Florence Sabin

Posted by amanda on Monday, March 8th, 2010

Today is International Women’s Day, where women are celebrated globally for their economic, social, political, and scientific achievements. This post is in continuation of my own celebration of National Women’s History Month.
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Florence Sabin

Florence Rena Sabin’s life was full of firsts. In 1896, after saving up money for 3 years as a schoolteacher, Florence Rena Sabin enrolled in Johns Hopkins Medical School. From a mining town in Colorado, Sabin was the first woman to graduate with an M.D. from Johns Hopkins. After graduation, she joined the Department of Anatomy with the support of a fellowship from the Baltimore Association for the Promotion of University Education of Women. She was the first woman faculty member at Johns Hopkins, the first woman to hold the rank of full professor, the first woman president of the American Association of Anatomists, the first woman elected to membership in the National Academy of Sciences, and the first woman to be appointed a full member at the Rockefeller Institute. In her obituary in the British Medical Journal, she was referred to as “the greatest living woman scientist and one of the foremost scientists of all time”.

Her research contributed more than a hundred papers to the literature on the lymphatic system, tuberculosis, blood vessels, cells, and connective tissue. Contrary to popular belief at the time, Sabin demonstrated that the lymphatic system structure was formed from an embryo’s veins rather than from other tissues. Among her other research, she perfected a cell staining technique use to visualize live cells. As a scientist at the Rockefeller Institute, she made major contributions to the understanding of the human immune response to tuberculosis.

Upon accepting the Pictorial Review achievement award in 1929, Sabin said:

I hope my studies may be an encouragement to other women, especially to young women, to devote their lives to the larger interests of the mind. It matters little whether men or women have the more brains; all we women need to do to exert our proper influence is just to use all the brains we have.

Rest assured, Dr. Sabin, you are an encouragement.

See the National Library of Medicine for a more detailed biography of Sabin.

Regression in the Dark

Posted by amanda on Friday, March 5th, 2010

Why don’t humans have tails or gills? Why aren’t we covered in hair? Why don’t we have all the traits of our primitive ancestors? When we think of the advance of evolution, we may think of increasing complexity, but many traits are lost due to regressive evolution. Regressive evolution is the disappearance of an ancestral trait or characteristic over time.

Surface FishCavefish

A. mexicanus Surface Fish and Cavefish; Courtesy of William Jeffery

In order to better understand how regressive evolution occurs, scientists have found a model organism among cave-dwelling animals. Cavefish, like most cave-dwelling animals, have lost their eyes and pigmentation over time. And interestingly, they can interbreed with their surface-dwelling counterparts who still have eyes and normal pigment, making them a model tool for understanding the genetics of trait loss.

How are traits lost in evolution? It may be that genes responsible for these traits are mutated or lost due to their lack of advantage. Or perhaps it is somehow more beneficial to not have the lost trait due to energy conservation. A third theory is that lost traits may be negatively linked to other traits that now benefit the organism in a new environment. When one gene affects many traits, this is known as pleiotropy.

In a recent review in the journal Annual Review of Genetics, William Jeffery, a professor at the University of Maryland’s Department of Biology, discusses regressive evolution in the cavefish Astyanax mexicanus. Known as the Blind Tetra, A. mexicanus is native to 30 known caves in Mexico but can now be found in laboratories around the United States due to its short reproduction time, simple diet, and frequent spawning. Although cavefish appear eyeless, they actually have small nonfunctional eyes in a smaller eye socket completely covered with skin. In Jeffery’s lab, when a cavefish embryo is transplanted with a surface fish lens, the cavefish is able to develop an eye, containing a retina lacking pigment. The lens of the eye prevents cell death in the retina. Because the surface fish lens was able to rescue eye development, this suggests that the lens has a fundamental role in regulating eye degeneration and may be the crucial trait that is lost in the regressive evolution of eyesight.

From genetic studies, it is estimated that up to twelve separate genes are responsible for eye loss. One of these genes (known as shh), affects both eye degeneration and the enhancement of oral and taste bud development, traits that would be advantageous to a cave-dwelling fish. This indicates that pleiotropy may play a role in eye regressive evolution. Jeffery stresses that more than one of the three possible theories for regressive evolution may be responsible for eye loss in cavefish. The search to identify all of the genes that affect eye degeneration in A. mexicanus is underway and may lead to insights about our own regressive evolution.

