go back to work the next day?

I just hope Monday comes and goes really quickly. All I seem to be doing is wishing my life away, as I go from test to test.

It will be a massive relief one way or another to know what is wrong or if something is wrong.

Needle Biopsy - lymph nodes in neck

Hi, I’ve had a few of these biopsies, you shouldn’t feel anything after they numb you, it’s over in ten minutes. You will be absolutely fine to go back to work. Just close your eyes and don’t watch the needle go into node like I did the last time.

Good luck on Monday hope it goes ok for you.

Needle Biopsy - lymph nodes in neck

Thank you scones! I can do ten minutes! Hope you are well!

Needle Biopsy - lymph nodes in neck

Good luck! I hope it goes well for you! I had my ct scan on Tuesday and I have my ultrasound and biopsy next week. Haven’t had results from the ct yet as I have an appointment with the consultant a week on Wednesday so would imagine I will get the ct, ultrasound and biopsy results all on that date. Hopefully your biopsy is painless and results come through quickly x x

Needle Biopsy - lymph nodes in neck

Hi Bec2019, so we're on the same rollercoaster. I had an ultrasound first, so our tests are in different order. My CT scan results took 8 days. Blood work 5 days. The ultrasound results were immediate. The biopsy can take a while, they tell me. I feel that I am overthinking this experience. I think that as I go through test to test, I'm just waiting to hear that I'm well. The imbetween 'waits' are pretty horrific.

Let me know how you are, I'll do the same! Either way!

Needle Biopsy - lymph nodes in neck

The waiting is awful I was worried that by just feeling it he felt it warranted a full chest and neck ct done ASAP and ultrasound and biopsy as I’ve heard people having an ultrasound and biopsy that’s inconclusive and then being sent for a ct for a further look but not normally the other way around. Feel like the wait for next weeks ultrasound is taking forever .

the needle biopsy I have had before in my breast and it was painless so I hope yours goes well on Monday! Fingers crossed it all goes well and your results are quick and good news! Keep me updated I will also let you know how I get on next week x x

Needle Biopsy - lymph nodes in neck

I think each doctor has his / her own way of testing? My lumps were found during a random check after I was admitted to hospital for a hernia. I told my GP that I had to go back for tests and he said to just get a blood test first and take a round of antibiotics before getting anything else done. But at the hospital they had already taken a full round of blood tests, had me in for a day in hospital for tests for allergies and had scheduled a CT with contrast. I asked him for a day off work to have the CT and he said 'whatever are you doing?', as the hospital haven't been in contact with him, and I haven't taken the antibiotics as he suggested, I think he's confused.

But I am quite relieved that if I actually do have something wrong with me, I'm further along the testing stage than I would have been if I had done what my GP suggested. I said many times to the DR at the hospital, my GP thinks I need to take antibiotics and wait. I hate the idea that I am wasting hospital time and money if I should have just tried antibiotics.

The radiologist asked me before the CT how antibiotic therapy had gone. I said I hadn't taken any. He looked miffed. After I asked, should I take antibiotics starting this week? He said no need, and he was suggesting a biopsy in his report.

I've asked my ex husband to go away with our daughter this weekend, so I can lay low and do some cleaning. I decided not to discuss any of the 'what ifs' with my daughter, I have a new hernia in my back, so she thinks I'm sick because of my back and all the tests I've being having are for something she's used to me having.

I hope time passes for us both, and that we are found to be healthy at the end of it all. I am truly convinced I have nothing as I haven't lost any weight, I don't have night sweats and I wasn't even aware I had large lymh nodes until last month. Now I can see my neck is considerably swollen on the right, but I don't see the 6 3.5 cm lumps they say I have!


Seeking the Source of Ebola

The latest Ebola crisis may yield clues about where it hides between outbreaks.

Ebola Map

A map of the 2014-2015 Ebola outbreak and how it is believed to have spread throughout Africa.

Graphic by James Lauren E.

No one foresaw, back in December of 2013, that the little boy who fell ill in a village called Méliandou, in Guinea, West Africa, would be the starting point of a gruesome epidemic, one that would devastate three countries and provoke concern, fear, and argument around the planet.

No one imagined that this child&rsquos death, after just a few days&rsquo suffering, would be only the first of many thousands. His name was Emile Ouamouno. His symptoms were stark&mdashintense fever, black stool, vomiting&mdashbut those could have been signs of other diseases, including malaria. Sad to say, children die of unidentified fevers and diarrheal ailments all too frequently in African villages. But soon the boy&rsquos sister was dead too, and then his mother, his grandmother, a village midwife, and a nurse. The contagion spread through Méliandou to other villages of southern Guinea. This was almost three months before the word &ldquoEbola&rdquo began to flicker luridly in email traffic between Guinea and the wider world.

The public health authorities based in Guinea&rsquos capital, Conakry, and the viral disease trackers from abroad weren&rsquot in Méliandou when Emile Ouamouno died. Had they been, and had they understood that he was the first case in an outbreak of Ebola virus disease, they might have directed some timely attention to an important unknown: How did this boy get sick? What did he do, what did he touch, what did he eat? If Ebola virus was in his body, where did it come from?

Among the most puzzling aspects of Ebola virus, since its first recognized emergence almost four decades ago, is that it disappears for years at a time. Since a 1976 outbreak in what then was Zaire (now the Democratic Republic of the Congo) and a simultaneous episode with a closely related virus in what was then southern Sudan (now South Sudan), the sequence of Ebola events, large and small, has been sporadic. During one stretch of 17 years (1977-1994) not a single confirmed human death from infection with Ebola virus occurred. This is not a subtle bug that simmers delicately among people, causing nothing more than mild headaches and sniffles. If it had been circulating in human populations for those 17 years, we would have known.

