epithelial cell

Anatomy & Physiology Overview - The Ear

Outer ear 

  • Pinna (auricle) - visible part of the ear outside of the head.  
  • External auditory canal 
  • Ceruminous glands - specialized sudoriferous glands (sweat glands) located subcutaneously in the external auditory canal. They produce cerumen (earwax) by mixing their secretion with sebum and dead epidermal cells.

 Middle ear: air filled 

  • Tympanic membrane -  vibrates in response to sound waves 
  • Malleus, incus and stapes - 3 small bones that transmit vibrations to each other

Inner ear: fluid filled 

  • Mechanoreceptor for hearing and balance 
  • Vesibular apparatus - balance
  • Semicircular canals 
  • Cochlea
  •  • Organ of Cor -  sensory epithelial cell


  • Perilymph = similar in compositon to plasma – Na+ 
  • Endolymph = high in K+ 
  • Organ of Cor: contains hair cells – move due to pressure waves 
  • 50-100 stereocilia on each cell 
  • Longest embedded in tectorial membrane 

In the cochlea that the vibrations transmitted from the eardrum through the tiny bones are converted into electrical impulses sent along the auditory nerve to the brain. 

  • The cochlea is a tapered tube which circles around itself 
  • The basilar membrane divides the tube lengthwise into two fluid-filled canals joined at the tapered end. 
  • ossicles transmit vibration to the cochlea where they attach at the oval window
  • resultant waves travel down the basilar membrane where they are “sensed” by  16-20,000 hair cells (cilia) attached to it which poke up from a third canal called the organ of Corti
  • Organ of Corti transforms the stimulated hair cells into nerve impulses 
  • Waveforms travelling down the basilar membrane peak in amplitude at differing spots along the way according to their frequency 
  • Higher frequencies peak out at a shorter distance down the tube than lower frequencies
  • The hair cells at that peak point give a sense of that particular frequency
  • The distance between pitches follows the same logarithmic distance as our perception of pitch i.e. the placement of octaves are equidistant.
Wet or sticky? What your discharge is telling you

Tracking your cervical fluid can give you clues about what hormonal changes and events are happening in your body right now. Understanding your own patterns can help you to know when ovulation has occurred, and when you might be able to skip the lube. Getting to know your fluid can also allow you to recognize when something may be off — from an infection or hormonal issue, for example.

The ebbs and flows of cervical fluid

The cervix is the passageway between your lower and upper reproductive tract. It has glands in and around it which produce fluid. The quality, consistency, and volume of this fluid changes along with your cycle. The pattern and experience of these changes is different for everyone but cervical fluid tends to follow a consistent cyclical pattern. It changes in quality, quantity and function. This happens in response to your changing hormones. At different times, cervical fluid acts to facilitate or prevent sperm from moving past your cervix (1). It also contains antibodies, and helps to keep out unhealthy bacteria and viruses (2).

A fluid timeline

1. Menstruation: Start of cycle

On day one of the cycle, both estrogen and progesterone are low. The cervix is not likely producing much fluid, but you won’t be able to tell, as it’s mixed in with blood, endometrial tissue and dissolved remnants of a disintegrated egg.

2. Dry/Sticky: Early-to-mid follicular phase

In the early follicular phase, estrogen starts to rise (it’s produced by your follicles as they grow). This rising estrogen leads to increased production of fluid. You probably won’t notice much of it in the days after your period — these are “dry” fluid days for many people — some might notice “sticky” fluid. Typically, cervical fluid first becomes noticeable around the middle of the follicular phase (day ~7 in a 28 day cycle) (3).

3. Creamy: Mid-to-late follicular phase

It may start sticky, but as estrogen and water content rises fluid tends to become ‘creamy,’ cloudy (not clear) and whitish or yellowish. Research has shown sperm can start to swim through cervical fluid on about day ~9 of a 28 day cycle (1).

4. Egg White/Wet: Late follicular phase/mid-cycle

As ovulation approaches, more cervical fluid is produced. Fluid becomes stretchier, clearer and more wet and slippery — like an raw egg white. This fluid tends to “peak” about 1–2 days before ovulation, when estrogen is highest (3). Around that time fluid can often be stretched several inches between your finger and thumb. For others it may be more watery. The amount of peak fluid the body produces is different for everyone, but it can be up to 20x more in some cases (4). This fluid is about 95% water in weight, and 5% solids (electrolytes, organic compounds and soluble proteins)(2). If you’re having sex and using lube, you may notice you need less around this time. *Note that the presence of fertile-type cervical fluid alone cannot confirm ovulation — it’s not accurate enough on its own to use for a FAM method or pregnancy prevention.

