TEACHABLE MEDICAL NEWS

How can a weight-loss drug fight sleep apnea?

On June 27, 2025

In muscular system, nervous system, respiratory system

Teachable moment in classrooms:

respiratory system chapter – anatomy of the upper airways
muscular system chapter – anatomy of the muscles of the tongue and pharynx
nervous system chapter – location of satiety center in the hypothalamus

The news item: Recently the following report appeared online:

FDA approves weight loss drug Zepbound for sleep apnea

Zepbound, Eli Lilly’s weight loss drug, can now be used to treat obstructive sleep apnea in adults with obesity, the FDA said.

The report states that 39 million adults with obesity in the USA might benefit from this drug treatment. Studies showed that Zepbound significantly reduced the obstruction events in patients. The article also provides a brief description of apnea events, and alternative treatment methods of sleep apnea.

So, Why Do I Care?? Sleep apnea, or more precisely, obstructive sleep apnea, is a sleep disorder that affects millions of adults in the US who suffer from obesity. Those people are not just losing sleep, but are at higher risk for several cardiovascular diseases, and for daytime sleepiness. While there are limitations (such as side effects) to the wide use of this drug treatment, it adds to the list of possible treatment options physicians can subscribe.

Plain English, Please!!! First, let’s talk about sleep apnea. Apnea is a brief closure of the airways where the closure stops air from getting into the lungs. The lower portion of our airways have solid cartilage framework (trachea, bronchi), so narrowing rarely occurs; it is always open, like a steel pipe. However, in the upper airways (mouth, soft palate) we have muscles that surround those airways, and the inappropriate relaxation of the muscles can lead to closure of the upper airway; imagine putting on a sock: it’s easy when we open it up with our fingers, but it’s harder to put our toes through it when the sock is collapsed on the floor. The loss of oxygen flow awakens the person, and repeated instances of apnea leads to poor quality sleep.

Second, let’s talk about throat muscles. Skeletal muscles in the throat (anatomically called pharynx) and in the soft palate (by specific names: the tensor palatini, levator palatini muscles), and in the tongue

Can we really get pneumonia just by inhaling water mist?

By admin

On May 24, 2025

In cellular basis of life, lymphatic and immune system, microbiology, respiratory system

Teachable moment in classrooms:

microbiology – Legionella bacterium
lymphatic and immune system chapter – development and role of macrophages in immune defense
respiratory system chapter – cells that make up the alveoli
cellular basis of life chapter – functions of lysosomes

The news item: Recently the following article appeared online:

3 dead in Legionnaire’s disease outbreak at New York assisted living facility

Since the discovery of Legionella bacteria at the Albany facility, 20 people have been hospitalized and three of those who tested positive have died.

The article states that at the time of the writing of the report 3 people have already died from Legionnaire’s disease in an assisted living facility, and that the infection likely spread to residents by them inhaling mist contaminated by the Legionella bacterium.

So, Why Do I Care?? While the name “Legionnaire’s disease” make it sound like it has an uncommon occurrence, but this bacterial infection, and the pneumonia it causes, is responsible for over 10,000 yearly hospitalizations in the USA. The bacterium specifically disables macrophages, so understanding how this happens may help us design pharmaceuticals or other interventions to help infected people, and to apply this knowledge to other disorders where macrophages have a role.

Plain English, Please!!! First, let’s talk about how macrophages are involved in the defense of our lungs. We find resident macrophages in the lumen of the cup-shaped, microscopic alveoli of the lungs. Macrophages there internalize, phagocytose, microorganisms that invaded the alveoli. The internalization brings the microbes into microscopic bubbles called phagosomes, and once that phagosome fuse with a lysosome full of acid and digestive enzymes, the microbes will be digested into their molecular components. To picture a macrophage in action, imagine a vacuum cleaner where the microbes are “internalized” into a vacuum cleaner bag (the phagosome) which would be merging with a zip-lock bag full of acid and digestive enzymes. Digesting viruses, bacteria, fungi keep the alveoli free of harmful microbes.

Second, let’s talk about how Legionella bacterium infects macrophages. Once inside the phagosome, the Legionella bacteria delay the fusion with the lysosome, and that delay gives enough time for the bacteria

Can we use gene therapy to prevent hearing loss?