A virus can&rsquot survive for long, or replicate at all, except within a living creature. That means it needs a host&mdashat least one kind of animal, or plant, or fungus, or microbe, whose body serves as its primary environment and whose cell machinery it can co-opt for reproducing. Some harmful viruses abide in nonhuman animals and only occasionally spill into people. They cause diseases that scientists label zoonoses. Ebola is a zoonosis, an especially nasty and perplexing one&mdashkilling many of its human victims in a matter of days, pushing others to the brink of death, and then vanishing. Where does it hide, quiet and inconspicuous, between outbreaks?

Not in chimpanzees or gorillas field studies have shown that Ebola often kills them too. Dramatic die-offs of chimps and gorillas have occurred around the same time and in the same area as Ebola virus disease outbreaks in humans, and some carcasses have tested positive for signs of the virus. Scavenging ape carcasses for food, in fact, has been one of the routes by which humans have infected themselves with Ebola. So the African apes are highly unlikely to harbor Ebola. It hits them and explodes. It must lurk somewhere else.

The creature in which a zoonotic virus exists over the long term, usually without causing symptoms, is known as a reservoir host. Monkeys serve as reservoir hosts for the yellow fever virus. Asian fruit bats of the genus Pteropus are reservoirs of Nipah virus, which killed more than a hundred people during a 1998-99 outbreak in Malaysia. Fruit bats also host Hendra virus in Australia, where it drops from bats into horses, with devastating effect, and then into horse handlers and veterinarians, often killing them. The passage event, when a virus goes from its reservoir host to another kind of creature, is termed spillover.

As for the reservoir host of Ebola&mdashif you have heard that fruit bats again are the answer, you&rsquove heard supposition misrepresented as fact. Despite arduous efforts by some intrepid scientists, Ebola virus has never been tracked to its source in the wild.

&ldquoWhere is it when it&rsquos not infecting humans?&rdquo Karl M. Johnson said to me recently. Johnson is an eminent virologist, a pioneer in Ebola research, the former head of the Viral Special Pathogens Branch at the Centers for Disease Control and Prevention (CDC). He led the international response team against that initial 1976 outbreak in Zaire, a harrowing venture into the unknown. He also led a team that isolated the virus in a CDC lab, demonstrated that it was new to science, and named it after a modest Zairean waterway, the Ebola River. Johnson wondered back then about its hiding place in the wild. But the urgency of human needs during any Ebola outbreak makes investigations in viral ecology difficult and unpopular. If you&rsquore an African villager, you don&rsquot want to see foreigners in moon suits methodically dissecting small mammals when your loved ones are being hauled away in body bags. Thirty-nine years later, although we&rsquore beginning to learn a bit, Johnson said, the identity of the reservoir host &ldquois still largely a monster question mark out there.&rdquo

A Rain of Bats

In April 2014, soon after word spread that the cluster of deaths in southern Guinea involved Ebola, Fabian Leendertz arrived there with a team of researchers. Leendertz is a German disease ecologist and veterinarian, based at the Robert Koch Institute in Berlin, who studies lethal zoonoses in wildlife, with special attention to West Africa. He reached southern Guinea by driving overland from Ivory Coast, where he has worked for 15 years in Taï National Park on disease outbreaks among chimpanzees and other animals. He brought with him three big vehicles, full of equipment and people, and two questions. Had there been a recent die-off among chimps or other wildlife, possibly putting meat-hungry humans at risk from infected carcasses? Alternatively, had there been direct transmission from the Ebola reservoir host, whatever it was, into the first human victim? Leendertz knew nothing at that point about Emile Ouamouno. His team spoke with officials and local people and walked survey transects through two forest reserves, finding neither testimony nor physical evidence of any remarkable deaths among chimpanzees or other large mammals. Then they shifted their attention to the village of Méliandou, talked with people there, and heard a very interesting story about a hollow tree full of bats.

These were small bats, the quick-flying kind that echolocate and feed on insects, not the big creatures that fly out majestically at dusk, like a Halloween vision of nocturnal crows, to eat fruit. The locals called them lolibelo. They were dainty as mice and smelly, with wriggly tails that extended beyond their hind membranes. Showing pictures and taking descriptions, Leendertz&rsquos team ascertained that the villagers were probably talking about the Angolan free-tailed bat (Mops condylurus). These bats had roosted in great numbers within a big, hollow tree that stood beside a trail near the village. Then, just weeks before, the tree had been burned, possibly during an attempt to gather honey. From the burning tree came what the people remembered as &ldquoa rain of bats.&rdquo The dead bats were gathered up, filling a half dozen hundred-pound rice sacks, and might have been eaten except for a sudden announcement from the government that because of Ebola, consuming bush meat was now prohibited. So the Méliandou villagers threw the dead bats away.

And there was something else about that hollow tree, the villagers told Leendertz&rsquos team. Children, possibly including Emile Ouamouno, used to play in it, sometimes catching the bats. They would even roast them on sticks and eat them.

Leendertz consulted a colleague with expertise in recovering DNA from environmental samples, who told him it might be feasible to find enough beneath the tree to identify the bat species that had roosted there. &ldquoSo I started running around with my tubes and spoon collecting soil,&rdquo Leendertz told me. Back in Berlin, genetic sequencing confirmed the presence of Angolan free-tailed bats. So this creature&mdashan insectivorous bat, not a fruit bat&mdashjoined the list of candidates for the role of Ebola&rsquos reservoir host.

