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Primum Non Nocere

I do not own the rights of these photos. Have fun studying!.. =)

Cell Cycle and Mitosis

If you need to remember cell cycle and mitosis, here an excellent video!

scinote:

Some Like It Hot: A Look at Capsaiscin

If you’ve ever eaten a chili pepper— either because of a dare or by your own volition— you have no doubt come across the painful burning sensation that comes soon after. But what causes this pain? And why does it exist in the first place? Before we look at chemistry, we have to look at biology— specifically, evolution.
Capsaicin is found naturally in chili peppers, in varying quantities. To truly understand its purpose, we have to look at where it’s located. The amounts of capsaicin vary throughout the plant, but the highest concentrations are found in the placental tissues surrounding the seeds of the plant. This makes sense evolutionarily, as the seeds are the future generations of  these peppers. It makes sense that the plant would use whatever means are most effective to protect its progeny. Capsaicin, with its burning, itching, stinging side effects, acts as a perfect deterrent to possible predators looking for a tasty meal.
Now that we know why capsaicin exists - why does it burn? This is where the chemistry comes in. The burning, painful sensation attributed to capsaicin results from chemical interactions with sensory neurons. When introduced to the body, capsaicin binds to a specific receptor called the transient receptor potential cation channel subfamily V member 1 (TrpV1) or, more simply, the vanilloid receptor subtype 1. This receptor is a subtype of receptors that are present in peripheral sensory neurons. The vanilloid receptor 1 is usually reserved for detecting heat or physical abrasion. When heat is applied to the surface of the skin this TRPV1 ion channel opens, allowing cations (positively charged ions) into the cell. This inflow of cations activates the sensory neuron, which sends signals to the brain that there is a painful stimulus present. Capsaicin has a binding site on the receptor, and opens the cation channel just like if heat were applied. This results in a signal to be brain to alert you of a potential threat and produces a burning sensation where the capsaicin was introduced, but without an actual burn.
Interestingly, while the receptor works this way in most mammals, it is not activated by capsaicin in birds; therefore, birds are the largest distributors of capsaicin seeds in the natural environment.
This has just been a brief overview of some of the chemistry of capsaicin, but hopefully next time you bite into a jalapeno, you’ll take a moment to appreciate the science that’s occurring before you gulp down your milk!
References:
Pingle SC, et al. Capsaicin receptor: TRPV1 a promuscious TRP channel. Handbook of experimental pharmacology. 2007.(179):155-71.
Tewksbury JJ. et al. Ecology of a spice: Capsaicin in wild chilies mediates seed retention, dispersal and germination. Ecology. 2008. (89):107-117.

Submitted by thatoneguywithoutamustache
Edited by Ashlee R.

scinote:

Some Like It Hot: A Look at Capsaiscin

If you’ve ever eaten a chili pepper— either because of a dare or by your own volition— you have no doubt come across the painful burning sensation that comes soon after. But what causes this pain? And why does it exist in the first place? Before we look at chemistry, we have to look at biology— specifically, evolution.

Capsaicin is found naturally in chili peppers, in varying quantities. To truly understand its purpose, we have to look at where it’s located. The amounts of capsaicin vary throughout the plant, but the highest concentrations are found in the placental tissues surrounding the seeds of the plant. This makes sense evolutionarily, as the seeds are the future generations of  these peppers. It makes sense that the plant would use whatever means are most effective to protect its progeny. Capsaicin, with its burning, itching, stinging side effects, acts as a perfect deterrent to possible predators looking for a tasty meal.

Now that we know why capsaicin exists - why does it burn? This is where the chemistry comes in. The burning, painful sensation attributed to capsaicin results from chemical interactions with sensory neurons. When introduced to the body, capsaicin binds to a specific receptor called the transient receptor potential cation channel subfamily V member 1 (TrpV1) or, more simply, the vanilloid receptor subtype 1. This receptor is a subtype of receptors that are present in peripheral sensory neurons. The vanilloid receptor 1 is usually reserved for detecting heat or physical abrasion. When heat is applied to the surface of the skin this TRPV1 ion channel opens, allowing cations (positively charged ions) into the cell. This inflow of cations activates the sensory neuron, which sends signals to the brain that there is a painful stimulus present. Capsaicin has a binding site on the receptor, and opens the cation channel just like if heat were applied. This results in a signal to be brain to alert you of a potential threat and produces a burning sensation where the capsaicin was introduced, but without an actual burn.

Interestingly, while the receptor works this way in most mammals, it is not activated by capsaicin in birds; therefore, birds are the largest distributors of capsaicin seeds in the natural environment.

This has just been a brief overview of some of the chemistry of capsaicin, but hopefully next time you bite into a jalapeno, you’ll take a moment to appreciate the science that’s occurring before you gulp down your milk!

References:

Pingle SC, et al. Capsaicin receptor: TRPV1 a promuscious TRP channel. Handbook of experimental pharmacology. 2007.(179):155-71.

Tewksbury JJ. et al. Ecology of a spice: Capsaicin in wild chilies mediates seed retention, dispersal and germination. Ecology. 2008. (89):107-117.

Submitted by 

Edited by Ashlee R.

(via brains-and-bodies)

Understanding Williams Syndrome from a different point of view.

Williams syndrome is a genetic condition produced by microdeletion of chromosome 7q.

This condition is characterized by cardiovascular problems (SVAS), hypercalcemia, mild to moderate intellectual disability or learning problems, a distinctive “elfin facies” and well developed language skills.

One particular characteristic of this condition is the extreme friendliness they show to any person around them, even with strangers, or as the clip says a condition “where everybody wants to be your friend”

WILLIAMS SYNDROME

Congenital microdeletion of the long arm of chromosome 7, involving different genes, including ELN gene (ELASTIN).

W—->Well developed verbal skills
I——>Increased calcium
L——>Lfin facies(elfin facies)
L——>Lastin gene microdeletion(elastin gene)
I——>Increased sensitivity to vit.D
A——>Aortic stenosis
M——>Mental retardation
S——>Stranger friendliness

(Source: smartspeechtherapy.com)

Alport’s Syndrome

mynotes4usmle:

Light Microscopy (LM)

image

Immunofluorescence (IF)

image

Electron microscopy (EM)

image

In all 3 images, you can see the same pattern: alterning thick and thinning of the GBM (more clear in the EM picture, black arrows). Lamina densa splitting.

MARFAN SYNDROME

Autosomal dominant disease (AD), produced by a defect in the gene FBN1 (chromosome 15) which encodes fibrillin type 1 protein, (main componente microfrillin), important for the biogenesis of elastic fibers, thus affecting the connective tissue.  

PHOTO 1 The Steinberg (thumb) test is positive when the thumb, enclosed in the clenched fist, extends beyond the hypothenar border.

Photo 2. The Walker-Murdoch (wrist) sign is positive when there is overlap of the thumb and fifth digit as they encircle the opposite wrist.

Photo credit (2) http://www.medicalvideos.org/forum/gallery/image_page.php?album_id=5&image_id=87

(Source: njcponline.com)

MARFAN SYNDROME

Marfan syndrome is a connective tissue disorder characterised by a tall, slender body featured with long limbs and long thin fingers.

The most serious complications are the defects of the heart valves and the aorta, which could lead to an aortic rupture (due to too much stress on the aorta), which is usually fatal. 


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