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How can a weight-loss drug fight sleep apnea?

Teachable moment in classrooms:

  1. respiratory system chapter – anatomy of the upper airways
  2. muscular system chapter – anatomy of the muscles of the tongue and pharynx
  3. 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

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

Teachable moment in classrooms:

  1. nervous system chapter – functions of neurons
  2. nervous system chapter – function of synapses in neuronal communication
  3. immune system chapter – role of antibodies to speed up phagocytosis
  4. 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?

Teachable moment in classrooms:

  1. endocrine system chapter – concept of hormones interacting with receptors in order to change cell behavior
  2. brain chapter – anatomy and function of hypothalamus
  3. 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

How could we possibly slow down the weakening of skeletal muscles in myasthenia gravis ?

Teachable moment in classrooms:

  1. muscle tissue chapter – structural components of the neuromuscular junction
  2. muscle tissue chapter – role of acetylcholine receptor in muscle excitation
  3. immune system chapter – components and function of complement system

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

FDA approves drug for adults with generalized myasthenia gravis

AstraZeneca has announced FDA approval of Ultomiris, a long-acting C5 complement inhibitor for the treatment of adults with generalized myasthenia gravis. According to a company press release, Ultomiris (ravulizumab-cwvz) was approved for adult patients who are anti-acetylcholine receptor antibody-positive, which represents 80% of people with the disease.

The article states that the disease myasthenia gravis affects about 90,000 people in the US, and that Ultomiris is a long-acting C5 inhibitor that allows early treatment leading to lesser amount of damage.

So, Why Do I Care??  The article’s citation of the number of affected individuals shows that this is not a minor disease. In its advanced stage myasthenia gravis can be deadly, or at least life threatening; the loss of muscle strength prevents the patients from many daily activities, which causes a decreased quality of life.

Plain English, Please!!!  First, let’s talk about what myasthenia gravis is. Myasthenia gravis is an autoimmune disorder where the patient’s own immune system attacks and damages the neuromuscular junction. The target of the immune system is a molecule, the acetylcholine receptor, in the neuromuscular junction. The acetylcholine receptor physically binds to the messenger molecule called acetylcholine released by the neurons. So, destruction of the receptor makes it impossible for skeletal muscles to understand that they are supposed to contract. The damaged muscles no longer contract with normal force, thus the patients develop muscle weakness that affects movement, and can endanger inhalation causing respiratory distress.

Second, let’s talk about how myasthenia gravis causes damage. The first action of the immune system in myasthenia gravis is to make antibodies that stick to the acetylcholine receptors. The second action is that the antibodies in the neuromuscular junction attract the proteins of the complement system. The 9 complement proteins stick to each other, assemble on the cell membrane, and eventually open a hole in the muscle cell membrane. Imagine an excavation crew where all 9 members have to work together to dig a hole. Those holes in the muscle cell membrane cause the most significant damage to the neuromuscular junction.

Third, let’s talk about how Ultomiris works. The active ingredient in Ultomiris covers up a complement protein (#5), and prevents the piling up the rest of the complement proteins. Without the assembly of all of those proteins the excavation crew never starts to dig, the hole never forms in the muscle cell membrane, and the neuromuscular junction can stay relatively undamaged. That kind of protection slows deterioration, and preserve muscle strength in the patients.

 

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How could possibly a stroke cure addiction?

Teachable moment in classrooms:

  1. nervous tissue chapter – using neurotransmitters in synaptic communication between neurons
  2. nervous tissue chapter – anatomy of the brain, the five lobes
  3. nervous tissue chapter – basic cellular structures of neurons, axon, cell body

The news item:  Recently the following report appeared online:

Why a Brain Injury From a Stroke Cured a Smoking Addiction

Scientists are learning new ways we might be able to permanently cure addiction in the future.

The article states that in the USA over 27 million adults suffer from addiction to various substances, and that for a portion of those people current treatments are not effective. Researchers started a new study when sporadic evidence emerged that brain lesions caused addicted smokers to stop smoking. This article mentions the insular area, frontal lobe where brain damage correlated with cessation of addiction to smoking.

So, Why Do I Care??  To be more accurate than the article, over 27 million people in the USA suffered from addiction during the year 2022. The relapse rate (the return to addictive substance use) can reach as high as 60% of those people. The impact of addiction on the individual ranges from deterioration of health, problems of employability, and limited social interactions.  According to estimates, the yearly economic cost of addiction is over $500 billion for the US. There is also a cost on personal relationships, and this is difficult to measure. Finding new biological pathways that are part of addictions can result in new, more effective treatments.