The Hitchhiker

The first clues in this long mystery&mdashclues that seemed to point toward bats&mdasharose from disease outbreaks caused by Marburg virus, Ebola&rsquos slightly less notorious relative within the group known as filoviruses. The story of Ebola is closely connected with that of Marburg, according to a seasoned South African virologist named Robert Swanepoel, who has long studied them both.

&ldquoThe two are interlinked,&rdquo he said, as we sat before a computer screen in his Pretoria home, looking at photographs from his archive. Swanepoel, who hides a genial heart within a bearish exterior, is retired from the National Institute for Communicable Diseases (NICD), in Johannesburg, where he ran the Special Pathogens Unit for 24 years, but is still busy with research and bristling with ideas and memories.

Back in 1967, nine years before Ebola itself was recognized, a shipment of Ugandan monkeys intended for medical research arrived in Frankfurt and Marburg, in West Germany, and Belgrade, in Yugoslavia, bringing with them an unknown but dangerous virus. Laboratory workers became infected in each place, and then, secondarily, some family members and health workers. Among 32 confirmed cases, seven people died. The new virus, a spooky, filamentous thing, like a strand of toxic vermicelli, was given the name Marburg virus. Eight years later an Australian student died of Marburg virus disease in a Johannesburg hospital after a hitchhiking trip across Rhodesia (now Zimbabwe). He and his girlfriend&mdashshe got sick too but recovered&mdashhad done a few things that might have exposed them to infection: slept on the ground in a pasture, bought some raw eland meat, fed some caged monkeys. And they had visited the Chinhoyi Caves, a complex of caverns and sinkholes in northern Rhodesia that, like many caves in Africa, have been known to harbor bats. Along the way the hitchhiker also sustained some sort of insect or spider bite, which raised a painful red welt on his back. Investigation of his case in the immediate aftermath focused much on the bite, little on the caves.

Two other early cases of Marburg virus disease did cast some suspicion on caves and the bats that roost within them. In 1980 a French engineer who worked at a sugar factory near the base of Mount Elgon, in western Kenya, ventured into Kitum Cave, a deep passage into the volcanic rock of the mountain sometimes entered by elephants looking for salt. The engineer&rsquos cave visit was evidently a bad idea he died of Marburg in a Nairobi hospital. In 1987 a Danish schoolboy climbed the mountain and explored the same cave during a family vacation, and he died of an infection with a virus (now known as Ravn virus) closely related to Marburg. These events engaged the notice of Swanepoel, down in Johannesburg. In 1995 came another outbreak&mdashEbola this time, not Marburg&mdashcentered on the city of Kikwit in what is now the Democratic Republic of the Congo (DRC). The chain of human-to-human infections, which totaled 315 cases and 254 deaths, began with a man who farmed manioc and made charcoal in a forest area at the city&rsquos edge. Swanepoel flew to Kikwit, joining an international team of responders. He came down with malaria, went home, recovered, and in early 1996, with the support of the World Health Organization, returned. His primary task was to look for the reservoir host, searching the same ecosystem where the outbreak had begun at the same time of year. &ldquoAlready by that stage,&rdquo he told me, &ldquobats were on my mind.&rdquo

Swanepoel and his crew at Kikwit took blood and tissue not only from bats but also from a wide selection of other animals, including many insects. Screening those samples back at his lab in Johannesburg, he found no evidence of Ebola. So he tried an experimental approach, one that seemed almost maniacally thorough. Working in NICD&rsquos high-containment suite&mdashbiosafety level 4 (BSL-4), the highest&mdashhe personally injected live Ebola virus from the Kikwit outbreak into 24 kinds of plants and 19 kinds of animals, ranging from spiders and millipedes to lizards, birds, mice, and bats, and then monitored their condition over time. Though Ebola failed to take hold in most of the organisms, a low level of the virus&mdashwhich had survived but probably hadn&rsquot replicated&mdashwas detected in a single spider, and bats sustained Ebola virus infection for at least 12 days. One of those bats was a fruit bat. Another was an Angolan free-tailed bat, the same little insectivore that would later catch Fabian Leendertz&rsquos attention in Méliandou. It was proof of principle, though not of fact: These creatures could be reservoir hosts.

Ten Thousand Haystacks

The events in Kikwit highlighted an important difference between Marburg and Ebola viruses that has persisted: Whereas outbreaks of Marburg virus disease usually begin around caves and mines, Ebola virus disease outbreaks usually begin with hunting and carcass scavenging, which are forest activities. This suggests the two viruses may emerge from two different kinds of reservoir hosts&mdashor if bats are the hosts, two different kinds of bats, cave roosters and tree roosters.

The pattern was reaffirmed during a cluster of Marburg outbreaks from 1998 to 2000, centered on a derelict gold-mining town called Durba, in the DRC. Bob Swanepoel led another expedition and found multiple chains of infection, most or all of which started with miners who worked underground. Miners who worked at open pits in the daylight were far more likely to stay healthy. This led Swanepoel to suspect cave-roosting Egyptian fruit bats as the virus source, though he didn&rsquot publish his suspicion at the time.

