Are engineered organs finally becoming reality in medicine?

 The concept behind tissue engineering is simple: grow the patient’s stem cells in the laboratory, add them to a scaffold material, and you have a laboratory-grown organ. But few patients have benefited from this technology so far. Could change be on the horizon?

Scientific studies are frequently hailed as bringing novel, breakthrough treatments to patients. But the stark reality is that a long road must be travelled to turn a discovery in the laboratory into a viable clinical option.

For patients with severe gastrointestinal problems, new solutions are sorely needed; current medical treatments are marred with problems.

And complications such as this affect many people. For instance, babies with short bowel syndrome have a small intestine that is too short, making it unable to absorb nutrients properly. This condition affects around 25 in 100,000 newborns per year in the United States and can leave them with lifelong complications.

Short bowel syndrome can also occur when part of the intestine has to be removed due to cancer or other diseases.

Also, when the anal sphincter becomes damaged during childbirth – as a result of either cancer surgery or old age – patients can experience fecal incontinence. As many as 26 percent of women are reportedTrusted Source to experience fecal incontinence after vaginal birth.

To address these problems, a research team from the Wake Forest Institute for Regenerative Medicine in Winston Salem, NC, has been developing new therapies for both anal sphincter injuries and short bowel syndrome.

But what is the likelihood of these new therapies ever reaching the patients, many of whom are in desperate need of better treatment options?

Tissue-engineered bowel

Khalil N. Bitar, Ph.D., a professor of regenerative medicine, explains the team’s approach, saying, “Our goal is to use a patient’s own cells to engineer replacement tissue in the lab for devastating conditions that affect the digestive tract.”

The small intestine is a complicated tissue. It consists of muscle cells that are essential for the contraction and forward propulsion of the food, as it moves through the gut. These cells must be aligned in a precise way to allow contraction to happen. Nerves are essential to stimulate the muscle cells to contract.

Similarly, in the sphincter, both muscle and nerve cells need to work closely together for normal function. This co-operation between different cells is one of the biggest challenges in tissue engineering. Although cells naturally grow and work together in the body, different cells are mostly grown in isolation in the laboratory.

Dr. Bitar’s team has spent years developing a precise method that allows them to grow muscle cells that are precisely aligned in one direction, and connect with nerve cells when they are added to the cell culture a few days later.

In a recent paper in published in Tissue Engineering Part C: Methods, the researchers transferred sheets of both cell types to small hollow tubes, which would make up the structure of the small intestine.

The tubes were then implanted into the lower abdomen of rats for 4 weeks, to allow blood vessels to infiltrate the structure. After this acclimatization phase, the tubes were attached to the small intestine of the rats, where they stayed in place for 6 weeks.

Importantly, the researchers found that after this period, the cells of the lining of the gut, or epithelial cells – which are essential for nutrient uptake from food – had started to migrate into the tube.

They also found food in the tubes, indicating that digestion was taking place and that this food was actively being moved through the tubes.

“A major challenge in building replacement intestine tissue in the lab is that it is the combination of smooth muscle and nerve cells in gut tissue that moves digested food material through the gastrointestinal tract,” Dr. Bitar explains.

Source: Medical News Today

Eye lens regeneration from own stem cells: 'a paradigm shift in cataract surgery'

 A new study describes a pioneering new cataract treatment – tested in animals and in a small trial with human patients – where, after the cloudy lens is removed, the eye grows a new lens from its own stem cells.

The researchers – including teams from the University of California-San Diego (UCSD), Sun Yat-sen University in Guangzhou and Sichuan University, both in China – describe their new regenerative medicine approach in a paper published in the journal Nature.

The treatment was tested in 12 babies born with cataracts. It resulted in significantly fewer surgical complications than current treatments, say the researchers. Sight was improved in all 12 patients.

One of the study leaders, Kang Zhang, a professor of ophthalmology and chief of Ophthalmic Genetics at UCSD, says:

“We believe that our new approach will result in a paradigm shift in cataract surgery and may offer patients a safer and better treatment option in the future.”

Being born with a lens that is cloudy or shortly becomes so is rare, but it is a significant cause of blindness in children. Estimates suggest it affects around 3 out of 10,000 children, although this rate varies throughout the world.