I wish I could trade in my spleen for a tail…

Henrietta Lacks

Posted by amanda on Tuesday, March 2nd, 2010

March is National Women’s History Month. In celebration, I plan to make one post a week featuring women that contributed significantly to science in Baltimore.

Immortal Life of Henrietta Lacks

I want to start with Henrietta Lacks, a woman from Turner Station whose cancerous cells were taken and turned into one of the most powerful scientific tools we have today. The tumorous cells that were removed from Henrietta’s cervix at Johns Hopkins Hospital during her treatment in 1951 were the first immortal human tissue cells to be cultured. First grown in the lab of George and Margaret Gey, Henrietta’s cells can be maintained indefinitely and have been used for countless experiments to study everything from cancer to the effects of atomic radiation on human tissue. Named HeLa, these cells led to advances in human genetics, such as the numbering of chromosomes, as well as to the cell culture, cloning, and in vitro fertilization methods we use today.

The Immortal Life of Henrietta Lacks by Rebecca Skloot is an excellent read on the history of Henrietta and HeLa cells and highlights the moral and legal dilemmas of tissue collection. In her book, Skloot discusses how the Lacks family (who still reside in Baltimore) did not know about the use of HeLa cells until decades after their spread into laboratories around the world, and that while biotechnology companies that produce and sell HeLa continue to profit, the Lacks family has struggled with affording health insurance.

According to Skloot, there has never been an official effort by Johns Hopkins to honor Henrietta Lacks and her biological contribution to science. With the amazing press Skloot’s book has generated, I have a feeling this may change soon.

What’s in YOUR Water?

Posted by amanda on Sunday, February 28th, 2010

water drop

http://www.flickr.com/photos/hypergurl/ / CC BY-NC 2.0

In an article published last week in Current Opinion in Pediatrics, a well-respected professor at Mount Sinai School of Medicine in New York, Philip Landrigan, talks about the environmental chemicals implicated in neurodevelopmental disabilities. He discusses the possibility that environmental toxins may be contributing to autism, alerting the scientific community to the need for more research on the effects of common chemicals on brain biology. In his article, he states that synthetic chemicals that are ubiquitous at hazardous waste sites are commonly found in our air, food, and drinking water. And fewer than 20% of these have been tested for brain developmental toxicity.

As I sat reading the article, drinking my cup of tap water tea, I asked myself: What’s in your water?

According to the Environmental Working Group, a watchdog organization that compiles data from water utility companies and state departments, Baltimore ranks 69 out of 100 cities for quality of water with 1 being the best and 100 the worst. The list of chemicals found in the Baltimore City Department of Public Works water is astounding. In the past five years, two contaminants were found to be above legal limits with eleven others above health guidelines. A total of 22 pollutants were identified in Baltimore City water, 14 more than the national average. 22!

Let’s do a rundown on some of them:

  • Lead: Even my 2-year old daughter knows this one is bad. The EPA has a restriction of 15 ppb for drinking water, and levels above that value (at 19.3 ppb) were detected in Baltimore City water in the past 5 years with an average of 5.16 ppb overall. Lead is known to cause brain damage.
  • Total haloacetic acids (HAAs), Total trihalomethanes (TTHMs), Chloroform, Bromoform, and Trichloroacetic acid: Disinfectants that cause DNA damage and cell death. Carcinogens aplenty. Both HAAs and TTHMs were found above legal limits during the past 5 years. In fact, Baltimore City water ranks among the top 10 cities with the highest levels of TTHMs (at an average of 44.5 ppb).
  • Alpha Particle Activity and Radium-226: Radioactive. Any chemical with a number after it is generally bad. Luckily, the data is from only one test and is at very low levels that we probably don’t need to worry about.
  • Di(2-ethylhexyl) phthalate: Phthalates, found in soft plastics, have been in the news for awhile now, so you probably have heard their name. They are beginning to be phased out of products in both the United States and Europe due to their toxicity.  Phthalates can cause both reproductive and developmental problems. The level in Baltimore City water is at an average of 0.85 ppb. The danger lies in a build-up of phthalates within the body over time.