Then, beginning in late 2001 and extending into 2003, another series of small, independent outbreaks&mdashof Ebola again, not Marburg&mdashafflicted villagers in the densely forested borderlands of Gabon and the Republic of the Congo (which are west of the DRC, on the other side of the Congo River). Roughly 300 people became infected almost 80 percent died. Meanwhile gorillas, chimpanzees, and duikers, small forest antelopes, started turning up dead in the same region. Each human outbreak seemed to start with an unfortunate person, usually a hunter, who&rsquod handled an animal carcass.

&ldquoPeople were dying, and different animals were dying,&rdquo said Janusz Paweska, nowadays Swanepoel&rsquos successor as head of Special Pathogens at NICD, when I visited him in Johannesburg. &ldquoSo we thought, This is a good time to hunt for the Ebola reservoir.&rdquo

Swanepoel enlisted Paweska and others, then arranged a partnered expedition with Eric Leroy, a French virologist based in Gabon who had responded to earlier Ebola outbreaks there. He met with Leroy in Gabon&rsquos capital, Libreville, before heading into the field.

&ldquoI gave him a long story about how historically bats have been involved in Ebola and Marburg,&rdquo Swanepoel told me. His team, he informed Leroy, had found fragments of Marburg, for instance, in the underground bats at Durba. Swanepoel had brought rodent traps, mist nets, and other collecting gear to Gabon. &ldquoAlthough I was fixated on bats, I said we had to cover everything,&rdquo he recalled. That would include a variety of mammals, birds, mosquitoes, biting midges, and other insects. Swanepoel&rsquos group took home a third of the specimens and sent a third to the CDC in Atlanta, leaving a third to be tested by Leroy. The processing moved slowly in Swanepoel&rsquos lab and at the CDC, amid many other projects, and yielded no positives. &ldquoWe drew a blank.&rdquo

But Leroy&rsquos group went back. Eventually his team made three field trips to the border area, capturing and sampling more than a thousand animals, including 679 bats, on which Leroy too was now fixated. In 16 of those bats, belonging to three different fruit-eating species, they found antibodies&mdashproteins marshaled by the immune system&mdashthat had reacted against Ebola virus. In 13 other fruit bats they detected very short fragments of Ebola RNA. It&rsquos important to note that those two kinds of evidence, antibodies and viral fragments, are analogous to finding the footprints of a Yeti in snow. You might or might not have something real. Isolating live virus&mdashthat is, growing fresh and infectious Ebola from a tissue sample&mdashis the higher standard of evidence, almost like finding a real Yeti&rsquos foot attached to a real Yeti in a leghold trap. Leroy&rsquos group didn&rsquot succeed in growing live virus from any samples. Still, in 2005 the journal Nature published a paper on these results, written by Leroy but with Swanepoel and Paweska credited as co-authors, titled &ldquoFruit Bats as Reservoirs of Ebola Virus.&rdquo That paper, though cautious and provisional, is the primary source for all those careless, overly certain assertions you&rsquove seen in the popular media during the past year to the effect that Ebola virus resides in fruit bats.

Possibly it does. Or not. The paper itself says maybe.

&ldquoYou tried to isolate live virus?&rdquo I asked Leroy during my stop in Gabon. He&rsquos a courteous, dapper Frenchman, now director of the Centre International de Recherches Médicales de Franceville, who works in a white shirt and dark tie, at least when he&rsquos not wearing a full protective suit in his BSL-4 lab or Tyvek coveralls in the forest. &ldquoYes. Many, many, many times trying to isolate the virus,&rdquo he said. &ldquoBut I never could. Because it was&mdashthe viral load was very, very low.&rdquo Viral load is the quantity of virus in the solid tissues or blood of the creature, and it tends to be much lower in a reservoir host than in an animal or person suffering an acute infection.

That&rsquos just one of three reasons why finding a reservoir host is difficult, Leroy explained. The second is that, in addition to low viral load within each animal, the virus may exist at low prevalence within a population. Prevalence is the percentage of positive individuals at a given time, and if that happens to be as little as one animal in a hundred, then &ldquothe probability to detect and to catch this infected animal is very low.&rdquo If a single kind of animal amid the great diversity of tropical forests represents a needle in a haystack, then one infected individual within one population of animals amid such diversity represents one needle in ten thousand haystacks.

And the third constraint on the search for a reservoir host? &ldquoIt&rsquos extremely expensive,&rdquo Leroy said.

The Perfect Holiday

The cost of field operations in remote forest locations, as well as the competing demands upon institutional resources, has hindered even veteran researchers such as Swanepoel and Leroy from mounting long-term, continuous studies of the Ebola reservoir question. Instead there have been short expeditions, organized quickly during an outbreak or just as a crisis was ending. But going to the site of a human outbreak to do research on the ecology of the virus is logistically nightmarish and, as I&rsquove mentioned, offensive to local people. So those expeditions get delayed. The problem with delay is that the prevalence of Ebola virus within its host population, the viral load within individual hosts, and the abundance of virus being shed into the environment may all fluctuate seasonally. Miss the right season, and you might miss the virus.

Fabian Leendertz tried to address these difficulties by organizing a second field expedition, this one at roughly the same season as the fateful spillover that killed Emile Ouamouno, but a year later and in neighboring Ivory Coast. Angolan free-tailed bats are abundant there too, roosting beneath the roofs of village houses. Their very abundance in such close proximity to people suggests a further perplexing question, if the little-bat hypothesis is correct: With the virus so near, why don&rsquot spillovers occur far more often? Leendertz wanted to trap those bats, as many as possible, and sample them for evidence of Ebola. Photographer Pete Muller and I went with him.