Plain English, Please!!!  First, let’s talk about the anatomy of the nervous system linked to addiction. Addiction activates the reward centers in our brain, causing the perception of satisfaction, pleasure. Those centers are located in the brainstem, and in the basal ganglia, and the centers are made up of millions of neurons.  Those centers are receiving stimulation or inhibition from other parts of the brain, such as the frontal lobe of the cerebrum, and the amygdala. These areas also represent millions of neurons. Think about this like a spider (the mass of neurons of the reward center) sitting in the middle of the spider web made up by the millions of axons coming from those other brain parts. Imagine that the stimulating nerve impulses pull the spider web to the right, while the inhibiting nerve impulses pull the spider web to the left. The reward center (the spider) will move to the right to consume the addictive substance, or move to the left to resist the urge to consume.

Second, let’s talk about how different brain parts influence the reward center. The influence of inhibition or stimulation of the reward center is carried out by neurotransmitters that are small molecules acting at

How can a new combination drug treatment fight childhood brain cancer with increased effectiveness?

TeachableMedicalNews article 02272024

Teachable moment in classrooms:

  1. cellular basis of life chapter – cell cycle, and phases of mitosis
  2. cellular basis of life chapter – concept of gene mutation leading to protein malfunction
  3. cellular basis of life chapter – enzymes are proteins that catalyze chemical reactions
  4. nervous tissue chapter – functions of the neuroglial cells

The news item:  Recently this reporting appeared online:

Novartis drug combo shows promise in childhood brain cancer

An oral drug combination by Swiss pharmaceuticals company Novartis showed promise in treating a subgroup of patients suffering from a common childhood brain cancer in a trial.

 

The article describes a new drug combination for the treatment of childhood brain cancer, namely low grade glioma. The article states that about 1000 children are diagnosed yearly with this brain cancer, and that the study participants were between the ages 1 and 17. The new treatment slowed the cancer progression more than standard chemotherapy.

So, Why Do I Care??  Brain cancer in children is very disruptive to their development and education, and even worse, it can end their lives. In addition, parents, siblings, relatives, classmates all suffer emotional trauma. New treatments that slow the progression of these gliomas promise fewer disruptions and longer survival.

Plain English, Please!!!   First, let’s talk about what a glioma is. Inside our brain and spinal cord there are cells called neuroglia. They support the working of neurons. When mutations cause the neuroglial cells to divide continually, then an abnormal accumulation of neuroglial cells results, thus a glioma forms. The most frequent mutations in gliomas are the ones that activate MEK kinase and the BRAF kinase enzymes. The normal function of these enzymes is to act inside the cells to add phosphate groups to proteins. Those phosphorylated proteins stimulate the start of cell division.

Second, let’s talk about how mutations of the MEK and BRAF kinases contribute to glioma development. Under normal circumstances the kinases are active only during interphase when a growth stimulating

Can our genes influence what we like to eat?

Teachable moment in classrooms:

  1. cellular basis of life chapter – concept of one gene, one protein
  2. cellular basis of life chapter – concept of gene mutation leading to protein malfunction
  3. special senses chapter – taste receptors are in taste buds
  4. special senses chapter – role of G-proteins in sweet, bitter and savory taste receptors

The news item:  Recently this news article appeared online:

Bitter or Savory, Taste Genes Could Influence Your Diet

US News is a recognized leader in college, grad school, hospital, mutual fund, and car rankings. Track elected officials, research health conditions, and find news you can use in politics, business, health, and education.

 

The article states that a study was conducted to link previously described gene variations to the five basic taste types: sweet, sour, bitter, salty and savory. People with high sensitivity to bitter flavor ate fewer whole grains.  People with high sensitivity to savory flavor ate fewer vegetables. People with high sensitivity to sweet flavor had lower triglyceride levels.

So, Why Do I Care??  Changing ones diet have been part of many non-invasive prevention of diseases, and also part of maintaining a healthy lifestyle after surgery or after the start of new medication. However, changing ones diet is a challenging task, because of the stubborn food preferences we all develop. If those food preferences can be linked to genetic function, then dietary changes could be guided to accommodate those gene-influenced food preferences, and to give patients dietary prescriptions that we find easier to follow.

Plain English, Please!!!  First, let’s talk about the cells that detect tastes. On the surface of your tongue there are hundreds of small bumps called papilla, and inside each of those bumps sit taste receptor cells that detect chemicals around them. When those receptor cells detect taste-related chemicals, the cells then release neurotransmitters to start a nerve impulse in the axons of cranial nerve VII or IX.

Second, let’s talk about how taste receptors detect tastes. The five types of taste receptor cells are sensitive to different taste-causing chemicals (tastants). The “sour” receptor cells are sensitive to hydrogen ions, and the “salty” receptor cells are sensitive to sodium ions. For both of those receptors the

Can we really carry out vision tests with AR goggles and artificial intelligence app?

Teachable moment in classrooms:

  1. special senses chapter – location of retina, the third tunic of the eye
  2. special senses chapter – location and importance of macula lutea
  3. special senses chapter – the retina needs blood supply to bring oxygen and nutrients to the neurons of the retina
  4. special senses chapter – location of liquid-filled spaces inside the eye
  5. special senses chapter – the sensory cells called rods and cones of the retina detect light

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

 

Duncansville Eye Practice Using AR-Type Headset to Diagnose Major Eye Issues

A Duncansville eye practice is using a new augmented-reality device made by Florida-based company Heru to diagnose severe conditions in patients. This AR-like headset can detect serious eye diseases like Glaucoma in minutesand it’s being used right here in Blair County.

