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Can a copper injection really cure a genetic disease?

On January 24, 2026

In cardiovascular system, cellular basis of life, metabolism, nervous system, skeletal system, tissues

Teachable moment in classrooms:

cellular basis of life chapter – concept of one gene, one protein
cellular basis of life chapter – concept of gene mutation leading to protein malfunction
cellular basis of life – active transporter proteins use ATP to move substances against concentration gradient
tissues chapter – collagen fibers in connective tissues
nervous system chapter – function of the blood-brain barrier

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

Zydus Lifesciences Sentynl Gets USFDA Approval for ZYCUBO for Menkes Disease First Approved Therapy in United States – CNBC TV18

The US drug regulator approval is backed by positive clinical data showing a nearly 80% reduction in the risk of death in patients who received early treatment with ZYCUBO®, compared with an untreated external control group.

The article states that the newly-approved drug, Zycubo, is for the treatment of X-linked Menkes disease that is characterized by impaired copper transport.

So, Why Do I Care?? Menkes disease affects about 3000 children yearly in the USA. Most children die by the age of three, and that is the best evidence that treatment attempts have not been successful in fighting this disease. The relatively simple drug, Zycubo, by simple injection has proven successful in reducing disease severity and increasing survival to past age 6. This gives hope for the patients and the parents, and opens the door to future treatments that may be even more effective.

Plain English, Please!!! First, let’s talk about why copper is important for our bodies. Copper is a cofactor for several enzymes. A cofactor is a small atom or molecule that change the active site of the enzyme to make the enzyme more efficient. Picture the enzyme as a hand drill. The hand drill cannot work without a drill bit, that twisting piece of steel that has to be inserted into the hand drill. In this case the drill bit is the cofactor. One such copper-dependent enzyme, superoxide dismutase, removes harmful oxidizing chemicals from the cells. When this enzyme is disabled by copper deficiency, the neurons lower their activities leading to the deterioration of the nervous system we see in Menkes disease. Another enzyme, lysine oxidase, cross-links, strengthens collagen fibers, and when this enzyme is disabled by copper deficiency, weak collagen fibers are created leading to the weakened aorta and bones in Menkes disease.

Second, let’s talk about the nature of the genetic mutation in Menkes disease. When we think about copper deficiency, first we think about the possible deficiency of absorption from the small intestine. Copper absorption from the small intestine

Can we train the body’s immune system to fight melanoma?

By admin

On December 29, 2025

In integumentary system, lymphatic and immune system

Teachable moment in classrooms:

integumentary system chapter – location and function of melanocytes in skin
lymphatic and immune system chapter – the role of T lymphocytes (T cells) in the immune defense reaction
lymphatic and immune system chapter – mechanism of cell killing by cytotoxic T cells

The news item: Recently this report appeared online:

Patient is first treated with drug newly OK’d for melanoma

A Stanford Medicine melanoma patient is first in the nation to receive a cell-based therapy the FDA has approved for treating solid tumors.

The article informs us that a new therapy called “lificel” is being employed to treat patients with metastasized melanoma. The therapy includes removing a portion of the melanoma, extracting T cells from the tumor, stimulating the T cells to multiply into the millions, and infusing the new T cells into the patient.

So, Why Do I Care?? There are about 1.4 million people in the US alone living with melanoma, and the yearly new diagnosed cases are over 100,000. There are about 8,000 deaths from melanoma yearly. The metastasized stage of melanoma has a 5-year survival rate of about 20%. It is important to evaluate new therapies, because we want to increase the survival rate.

Plain English, Please!!! First, let’s talk about what metastasized melanoma is. Normally melanocytes reside in the epidermis layer of the skin where they produce the dark substance called melanin which protects the cells from UV light. When melanocytes start to divide uncontrollably, a cancer called melanoma forms. Melanomas have the tendency to release clumps of cancer cells, and those clumps spread through lymphatic vessels and grow into new cancer lump. Those new cancer lumps are called metastasis. Traditional chemotherapy drugs have been unable to kill off metastasized melanomas.

Second, let’s talk about how our immune system fights melanoma. Whenever cancer cells form, they produce modified proteins and sometimes new proteins,

Can we fight long-Covid by slowing scar tissue formation?

By admin

On November 27, 2025

In cellular basis of life, respiratory system, tissues

Teachable moment in classrooms:

tissues chapter – elastin and collagen fibers in connective tissues
respiratory system chapter – microscopic structure of alveoli
respiratory system chapter – changes in lung volume during ventilation
cellular basis of life chapter – general action of receptors on cell surface

The news item: Recently the following article appeared online:

Overactive genes contribute to long COVID lung fibrosis

A handful of overactive genes that regulate the immune response cause debilitating lung fibrosis, researchers find.

The article describes research that identified interleukin 6, CD47 and pJUN genes that make COVID-19 survivors’ lungs resemble the lungs with pulmonary fibrosis. The article also states that those three genes are active in scar formation, and that in mice the fibrosis was stopped by blocking interleukin 6 and CD47 action.