5. Dry/Sticky: Luteal phase

As soon as ovulation is over, fluid changes — even before you notice a visual change, it will already have become more fibrous and less penetrable for sperm (1). In the day or two after ovulation (the first days of the luteal phase), cervical fluid lessens and becomes much thicker. Progesterone, the dominant hormone in this phase, acts to inhibit the secretion of fluid from the epithelial cells (1). You may notice little fluid, or it may be sticky (or something else unique to you).

Note that every body is unique — these changes may show up differently for you, or you may experience or interpret them in a different way.

To swim or stick — the changing role of fluid

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Soy milk: Grow and harvest soybeans and process them into a liquid

Cow’s milk: Artificially inseminate or dictate the reproduction of a cow. If a bull calf is born, shoot them or sell them for cheap meat. If a heifer calf is born, take her away immediately after she had suckled her colostrum (first milk), put her in a pen, and feed her discarded, diseased milk or a milk replacer until the earliest age that she can be weaned onto grain and pasture. Start breeding and milking her when she is 2-3 years old and don’t stop until her body starts to show the strain either through lameness, higher cell counts in the milk, recurrent mastitis, or emaciation, usually when she is between 5 and 10 years old. Send her to slaughter to be killed for cheap meat. Milk every cow twice a day and make sure to provide supplementary energy in the form of grains, silage, and molasses combined with additional minerals to prevent any deficiencies from the unnaturally long, repetitive, and voluminous lactation periods. Make sure to heat the milk collected in order to destroy or deactivate somatic cells (epithelial and inflammatory cells shed into the milk), infectious bacteria, and generally make it safe for humans to consume.

Pharmacokinetics Overview

(Absorption and distribution of drugs)

The study of the time course of drugs and their metabolites in the body (what the body does to the drug) consisting of:

  • administration
  • absorption
  • distribution
  • metabolism
  • excretion


Enteral (passes through intestine)

  • oral (mouth)
  • buccal/sublingual (applied in cheek/under tongue)
  • Gastrosomy (surgical opening through the abdomen into the stomach)

Topical (applied directly)

  • Nasal
  • Rectal
  • Ophthalmic (eyes)

Parentral (injection)

  • Intravenous (into veins)
  • intramuscular (into muscles)
  • intradermal (within layers of skin)
  • subcutaneous (under the skin)

Drug molecules move around the body either through bulk flow (bloodstream, lymphatics or cerebrospinal fluid) or diffusion (molecule by molecule over short distances)


Passage of drug from its site of administration into plasma - important for all routes except intravenous injection.


  • IV = fastest route of administration
  • bolus injection = very high concentration of drug
  • rate limiting factors = diffusion through tissues and removal by local blood flow

Drugs need to pass through membranes (cell membranes, epithelial barriers, vascular endothelium, blood-brain barrier, placenta barrier etc) via

  • passive diffusion through lipids
  • carrier-mediated
  • passage through membrane pores/ion channels
  • pinocytosis (ingestion into a cell by the budding of small vesicles from the cell membrane)

Diffusion through lipid

  • non-polar molecules can dissolve freely in membrane lipids
  • the rate is determined by the permeability coefficient (P)(solubility in the membrane and diffusibility) and the concentration difference across the membrane

pH and Ionisation

  • Many drugs are weak acids or weak bases
  • exist in unionised or ionised forms
  • pH = balance between the two forms
  • ionised forms have low lipid solubility
  • uncharged however the drug is usually lipid soluble

ionisation affects:

  • rate of drug permeation through membranes
  • steady state distribution of drug molecules between aqueous compartments if pH difference exists between them


  • urinary acidification accelerates the excretion of weak bases and slows that of weak acids
  • alkalisation has opposite effect
  • increasing plasma pH causes weak acids to be extracted from CNS into plasma
  • Reducing plasma pH causes weakly acidic drugs to become concentrated in CNS, increasing neurotoxicity


  • Bioavailibility (F) indicates the fraction of an orally administered dose that reaches systemic circulation intact, taking into account both absorption and local metabolic degradation
  • determined by comparison between oral and IV absorption

affected by:

  • drug preparation
  • variation in enzyme activity of gut
  • gastric pH
  • intestinal motility

Volume of Distribution

Vd is defined as the volume of fluid required to contain the total amount, Q, of drug in the body at the same concentration as that present in the plasma, Cp

  • determined by relative strength of binding between drug and tissue compared with drug and plasma proteins
  • tight binding to tissue but not plasma –> drug appears to be dissolved in large volume –> large Vd (eg chloropromazine)
  • tight binding to plasma –> V can be very close to blood volume –> low Vd (eg warfarin)

Planets inside of you aka epithelial tissues. 