In his article, Landrigan stresses that in the examples of known chemicals that are relevant to autism (where women were taking certain medications that lead to a higher incidence of autism in their children, such as thalidomide, misoprostol, and valproic acid), exposure occurs prenatally, very early in the first trimester of pregnancy. Therefore, this may be the most important time to avoid harmful chemicals that can affect fetal brain development. Whether or not other chemicals or known neurotoxins, such as phthalates, organophosphate pesticides, and BPA, cause an increase in autism or other specific brain development disorders is not known, and Landrigan encourages future toxicological studies to answer these questions.

But I know one thing for sure: I’m off to get a water filter.

Nano Nano

Posted by amanda on Thursday, February 25th, 2010

Carbon Nanotube

Carbon Nanotube; http://www.flickr.com/photos/ghutchis/ / CC BY-ND 2.0

Imagine a tiny tube. Now imagine it even tinier than that — so tiny that not even a single molecule of caffeine can pass through it. Carbon nanotubes, some only fractions of a nanometer (one billionth of a meter) in diameter, consist of seamless graphite layers shaped in cylinders with one capped end that can extend several centimeters.

Discovered accidentally in 1991 by Sumio Iijima, carbon nanotubes, despite their small size, have the strongest tensile strength of any known material. Their extremely high thermal conductivity, electrical superconductivity, precise positioning of atoms, light weight, and potential for molecular transport provide numerous applications in electronics, aerospace, and medicine. They may even be used for the construction of space elevators, providing material for the cable to move things between Earth and space. (Not humans, though, unless we do something about that nasty space radiation.) In the US, the potential of carbon nanotubes was recognized in 2001 with the establishment of the National Nanotechnology Initiative program.

Carbon nanotubes can have single or multiple walls. Single walled tubes have higher thermal conductivity and more desirable electrical properties for use in electronics and heat transport. Multiwalled tubes have potential as biosensors in medicine and laboratory science used to detect microscopic amounts of chemical or biological compounds. Nanotubes have potential in drug delivery and targeted treatment, although studies have shown nanotubes to be toxic in mice if they reach the lungs.

Unruly Mass of Nanotubes

NASA Goddard Photostream; Image credit: Yuki Kimura, Tohoku University

With the immense interest in carbon nanotubes, a revolution of sorts in industry has occurred. The synthesis of carbon nanotubes generally requires the use of a cobalt or nickel catalyst. But most recently, Joseph Nuth of NASA Goddard in Greenbelt and colleagues described a new form of nanotube synthesis in Astrophysical Journal Letters that results from the recycling of carbon in space when supernovas explode. Instead of requiring a metal catalyst, a mass of nanotubes were produced when graphite dust particles were exposed to a mixture of carbon monoxide and hydrogen gases (using a known method for making  liquid fuel from coal). This research was spawned by the discovery of graphite whiskers, large carbon nanotubes, that were found associated with meteorites. If this new form of synthesis can result in lightweight and orderly tubes, it may mean an innovation for the nanotube industry.

In addition, the formation of these large nanotubes may be the reason supernovas appear dimmer than we expect from their distance alone. Imagine that: A nanotube-haze in space.

Read an article in the Baltimore Sun on Nanotechnology here.

How do we taste?

Posted by amanda on Monday, February 22nd, 2010

What tastes good to you right now? A sweet carrot? A bitter beer? Or maybe some salty pretzels? Whatever it is, how it tastes to you is determined by your cells. So how do we taste?

boy eating cookies

We separate tastes for humans (and probably most mammals) into five categories: bitter, sour, sweet, salty, and umami (the taste generated when you consume certain amino acids, such as MSG). Our taste preferences when we are born are genetically encoded. We prefer sweet tastes as babies, because “sweet” is associated with healthy foods that contain proteins and energy. We avoid bitter and sour things, because these are associated with toxins and acidic foods, like spoiled fruits or harmful plants. Humans (and mice) generally prefer salty foods when our bodies are low in sodium with our tastes fitting our physiological need. As we mature (or most of us anyway), we acquire tastes for more bitter and sour things, such as coffee and lemons, and may prefer salty and sweet foods even though we really don’t need to build up our salt or sugar supply.