So, Why Do I Care?? Currently, approximately 23 million people in the US have long-COVID (defined by having disease symptoms longer than 3 months after the initial infection). Many of these people have respiratory symptoms such as debilitating shortness of breath and difficulty breathing. Research into the causes into the molecular details of the chronic fibrosis might lead to remedies that greatly improve the quality of life of long-COVID patients.

Plain English, Please!!! Let’s talk about what the nature of the fibrosis is seen in the lungs of long-COVID patients. In the walls of alveoli, away from the respiratory membrane, there is a layer of connective tissue normally dominated by the stretchable elastic fibers. In lung fibrosis the elastin fibers are degraded and replaced with collagen fibers that are not stretchable. The cells that make the connective tissue are called fibroblasts. The increased volume of collagen-rich connective tissue and increased number of fibroblasts is the hallmark of fibrosis we observe in the lungs of long-COVID patients. Apparently, this process is similar to scar formation in the skin.

Second, let’s talk about how fibrosis limits lung function. The accumulation of fibrotic tissue in the lung doesn’t affect the gas exchange process in the alveoli, but, rather, it makes ventilation more difficult.

How can a radioactive infusion chase down metastatic prostate cancer cells?

By admin

On October 24, 2025

In cellular basis of life, lymphatic and immune system, reproductive system, urinary system

Teachable moment in classrooms:

cellular basis of life chapter – location of transmembrane proteins
cellular basis of life chapter – endocytosis moves large number of molecules into the cell
urinary system chapter – structures of the male urethra
male reproductive system chapter – structure and function of the prostate
lymphatic and immune system chapter – anatomy of lymphatic vessels

The news item: Recently this report appeared online:

A new approach to prostate cancer offers patients more time and energy

John Grim fought prostate cancer for six years. He did radiation. He did hormone therapy. He did chemotherapy. It felt like a losing battle. The West York man lost 50 pounds. He felt weak and exhausted. The cancer spread to his bones, causing a tumor in his spine.

The article states that a prostate cancer patient was given 6 months to live because his cancer metastasized to his bones. Pluvicto treatment extended his life expectancy, allowed him to continue to work, lowered his PSA levels to 22 from 491 and restored his body weight. The article also states that the medication is radioactive, and it seeks out and kills the prostate cancer cells.

So, Why Do I Care?? In the US alone prostate cancer develops in more than 300000 people each year, and, according to the National Cancer Institute, it causes over 35000 deaths. So, developing new approaches to kill prostate cancer cells are always welcome. This is especially the case when it comes to prostate cancer cells that spread over the body.

Plain English, Please!!! First, let’s talk about what the prostate is. The prostate gland (or prostate) is a cherry sized gland wrapped round the male urethra. The prostate functions as a gland producing a secretion that will be incorporated into the semen. The gland itself is mostly epithelial tissue, and is a site of frequent cancer formation. Both the normal and the cancerous cells of the prostate have in their cell membranes transmembrane proteins; these proteins sticks out of the cell just like the fuzz sticks out from a tennis ball. However, the prostate cancer cells have unique transmembrane protein called the Prostate Specific Membrane Antigen, or PSMA.

Second, let’s talk about what metastasis is. Some cancer cells lose their connection to the mass of growing cancer cells, and those detached cells enter the lymphatic capillaries, and travel throughout the

Can we really replace an damaged iris with a silicone one in the human eye?

By admin

On September 28, 2025

In special senses, tissues

Teachable moment in classrooms:

tissue chapter – characteristics and locations of smooth muscle
special senses chapter – structures inside the eyeball
special senses chapter – location of the iris and the action of smooth muscle to change pupil diameter

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

Independence woman regains sight after first-of-its-kind surgery in Missouri

In 2010, Jennifer Sanders suffered an orbital globe rupture which destroyed 95% of the iris in her right eye.

The article states that a woman whose eye ruptured in an accident suffered from poor vision and light sensitivity because of a destroyed iris. An artificial iris implanted into her eye resulted in much improved vision.

So, Why Do I Care?? In addition to trauma-caused damage of the iris, about 1% of cataract surgeries damage the iris, and there is a developmental disorder called aniridia that results in the underdevelopment of the iris. Thus, there are tens of thousands of people who suffer from the absence or malfunctioning of the iris. Poor vision affects the ability to learn in school, to get a job, to drive a car, among other things, so it is important to seek out solutions for these conditions.

Plain English, Please!!! First, let’s talk about the location and function of the iris. The iris is a flat, thin ring inside the eye. For the shape just think about a donut that somebody sat on. The forward-looking surface of the “flattened donut” is the visible, colored part of the iris; this gives us the color of the eye. The backward-looking surface of the iris is made up of a thin layer of smooth muscle. The circle-shaped opening in the “flattened donut” is the pupil where light passes through towards the deeper portion of the eye. Because of the action of the smooth muscle, the pupil can be made wider or narrower. A narrow pupil prevents large amount of light entering the eye as that light would overload the photoreceptors in the retina. A wide pupil allows more light into the eye in a dim environment, so the photoreceptors can receive enough light for producing visual experience.