The report states that the HERU is a headset with goggles, and the equipment projects flashes of light in the visual field of the eye, and asks the test subject to respond when they see the light. Among other conditions, glaucoma can be diagnosed with the device.

So, Why Do I Care??  Deterioration of vision is a major threat to quality of life in an aging population. The most serious causes of vision loss are glaucoma and age-related macular degeneration, affect over 13 million people in the US. Faster and easier to perform diagnostic process can ensure that people can get an early diagnosis, and more effective treatment. In addition to those two eye disorders the HERU device can diagnose 7 additional eye disorders, indicating the versatility of the device.

Plain English, Please!!!  First, let’s talk about what glaucoma is. This eye disorder develops because of the increased pressure inside the eye. The pressure is coming from the accumulation of aqueous humor in the front (anterior) cavity inside the eye. The increased pressure is then transferred to the vitreous humor of the posterior cavity.  The vitreous humor compresses the blood vessels on the surface of the retina, and that slows the flow of oxygen and nutrients to the light-sensing cells (rods and cones). Picture a garden hose with water flowing through it. If someone steps on the hose the water flow slows down. The same happens to blood vessels of the retina if they are compressed. Without enough oxygen and nutrients the rods and cones start dying, and they no longer detect light, and that leads to vision loss.

Second, let’s talk about what age-related macular degeneration is. This eye disorder develops when a small patch of the retina, the macula lutea, malfunctions. The cause of macular degeneration is

Can we really diagnose concussion from a blood test?

TeachableMedicalNews article 05292023

Teachable moment in classrooms:

  1. cellular basis of life chapter – intermediate filaments are part of the cytoskeleton
  2. nervous system chapter – neurons and astrocytes are cells of the nervous system
  3. brain chapter – meninges are protective coverings of the central nervous system
  4. cardiovascular system chapter – reabsorption during capillary exchange brings degraded proteins into blood circulation
  5. brain chapter – cerebrospinal fluid is absorbed into venous sinus

The news item:  Recently the following report appeared online:

https://www.nbc12.com/prnewswire/2023/03/07/abbott-receives-fda-clearance-first-commercially-available-lab-based-blood-test-help-evaluate-concussion/?outputType=amp

The article states that a new blood test is available for patients who are suspected to have suffered concussion because of an impact injury, and that this test may help to find the patients who might need a CT scan for further evaluation. The test works by analyzing two biomarkers.

So, Why Do I Care??  Concussion happens frequently with over 2 million concussions occurring yearly in the USA. Whether it is from a car accident, from a fall, or from a collision at a sporting event, the consequence is impaired brain function. That comes with a price tag of over $40 billion per year medical cost and lost income in the USA.

Plain English, Please!!! First, let’s talk about what concussion is. An injury to the brain from a physical impact is called concussion. The symptoms can be a brief loss of consciousness followed by headache, memory impairment, loss of orientation, loss of cognitive functions, depression. The most dangerous aspects of concussion are the long-lasting effects.

Second, let’s talk about how the brain is injured by mechanical forces. While it is true that the meninges, the membrane-like covering of the brain, provide a moderate level of protection against sudden

How could the lead contamination in blueberries harm us?

TeachableMedicalNews article 04052023

Teachable moment in classrooms:

  1. nervous system chapter – axons and synapses as structures of neurons
  2. nervous system chapter – transmission of a nerve impulse using a chemical synapse
  3. nervous system chapter – formation of myelin sheet along axons
  4. cellular basis of life chapter – zinc-finger proteins in gene regulation
  5. endocrine system chapter – protein kinases are important for cellular actions

The news item:  Recently this report appeared:

Freeze-dried blueberries recalled due to potential lead contamination

The voluntary recall covers packages of organic blueberries sold under the brand name Natierra, with expiration dates of December 2022 and January 2025.

The article states that long term exposure to lead in children may affect the central nervous system causing learning disabilities, developmental defects, and in adults causing damage to the nervous system and internal organs.

So, Why Do I Care??  Long term exposure to lead harms about 500,000 children in the USA alone. The consequences last for decades, and can not be undone. It is good to understand why the metal lead poses such severe consequences.

Plain English, Please!!!  First, let’s talk about how lead (Pb in the periodic table) gets into our bodies. Typically, lead comes into our bodies through eating lead-contaminated food or drinking water, because lead compounds are soluble in water. The heavy metal lead has similar chemical properties to the biologically important metal calcium. Because of that similarity the small intestine readily absorbs lead just as it absorbs calcium.

Second, let’s talk about what biological processes are harmed by lead. Once absorbed into the bloodstream the lead ions take the place of the calcium and zinc ions. Here are a few examples. A. Lead

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