The clouded lens stops light getting to the retina, resulting in significant loss of vision. Current treatments can be difficult and result in complications in very young patients. Most children need to wear glasses after cataract surgery.

Method uses stem cells in the eyes to grow new lens

In the new study, the team used the ability of stem cells to grow new tissue. They did not use the more common approach – where stem cells are taken out of the patient, grown in the lab and then put back in the patient. This method can introduce disease and raise the risk of immune rejection.

Instead, the team coaxed stem cells in the patients’ eyes to regrow the lenses. So-called endogenous stem cells are stem cells that are naturally already in place, ready to regenerate new tissue in the case of injury or some other problem.

In the case of the human eye, the endogenous stem cells – known as lens epithelial stem cells (LECs) – generate replacement lens cells throughout a person’s life, although production wanes with age.

Current approaches to cataract surgery remove LECs along with the faulty lens – any few that are left can generate some lens cells, but the growth is random and disorganized in infants, resulting in no useful vision, note the researchers.

The approach the researchers describe in their paper has two important differences to conventional cataract surgery: it leaves the lens capsule intact, and it stimulates LECs to form a new lens. The lens capsule is a thin membrane that helps give the lens its required shape to function.

Source: Medical News Today

Functional human body parts built using 3D-bioprinting technique

 In what has been hailed a breakthrough in regenerative medicine, scientists have developed functional ear, bone and muscle structures using 3D-bioprinting technology.

The research team, from the Wake Forest Baptist Medical Center in Winston-Salem, NC, say their novel technology – named the Integrated Tissue and Organ Printing (ITOP) system – and the resulting creations mark “an important advance” in growing replacement tissue and organs for patient transplantation.

Senior study author Dr. Anthony Atala, director of the Wake Forest Institute for Regenerative Medicine (WFIRM), and colleagues explain how they created the 3D-printed body parts in the journal Nature Biotechnology.

In recent years, 3D printing has emerged as a promising strategy for the growth of complex tissues and organs that can replicate those of the human body.

However, Dr. Atala and colleagues note that current 3D printers are unable to produce human tissues and organs that are strong enough to be transplanted in the body or that can survive following transplantation.

The team believes that their ITOP technology, however, could help overcome such problems.

Functional ear, bone and muscle created with ITOP

The researchers have spent the last 10 years developing the ITOP system.

The 3D-printing technology combines a biodegradable, plastic-like material and an optimized water-based gel. The plastic forms the shape of the 3D structure, while the gel contains tissue cells and encourages them to grow.

The 3D prints also consist of micro-channels, which act as a sponge to soak to up the body’s nutrients and oxygen after transplantation. This helps the structures survive as they develop a blood vessel system, which they need in order to function in the human body.

In their study, Dr. Atala and colleagues used the ITOP system to build baby-sized human ear structures – around 1.5 in – and implanted them beneath the skin of mice.

Within 2 months after transplantation, the ear structures – the shape of which were well maintained – had formed cartilage tissue and a system of blood vessels.

For comparison, previous research had shown that a 3D-printed tissue structure without a pre-existing blood vessel system needed to be smaller than 200 microns (0.007 in) in order to survive in the human body.

“Our results indicate that the bio-ink combination we used, combined with the micro-channels, provides the right environment to keep the cells alive and to support cell and tissue growth,” says Dr. Atala.

The researchers also used the ITOP system and human stem cells to build jaw bone fragments, which the team notes were the size and shape required for human facial reconstruction. Five months after being implanted in rats, the bone fragments had formed blood vessels.

Additionally, the researchers printed muscle tissue and implanted it in rats. The tissue had formed blood vessels and triggered nerve formation in only 2 weeks, and its structural characteristics were maintained.

Source: Medical News Today

What are stem cells and why are they important?

 The idea of a miracle cure and bodies healing themselves holds a particular fascination. Stem cell research brings regenerative medicine a step closer, but many of the ideas and concepts remain controversial. So what are stem cells, and why are they so important?

Stem cells are a type of cell that can develop into many other types of cell. Stem cells can also renew themselves by dividing, even after they have been inactive for a long time.

The human body requires many different types of cell to function, but it does not produce each cell type fully formed and ready to use. Instead, it produces stem cells that have a wide range of possible functions. However, stem cells need to become a specific cell type to be useful.