Second, let’s talk about the implant itself. The implant is made of silicone, and shaped like the biological iris. It is placed into its normal location, immediately in front of the lens. Because silicone doesn’t

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

By admin

On August 25, 2025

In lymphatic and immune system

Teachable moment in classrooms:

cellular basis of life chapter – DNA specifies protein structure
blood chapter – role of red bone marrow in hemopoesis
immune system chapter – development of T and B cells and their role in the immune response
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 a surgical implant in the heart prevent blood clot formation during atrial fibrillation?

By admin

On July 27, 2025

In cardiovascular system

Teachable moment in classrooms:

heart chapter – description of blood flow through the chambers of the heart
blood chapter – mechanism of blood clotting
hemodynamics chapter – connection of atria to systemic veins and systemic arteries

The news item: Recently the following report appeared online:

Durham VA Performs Second Watchman Procedure in North Carolina, First in VISN 6 | VA Durham health care | Veterans Affairs

On August 21, 2023, the Durham VA Health Care System achieved a significant medical milestone as it became the second hospital in North Carolina and the first facility in VA’s Mid-Atlantic Health Care Network to perform the Watchman FLX Left Atrial Appendage Closure Device procedure.

The article describes the first implantation of the Watchman FLX Pro device for left atrial appendage closure, and that the device is used to reduce the incidence of stroke in patients with atrial fibrillation who can not tolerate long-term use of blood thinners. The article also describes atrial fibrillation as a form of arrhythmia.

So, Why Do I Care?? There are over 10 million Americans with atrial fibrillation, and all of them have an increased risk of stroke. Because strokes can have debilitating consequences, it is important to prevent atrial fibrillation or stop the process of blood clot formation. While pacemakers and blood thinners serve to prevent atrial fibrillation in most people, in patients who cannot tolerate long-term blood thinner treatment other treatment alternatives must be used.

Plain English, Please!!! First, let’s talk about the connection between stroke and the atria of the heart. A stroke is a consequence of a blood clot blocking blood flow through an artery in the brain. During atrial fibrillation the muscle of the atria shivers, and the ejection of blood from the atria slows down. Think about when your teeth chatter in the cold. Your jaw muscles shiver and cannot create force. Similarly, the atria cannot create force to push out blood. Blood clots form with ease in such very slowly flowing blood. The critical location for the formation of blood clots can be pinpointed to the appendage of the left atrium. From there normal blood flow takes the blood clots from the left atrium to the arteries of the brain.

Second, let’s talk about the atrial appendage. While the atrium is a chamber shaped like a wide-open cave, the appendage is shaped like a pocket of a pita bread. The opening of the pocket is connected to the

How can a weight-loss drug fight sleep apnea?

By admin

On June 27, 2025

In muscular system, nervous system, respiratory system

Teachable moment in classrooms:

respiratory system chapter – anatomy of the upper airways
muscular system chapter – anatomy of the muscles of the tongue and pharynx
nervous system chapter – location of satiety center in the hypothalamus

The news item: Recently the following report appeared online:

FDA approves weight loss drug Zepbound for sleep apnea

Zepbound, Eli Lilly’s weight loss drug, can now be used to treat obstructive sleep apnea in adults with obesity, the FDA said.

The report states that 39 million adults with obesity in the USA might benefit from this drug treatment. Studies showed that Zepbound significantly reduced the obstruction events in patients. The article also provides a brief description of apnea events, and alternative treatment methods of sleep apnea.

So, Why Do I Care?? Sleep apnea, or more precisely, obstructive sleep apnea, is a sleep disorder that affects millions of adults in the US who suffer from obesity. Those people are not just losing sleep, but are at higher risk for several cardiovascular diseases, and for daytime sleepiness. While there are limitations (such as side effects) to the wide use of this drug treatment, it adds to the list of possible treatment options physicians can subscribe.

Plain English, Please!!! First, let’s talk about sleep apnea. Apnea is a brief closure of the airways where the closure stops air from getting into the lungs. The lower portion of our airways have solid cartilage framework (trachea, bronchi), so narrowing rarely occurs; it is always open, like a steel pipe. However, in the upper airways (mouth, soft palate) we have muscles that surround those airways, and the inappropriate relaxation of the muscles can lead to closure of the upper airway; imagine putting on a sock: it’s easy when we open it up with our fingers, but it’s harder to put our toes through it when the sock is collapsed on the floor. The loss of oxygen flow awakens the person, and repeated instances of apnea leads to poor quality sleep.

Second, let’s talk about throat muscles. Skeletal muscles in the throat (anatomically called pharynx) and in the soft palate (by specific names: the tensor palatini, levator palatini muscles), and in the tongue

Can we really get pneumonia just by inhaling water mist?

By admin

On May 24, 2025

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

Teachable moment in classrooms:

microbiology – Legionella bacterium
lymphatic and immune system chapter – development and role of macrophages in immune defense
respiratory system chapter – cells that make up the alveoli
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 use gene therapy to prevent hearing loss?

By admin

On April 14, 2025

In cellular basis of life, special senses

Teachable moment in classrooms:

cellular basis of life chapter – concept of one gene, one protein
cellular basis of life chapter – concept of gene mutation leading to protein malfunction
cellular basis of life – cells can die through programmed cell death
special senses chapter – regions of the hearing apparatus
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