In order:

Kidney, simple cuboidal epithelial

Pancreas; simple cuboidal epithelial

Lung; pseudostratified ciliated columnar epithelial

Lung; simple squamous epithelial

Bowman’s capsule; simple squamous epithelial

Small intestines; simple columnar epithelial

Transitional epithelial

Ciliated simple columnar epithelial

Epstein-Barr Virus (EBV)

Epstein-Barr Virus (EBV) is the cause of infectious mononucleosis (aka mono), and it is in the herpes family. This disease is particularly harmful because it can also cause cancer of the head and neck and it increases one’s likelihood of getting autoimmune diseases such as HIV, multiple sclerosis, and rheumatoid arthritis. And since EBV attacks epithelial cells lining the throat, short-term flu-like symptoms associated with mono such as fatigue, sore throat, fever, abdominal pain, sore muscles and headache as well as the long-term conditions associated with EBV may develop. The Epstein-Barr Virus may be transmitted through the exchange of saliva and/or genital secretions, but even though mono is called the kissing disease, it can be spread by sharing a drink or food as well. This is why 50% of children in the US and England test positive for EBV at age 5, and 90% of adults 35-40 have been infected at one point in their lives. The primary target for EBV is college students, so be careful out there. Unfortunately, EBV does not have a vaccine, so the best prevention is keeping food and drink to oneself. Fortunately, most often symptoms disappear on their own. If symptoms persist, a doctor visit is required.


The split skin graft; it involves the harvesting of a sheet of skin comprising epidermis and varying thickness of dermis, naturally this process involves the creation of a superficial wound that is the donor site, the donor site heals by a process of re-epithelialization; epithelial cells migrate across the wound surface from the rim of the wound and the edges of various structures in the dermal layer, such as sebaceous glands and hair follicles, this process results in an epithelial cover of the split-thickness skin graft donor site usually within 7–14 days. 

Cancer pt 1

A cancer-y overview

  • the second most common cause of death in developed countries 
  • 29% of all mortality (13% worldwide) 
  • 12.7 million cases, 7.6million deaths in 2008 
  • 14.1 million cases 8.2 million deaths in 2012 

Tumours originate in epithelial cells, cells of the blood and lymph system, connective tissue cells and neural cells

Hallmarks of cancer

Genetic Factors

  • Cancer Producing Genes are known as oncogenes - “Any mutated gene that contributes to neoplastic transformation” 
  • These genes are activated in cancer 
  • Often promote cell growth & survival 
  • “Remove the brakes” from normal tissue homeostasis 
  • Often repress cell death and differentiation
  • Result = lots more cells


Prior to mutation these are known as “Proto-oncogenes”. Activation can occur by altering gene expression or protein structure (e.g. constitutive activation). Many common oncogenes promote mitosis/progress through cell cycle OR the evasion of death signals.

Activation is caused by genetic changes, including:

  • Point mutations: can result in production of an abnormally functioning protein product.  
  • Deletions: of a few base pairs to loss of an entire chromosome 
  • Gene amplification: resulting in excessive production of oncogene product 
  • Chromosomal translocations: gene is activated inappropriately by another promoter region; caused by rearrangement of parts between nonhomologous chromosomes

Active oncogenes are found in tumours and are thought to be early events in malignant transformation.

Environmental Factors

Carcinogenesis - the process of initiating and promoting cancer

  • Initiationirreversible genetic alteration of a cancer-related gene (oncogene or tumour suppressing gene (TSG)) 
  • Promotion – clonal expansion of the initiated cell (i.e. stimulation of growth) 
  • Progression – stable alteration of an initiated cell. Gaining ability to invade and metastasise 

Carcinogenic agents (will go into detail in future posts)

  • Chemical Carcinogens 
  • Dietary factors 
  • Biological 
  • Viruses
  • Physical 
  • Exposure to ionising radiation

Following exposure to a carcinogenic agent there can be a long latent period before neoplasia develops. This is because the steps of carcinogenesis must be in the right order (initiation, promotion, progression). eg if exposed to a promoter and then an initiator, all is good until exposed to another promoter after the initiator.

