TEACHABLE MEDICAL NEWS

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

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On January 14, 2025

In lymphatic and immune system

Teachable moment in classrooms:

  1. immune system chapter – characteristics of IgG and IgE antibodies
  2. immune system chapter – there are different types of white blood cells in the immune system
  3. 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

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How can Opzelura reverse skin discoloration in vitiligo?

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On December 25, 2024

In endocrine system, integumentary system, lymphatic and immune system

Teachable moment in classrooms:

  1. integumentary system – layers/strata of epidermis
  2. integumentary system – melanocytes produce melanin for skin pigmentation
  3. immune system chapter – the white blood cells called cytotoxic (CD8) T lymphocytes can kill invaders and infected cells
  4. 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

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

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On November 26, 2024

In cellular basis of life, skeletal system

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. skeletal system chapter – mechanisms of intramebraneous and endochondral ossifications
  4. 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

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

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On October 29, 2024

In lymphatic and immune system, nervous system

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

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

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On September 29, 2024

In endocrine system, nervous system

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

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

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On August 30, 2024

In lymphatic and immune system, muscular system, nervous system

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 can infusion of Tzield slow the progression of type I diabetes?

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On July 24, 2024

In endocrine system, lymphatic and immune system

Teachable moment in classrooms:

  1. endocrine system chapter – role of insulin in lowering high blood sugar levels
  2. endocrine system chapter – location of insulin-producing beta cells in the pancreas
  3. immune system chapter – role of T-lymphocytes in the immune system

The news item:  Recently the following report appeared online:

FDA approves 1st drug to delay onset of Type 1 diabetes

For the first time, the U.S. Food and Drug Administration on Thursday approved a treatment that can delay the onset of Type 1 diabetes.

The article states that the drug was approved to treat stage 2 type I diabetes in order to avoid progression to stage 3. The article states that type 1 diabetes is a chronic autoimmune condition where the pancreas doesn’t produce insulin. When diagnosed by the detection of autoimmune antibodies, patients develop insulin-dependence within 5 years. Tzield is administered as an infusion. The article also states that 64,000 people in the US are diagnosed with type 1 diabetes each year, and currently 1.6 million people are using insulin.

So, Why Do I Care??  Insufficient production in type 1 diabetics happens to many people, as we see from the statistics in the online report. Large number of current and future patients could benefit if a new treatment could delay the starting point of insulin dependence. Then their lifestyle could be preserved, and the need for injected insulin could be delayed, and the cost to society be reduced.

Plain English, Please!!!  First, let’s talk about why type 1 diabetes develops. Our immune system is normally programmed to recognize and then destroy invaders such as bacteria, fungi, viruses, worms, and others. Attack on the body’s own cells is prevented by a set of molecular “hand brakes”. When you apply the hand brake on your car, the car is immobilized, and the same way the CD3 molecules on T-lymphocytes prevent the destruction of the body’s cells. In an autoimmune disorder, such as type I diabetes, the hand brakes are released, and the T-lymphocytes attack and destroy the body’s own cells. In type I diabetes the beta cells of the pancreas are attacked and destroyed. Because the beta cells are the only cells that make the hormone insulin, when they are destroyed, the insulin levels decrease, and lowering a high blood sugar level becomes difficult.

Second, let’s talk about the stages of type 1 diabetes. In stage 1 the immune system is beginning its attack on the beta cells of the pancreas, there are no symptoms yet, but a blood test can discover the signs of an

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Can you die by drinking too much stimulants like charged lemonade?

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On June 26, 2024

In cardiovascular system

Teachable moment in classrooms:

  1. heart chapter – order of contraction of chambers during cardiac cycle
  2. heart chapter – contraction of cardiac muscle cells are causing the contraction of heart chambers
  3. heart chapter – structures in the conduction system of the heart
  4. heart chapter – relationship of the ECG wave forms to contraction of heart chambers

The news item: Recently the following news appeared online:

Family sues Panera Bread after college student who drank Charged Lemonade dies

Panera Bread is facing a lawsuit from the family of 21-year-old University of Pennsylvania student Sarah Katz, who died after drinking a “charged lemonade.”