Leendertz and his team, including a graduate student named Ariane Düx, focused on two villages outside the city of Bouaké, a trade hub near the country&rsquos center. After shopping for trap materials in Bouaké&rsquos market, scouting the villages for bat-filled houses, and paying respects to village elders, the team assembled their apparatus late one afternoon, in time for the fly out at dusk. The traps were cone-shaped structures, jerry-built of long boards and translucent plastic sheeting, designed to capture bats as they emerged from a roof hole and funnel them down into a plastic tub. Amazingly, the system worked. At 6:25 p.m. on the first evening one trap came alive like a popcorn popper, as dozens of small gray bodies slid down the sheeting and thumped into the tub.

For the next phase Leendertz and Düx suited up in medical gloves, respirator masks, gowns, and visors. With a naked lightbulb hanging above their makeshift lab table, they began processing bats: weighing and measuring each animal, noting sex and approximate age, injecting an electronic chip the size of a caraway seed for later identification, and most important, drawing blood from a vein in the animal&rsquos tiny arm. One well-aimed poke with a delicate needle, and a blood drop would appear, to be gathered with a fine pipette. Düx and Leendertz worked together at close range, trustingly sharing tasks, and it occurred to me that if she poked twice at the vein and missed the second time, jabbing Leendertz&rsquos finger instead, he could have an Ebola-related needle-stick injury. But she didn&rsquot miss.

The blood went into small vials, for freezing immediately in a liquid-nitrogen tank and eventual screening back in Berlin. A small fraction of all the captured bats would be killed and dissected, so that snippets of their internal organs, especially liver and spleen, where viruses often concentrate, could be added to the trove of frozen samples. The other bats would be released. If a blood sample from one dissected individual later tested positive for antibodies or viral fragments, its organs would then be used in an attempt (more dangerous and more expensive, done only in a BSL-4 laboratory) to isolate live Ebola virus.

After a few bats Leendertz stepped back from the processing work and allowed an Ivorian graduate student, Leonce Kouadio, tall, mild mannered, and thin as a candle, to take his place. This was a training mission as well as a scientific investigation, after all, and Leendertz wanted to give his protégés a richness of experience. Kouadio had good skills already, and as he got into rhythm, sharing these exacting tasks in the warm African night, I noticed the T-shirt beneath his medical gown, which carried some sort of resort logo and said, It&rsquos the perfect holiday. For him, maybe, but not for everybody.

A Strange Host

Back in the United States, I spoke with more experts during a stop at the CDC in Atlanta and by telephone. When I asked why it&rsquos important to identify the reservoir host of Ebola virus, they all agreed: because that information is essential to preventing future outbreaks. On other points they diverged. The most unexpected comment came from Jens Kuhn, a brainy young virologist now at the National Institutes of Health and, by way of his tome Filoviruses, arguably the preeminent historian of Ebola. I&rsquove known Kuhn as a candid source but also a lively and generous friend since we met at a conference hosted by Eric Leroy. Why do you think that after 39 years, I asked him, the reservoir of Ebola is still unidentified?

&ldquoA strange host,&rdquo I repeated, not sure I&rsquod heard right.

His logic was complex, but he sketched it concisely. First, outbreaks of Ebola virus disease have been relatively infrequent&mdashonly about two dozen in nearly 40 years. Rare occurrences. Almost everyone was traceable to a single human case, infected from the wild, followed by human-to-human transmission. This suggests, he said, that the sequence of events yielding spillover has to be &ldquoextraordinary and weird.&rdquo Highly unusual circumstances, an unlikely convergence of factors. Second, there&rsquos &ldquothe remarkable genome stability of the virus over the years.&rdquo It didn&rsquot change much, didn&rsquot evolve much, at least until the human case count in West Africa started going so high, providing many more opportunities for the virus to mutate. That stability might reflect &ldquoa bottleneck somewhere,&rdquo Kuhn said&mdasha constraining situation that keeps the virus scarce and its genetic diversity low. One possible form of bottleneck would be a two-host system: a mammal host such as a bat species that becomes infected only intermittently, when it gets bitten by a certain insect or tick or other arthropod, perhaps relatively rare or narrowly distributed, which is the ultimate host of the virus. As we both knew, this harked back to that hitchhiker in Rhodesia in 1975 who suffered an odd little bite and then died of Marburg. It evoked the spider in Bob Swanepoel&rsquos lab that carried Ebola for two weeks.

What would you do, I asked him, if you had a big research grant for nothing but finding Ebola&rsquos reservoir? Kuhn laughed.

&ldquoI&rsquom going to make myself unpopular,&rdquo he said, &ldquobut I would still look into insects and other arthropods.&rdquo

He doesn&rsquot have that big grant, nor does anyone else. The mystery remains. The stakes are high. The samples from Ivory Coast have so far yielded no positives. The search continues.

Originally published by National Geographic Magazine and natgeo.com in July 2015.

A map of the 2014-2015 Ebola outbreak and how it is believed to have spread throughout Africa.


Chilling Out with Cold Plasmas

There are two things people think about when they hear the word "plasma." The first is blood plasma, the liquid part of blood that holds blood cells in suspension. The second, if you love physics, is an ionized gas (if you love geology, you'll think of a bright green chalcedony stone), usually at fairly high temperatures. The sun shoots out plasma arcs, for example. You can find them in plasma TV displays, you can use them to create antennae, and fans of science fiction likely fantasize about shooting them firearms as a high-tech weapon. (Lightning is a form of plasma.)

