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Can we chase down and kill the hiding cancer cells in our bodies?

Teachable moment in classrooms:

  1. cellular basis of life chapter – DNA specifies protein structure
  2. blood chapter – role of red bone marrow in hemopoesis
  3. immune system chapter – development of T and B cells and their role in the immune response
  4. immune system chapter – structure of antibodies and their binding to specific target molecules

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

Talvey Giving Patients With Heavily Pretreated Multiple Myeloma ‘a New Lease on Life’

The recent FDA approval of Talvey for heavily pretreated multiple myeloma results in an improved response to therapy and a manageable side effect profile.

The report describes that the Talvey treatment is given to multiple myeloma patients whose cancer returned despite several previous treatment with conventional drugs. The report also describes the several side effects of Talvey treatment.

So, Why Do I Care??  Every year multiple myeloma kills over 12,000 people in the USA alone. This type of cancer frequently reappears after conventional cancer treatments, and any new treatment that extends patient life after previous treatments are exhausted, is important to research.

Plain English, Please!!! First, let’s talk about what multiple myeloma is. This disorder represents a cancerous, uncontrolled cell division of plasma cells in the red bone marrow. A plasma cell is a type of white blood cell that produces antibodies during immune response. When the cancerous plasma cells quickly multiply and overtake the red bone marrow, fewer red blood cells and platelets are made, leading to fatigue, tiredness and easy bleeding.

Second, let’s talk about how Talvey works. If we want the immune system to kill cancer cells it would make sense to bring the immune system’s cells right to the cancer cells. Metaphorically speaking, picture

Can we really get pneumonia just by inhaling water mist?

Teachable moment in classrooms:

  1. microbiology – Legionella bacterium
  2. lymphatic and immune system chapter – development and role of macrophages in immune defense
  3. respiratory system chapter – cells that make up the alveoli
  4. 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 predict from a blood test when someone may outgrow peanut allergy?

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

How can Opzelura reverse skin discoloration in vitiligo?

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

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

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 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

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.

Can a protein from pig skin restore vision to blind people?

TeachableMedicalNews article 01152023

Teachable moment in classrooms:

  1. special senses chapter – tunics/layers of the eye
  2. special senses chapter – structure of the cornea
  3. tissues chapter – collagen is found in the extracellular matrix of many connective tissues
  4. immune system chapter – recognition of non-self antigens
  5. immune system chapter – role of lymphocytes for immune functions

The news item:  Recently this news item was online:

Eye implant made from pig protein restored sight in 14 blind people

Twenty people with diseased or damaged corneas saw improvements to their vision after receiving implants engineered out of protein from pigskin.

The article states that collagen from pig skin was helpful in restoring vision to people with the disorder called keratoconus, that this disease represents a bulging of the front of the eye, that about 50-200 from 100,000 people have this disease, and that the treatment includes injection of this collagen into the cornea.

So, Why Do I Care??  Our vision is the most precious sense, so, any loss of visual capacity has a major effect on our quality of life. The misshaped cornea causes loss of sharp vision.  As the article states keratoconus is a relatively rare disorder, nonetheless it is important to keep an account of any remedy that restores vision.

Plain English, Please!!! First, let’s talk about what keratoconus is. At the front of the eyeball there is a transparent sheet called cornea. From the side it looks like a flat bubble. The cornea focuses light into the eye. In some people the cornea has a pointy shape like a small ice cream cone. This keratoconus condition prevents the focusing of light, so, blurred, cloudy vision is the result.

Second, let’s talk about the injection into the cornea. While the cornea is a very thin sheet of tissue, it is possible to inject materials into the sheet.  Because the cornea is flexible, injection of the proper amount

Why are we trying to transplant pig hearts into human beings?

TeachableMedicalNews article 10222022

Teachable moment in classrooms:

  1. chemical basis of life chapter – genetic engineering can remove genes from, or add genes to DNA molecules (the chromosomes)
  2. cellular basis of life chapter – removing a gene removes a protein, while adding a gene adds proteins to the functional toolkit of cells
  3. hear chapter – blood pumping action of left ventricle delivers oxygen, nutrients to all organs
  4. immune system chapter – role of HLA proteins in the recognition of self and non-self antigens

The news item:  Recently the following news article was published:

Two pig heart transplants succeed in brain-dead recipients

Surgeons at New York University (NYU) have successfully transplanted genetically-engineered pig hearts into two brain-dead people, researchers said on Tuesday, moving a step closer to a long-term goal of using pig parts to address the shortage of human organs for transplant.

The article states that experimental transplantation of pig hearts into brain dead humans was carried out, and the hearts remained functional for the three days of the study.  The article also states that the transplanted hearts came from genetically engineered pigs in which 4 genetic alterations were done to prevent rejection, and 6 genetic modifications were done to prevent incompatibilities between pigs and humans.

So, Why Do I Care??  There are about 600,000 people in the US whose heart is about to give out (end stage heart disease), but there are only about 3800 heart transplant operations. Several people die each day because suitable donor hearts are not available for transplantation. If we could routinely transplant pig hearts into humans that would save thousands of lives.

Plain English, Please!!!  First, let’s talk about why people need a heart transplant. End stage heart disease happens either because of the degeneration of heart muscle from coronary artery disease or from viral infection, or because of heart valve problems.  Once the pumping efficiency of the heart drops

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