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

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

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

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

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

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

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

Can we use gene therapy to fight the skin disorder epidermolysis bullosa?

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. tissue chapter – the basement membrane is a thin layer of tissue in-between epithelium and the underlying connective tissue
  4. integumentary system chapter –the integrity of the skin depends on the secure connection of the dermis to the basement membrane

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

U.S. FDA approves Krystal Biotech’s skin-disorder gene therapy

(Reuters) -The U.S. Food and Drug Administration on Friday approved Krystal Biotech Inc’s first-of-its kind topical gene therapy for patients with a genetic skin disorder, sending its shares up 7% in afternoon trading. Patients with the rare dystrophic epidermolysis bullosa disorder suffer from open wounds, causing skin infections and are at an increased risk of vision loss, scarring and skin cancer.

The article states that the therapy named Vyjuvek healed skin wounds in 65% of dystrophic epidermolysis bullosa patients as opposed to 22% healing rate with placebo treatment. The article also states that about 10,000 people world-wide, and 3000 people in the USA suffer from the disorder.

So, Why Do I Care??  While severe forms of epidermolysis bullosa are life-threatening, moderate forms are devastating to the quality of life, as they it creates painful wounds or blisters on the skin, or in the mouth, and the healing wounds lead to widespread scarring. That makes dressing into clothes, wearing shoes, eating difficult. For dystrophic epidermolysis bullosa patients the promise is the possibility of returning to a normal lifestyle after this new treatment.

Plain English, Please!!!  First, let’s talk about epidermolysis bullosa. This is a group of diseases with the shared symptoms of fragile, easy to break skin and blistering of the skin. The three-layered area of epithelium-basement membrane-dermis is made sturdy by several molecules, and if one is malfunctioning because of a mutation, then fragility of the skin results. The many types of epidermolysis bullosa are caused by a variety of genetic mutations.

Second, let’s talk about the cause of dystrophic epidermolysis bullosa. In this type of the disease the missing component is type VII collagen, the molecule that secures the basement membrane to the dermis. Imagine a large picnic table where the table cover is clamped to the table so the wind wouldn’t blow the cover away. Type VII collagen acts like those clamps securing the dermis (the table) to the table cover (the basement membrane). When the type VII college gene suffers mutations, the resulting type VII collagen protein clamp has a distorted shape, and cannot secure the basement membrane to the dermis, and the skin blisters to form open wounds.

Third, let’s talk about how Vyjuvek treatment works. This treatment is delivering a normal type VII collagen gene to the fibroblast cells of the dermis. The gene is enclosed in an inactivated virus, and the viruses are mixed into a gel, and that gel is applied to the wound surface.  Once that virus enters inside the fibroblast in the person’s dermis, then the normal gene is used to make the type VII collagen protein. With time the newly-made, normal type VII collagen “clamps” will secure the dermis to the basement membrane, and prevent new blistering or breaking of the skin.

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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 we really grow blood in a laboratory?

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. cardiovascular system chapter – formation of red blood cells by stem cells in red bone marrow
  4. respiratory system chapter – oxygen transport by hemoglobin in red blood cells

The news item:  Recently the following report appeared online:

Lab-grown blood given to people in world-first clinical trial

It is hoped the blood could revolutionise care for people who need regular donations.

The report described the need for blood transfusion for repeated infusions such as those for sickle cell anemia patients, and the shortage of minor blood types for transfusion. The report briefly described the lifespan of the red blood cells, and the process of growing blood in the lab.

So, Why Do I Care??  Blood transfusion, the administering of blood or red blood cells into the vein of the recipient, is a life saver when the recipient lost lot of blood, or when the red blood cells of the recipient are being damaged because of a disease. As the transfused blood is derived from blood donors who are not always available to donate, the volume of donated blood can be so low as to create a blood shortage.  It would be a great improvement if red blood cells could be “manufactured” on demand.  That would make blood shortages obsolete. In the US 100,000 people suffer from sickle cell anemia.

Plain English, Please!!!  First, let’s talk about why blood transfusion is a lifesaver clinical intervention, in general. We need red blood cells to transport oxygen from the lungs to all organs of our body. When blood loss or damage to red blood cells (like in sickle cell anemia) decrease the number of oxygen transporter cells, the organs do not receive enough oxygen for normal functioning. It’s like a fleet of trucks delivering bread to a store. If the trucks break down, the bread never get’s to the stores, and the functioning of the store will suffer. In this case the red blood cell trucks deliver oxygen to organs of the body. The most noticeable effect of oxygen deficit is on the skeletal muscles (loss of muscle strength) and on the nervous system (fatigue, tiredness). Restoring the number of red blood cells to normal helps to return the functioning of the body to normal. This why most transfusions do not transfuse whole blood, but only red blood cells.

Second, let’s talk about why sickle cell anemia patients need frequent blood transfusions. In sickle cell anemia patients the mutation of the globin protein of hemoglobin causes the red blood cells to change

Can we use an antibody to strengthen patients’ own immune system to fight childhood soft tissue cancer?

Teachable moment in classrooms:

  1. tissue chapter – general characteristics of epithelial and connective tissues
  2. cellular basis of life chapter – proteins in cell membranes can serve as receptors
  3. immune system chapter – CD8-T-cells actively destroy target cells
  4. immune system chapter – antibodies can be engineered to bind to specific targets

The news item:

Recently a newly approved treatment for childhood soft tissue cancer was reported:

Drug Approved to Help Young Patients Battle a Rare Cancer

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 the drug Tecentriq was approved for use against alveolar soft part sarcoma (a soft tissue cancer). About 80 children and adults in the USA are diagnosed each year with his sarcoma, and most conventional treatments fail to fight it. The article also states that Tecentriq is an anti-PD-L1 inhibitor, and works by helping the immune system respond more strongly to cancer.

So, Why Do I Care??  While the overall number of cancer patients diagnosed with alveolar soft part sarcoma is low, these patients could not be helped by regular cancer treatments. Finding new cancer treatment approaches for these patients opens the possibility to treat other cancers where traditional cancer treatment failed.

Plain English, Please!!!  First, let’s talk about what a sarcoma is. The sarcoma type of cancers start from connective tissue, as opposed to the carcinoma type of cancers that start from epithelial tissues. The general course of the sarcomas is similar to other cancers, and that includes local growth, and the spreading, metastasizing throughout the body. Alveolar soft part sarcoma was named such, because the cancer cells form baggy, alveolus-looking microscopic structures.

Second, let’s talk about how cancer cells can slow down the immune system. One normal function of our immune system is to detect and destroy cells that show evidence of infection or abnormal components.

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