From studies in mice, it is thought that the five tastes are determined by separate taste-receptor cells (TRCs) in the mouth each tuned to a specific taste. TRCs are organized into taste buds, composed of 50-100 cells, and these taste buds are housed within papillae (the bumps on your tongue). Taste buds from all regions of the mouth contain cells that respond to the five tastes and are connected to nerves that carry taste information to your brain stem and into the primary gustatory cortex (where your response to a food and your perception of flavor is dictated). Contrary to popular belief, there is no “taste map” on the tongue.

Recently published online in Nature, Jayaram Chandrashekar and colleagues (including scientists from the National Institute of Health in Bethesda) illustrate how salty taste occurs in sodium sensing in mice. Each TRC that determines a salty taste contains a sodium channel (or sodium transporter). This channel is present in many cells within your body, including your kidneys, lungs, and sweat glands, and is important in salt transport. Its role is so important that if this channel is made completely nonfunctional in mice, death occurs soon after birth. In order to study the importance of this channel in taste, scientists used a clever technique (attaching the channel mutation-causing agent to a known TRC-specific gene) to generate mice that were missing the sodium channel only in their taste buds. Unlike their ‘normal’ peers, these mice displayed a complete loss of salt attraction and sodium taste response while responding normally to the other four tastes. And most importantly, all of the TRC cells that carried the mutated salt channel did not carry any markers for the other four taste sensors, showing again that individual TRC cells are only able to determine one taste.

Whether or not this specific sodium channel is as important to salty tastes in humans as it is in mice is unknown. Due to our molecular similarities, the authors note that it is likely. But unlike mice, our innate responses to salty taste may be overridden by our high-salt diets.

Now, pass me those fries. All this talk of salt has made me hungry.

The Genetics of Stuttering

Posted by amanda on Thursday, February 18th, 2010

When we think of genetically affected characteristics, we often think of hair and eye color, height, and the size of our nose. But what about speech? This week, Changsoo Kang and Dennis Drayna, from the National Institute on Deafness and Other Communication Disorders in Bethesda, and colleagues report on the genetics of stuttering in the New England Journal of Medicine.

Stuttering is found in all cultures and languages, affecting 5% of children in twice as many boys as girls. Nearly 80% of childhood stuttering resolves itself, mostly in girls, leaving male stutterers outnumbering female stutterers 4:1. 60 million people in the world are stutterers, and Winston Churchill, John Updike, King George VI and James Earl Jones join their ranks. The history of stuttering is fraught with erroneous theories and damaging medical practices. The ancient Greeks thought that stuttering resulted from tongue dryness and recommended enlargement of the veins by surgical or chemical means. In the 1800s, stuttering was thought to be an anatomical defect, and surgical treatments were popular. By the 1900s, stuttering was ruled a psychological disorder and treated with conditioning and psychoanalysis that were eventually proven ineffective. The modern theory is that stutterers have a neurophysical problem that disrupts the precise timing in speech.

human chromosomes

Human chromosomes; NIH

The evidence for a genetic component to stuttering is apparent, such as the existence of identical twin stutterers and a high incidence of stuttering in first degree relatives. Approximately half of stutterers have a family history of the disorder. By examining genetic linkage in families of stutterers, geneticists have honed in on several chromosomes that may be involved in stuttering.

recycling

In Kang and Drayna’s most recent study, they’ve focused on chromosome 12 to examine the genes involved in stuttering in the largest well-studied group of stutterers, a Pakastani family simply known as PKST72. By comparing the DNA of stutterers in the family to non-stuttering control subjects, the researchers were able to pinpoint the genetic sequences affected in stuttering individuals. Interestingly, the genes they identified affect the cell’s recycling center, the lysosome. The lysosome takes unwanted material in the cell, such as old proteins, and breaks them down into something more usable. In this family of stutterers, the genes that direct proteins to the lysosome for recycling are mutated, most likely resulting in a build-up of this cell litter in other compartments of the cell. Somehow this accumulation of trash in cells leads to speech disturbance. The way this occurs is unknown, and the implication of these results for both treatment of stuttering and future studies is profound.

One other thing of note is that all but two of the stutterers with these mutations were heterozygous, meaning that the mutations were only found on one of the two strands of chromosome 12. If the mutations were found on both strands of DNA, the affected persons may have had a severe lysosomal storage disease called mucolipidosis.

DNA is amazing.