By admin

On April 14, 2025

In cellular basis of life, special senses

Teachable moment in classrooms:

cellular basis of life chapter – concept of one gene, one protein
cellular basis of life chapter – concept of gene mutation leading to protein malfunction
cellular basis of life – cells can die through programmed cell death
special senses chapter – regions of the hearing apparatus
special senses chapter – functioning of hair cells in the cochlea

The news item: Recently the following news item appeared:

Gene Therapy Restores Hearing in Mice – University of Miami Medicine Magazine

esearchers from the Miller School and Harvard Medical School report successfully using gene therapy to help restore hearing in a mouse model mimicking genetic hearing loss in humans. The next step is to study the therapy in humans with a common type of genetic hearing loss.

The article states that very similar to humans, mutations in the gene TMPRSS3 causes late-onset hearing loss in mice. The article also states that this gene affects the survival of inner ear hearing nerve cells, and mutations are responsible for 9% of genetic hearing loss. The article adds that gene therapy in mice was successful in reversing the hearing loss.

So, Why Do I Care?? In the USA over 10,000 babies are born with hearing loss, and 37 million people have hearing loss ranging from mild to severe. Because verbal communication is an important part of information gathering and social activities, hearing loss can lead to a decrease in the quality of life, and social isolation. While hearing aids and cochlear implants have been helpful to restore some degree of hearing, the possibility of gene therapy provides new opportunities to remedy hearing loss.

Plain English, Please!!! First, let’s talk about the location of the hair cells where the gene mutation causes abnormal functioning leading to hearing loss. Our hearing apparatus is made up of three regions: the external ear where the eardrum is, the middle ear where the auditory ossicles are, and the inner ear where the sensory hair cells are located. When we take a closer look we see that the hair cells are found inside a snail-shaped structure called the cochlea. These hair cells are essential for hearing, because they release neurotransmitters to create nerve impulses by the neurons inside the cochlea.

Second, let’s talk about how the TMPRSS3 mutation affects the hair cells. The normal TMPRSS gene encodes for a protein that is a protease. There is no final word on this, but some research suggest that

How can finerenone help patients with both kidney disease and heart disease?

By admin

On March 30, 2025

In cardiovascular system, endocrine system, urinary system

Teachable moment in classrooms:

urinary system chapter – parts of the nephron and their functions
endocrine system chapter – location and action of receptors for lipid-soluble hormones
heart chapter within cardiovascular system – location of myocardium in the heart wall

The news item: Recently the following article appeared online:

Utilization of Finerenone by Patients With T2D, CKD | Docwire News

Two years after its approval, researchers studied the use of finerenone in adults with type 2 diabetes and chronic kidney disease (CKD).

The report states that finerenone – a mineralocorticoid receptor antagonist – is approved for several medical conditions (type 2 diabetes, chronic kidney disease, end-stage renal disease, heart failure) where glomerular filtration rate was declining. The author states that utilization rate is still low for this drug.

So, Why Do I Care?? In the USA alone the combined number of people suffering from type II diabetes, chronic kidney disorder (CKD), end-stage renal disease (ESRD) and heart failure is over 100 million. Those disorders cause the death of over 500,000 people every year, and force many patients into hospitalizations, and into major changes in the quality of life. Therefore, it is worth finding and using new pharmaceutical treatments that may lower those disease and death numbers.

Plain English, Please!!! First, let’s talk about what is the shared, common, physiological malfunction in CKD, ESRD, and heart failure. In all three disorders damaged cells start inflammation, and the tissue is repaired by formation of scar tissue. In the case of CKD and ESRD the kidney accumulates unusually large amount of connective tissue (develops fibrosis) made by overstimulated fibroblast. In heart failure the myocardium portion of the heart wall accumulates unusually large amount of connective tissue. In the kidneys the filtration by the nephrons is slowed down by fibrosis, while in the heart the contraction of the ventricles is made difficult by the fibrosis.

Second, let’s talk about why fibrosis appears in the kidneys and in the heart. During early stage kidney disease and early-stage heart disease the cells of the nephron in the kidneys, and the cardiac muscle cells

Can we lower the need for hospitalization by preventing the clumping of proteins in the heart?