There are also so-called "cold plasmas." I wrote about this topic back in 2007, both in Physics Today and at Cocktail Party Physics, focusing on their potential to kill bacteria, remove dental plaque, loosen the connections between cells that make up biological tissue, help coagulate blood and reduce bleeding following a wound, or during surgery, and perhaps even remove cancerous tumors. And an October paper in the Journal of Physics D: Applied Physics describes a potentially revolutionary new cold plasma device, similar to a blowtorch, for treating blood cancer leukemia.

"We have a really amazing device," lead author Mounir Laroussi (Old Dominion University) told the folks at Physics Buzz. "We can generate a beam of plasma that is around room temperature. It doesn't burn anything it doesn't destroy or poke holes. You can touch it with your hand." Laroussi's results are pretty startling: after a mere 10 minutes' exposure to the cold plasma, more than 90% of leukemia cells in the study were destroyed.

The term "cold" can be a bit misleading. (Eg, "high-temperature superconductivity" takes place at temperatures common to liquid nitrogen.) Many cold plasmas are "cold" compared to, say, the sun, but still pretty hot: on the order of 70 to 100 degrees Celsius. Apply that to living human tissue, and it's gonna burn. Badly.

Still, they're useful for things like sterilizing drinking water and decontaminating industrial surfaces. That's because they kill ("inactivate") bacteria by destroying the bacterial cell membrane via a lethal combination of charged particles, free radicals and UV radiation. They work fast, too: the Air Force has an active cold plasma research program, using them to break down the chemicals found in toxins like anthrax in mere minutes, compared to several hours for other methods.

Sometime in the late 1990s, researchers figured out how to create truly room-temperature cold plasmas in the laboratory, so for the first time, they could be tested on biological tissue. And that's the focus of Laroussi's research. Per Physics Buzz:

There was an intriguing delayed effect with the plasma blowtorch. While the leukemia cells seemed fine immediately after being blasted with the cold-plasma plume for ten minutes, within four to eight hours they started to die. Laroussi hypothesizes that the plasma plume might trigger a biochemical reaction of sorts, inducing cell death in the leukemia cells while leaving normal cells intact.

According to George Washington University's Michael Keidar, among the molecules in a cold plasma is ozone, which is especially reactive -- hence the effectiveness of cold plasmas in treating bacterial infections. Keidar studies plasma treatments for cancer and thinks that because cancerous cells have higher metabolisms than healthy cells, they have more ozone. So the addition of even more ozone molecules via the cold plasma plume puts the cancer cells over the threshold and triggers cell death, whereas healthy cells can withstand the blast just fine.

Previously, Laroussi developed a helium-filled plasma pencil capable of creating a long plasma plume of 2 to 3 inches, which can kill bacteria on the delicate surface of human skin without damaging the surrounding tissue. Laroussi has used it on e coli bacteria. Other groups working with cold plasma "jet guns" have demonstrated the destruction of salmonella and even a few viruses.

Those decontamination properties are incredibly useful in helping accelerate wound healing, which has roughly three stages. There's an inflammatory stage, where everything is red and/or swollen and painful, in which it might seem like little healing is actually taking place -- in fact, it's easy to confuse with actual infection.

But there's all kinds of things going on to prompt the body into the second stage: producing collagen to strengthen the wound. This can take several weeks, depending on the severity of the injury, and thick scars can develop.

The final stage is called the remodeling phase, in which the body gets rid of the excess scar tissue. Sometimes a heavy raised (keloid) scar still remains, if the wound was especially deep and nasty. Being able to kill bacteria reduces the chance of infection, and being able to remove dead cells and replace them with healthy ones can significantly speed up this weeks-long process.

Back in 2010, researchers at the Gamaleya Institute of Epidemiology and Microbiology in Moscow used a cold plasma torch on two common bacteria, Pseudomonas aeruginosa and Staphylococcus aureus, both antibiotic-resistant strains (thanks to a biofilm) that are common in wound infections. Per Discovery News: "After five minutes, the plasma torch killed 99 percent of bacteria grown in a Petri dish, and after ten minutes, it killed 90 percent of bacteria present in the wounds of a rats. And because the torch can be directed at a specific, small area of infection, surrounding tissue is left unharmed."

Eva Stoffels-Adamowicz of Eindhoven University of Technology in the Netherlands developed a handy little device called a plasma needle -- basically a thin tungsten wire about 50 millimeters long, inside a gas-filled quartz tube -- that enables her to precisely remove or manipulate biological cells. She calls it "surgery without cutting." Just drive a voltage through the needle and voila! A small plasma spark is generated at the tip.

Neither the plasma needle nor the plasma pencil are using a cold plasma to do actual cutting. But a company called Peak Surgical has a prototype device called the Plasma Blade that actually uses cold plasmas to cut biological tissue. Surgical scalpels have served us well for a very long time, but while they cut very precisely, they can't control bleeding. There are alternative electrosurgical devices that can do both, but there's usually some accompanying thermal damage to surrounding tissue.

The Plasma Blade cuts, cauterizes, and doesn't burn surrounding tissue, plus you've got those built-in decontamination attributes to fight infection and reduce inflammation, thereby accelerating the healing process. Peak has tested their Plasma Blade on both retinal tissue and on pig skin.

Cold plasmas kill bacteria and save lives, which makes them pretty cool.

Barekzi, N. and Laroussi, M. (2012) "Dose-dependent killing of leukemia cells by low-temperature plasma," Journal of Physics D: Applied Physics 45 422002.