When a stem cell divides, the new cells may either become another stem cell or a specific cell, such as a blood cell, a brain cell, or a muscle cell.

Scientists call a stem cell an undifferentiated cell because it can become any cell. In contrast, a blood cell, for example, is a ‘differentiated’ cell, because it is already a specific kind of cell.

Stem cells in therapy

In some tissues, stem cells play an essential role in regeneration, as they can divide easily to replace dead cells.

Scientists believe that knowing how stem cells work may lead to possible treatments for conditions, such as diabetes and heart disease.

For instance, if someone’s heart contains damaged tissue, doctors might be able to stimulate healthy tissue to grow by transplanting laboratory-grown stem cells into the person’s heart. This could cause the heart tissue to renew itself.

Researchers on a small-scale study published in the Journal of Cardiovascular Translational Research tested this method.

The results showed a 40 percent reduction of the size of scarred heart tissue caused by heart attacks when doctors transplanted stem cells to the damaged area.

Doctors have always considered this kind of scarring permanent and untreatable.

However, this small study involved only 11 participants. This makes it difficult to tell whether the improvement in heart function resulted from the transplantation of stem cells or whether it was due to something else.

For example, all of the transplants took place while the individuals were undergoing heart bypass surgery, so it is possible that the improvement in heart function was due to the bypass rather than the stem cell treatment.

To investigate further, the researchers plan to do another study. This study will include a control group of people with heart failure who undergo bypass surgery but who do not receive the stem cell treatment.

Another investigation, published in Nature CommunicationsTrusted Source in 2016, has suggested that stem cell therapies could be the basis of personalized diabetes treatment.

In mice and laboratory-grown cultures, researchers successfully produced insulin-secreting cells from stem cells derived from the skin of people with type 1 diabetes.

Jeffrey R. Millman, assistant professor of medicine and biomedical engineering at Washington University School of Medicine and first author, says:

“In theory, if we could replace the damaged cells in these individuals with new pancreatic beta cells — whose primary function is to store and release insulin to control blood glucose — patients with type 1 diabetes wouldn’t need insulin shots anymore.”

Jeffrey R. Millman

Millman hopes that these stem cell-derived beta cells could be ready for research in humans within 3 to 5 years.

“What we’re envisioning is an outpatient procedure in which some sort of device filled with the cells would be placed just beneath the skin,” he said.

Stem cells could have vast potential in developing new therapies.

Stem cells in drug development

One way that scientists use stem cells at the moment is in developing and testing new drugs.

The type of stem cells that scientists commonly use for this purpose are called induced pluripotent stem cells.

These are cells that have already undergone differentiation, but which scientists have genetically “reprogrammed” using viruses, so they can divide and become any cell. In this way, they act like undifferentiated stem cells.

Scientists can grow differentiated cells from these pluripotent stem cells to resemble, for instance, cancer cells. Creating these cells means that scientists can use them to test anti-cancer drugs.

Researchers are already making a wide variety of cancer cells using this method. However, because they cannot yet create cells that mimic cancer cells in a controlled way, it is not always possible to replicate the results precisely.

Source: Medical News Today

What's to know about DiGeorge syndrome?

 DiGeorge syndrome is a chromosomal disorder that typically affects the 22nd chromosome. Several body systems develop poorly, and there may be medical problems, ranging from a heart defect to behavioral problems and a cleft palate.

The condition is also known as 22q11.2 deletion syndrome. Around 90 percent of people with the condition have a small deletion on the 22nd chromosome at the q11.2 location.

This deletion is now known to be responsible for several previously-named syndromes that now all fall under the 22q11.2 deletion syndrome.

Other names include velocardiofacial syndrome, conotruncal syndrome, Shprintzen syndrome, and CATCH22.

DiGeorge syndrome is thought to affect 1 in 4,000 people. However, the features vary widely. As a result, underdiagnosis and misdiagnosis are likely to occur.

Fast facts on DiGeorge syndrome

Here are some key points about DiGeorge syndrome.

• DiGeorge syndrome is typically referred to as 22q11.2 deletion syndrome, as this most accurately reflects its origins
• The deletion of genes from the 22nd chromosome usually occurs randomly, and the condition is rarely inherited.
• The symptoms depend on the organ system that is affected.
• DiGeorge syndrome is often diagnosed with a specific blood test.
• Treatment will depend on the symptoms and the systems affected.