Think of an Eye

In this macro close-up of a human eye, two major elements are visible: the pupil and the iris. The pupil, of course, is the central aperture through which light passes to strike the retina. It appears dark because light rays entering the pupil are either absorbed by tissues inside the eye directly or absorbed after diffusely bouncing around inside the eye, with very little of the light escaping the same way it came in.

The pupil is a marvel, but it’s really just a hole. The work of adjusting the size of that hole – and thus the amount of light allowed inside the eye – falls to the iris. If the pupil is the aperture, the iris is the diaphragm that serves as the aperture stop.

The iris consists of two layers: the front pigmented fibrovascular (a combination of fibrous and vascular tissues), known as the stroma, and a two-cell-thick layer of underlying pigmented epithelial cells. In fact, pigment granules are found in dark colored eyes; blue eyes and those of albinos lack pigment.

Two types of muscle occupy the stroma: a sphincter that contracts the pupil in a circular motion to reduce incoming light and a set of dilator muscles that pull the pupil open, like a ring of grabbing hands, to allow in more light.  

Could stem cells heal IBD?

Surface of the mouse colon repaired by stem cells after a flare of ulcerative colitis. The different colors show the contributions of individual stem cells as they have multiplied to patch the breaks, or ulcers, in the colonic surface. These ulcers were originally caused by the rampant inflammation that happens repeatedly in patients that suffer from inflammatory bowel disease.

Inflammatory bowel disease, which includes Crohn’s disease and ulcerative colitis, affects more than 1.4 million Americans and is globally becoming more common.

Current medication targets the chronic inflammation that causes destruction of the intestinal lining, but a new approach for therapy is to heal the intestine directly.

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Sources of DNA for Forensics Investigations

The different regions of the body in which DNA can be extracted and used as an effective identifier.  

Saliva this contains cellular material and is easy to extract and can be taken from bite marks, postage stamps, cigarette butts and even envelop flaps!

Teeth contain DNA and is an excellent source as it remains long after the rest of the body has decomposed.

Blood is an excellent source of human DNA. However it is only present in the white blood cells. Red blood cells don’t contain DNA as they have no nuclei.

Sperm this is very important for sexual assault cases in particular. DNA is located in the head of the sperm and a special extraction methods are required to release the DNA.

Hair follicles located at the base of human hairs contains cellular material rich in DNA. In order to be used for DNA analysis, it has to have been removed from the body, broken pieces do not contain DNA as it is only found in the follicle. 

Body tissue a little more obvious but if it hasn’t been degraded any form of body tissue will contain DNA.

Bone is one of the best sources of DNA from decomposed human remains. Even after the flesh is decomposed, DNA can often be obtained from demineralized bone.

Urine does not contain DNA however sometimes it does contain epithelial cells which do but this is only if the individual is of poor health.

spillyourgutsplease-deactivated  asked:

Is it possible to have a male orgasm with a phalloplasty ? (Like, ejaculation)

What is the male orgasm?
Physiologically speaking, the male orgasm consists of the contraction and pulsating most guys feel in their penis, prostate and pelvic region. These sensations are met by increased heart rate, rapid breathing, muscle tensing, anal, sphincter and PC muscle contractions, and an increase in blood pressure, which then result in a sudden release of tension.
Did you know that ejaculation and orgasm are two separate things?
Right before orgasm, seminal fluids build up at the base of the penis in the urethral bulb. This reaps the familiar feeling that you’re about to ejaculate. Then, whilst reaching orgasm, your testicles tighten up close to your body, and your urinary tract shuts down so that your ejaculate can exit from your penis rather than your bladder. And of course, all those muscle contractions signify that orgasm is taking place.
Ejaculation, however, is a spontaneous muscle spasm: A reflex that arises at the base of the spine and causes the ejection of semen.

YES. Post-operative trans men can experience the typical signs of arousal, as well as orgasm, and even ejaculation in some men, as indicated by anecdotal reports. The ejaculate is chemically different from seminal fluid however, coming from the paraurethral ducts then down the urethra.

This 2006 study reported that “testosterone has a stimulatory effect on the female prostate, inducing epithelial cell proliferation, differentiation, secretory activity, and dysplasia.”