By admin

On February 25, 2025

In cardiovascular system, cellular basis of life

Teachable moment in classrooms:

cellular basis of life chapter – concept of one gene, one protein
cellular basis of life chapter – concept of gene mutation leading to protein malfunction
heart chapter – layers of the heart wall
heart chapter – conduction system of the heart and arrhythmias

The news item: Recently the following article appeared online:

NHS England ” First ever life-saving treatment for rare heart condition available on the NHS

NHS patients with a life-threatening heart condition are set to benefit from a cutting-edge new medicine which can significantly reduce the risk of hospitalisation and death. The drug, tafamidis, is the first ever approved treatment for a cohort of patients in England with a rare heart condition known as transthyretin amyloidosis cardiomyopathy (ATTR-CM), where clumps […]

The reporting states that the drug tafamidis treats patients with transthyretin amyloidosis cardiomyopathy (ATTR-CM), and that this disease comes from deposition of clumped proteins in the heart, presents symptoms of shortness of breath, fatigue, fainting, and may result in heart failure and death. In clinical trials tafamidis reduced hospitalizations by 41%.

So, Why Do I Care?? ATTR-CM currently affects about 6 million people un the USA, and 5-7000 new diagnoses happen each year. Heart disease limits daily activity of the patients, and lower their quality of life; therefore, designing treatments is always a positive development. Because amyloidosis can appear in many organs, tafamidis might show the potential path to the treatment of those disorders.

Plain English, Please!!! First, let’s talk about what amyloidosis is. In general terms, amyloidosis is an abnormal accumulation of proteins into clumps large enough to be seen through a light microscope. Many times those clumps interfere with the normal functioning of organs. In the case of ATTR-CM the transthyretin gene has mutations that cause the transthyretin protein to be misshaped. The normal transthyretin proteins join together in groups of four, because some amino acids create sticky surfaces that hold the four proteins together. Picture four eggs, each having a drop of glue at the pointed end. When four eggs are touching each other at their pointed ends they are stuck together like the four transthyretin proteins, and because the sticky surfaces are all covered up, no more eggs can be part of this complex. When the transthyretin protein is misshapen, the positions of the sticky surfaces change on the protein, and thousands of eggs (proteins) would stick to each other randomly, forming large clumps of eggs (proteins), the amyloids.

Second, let’s talk about how amyloidosis damages the heart. The clumps of transthyretin pile up in between the cardiac muscle cells, and with time connective tissue builds up next to the amyloids. The

Can we predict from a blood test when someone may outgrow peanut allergy?

By admin

On January 14, 2025

In lymphatic and immune system

Teachable moment in classrooms:

immune system chapter – characteristics of IgG and IgE antibodies
immune system chapter – there are different types of white blood cells in the immune system
immune system chapter – some T lymphocytes secrete stimulatory chemicals called cytokines

The news item: Recently a new report appeared online:

How antibody levels can predict which children will outgrow their peanut allergy

Australian researchers have discovered how changes in antibody levels over time can predict which children are likely to outgrow their peanut allergy.

The article reported research findings from an Australian research group, and stated that some children outgrow peanut allergies by age 6, and that following changes of two antibody biomarkers sIgG4 and sIgE in children revealed who will outgrow their peanut allergy.

So, Why Do I Care?? Allergic reaction to peanut is the most frequent allergy to food components. In the US it is estimated that between ages 6 and 10 there are over 400,000 children with peanut allergy. As the article describes, an allergic reaction in children may set off panicking of the parents, and can endanger the life of the children. Predicting when a child may outgrow peanut allergy can mean the return to normal dietary habits of those children.

Plain English, Please!!! First, let’s talk about what an allergy is. Some chemicals, the allergens, have the ability to activate the T lymphocytes (T cells). Those activated T cells secrete cytokines that stimulate mast cells to make a protein called immunoglobulin E (IgE). The cytokines act through receptors on the mast cells; so, imagine the mast cell as a soda fountain, and when you push a button on the fountain (your finger is a cytokine molecule binding to its receptor the button), a liquid comes out, the mast cell secrete IgE. After such sensitization, when the allergen enters the body through digestion and absorption, those allergens will stick to IgE molecules and those IgE molecules bind to their receptors in the cell membrane of mast cells. The receptors, in turn, instruct the mast cells to make a chemical called histamine. Here the allergen-IgE combo is your finger, the IgE receptor is the button on the soda fountain, and histamine is flowing out of the mast cell. Histamine spreads throughout the body, and causes coughing, tear production, sneezing, and itchy skin.