Causes

DiGeorge syndrome results from the deletion of the 22q11.2 segment in one of the two copies of chromosome 22. It affects approximately 30 to 40 genes.

Many of these genes are not yet fully understood.

The syndrome usually starts as a random event during fertilization, either on the maternal or paternal side. It may happen during the time of fetal development.

Most cases are not inherited, and there is rarely a family history of the condition.

However, in around 10 percent of cases, it is passed from a parent to a child.

Symptoms

If a child has DiGeorge syndrome, parents or caregivers may notice that they have:

• delays in learning to walk or talk and other developmental and learning delays
• hearing and vision problems
• mouth and feeding problems
• short stature
• frequent infections
• bone, spine, or muscle problems
• unusual facial features, including an underdeveloped chin, low-set ears, and wide-set eyes
• a cleft palate or other palate disorders

Heart problems are most likely to affect the aorta.

They may include:

• ventricular septal defect, a hole between the lower heart chambers
• truncus arteriosus, a missing heart vessel
• tetralogy of Fallot, a combination of four abnormal heart structures

The syndrome can involve a wide range of signs and symptoms.

They include:

• respiratory difficulties
• mouth, arm, throat or hand spasms
• frequent infections
• delayed growth
• poor muscle tone
• a higher risk of some behavioral problems, such as ADHD
• a higher risk later in life of some psychiatric disorders such as schizophrenia
• autoimmune diseases such as idiopathic thrombocytopenia purpura, autoimmune hemolytic anemia, autoimmune arthritis and autoimmune thyroid disease
• parathyroid gland abnormalities, usually hypoparathyroidism, causing abnormal calcium and phosphorus metabolism and sometimes seizures
• thymus gland abnormalities, such as a small, underactive thymus
• blue skin color (cyanosis), due to poor circulation caused by heart defects

Other symptoms may include hearing impairment, visual abnormalities, and altered kidney function

Due to the significant variability of DiGeorge syndrome, the type and severity of symptoms are typically determined by the organ system affected.

DiGeorge syndrome can become evident at birth, in infancy or during early childhood.

Diagnosis

DiGeorge syndrome is most commonly diagnosed with a blood test called a FISH analysis (Fluorescent In Situ Hybridization).

A health care provider is likely to request a FISH analysis if a child has symptoms that may indicate DiGeorge syndrome, or if there are signs of a heart defect. Certain types of heart defect are strongly associated with the condition.

Source: Medical News Today

'Leaky' blood-brain barrier may contribute to schizophrenia

 

• The blood-brain barrier shields the central nervous system, which comprises the brain and spinal cord, from the immune system.
• In a new study, researchers have hypothesized that if this barrier is compromised, it could cause inflammation in the brain, which may, in turn, trigger schizophrenia.
• To investigate this relationship, they used cells isolated from healthy individuals and from people with a rare genetic disorder that increases the risk of schizophrenia.
• The blood-brain barriers derived from cells of the latter group were more ‘leaky’ and produced more inflammatory molecules.

Schizophrenia is a psychiatric condition that is characterized by “positive” symptoms, such as hallucinations and delusions, and “negative” symptoms, such as social withdrawal and apathy.

For almost a century, scientists have speculated about a possible link between the immune system and schizophrenia.

Several lines of evidenceTrusted Source suggest that the inflammation provoked by a viral infection, either before birth or during childhood, could trigger the condition in adulthood.

Some studiesTrusted Source have also found changes in the blood-brain barriers of people with schizophrenia.

The blood-brain barrierTrusted Source comprises the tightly packed layer of cells that line the blood vessels in the brain and spinal cord. It prevents blood-borne immune cells from gaining entry to the central nervous system.

This is sometimes known as conferring “immune privilege” on the brain — in other words, protecting it from harmful inflammation.

Researchers at the University of Pennsylvania’s School of Veterinary Medicine in Philadelphia wondered whether a compromised blood-brain barrier in people with a rare genetic disorder known as DiGeorge syndrome or 22qDS, a genetic deletion syndrome, could be responsible for their increased risk of schizophrenia.