Lastly, results of a 2014 study into satisfaction after Phalloplasty:

  • All patients that could achieve orgasm before GCS with clitoral transposition could achieve orgasm after surgery, and the vast majority reported preserved quality of erogenous sensation by our transposition technique.
  • Inflatable penile prosthesis placement was not associated with decreased erogenous sensation/orgasm.
  • All RFF and 9/10 abdominal phalloplasty patients reported masturbation with their phallus.

Source: Overall Satisfaction, Sexual Function, and the Durability of Neophallus Dimensions

Toxoplasma gondii

Toxoplasma gondii. 7 syllables sure to strike fear in to any pregnant woman’s heart. I thought I’d do a little post today to summarise what toxoplasma actually is and how it affects us and the animals around us.

Toxoplasma gondii is a single celled parasite known as a protozoa. It has a complex lifecycle involving felines as its only final host. It does, however, have a vast array of ‘intermediate hosts’ thought to include virtually all warm blooded animals. It’s a very successful parasite infecting animals and humans worldwide. In France, 84% of people are thought to be infected.

Its lifecycle is as follows:

  • A cat becomes infected through consuming the raw meat of infected prey
  • The parasite infects the epithelial cells of the cat’s gut, sexually reproducing in these cells
  • Sexual reproduction produces oocysts which are shed in the cat’s faeces. The time period from consumption to shedding is around 3-10 days. Shedding only occurs for a few weeks before the cat’s immune system fights off the parasite, resulting in a persistent but non-shedding infection that can remain for life. After one infection it is highly unlikely the cat will get infected and shed again due to its raised immune response, however immunosuppression can result in subsequent shedding
  • These oocysts develop in the environment and after 1-5 days are developed enough to infect an intermediate host
  • Intermediate host ingests the oocysts through consumption of an item or fluid infected with cat faeces. Intestinal enzymes break down the oocyst wall releasing the parasite in to the gut
  • Acute asexual multiplication occurs in the intermediate host cells and the parasite is spread around the body in the blood
  • After around 2 weeks the host develops immunity but the infection enters a chronic phase as slow-growing forms of the parasite are ‘walled off’ into what is known as a cyst, protected from the immune system. These can remain infectious for months to years and can revert to the acute form if the host’s immune system becomes depressed (FIV, AIDs, canine distemper). They are often found in the brain and muscle.
  • This cyst-infected meat is consumed by the cat and the whole cycle begins again

Cats can also get infected by consuming oocysts from other cats, however they are a lot less susceptible to this than other intermediate hosts so a large number of oocysts would need to be consumed. To make it even more confusing, intermediate hosts can get infected via carnivorism/ scavenging when they consume meat infected with cysts (e.g. a human eating undercooked, infected pork). As well as this, transplacental transmission can occur in some host species during the acute phase of the infection (however this is not seen in dogs or cats). This creates a complex web of infection. The cysts are killed when meat is cooked.

Toxoplasmosis is most often asymptomatic, with flu-like symptoms possible during the acute phase. It can be fatal in immunosuppressed individuals, however this is rare. You may have heard the parasite’s name mentioned in relation to sheep. If a non-immune ewe is infected during pregnancy it can cause foetal death, reabsorption, abortion, mummified foetuses, still births and weak lambs, depending on when in pregnancy the ewe was infected. In cases of abortion, you can see tiny white spots on the placenta and foetal tissue. Diagnosis can be confirmed through stained impression smears or serological examination of the foetal fluid or blood from the ewe. Prevention in sheep includes a vaccine which primes the immune system to the parasite. Sheep are often infected from eating infected hay or concentrates, so keeping cats away from these can help reduce infection rates.

Toxoplasma is also a favourite in the press, who claim that it ‘controls our brains’ and causes abortions and deformities. Like in sheep, infection of a non-immune, pregnant mother can indeed cause deformities in her child. Does this mean we should all kill off our cats when expecting? Definitely not, and I’ll explain why.

As I stated earlier, infected cats will only shed for 2-3 weeks in their entire lifetime, unless immunologically supressed. To become infected by your cat, you would need to have never been infected before yourself (because if you have, your immune system is primed and ready to fight it off), your cat would have to be in the shedding phase and you’d have to ingest oocytes (that take 1-5 days to become infective, so changing the litter box daily can hugely reduce this risk).  If worried, a blood test to see if you’ve been previously exposed and a blood test in your cat to see if they’ve been previously exposed may put your mind at rest. Indoor cats are less likely to become infected if their only food is tinned or dried. Humans are much more likely to be exposed to the infection through handling and eating undercooked infected meat, soil infected with cat faeces and unwashed vegetables. If you’re a vet in the making and have been on a lambing placement, you may well have been asked if you’re pregnant. This is because being in contact with aborted material from sheep with toxoplasmosis is another way to contract the infection.