Clearing the Water

Posted by amanda on Tuesday, February 16th, 2010

K. veneficum

Karlodinium veneficum aka Gymnodinium galatheanum aka Karlodinium micrum; Courtesy of Prof. Allen Place

There’s a predator in Maryland waters. In 1996, 1997, and 1999, thousands of fish were killed at the HyRock Fish Farm on the Eastern Shore of the Chesapeake Bay. Water samples revealed the presence of two potential culprits, and after an initial case of mistaken identity, Karlodinium veneficum (then called Gymnodinium galatheanum) was found to be the cause. K. veneficum, a free-swimming phytoplankton or dinoflagellate, was first identified in Walvis Bay, Namibia in 1950 during the second Danish “Galathea” Deep Sea expedition. In South Africa, it caused periodic massive fish deaths, leaving the beaches covered with rotting fish and turning the water red with its thick algal blooms (colloquially known as red tide). In 2008, five fish kills in Chesapeake Bay and the Potomac occurred due to the presence of K. veneficum. This algae species is now considered a long term resident of Chesapeake Bay, and blooms (sometimes resulting in a “mahogany tide”) are monitored by the Maryland Department of Natural Resources.

Map of Algal Cell Counts on 6/29/09

Map of algal cell counts in the Bay on 6/29/09, K. veneficum marked by green triangles; Maryland DNR

Like many dinoflagellates, K. veneficum produces toxins, known as karlotoxins. Karlotoxins causes cells to rupture by increasing the ionic permeability of biological membranes (making them leaky until they explode). Fish are killed by damage to the gill epithelia. K. veneficum can gain energy both by photosynthesis and by the consumption of single-celled organisms. The production of toxins was hypothesized to be a self-defense system against other organisms in the phytoplankton grazing territory with local fish as the unlucky bystanders. Karlotoxins were identified and characterized in the lab of Allen Place of the Institute of Marine and Environmental Technology at the University of Maryland Center for Environmental Science.

In the February 2nd issue of the Proceedings of the National Academy of Sciences, Place and colleagues from the University of Minnesota, The Johns Hopkins University and the University of Hawaii show that karlotoxins are not just used by K. veneficum in self-defense. The toxic predatory strains use karlotoxins as a means of stunning their cryptophyte prey (Storeatula major) before ingesting it. Thus, the presence of prey leads to the presence of toxin. Therefore, by reducing the amount of K. veneficum prey in the Chesapeake and other infected waterways, K. veneficum may produce less toxin, leaving the fish to swim in peace.

Prey reduction (in conjunction with the input of native feeders) may help in developing effective management strategies against other predatory dinoflagellates in Maryland waters. According to the Maryland Department of the Environment, another dinoflagellate, Gyrodinium uncatenum, caused the largest fish kills in the state in 2008, resulting in 142,365 fish deaths. Unlike K. veneficum, G. uncatenum is non-toxic, and fish kills are thought to be caused by low dissolved oxygen produced from the large algal blooms. Like K. veneficum, G. uncatenum could gain energy from photosynthesis alone, but a reduction in prey may reduce the size of algal blooms and fish deaths.

How dinoflagellate prey reduction will be implemented without damaging the Bay ecology or industry is another scientific challenge that I hope I will have the pleasure of blogging about someday.

Studying the Sun

Posted by amanda on Saturday, February 13th, 2010

UV image of the sun

Ultraviolet image of the Sun; Credit: NASA

While many of us were huddled at home during last week’s snowstorm, some employees at NASA Goddard Space Flight Center in Greenbelt were preparing for a mission of cosmic proportions. On February 11th, the Atlas V launched from Cape Canaveral to send the Solar Dynamics Observatory (SDO) into space on its mission to better understand the sun. Although no shuttles or satellites are actually launched in Maryland, Goddard provides critical mission support for shuttle launches and missions like SDO from its Mission Operation Center and Network Integration Center. In the lead up to a mission, the center is staffed 24 hours a day as they prepare for a launch.