People born with the condition have a 1 in 4 risk of developing schizophrenia later in life. This is compared with an overall risk of schizophrenia of around 1 in 100 in the wider adult population.

People with 22qDS have a small section of DNA missing from chromosome 22 of their genome.

Leaky barrier

To test their hypothesis, the researchers isolated cells from people with DiGeorge syndrome and schizophrenia and from healthy matched controls. They then turned these cells into pluripotent stem cells, which can develop into any type of cell in the body.

In the laboratory, they transformed the stem cells into the type of cells that line the blood vessels in the brain. These are the cells that together function as the blood-brain barrier.

The researchers found that the cells derived from people with DiGeorge syndrome and schizophenia created a less effective, more “leaky” barrier than those derived from the healthy controls.

In addition, the cells produced more of a type of molecule that promotes inflammation. This allowed more immune cells to penetrate the barrier.

The researchers obtained similar results when they investigated the integrity of the blood-brain barrier in a mouse model of DiGeorge syndrome.

Finally, they performed the same tests in postmortem brain tissue from three people who had DiGeorge syndrome and from three age-matched healthy controls.

They found evidence that the effectiveness of the actual blood-brain barrier of these people had indeed been compromised.

The research, which doctoral student Alexis Crockett led, now appears in the journal Brain.

Other brain disorders

The study authors speculate that a compromised blood-brain barrier may interact with environmental or other genetic risk factors to increase the likelihood not only of psychosis but also of other brain disorders in the case of people with DiGeorge syndrome.

“[W]e think these findings could also be used to understand how the blood-brain barrier and neurological processes impact not only schizophrenia but mental disorders at large,” says senior study author Prof. Jorge Iván Alvarez, from the School of Veterinary Medicine.

In 2019, Medical News Today reported on a study that suggested that a faulty blood-brain barrier in aging mice triggered brain inflammation and cognitive impairment in the animals.

Prof. Alvarez speculates that further research into the link between inflammation and neuropsychiatric disease could lead to new therapies for these conditions.

Anti-inflammatory and immunotherapy drugs have already shown some promiseTrusted Source as treatments for schizophrenia, alongside standard treatments.

Source: Medical News Today

Antipsychotic drugs may provide COVID-19 protection

 

• Antipsychotic drugs could have a protective effect against COVID-19.
• People treated with these drugs may have a lower risk of contracting the new coronavirus.
• People using these drugs may be more likely to experience a milder form of COVID-19 if they do get the virus.
• Antipsychotic drugs may reduce the activation of genes involved in inflammatory and immunological pathways associated with severe SARS-CoV-2 infections.

A group of researchers — led by scientists from the Mental Health Unit of the Virgen del Rocio University Hospital in Seville, Spain — have found that antipsychotic drugs could have a protective effect against COVID-19.

People treated with these drugs may have a lower risk of contracting the virus or may have milder symptoms if they do get the virus.

Some of the findings appear in the journal Schizophrenia Research.

“These are very interesting findings that reflect a clinical reality where we see few patients with severe COVID-19, despite the presence of various risk factors,” says Manuel Canal Rivero, a clinical psychologist and lead author of one of the two papers.

Vulnerable group for COVID-19?

Many researchers have spent the past year studying whether or not individuals with severe mental health conditions might be more likely to contract SARS-CoV-2 and develop severe symptoms from COVID-19.

In the issue of Schizophrenia Bulletin published April 28, 2020, a team from the Centre for Addiction and Mental Health in Toronto, Canada, discussed why they believed people with schizophrenia and related disorders were likely to have a higher risk of contracting SARS-CoV-2.

They pointed to features of the condition, such as experiencing hallucinations and possessing a lower awareness of risk. They added that living in crowded settings, such as congregate housing or prisons, where social distancing is difficult, may increase the risk of contracting SARS-CoV-2.

The team wrote that they believed individuals with schizophrenia and related disorders would be more likely to have poor outcomes from COVID-19. This is because they are more likely to have poor physical health, are disadvantaged socioeconomically, and experience stigma and social isolation. Scientists believe that these factors likely elevate mortality from COVID-19.

People with severe mental illness are more likely to have conditions such as cardiovascular disease, diabetes, and chronic respiratory disease. The researchers also pointed out that people with schizophrenia are more likely to smoke, a habit that several studies have linked to developing a more severe form of COVID-19.