Second, let’s talk about how peanuts cause allergy. The seed of the peanut plant is rich in proteins, and some of those proteins, such as vicillins and prolamines, can bind to the IgE in the tissues of the small

How can Opzelura reverse skin discoloration in vitiligo?

By admin

On December 25, 2024

In endocrine system, integumentary system, lymphatic and immune system

Teachable moment in classrooms:

integumentary system – layers/strata of epidermis
integumentary system – melanocytes produce melanin for skin pigmentation
immune system chapter – the white blood cells called cytotoxic (CD8) T lymphocytes can kill invaders and infected cells
endocrine system chapter – some hormone receptors in the cell membrane send chemical signals to the inside of the cell

The news item: Recently the following new item appeared online:

More Vitiligo Patients Respond with Longer Use of Opzelura

Longer-term use of Opzelura was well tolerated, with no serious treatment-related adverse events, according to a poster presented at the annual dermatology meeting.

The article states that vitiligo is a disorder where skin loses color, and that it is likely an autoimmune reaction. The article also states that Opzelura is a Janus kinase (JAK) inhibitor, and that JAK signaling is responsible for inflammation in vitiligo.

So, Why Do I Care?? While vitiligo is not a life-threatening condition, the appearance of “bleached” white spots on the face or hands hinders social interactions, and may cause social withdrawal, and associated psychological stress of vitiligo sufferers. The improved coloration of the skin through medical treatment increases quality of life by lowering the psychological stress.

Plain English, Please!!! First, let’s talk about how normal skin pigmentation is created. The deepest layer of the epidermis is called stratum basale, and in that layer, scattered among keratinocytes, we find the cells called melanocytes that make the brownish pigment called melanin. Melanin is exocytosed, secreted, from melanocytes, and then neighboring keratinocytes of stratum basale and stratum spinosum endocytose, soak up melanin. Inside the keratinocytes melanin protects the DNA from UV light.

Second, let’s talk about how vitiligo changes skin pigmentation. People with vitiligo has melanocytes that are more sensitive to UV light or chemical stress. The stressed melanocytes release stress-related

How can the drug Sohonos treat a disease where muscles are turning into bone?

By admin

On November 26, 2024

In cellular basis of life, skeletal system

Teachable moment in classrooms:

cellular basis of life chapter – concept of one gene, one protein
cellular basis of life chapter – concept of gene mutation leading to protein malfunction
skeletal system chapter – mechanisms of intramebraneous and endochondral ossifications
skeletal system chapter – differentiation of mesenchymal cells into osteoblasts during bone formation.

The news item: Recently the following report appeared online:

US FDA approves French drugmaker Ipsen’s rare bone disorder drug

(Reuters) -The U.S. Food and Drug Administration (FDA) on Wednesday approved French drugmaker Ipsen’s drug for a rare bone disorder, making it the first treatment available to patients with the condition that causes abnormal bone growth.

The article states that the drug that was approved by the FDA treats a rare, genetic bone disorder called fibrodysplasia ossificans progressiva. The article also states that there are about 800 people worldwide with this disease, which is characterized by abnormal bone formation.

So, Why Do I Care?? While there are relatively few people directly affected by this disorder, the family members also suffer the emotional trauma of seeing a child or young adult becoming immobilized by this disease, as there is no reversal of the formation of unwanted bone. In addition, research into finding pharmaceuticals that regulate bone formation may enlighten us to find treatment for other disorders of bone growth.

Plain English, Please!!! First, let’s talk about how bone forms under normal circumstances. Bone formation is started by local hormone-like proteins, the bone morphogenetic proteins (BMPs) instructing fibroblast-like cells, the mesenchymal cells, to change into chondrocyte (cells of the cartilage) and then into osteoblast. The instruction of BMPs is transmitted to the cell through a receptor (named ACVR1) on the fibroblast and chondrocyte cell surface. Picture a garage door-opener button on the wall of a house. The finger the pushes that button is the BMP protein, and the button is the ACVR1. When finger contacts the button, changes will happen in the house: the electric motor is turned on, and a chain pulls the garage door upward. When the BMP protein contacts the ACVR1, several chemical changes will happen in the cell, and the cell restructures itself into a chondrocyte, and then into an osteoblast, the cell that makes the mineralized bone material.