Layers of the Sun

Layers of the Sun; Credit: NASA

Although it is the center of our solar system and our closest star, there is still much to learn about the Sun. We know the Sun is a ball of gas composed of the same elements found on Earth (mainly hydrogen and helium) that get denser as they move inward to the Sun’s core. We also know it is composed of distinct layers, but we can only observe the Sun’s outer layers directly. These include the deepest layer we can see, the photosphere, the next outer layer, the chromosphere, and the outermost region of the atmosphere, the corona, which can be viewed as a halo during an eclipse. Although temperature generally decreases as you move out from the core of the Sun, the chromosphere can reach temperatures higher than the photosphere, and the corona can reach millions of Kelvin. The corona is so hot that the majority of radiation is emitted at ultraviolet and X-ray wavelengths. (The atmosphere of the Earth can block most of this light, which is why we aren’t constantly sunburned.) We don’t yet understand why the corona is so hot. It may be because of the Sun’s magnetic field, but the mechanism is still unknown.

Most important to space weather (and therefore, Earth weather) is the Sun’s solar activity, which is measured by the amount of sunspots present on the Sun. Sunspots are cooler regions on the Sun’s photosphere and so appear to be darker than the photosphere. Although sunspots are locally cooler, their presence is associated with greater overall solar temperatures. They form in cycles of an average of 11.1 years, where at the maximum over 100 sunspots can be seen, and sometimes no spots are observed at the minima. The cycle of sunspots is closely related to the magnetism of the Sun and form in regions of intense magnetic activity. Solar flares and coronal mass ejections, large explosions in the Sun’s atmosphere, often occur in these magnetically intense areas. During extended periods of low solar activity, the Earth can experience cold temperatures (such as during the Little Ice Age in the 17th century).

The NASA Goddard-managed SDO will aid in understanding the Sun’s magnetic changes. The spacecraft is built to fly for five years but will probably outlast itself like previous satellites. SDO is the first satellite to launch under the Living With a Star program at NASA aimed to understand the relationship of the Sun to space weather. By measuring the properties of the Sun and solar activity, SDO plans to determine how the magnetic field is generated and structured and how the stored magnetic energy is released outward from the Sun into space. SDO data and analysis will be used to help predict the solar variations that influence life on Earth. Among other things, SDO will examine sunspots, solar flares, and coronal mass ejections like the one observed less than a month ago from another Goddard-associated satellite:

YouTube Preview Image

STEREO satellite movie from NASA

We could certainly use more of the Sun around Baltimore right now.

For more detailed explanations of the Sun and its properties, see NASA or Wikipedia.

The Sound of Science

Posted by amanda on Thursday, February 11th, 2010

white-crowned sparrow in snow

White-crowned sparrow http://www.flickr.com/photos/lostinfog/ / CC BY-SA 2.0

In the middle of a snowstorm in Baltimore, there is a lack of sound. There are no moving cars, no birdsong in the trees, and the insulating snow dampens any cross-street conversation. Even the sirens seem more silent than usual. Luckily, we have the University of Maryland to remind us of the importance of urban sound. Published in the February issue of the Proceedings of the Royal Society B, David Luther from UM-College Park and Luis Baptista from the California Academy of Sciences report on their study on the effect of urban noise on white-crowned sparrows.

Human-made noise has long been suspected to have an impact on bird populations. Bird species are less abundant near highways and urbanization limits bird distribution. Noise has been shown to reduce nesting success and affect species interactions. Urban birds sing at a higher minimum frequency than rural birds to be heard above the low-pitched human-caused noise. (Think of the hum of the city.)

Birds, like humans, speak in vocal dialects that change with geographical region and often differ between neighboring populations. The alteration or change in learned songs between one generation and the next is described as the cultural evolution of songs. Some species of birds, such as the indigo bunting, are capable of changing dialects within less than a year, whereas others maintain their songs for decades or longer.

Luther and Baptista’s study is the first long-term study to document an increase in the minimum pitch of song over multiple generations of urban sparrows with a mixture of three dialects. By examining urban sparrow birdsong recordings spanning almost 30 years (1969, 1970, 1990, and 1998), they essentially observed the cultural evolution of sparrow song in a small San Francisco population. (Sparrows only live for 2 years, eliminating the possibility of recording the same individuals from the beginning to the end of the study.) Luther and Baptista found that the lowest frequency of birdsong rose over time with a shift to the dialect previously found within the most urban environment with the greatest ambient noise. This result of shifting dialect indicates an adaptation to the local acoustic environment over multiple generations. Songs (or dialects) change to a higher pitch to transmit more effectively in ambient noise.

So if urban noise affects bird dialects, does this mean that Baltimoreans will be speaking a higher pitch of Bawlmerese in 250 years? Maybe… if our breeding depended on it.