Another recent study published in JAMA PsychiatryTrusted Source reported that individuals with schizophrenia are at a significantly increased risk of dying from COVID-19.

In contrast, a South Korean study that appears in The Lancet PsychiatryTrusted Source found that a mental illness diagnosis has no associations with an increased likelihood of testing positive for COVID-19. The study also concluded that people with a severe mental illness had only a slightly higher risk for severe clinical outcomes from COVID-19.

Therefore, “Previous investigations to assess the prevalence of COVID-19 in [the population with severe mental health conditions] have yielded to inconsistent results,” the Seville researchers wrote.

Lower risk

For the new study, which appears in Schizophrenia Research, the research team examined data for a representative Spanish population of 557,576 adults.

Of these, 23,077 (4.1%) tested positive for COVID-19 between February and November 2020. There were 1,953 (8.5%) hospitalizations related to COVID-19 and 254 deaths (1.1%).

Among 698 people with severe mental health conditions who received treatment with long-acting injectable (LAI) antipsychotic treatment, 9 (1.3%) tested positive for COVID-19. Only one member of that group displayed COVID-19 symptoms. None had to go to the hospital, and none died due to COVID-19.

This suggests people treated with these drugs may have a lower risk of acquiring a SARS-CoV-2 infection and may be more likely to have a milder form of the disease if they do get the virus, say the researchers.

“The number of COVID-19 patients is lower than expected among this group of people, and in cases where a proven infection does occur, the evolution is benign and does not reach a life threatening clinical situation,” says Canal Rivero. “These data as a whole seem to point to the protective effect of the medication.”

Source: Medical News Today

Lack of trial data exacerbates COVID-19 vaccine inequality

 

• According to an opinion piece in the BMJ, inequalities in the supply of vaccines to middle- and low-income countries have been compounded by a lack of access to data from clinical trials.
• The author warns that this lack may stoke anti-vaccine conspiracy theories.
• He argues that poor vaccine supply and public skepticism are likely to fuel the spread of new, more dangerous strains of the virus.

In the past month, more than 1,000 scientific, public health, and legal experts have joined a call to global leaders to ensure access to COVID-19 vaccines for low- and middle-income countries.

“The COVID-19 pandemic will not be over for us until it is over for everyone,” the authors wrote in an open letter.

Now, a health expert in Argentina argues in the BMJ that, on top of supply problems, Latin American countries face an additional challenge due to a lack of publicly available data about vaccines from Russia and China.

Dr. Juan Víctor Ariel Franco, the editor-in-chief of BMJ Evidence-Based Medicine and a lecturer in research methodology, family medicine, and public health at the Instituto Universitario of the Hospital Italiano de Buenos Aires, in Argentina, points out that high-income countries have not had to face this difficulty.

“The lack of publicly available data on these vaccines adds another layer of inequality: We are administering vaccines to millions of individuals in Latin American countries for which we have little to no information beyond press releases,” he writes.

If the virus is allowed to spread unchecked in low- and middle-income countries, Dr. Franco warns, it will mutate into variants that evade the immune protection from vaccines.

Rollout of COVID-19 vaccines

Despite extreme political, economic, and social difficulties in Latin America, the rollout of COVID-19 vaccines started at the end of 2020 due to direct agreements between national governments and vaccine manufacturers.

Dr. Franco notes that the Pfizer-BioNTech and Oxford-AstraZeneca vaccines have been generally well-received because regulators such as the Food and Drugs Administration (FDA) and European Medicines Agency provided free access to the evidence on which they based their approvals.

However, he highlights an initial lack of information about the phase 3 trial of the Russian Sputnik V vaccine, which was distributed in Argentina between December 2020 and January 2021.

At the time, the only publicly available data was in a press release from the Gamaleya Research Institute of Epidemiology and Microbiology, in Moscow, which had developed the vaccine, and a two-page report from the Argentinian medicines regulatory agency.

Dr. Franco says that the publication of an interim analysis of the results in The LancetTrusted Source in early February 2021 allayed some concerns, but the full protocol for the trial has still not been released.