Brok, W.J.M. et al. (2005) "Numerical description of discharge characteristics of the plasma needle," Journal of Applied Physics 98: 013302.

Ermolaeva, Svetlana A. et al. (2011) "Bactericidal effects of non-thermal argon plasma in vitro, in biofilms and in the animal model of infected wounds," Journal of Medical Microbiology 60(1): 75-83.

Laroussi, M. et al. (2006) "Inactivation of bacteria by the plasma pencil," Plasma Proc. Polym. 3: 470-473.

Laroussi, M. et al. (2008) "The plasma pencil: a source of hypersonic cold plasma bullets for biomedical applications," IEEE Transactions: Plasma Science 36(4): 1298-1299.

Stoeffels, E., Kieft, I.E., Sladek, R.E.J. (2003) "Superficial treatment of mammalian cells using plasma needle," Journal of Physics D: Applied Physics 36: 2908-2913.

[Adapted in part from a 2007 post on the archived Cocktail Party Physics blog.]

The views expressed are those of the author(s) and are not necessarily those of Scientific American.

ABOUT THE AUTHOR(S)

Jennifer Ouellette is a science writer who loves to indulge her inner geek by finding quirky connections between physics, popular culture, and the world at large.


26 Answers 26

The "poison" is actually harmless A.

The body converts A to B, also harmless.

The body converts B to C, deadly.

Once the A->B path has saturated you get an A->D path.

B is eliminated from the body faster than D.

While I am not aware of anything with this behavior there are things that exhibit part of it. I don't know if it's still the case but the treatment for methanol poisoning is ethanol. Saturate the reaction path with the ethanol and the methanol doesn't kill you.

Also, consider acetaminophen. With the usual dose the preferred pathway produces a chemical that is of little threat. However, there's a second pathway that produces N-Acetylimidoquinone which is a nasty customer. While this is always produced it is usually in small quantities and quickly neutralized. However, the primary pathway can saturate, once it does all the remainder gets converted to the N-Acetylimidoquinone which destroys your liver and thus kills you if you don't promptly get a liver transplant.

It occurs to me that if such a chemical actually exists it probably would be unknown. After all, why would you test above the dose that kills all your test animals? And in humans such exposure would be extremely rare. Even if there is a case of unexpected survival it's unlikely they would spend the effort to figure out why.

What you're looking for is an emetic - a substance that induces vomiting. This is the specific reason why, as @Alberto Yagos already stated in his answer, suicide-by-pills doesn't always work - many pills are coated in a small amount of emetic so you'll throw them up if you take too many.

In the case of your poison, a large enough dose would cause you to throw it all back up, thus saving your life. A small enough dose, however, would just slowly digest in your stomach, and once it's in your bloodstream, it's lethal.

A cursory search hasn't found me any real-life emetics that would kill you if you didn't take enough of them. The closest I can find is copper sulfate, but it only becomes dangerous way past the point at which it makes you throw up, and doesn't seem to do anything below that threshold. The good news is, this means you can invent your own emetic poison, and tweak the numbers (how long it sits in the stomach for, how much is required to induce vomiting) until they're just right for your story.

This is perfectly possible, and I guess it could be readily done with modern technology. For less technical settings, you just need to say that some plant happens to produce the poison, it's believable enough.

So how does it work?
Your poison needs to be a drug (let's call it P) that targets two different compounds in the human body (call them A and B). Think of a large molecule with two different functional groups, each of which are responsible for one of the two reactions. Such molecules should be quite easy to produce with modern methods.

Compound A is rare in the human body. P strongly interacts with A to produce the evil, deadly compound E.

The evil compound E needs some time to do its destructive work, though.

Compound B is abundant in the human body, but P only weakly interacts with it to form some other compound R.

When compounds E and R meet, the E is destroyed for good.

With these traits and reactions, you would get the following behavior:

A low dose of P will mostly interact with A to form the evil E, killing the victim.

A big dose of P will quickly interact with all the A that's available to form E. Once the reservoir of A is depleted, no more E can be formed. The rest of the dose of P then interacts with B instead, forming large quantities of R. The R proceeds to eliminate the E before it can do too much harm.

After a large dose of P, the body will be flooded with R, granting immunity to P for a limited amount of time.

If you want to optimize, you may also skip the compounds B and R, and have P directly inhibiting E. In this case, the toxicity of small doses would rely on P turning A into E more quickly than it can eliminate the produced E. The non-toxicity of large doses would rely on P quickly depleting A, so it destroys the produced E instead.

The two path reaction seems easier to explain to me, though.

There is one possibility: your lethal substance is an ingested poison. With a low dose, it goes into the bloodstream and kills you. In a large dose, it is so harmful your stomach immediately throws it up, saving your life.

It isn't pretty, but it is reason some suicides with pills failed. And as another example, Napoleon tried to kill himself during his exile and he took so much poison he threw it up and survived (to be murdered by another poison later).

What you're proposing is certainly possible, although I don't know of a case that demonstrates this exactly. The behavior of biologically active molecules (drugs or toxins) can be very complex (see pharmacokinetics on Wikipedia). Many poisonous substances are detoxified or made toxic by enzymes in the body (drug metabolism). For instance, ethanol, the active component of beer, is converted by the liver enzyme alcohol dehydrogenase to acetylaldehyde (more toxic than ethanol) and then by the enzyme acetaldehyde dehydrogenase to acetic acid (nontoxic and naturally occurring in the body).