Second, let’s talk about how fibrodysplasia ossificans progressiva comes about. In this disorder abnormal, unwanted cartilage and bone masses form around joints and inside skeletal muscle. While we

How can the pharmaceutical Leqembi slow the progression of Alzheimer’s disease?

By admin

On October 29, 2024

In lymphatic and immune system, nervous system

Teachable moment in classrooms:

nervous system chapter – functions of neurons
nervous system chapter – function of synapses in neuronal communication
immune system chapter – role of antibodies to speed up phagocytosis
blood chapter – function of neutrophils, monocytes and macrophages

The news item: Recently the following report appeared online:

First Alzheimer’s drug to slow disease, Leqembi, gets full FDA approval

Leqembi is not a cure, but it is the first drug shown to slow the progression of Alzheimer’s disease. It first received an accelerated approval from the FDA earlier this year.

The article states that Leqembi slows the progression of Alzheimer’s disease in early stage Alzheimer’s patients, because Leqembi can remove the disease-causing plaques from the brain, and prevent their formation. The article also states that the plaques prevent neurons from talking to each other.

So, Why Do I Care?? Alzheimer’s disease (dementia) affects almost 7 million people in the USA. The memory loss at first reduces the quality of life, and then makes the patients dependent on daily nursing care. All the while the patients no longer recognize family members, or items in their environment, making it difficult on the families. Because there is no effective treatment or prevention for it, pharmaceuticals even with moderate effectiveness can have positive impact on both the patients and the families.

Plain English, Please!!!

First, let’s talk about what Alzheimer’s disease is. Recalling memories is a function assigned to groups of neurons, sometime called neuronal circuits. Each circuit may have thousands or millions of neurons, and the communication between the members keep the circuit functioning. Each time you remember something, neurons of a memory circuit are activated. Think about the “wave” you see in sporting events where the spectators stand up and raise their arms and then sit down forming a moving “wave. Each spectator is a neuron, and their collective action produces a “wave”, the recalling of a memory. In Alzheimer’s disease the neurons of the memory circuits malfunction, and when those neurons try to act in a coordinated fashion, their activity, their “wave”, their recall of memory becomes weaker leading to loss of memory. A few years into the disease large number of neurons may malfunction and die and complete the loss of memory may happen.

Second, let’s talk about why neurons are thought to die in Alzheimer’s disease. The most widely accepted theory is that the buildup of clumps of amyloid peptide, also called senile plaques, outside the neurons

Can we moderate the intensity of hot flashes by influencing the hypothalamus?

By admin

On September 29, 2024

In endocrine system, nervous system

Teachable moment in classrooms:

endocrine system chapter – concept of hormones interacting with receptors in order to change cell behavior
brain chapter – anatomy and function of hypothalamus
metabolism chapter – role of hypothalamus in thermoregulation

The news item: Recently the following news report appeared online:

FDA approves nonhormonadrug to treat hot flashes and night sweats

The new drug, fezolinetant, could be a “game-changer” for women who don’t want to take hormone replacement therapy or who have been treated for hormone-sensitive cancers.

The article states that a new pharmaceutical called Veozah was approved for use to combat hot flashes in women undergoing menopause. The article states that while estrogen supplementation is the most effective treatment for hot flashes, breast cancer survivors can not take estrogen, and for those women now there is an alternative; Veozah was effective in 48% of the patients. The article also states that Veozah blocks a receptor in the brain.

So, Why Do I Care?? There are 4 million breast cancer survivors who can now take advantage of this treatment. Hot flashes can lower one’s quality of life to the degree that holding down a job, or socializing is difficult.

Plain English, Please!!! First, let’s talk about what are “hot flashes”. Hot flash is a brief feeling of being overheated even when the environment has a normal temperature. During hot flashes the body creates sweating and vasodilation, the normal responses to true overheating. Because there is no real overheating of the body, hot flashes are considered instances of abnormal temperature regulation. Commonly, hot flashes happen in menopause when estrogen levels decrease in women.

Second, let’s talk about how our bodies normally respond to overheating. Our core body temperature is maintained at 100 ^oF by a biological thermostat. Picture the thermostat in our homes: when the house is