TEACHABLE MEDICAL NEWS

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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.

Why the test to predict preeclampsia is hailed as a great news?

Teachable moment in classrooms:

  1. blood vessel chapter – layers of the wall of arteries
  2. blood vessel chapter — blood pressure regulation through vasoconstriction and vasodilation
  3. urinary system chapter – filtering membrane of the glomerulus in the renal corpuscle
  4. development chapter – blood vessels in the placenta

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

FDA approves groundbreaking blood test for early preeclampsia detection in pregnant women

The FDA has approved a new blood test that can detect whether a mother will potentially get preeclampsia within 30 minutes.

The report describes preeclampsia as high blood pressure in pregnant women, and that in the state of Georgia hypertensive disorders are the leading cause of maternal death. The article describes the name of the test: BRAHMS sFlt1/PlGF KRYPTOR.

So, Why Do I Care??  The death of pregnant mothers is a tragic event that could cause the death of their unborn child as well.  When pregnancy-related high blood pressure appears, the medical response depends on how high the blood pressure is. Once a test predicts that preeclampsia will appear in a pregnant woman, the obstetrician can make preparations for monitoring and further possible actions. When the medical professionals are ready to make treatment choices, it is more  likely that the intervention will be successful, and both mother and baby will survive.

Plain English, Please!!!  First, let’s talk about why high blood pressure appears in pregnant women who had normal blood pressure before the pregnancy. By the end of the first month of pregnancy the fetus builds a placenta, an organ that incorporates a layer of the mother’s uterus as well. The purpose of the placenta to provide a place for exchange of oxygen and nutrients from the blood of the mother to the blood of the fetus, and for the exchange of carbon dioxide and other waste products from the blood of the fetus to the blood of the mother. This can be achieved only if a large number of fetal blood vessels and maternal blood vessels are part of the placenta. In the fetuses where the number of blood vessels is low in the placenta, the fetus will be deficient in oxygen, and the blood vessels release stress factors such as placenta growth factor (PlGF), and soluble fms-like tyrosine kinase-1 (sFlt1). Those stress factors reprogram the blood vessels of the mother to contract, and the contracting blood vessels increase blood pressure. Imagine a balloon filled with water. If you squeeze the balloon the force will increase water pressure to the point that balloon may burst. Smooth muscle cells in the wall of arteries do the squeezing (vasoconstriction) that increases blood pressure.

Second, let’s talk about why is preeclampsia harmful. High blood pressure in the mother can cause strokes by dislodging clots from large blood vessels and moving them to the brain where the clots block

Can our genes influence what we like to eat?

Teachable moment in classrooms:

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

The news item:  Recently this news article appeared online:

Bitter or Savory, Taste Genes Could Influence Your Diet

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

 

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

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

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

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

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

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

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

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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