As for the ‘mind control’, it has been found that mice infected with toxoplasma are attracted to the smell of cat urine and a lot less frightened of cats than those without infection. This is an incredibly clever mechanism and probably one of the reasons the parasite is so wide-spread. In humans, when analysing the number of people who are involved in car accidents, it was found that a significantly high proportion were infected with toxoplasma gondii. It has been suggested that the parasite is responsible for making people more reckless and argumentative. Toxoplasma cysts in the brain could definitely be responsible for parts of your personality, however conclusions at the moment suggest that although the infection may have some effect, the brain and concept of ‘personality’ are so complex and involve so many factors that its overall influence seems negligible.  

I hope this made sense, it’s quite confusing to explain! I’ve drawn a quick diagram to try and demonstrate the different scenarios in which we could become infected. Enjoy!


Cervical mass in a 11 year-old, male-castrated, black Labrador Retriever.  For the past two weeks the patient has been intermittently coughing, especially after voraciously eating his  kibbles.  He is described as healthy otherwise.  On physical examination his primary care veterinarian palpated a very large, 10cm firm mass in his ventral neck.  We got the aspirate samples of the mass and found….


…and found numerous apparently cohesive clusters of these mononuclear cells.  Their cohesive nature is typical of an epithelial population.  The cells look relatively bland - that is, they all appear very similar to their neighbor.  Such monomorphism suggests a more benign process…but we’ll come back to that interpretation!  Additionally, few clusters were associated with this brilliant magenta extracellular material - could be matrix, secretory product, or colloid.  What tumor type do think this is?!


Cytologic diagnosis: Neuroendocrine epithelial tumor.  Based upon the mass location, this is consistent with a Thyroid tumor.  Although the population looks relatively benign cytologically, canine thyroid tumors are usually aggressive adenocarcinomas.  Conversely, kitty thyroid tumors are usually benign and equine tumors a 50-50 shot on benign versus malignant.  No word yet on what therapy the owner has elected to pursue - but the prognosis is sadly grave :-(

On an aside, other neuroendocrine origin tumors (like insulin secreting pancreatic tumors or some adrenal tumors) have a very similar cytologic appearance. 

Herb of the Week-Aloe


Aloe Vera
Barbados Aloe
Curacao Aloe
Lu Hui
The herbaceous plant called the aloe finds wide usage in many herbal applications and remedies - it is often prescribed by herbalist for different conditions. The herb is also the main source for two commonly used herbal products that differ in their chemical composition as well as in therapeutic abilities - these two products however have very similar names which are inadvertently interchanged in the herbal literature. The gel or mucilage sourced from the aloe vera herb is a very thin and clear, jellylike material that is made from by the parenchymal tissues in the leaves of the herb - these water rich tissues make up the majority of the underlying inner portion of aloe leaves and stems. A variety of different procedures are utilized for the extraction of this gel that is prepared mainly from the leaves of the plant, on the basic level all of the these procedures consist of initial separation of the mucilage of the aloe not only from the internal cellular debris but specifically from specialized cells called the pericyclic tubules, these cells lie just underneath the epidermis or the rind of the leaves. Another useful herbal product from the aloe is derived from the dried remains of such cells. These pericyclic tubule cells posses a bitter yellow latex or juice, an active cathartic pharmaceutical herbal product known simply as the aloe, is prepared from these dried cells.

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Take a look at a living taste bud. The green objects are the taste receptor cells, red indicates blood vessels and blue is the collagen structure surrounding the bud. This is one of more than 2,000 taste buds scattered across the top of the tongue.

This 3-D rendering was part of a study at Harvard, the Australian National University and South Korea’s Sungkyunkwan University in which scientists captured the process of taste sensation live. In doing so, they provided more proof that the idea the tongue is broken into separate regions that sense salty, sour, sweet, bitter and umami is a myth.

They were able to watch taste reception by shining an infrared laser on a living mouse’s tongue and recording with a two-photon microscope what happened when they dripped sweet-tasting saccharin and acesulfame K or salt onto the buds. Each bud activated when exposed to both salty and sweet substances.

“With this new imaging tool we have shown that each taste bud contains taste cells for different tastes,” said Harvard Medical School’s Seok-Hyun Yun. Learn more and see photos below.

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