Drugs that can cause the body to make more of an enzyme are called enzyme inducers. Interestingly, some drugs can induce their own metabolism (for example, the anti-epileptic carbamazepine). This is called autoinduction of drug metabolism, meaning that the drug upregulates the same enzyme that degrades it. In fact, this is one mechanism for developing a tolerance to drugs.

So your poison could be a toxin that upregulates its own metabolism. The biological activities of drugs can be very nonlinear, so it is possible to have a situation where the toxic effects of your molecule are fatal at low concentration, while, at high concentrations, it highly upregulates the enzyme that metabolizes it, making it nontoxic before its effects are fatal. I don't know of any molecule that acts this way off the top of my head, but I wouldn't be surprised if something like this exists.

Homeopathy is the real world, but very, very mistaken, idea that "like cures like". An infinitesimal amount of a poison can cure the poison's symptoms. For example, mandrake root can cause hyperactivity and hallucinations, so a homeopathic "doctor" faced with a patient with such symptoms might produce a tincture of extremely diluted mandrake root. The more diluted the tincture, the more powerful the cure.

In reality this is hogwash. Homeopathic tinctures are so diluted statistically they often contain not even a single molecule of the original substance. Homeopathy "theorizes" that the alcohol or water retains the "memory" of the original substance, also hogwash. Homeopathy "worked" because doctors at the time would do more harm than good, and the "medicine" came with a long required list of healthy habits the patient must practice. Now it's just a placebo.

But in a fantasy world, why not?!

Homeopathy was developed in the 18th century, but "like cures like" goes back to Hippocrates so the concept would be around for a medieval setting.

Take the same approach as homeopathy, but now it's like kills like. In Homeopathy, diluting a poison is supposed to turn it into a cure. In your world, diluting a cure turns it into a poison! A large amount will save you, but an infinitesimally small amount will kill you. Perhaps the substance itself is the cure, but the diluted "solution" (in quotes because there's nothing of the original substance left) retains the "memory" of the disease it's meant to cure.

One possibility is that the substance binds to itself in large amounts but not so well in smaller amounts. Since it doesn't bind as well in small amounts it's able to interact with the body more so in those small amounts. It's poisonous in both situations, but significantly more so in small amounts.

The best description I can think of is this a thin layer of metal isn't very strong when stressed (like a chemical in a body would be) so it breaks with very little force into small pieces compared to a thick layer of that metal. It's been too long since chemistry class, so I can't say how accurate this description is.

You're missing a couple of elements here.

Effects vary depending on delivery method.

If the substance isn't readily digested, you might need large quantities to get any of it into the victim's system. In the extreme case, it might be completely ineffective that way. Taken in some other form - injected into the bloodstream, for the most obvious example, but more recently using coated microcapsules - you can get that substance to where it works.

Effects vary depending on surface area.

A bit of gravel stuck in a nostril is an annoyance. The same rock ground to a fine powder and inhaled over time gives you silicosis. Nanoparticles appear to have different characteristics to larger bulk stuff.

So smaller amounts can be more effective - but you'll need to use it differently.


If I keep on getting blood draws from the same vein, would it eventually scar the vein?

I've heard that drug users often have horrible scars on their veins because they inject things in their veins so much, and that worries me.

Now, I don't use drugs. And I don't get very many blood draws right now. But what about when I get old? The elderly often get repeated blood draws when they get in the hospital, and their veins are pretty fragile

YES. your veins will scar, but dont worry about it too much. This typically happens when people need to inject or draw blood repeatedly and dont give their veins time to heal.

First off, there are two methods in which the human body handles injury. The first is regeneration, in which native tissue cells grow over the injured site, and restore the tissue to native function. The second is repair, in which fibroblasts will invade the injured site, and deposit collagen in the form of scar tissue. You can think of it as either replacing a broken part in a machine, or super gluing back together. Obviously replacing the part is the best option, but its time consuming and expensive. Same thing happens in the human body.

Anyways, if you give repeated injuries to the same area of the same vein without letting the vein regenerate, the vein will be forced to repair (if you cant replace the part, you just have to superglue it together). When that happens, you get scarring. You probably dont need to worry about it unless you get very old (in which case, your regenerative abilities begin to weaken), or you are a drug user or you are on dialysis.

If you are on dialysis, scarring of the veins is actually a major issue. Not only does your vein scar, but repeated puncturing will also cause inflammation and collapsing of the vein. For dialysis patients, there are a number of techniques that are used to try and minimize these effects, some of which include surgically attaching a teflon tube to the vascular system to gain access to the blood supply without destroying the vein.

If anyone knows better and would like to add on to this or correct me where I'm wrong, feel free.


Change history

Ibáñez, A. J. et al. Proc. Natl Acad. Sci. USA 110, 8790–8794 (2013).

Aerts, J. T. et al. Anal. Chem. 86, 3203–3208 (2014).

Walker, B. N., Antonakos, C., Retterer, S. T. & Vertes, A. Angew. Chem. Int. Ed. Engl. 52, 3650–3653 (2013).

Lovrić, J. et al. ACS Nano (in the press).

Hiyama, E. et al. Anal. Sci. 31, 1215–1217 (2015).

Ali, A. et al. Anal. Sci. 32, 125–127 (2016).

Förster, J., Famili, I., Fu, P., Palsson, B. Ø. & Nielsen, J. Genome Res. 13, 244–253 (2003).


Watch the video: Q8: What would happen if the plasma membrane ruptures or breakdown? (August 2022).