The article states that a college student age 21 died of cardiac arrest as a consequence of drinking a “Charged lemonade” drink.The drink had 390 mg of caffeine. The article also states that the student has been suffering from long QT syndrome which is caused by a malfunctioning of the heart’s electrical system.  The syndrome causes fainting or heart palpitations upon excitement or exercise.

So, Why Do I Care??  Disorders of the heart may not show any symptoms during a sedentary life style. In the US alone there are over 100,000 people who has the long QT syndrome, and 2000-3000 people die a sudden death because of it. Because the symptoms appear mostly during stressful conditions, and therefore remain hidden in many people. If you know you have a heart disorder it is important to use your prescribed medications, and if you have symptoms of heart disorders then it is important to have them evaluated by medical professionals.

Plain English, Please!!!

First, let’s talk about heart rhythms. In order for the heart to move, to pump blood, the chamber must contract in a sequence during a single heartbeat.  The atria contract first, and then, after a short delay, the ventricles contract. This proper order of contractions is orchestrated by electric impulses from the heart’s natural internal pacemaker, the conduction system. This conduction system activates the muscle of atria or ventricles just like a band-leader of a marching band directs the use of musical instruments during a parade.

Second, let’s talk about long QT syndrome. The name of the syndrome comes from name of wave forms on electrocardiograms. The Q wave represents the first step in the contraction of the ventricles, and the

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Can we treat inflammatory bowel disease by holding the cells of the immune system captive?

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On May 24, 2024

In cellular basis of life, digestive system, lymphatic and immune system

Teachable moment in classrooms:

  1. cellular basis of life chapter – cell membrane proteins can function as receptors
  2. digestive system chapter – anatomy of the digestive system, location of large intestine
  3. digestive system chapter – layers of the gastrointestinal tract, location of mucosa
  4. immune system chapter – cell-based immunity depends on cytotoxic T-lymphocytes

The news item:  Recently the following article appeared online:

New drug for IBD, ulcerative colitis wins FDA approval: ‘Amazing results’

“We’re seeing pretty amazing results” with newer treatments, said one expert. “If you look over the last few years, it’s been game-changing.”

The article states that inflammatory bowel disease and ulcerative colitis are diseases of the lining of the large intestine and rectum where open sores develop, and while the precise cause is unknown, we consider this a consequence of the improper functioning of the immune system. The article describes the symptoms as diarrhea, abdominal pain, fatigue, and rectal bleeding. The article states that the current steroid and other injectable treatments are effective, but patients could be treated easier with oral medication.

So, Why Do I Care??  Each year over 70,000 people in the US are diagnosed with inflammatory bowel disease; currently about 2.1 million people are treated for the disease. Because the symptoms are debilitating, and treatment options have been limited to injectable drugs, the significance of Etrasimod (Velsipity) is that it provides a treatment option using oral medication instead of injections.

Plain English, Please!!!   First, let’s talk about what inflammatory bowel disease is. This disorder happens when the immune system overreacts to viruses or bacteria in the gastrointestinal tract (GI-tract), the tube-shaped part of the digestive system going from the mouth to the anus. Most of the time the large intestine and the rectum are the location for inflammation. The overactive immune system sends a large number of cytotoxic T-lymphocytes to the inner lining, the mucosa, of the GI-tract. Once there, those T-lymphocytes release inflammatory mediators that cause vasodilation, and eventually tissue damage. The damaged mucosa prevents absorption of nutrients and causes bleeding and diarrhea.

Second, let’s talk about how the immune system becomes overactive during the disease. Normally most of the T-lymphocytes reside in the lymph nodes limiting the number of T-lymphocytes released into

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How could possibly a stroke cure addiction?

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On April 27, 2024

In nervous system

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

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