Vaccines from China

With the second wave of COVID-19 sweeping across the region and variants spreading unchecked, Dr. Franco notes that regulators in Latin America have now approved two more vaccines, made by Sinopharm and Sinovac, in China.

But they did this in the absence of publicly available technical reports on phase 3 clinical trials or published data, he writes.

Dr. Franco points out that there is “little or no information” about the effects of these vaccines in particular subgroups of people or whether these vaccines are as effective against variants.

This is particularly important, he says, given that their efficacy against the original strain could be as low as 50%Trusted Source.

“This would not be acceptable for high-income countries who sign deals with the main manufacturers and align their regulators’ power to guarantee quality control and transparency in the approval process,” Dr. Franco writes.

He observes that this openness by the regulators in high-income countries is maintained “even in the most sensitive cases,” as with concerns about a possible link between the AstraZeneca vaccine and adverse events.

Source: Medical News Today

What is the latest research on autism?

 Doctors have defined autism spectrum disorder (ASD) as a neurobiological developmental condition that can impact communication, sensory processing, and social interactions. Although recent research has advanced the understanding of autism, there is much more to learn about the factors that influence this neurotype.

As of March 26, 2021, the Centers for Disease Control and Prevention (CDC) report that among 8-year-old children, one in 54Trusted Source are autistic. This number has increased from the one in 59 prevalence reported in previous estimates.

With autism rates on the increase, the scientific community has become all the more interested in uncovering the factors linked with autism.

Some scientists speculate that gene variantsTrusted Source cause autism, while others believe environmental factorsTrusted Source, such as exposure to toxinsTrusted Source, contribute to this neurotype. Still others theorize imbalances in the intestinal microbiomeTrusted Source may be at play.

The latest autism research includes investigations into factors associated with this neurotype, as well as genetic variants, gut biome imbalances, and neurological factors that may contribute to it.

In this Special Feature, Medical News Today examines the latest scientific discoveries and what researchers have learned about autism.

Exploring contributing factors

A multiyear study funded by the CDC is underway to learn more about factors potentially linked to autism.

The Study to Explore Early DevelopmentTrusted Source is a collaboration between six study sites in the United States. These sites are part of the Autism and Developmental Disabilities Research and Epidemiology network and focus on children aged 2–5 years.

One of the goals of the study is discovering what health conditions occur in autistic and neurotypical children and what factors are associated with the likelihood of developing ASD.

Another objective of the study is to differentiate the physical and behavioral characteristics of autistic children, children with other developmental conditions, and those without these conditions.

This ongoing research has already produced several published studies. The latest found an association between ASD and a mother’s exposure to ozone pollution during the third trimester of pregnancy.

Researchers also found that exposure to another type of air pollution called particulate matter during an infant’s first year also increased the likelihood of the infant later receiving a diagnosis of ASD.

Current research on genes

Other avenues of research on autism include investigations into gene variants that could play a role in the development of ASD.

A recent study analyzed the DNA of more than 35,584 people worldwide, including 11,986 autistic individuals. The scientists identified variants in 102 genesTrusted Source linked with an increased probability of developing ASD.

The researchers also discovered that 53 of the genes identified were mostly associated with autism and not other developmental conditions.

Expanding the research further, the team found that autistic people who carried the ASD-specific gene variantsTrusted Source showed increased intellectual function compared with autistic individuals who did not have the variants.

The gene variants the scientists identified mainly reside in the cerebral cortex, which is responsible for complex behaviors.

These variants may play a role in how the brain neurons connect and also help turn other genes on or off — a possible factor that may contribute to autism.

Investigating neurological factors

Biological research has unearthed some interesting findings linking certain types of cell malfunctions to ASD.

Scientists at the Lieber Institute for Brain Development in Baltimore, MD, discovered a decrease in the integrity of myelin, a protective sheath surrounding nerve cells in the brain, in mice with a syndromic form of ASD.

The study, published in Nature NeuroscienceTrusted Source, showed a gene variant-based malfunction in oligodendrocytesTrusted Source, which are cells that produce myelin.

This malfunction may lead to insufficient myelin production in the nerve cells and disrupt nerve communication in the brain, impairing brain development.

Using mouse models, researchers are now investigating treatments that could increase the myelination in the brain to see whether this improves ASD-associated behaviors that individuals may find challenging.

Source: Medical News Today