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Category: cellular basis of life Page 1 of 6

Can we really get pneumonia just by inhaling water mist?

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On May 24, 2025

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

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

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Can we use gene therapy to prevent hearing loss?

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On April 14, 2025

In cellular basis of life, special senses

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. cellular basis of life – cells can die through programmed cell death
  4. special senses chapter – regions of the hearing apparatus
  5. special senses chapter – functioning of hair cells in the cochlea

The news item:  Recently the following news item appeared:

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

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

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

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

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

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

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

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On February 25, 2025

In cardiovascular system, cellular basis of life

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. heart chapter – layers of the heart wall
  4. heart chapter – conduction system of the heart and arrhythmias

The news item:  Recently the following article appeared online:

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

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

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

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

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

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

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

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On February 27, 2024

In cellular basis of life, nervous system

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

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Can we really grow blood in a laboratory?

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On January 28, 2024

In cardiovascular system, cellular basis of life, chemical basis of life

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

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

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On December 18, 2023

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

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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How can a drug like Descovy prevent infection by the human immunodeficiency virus?

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On September 23, 2023

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

Teachable moment in classrooms:

  1. immune system chapter – role of CD4 Helper T cells in adaptive immunity
  2. chemical basis of life – structural characteristics of DNA and RNA
  3. cellular basis of life chapter – transcription of DNA into RNA during protein synthesis
  4. microbiology – structure of the viral protein envelope of HIV (human immunodeficiency virus)

The news item:  Recently the following report appeared online:

U.S. FDA approves Gilead’s Descovy for HIV prevention

The approval does not include use of the drug by women to prevent HIV infection. Descovy, a combination drug, was approved in 2016 to treat people already infected with HIV. It contains a newer formulation of a drug used in Gilead’s older medication, Truvada, which has been used to treat people infected with HIV since 2004.

 

The article states that Descovy is a pharmaceutical approved for pre-exposure prophylaxis, the  prevention of HIV infection in men. Descovy was found to be less toxic to the kidneys and bones than  previous drugs used to treat HIV infected people.

So, Why Do I Care??  In the US alone there are over 1 million people living with HIV (human immunodeficiency virus) infection, and each year there are 30,000 – 40,000 new HIV infections. The new infections happen despite the already available preventative measures. Therefore, pharmaceutical prevention of new infections is still important.

Plain English, Please!!! First, let’s talk about how Descovy is expected to prevent infection by HIV in highly exposed individuals. The clinical definition of HIV infection is that the HIV virus should be detectable in human bodily fluids. For HIV virus to appear in the blood or in other bodily fluids, the infected cells must make a swarm of new HIV viruses to spread through the body and enter into the blood and other bodily fluids. The ingredients of Descovy promise to prevent the cells from making new viruses, so there will be no swarm of new HIV viruses, there will not be enough viruses to spread through the body, so HIV viruses never enter bodily fluids. Therefore, even in people frequently exposed to the HIV virus the blood testing doesn’t find any HIV, and the person remains clinically uninfected, remains HIV-negative. This prevention of infection is called “pre-exposure prophylaxis”. An HIV-negative person cannot spread the virus to other people, so the number of new HIV infections are reduced.

Second, let’s talk about the ingredients of Descovy. Both active ingredients (emtricitabine, and tenofovir alafenamide) are inhibitors of the enzyme called reverse transcriptase of the HIV virus. That enzyme is

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How can the genetic engineering treatment of red bone marrow by Zynteglo help beta-thalassemia patients?

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On August 5, 2023

In cardiovascular system, cellular basis of life

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. cellular basis of life chapter – mRNA translation is needed for protein synthesis
  4. blood chapter – red blood cells are made in the red bone marrow
  5. blood chapter – the role of globin chains in hemoglobin function

The news item:  Recently the following report appeared:

https://timesnewscity.com/bluebirds-2-8m-gene-therapy-becomes-most-expensive-drug-after-us-approval/

The article states that about 1,500 patients need blood transfusion every 2-5 weeks, and that Zynteglo is a gene therapy.

So, Why Do I Care??

The most severe type of beta-thalassemia causes serious anemia with the symptoms of continuous lethargy, fatigue, tiredness. To fight this, the patients require regular blood transfusions. Those patients expected to live until about the age of 50. in the US there are about 1500-3000 such patients. New treatment approaches give the hope of longer life to those patients.

Plain English, Please!!! First, let’s talk about what beta-thalassemia is. This disorder is caused by the missing beta-globin protein in hemoglobin. The protein is missing because the beta-globin gene has mutations that prevent the mRNA formation for beta-globin. The outcome is that hemoglobin is abnormal, because it is formed only from the alpha-globin proteins. Such abnormal hemoglobin makes cells of the red bone marrow to burst, reducing the production of oxygen transporter red blood cells. The decreased oxygen transport cause anemia, the starvation of cells for oxygen.

Second, let’s talk about how red blood cells are made. The damage of the beta-thalassemia is done in the red bone marrow, where red blood cells are formed. In the red bone marrow the red blood cells move

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