HEALTH DIALOGUE
Thursday, 6 September 2018
Monday, 24 July 2017
Child Treated For HIV At Birth Remains Virus-Free Years After Final Treatment
A South African boy, believed to have been infected with HIV around the time of his birth, has remained free of the virus for 8½ years after early treatment — renewing hope among scientists that such outliers may hold clues to help end the decades-old epidemic.
The case study, described by researchers before a presentation Monday at an international AIDS conference in Paris, suggests a paradigm shift in the treatment of those infected. It establishes that HIV may be controllable in some way other than a daily and lifelong regimen of antiretroviral drugs.
“This is really the first step toward HIV remission and a cure,” said Deborah Persaud, a virologist at Johns Hopkins Children’s Center in Baltimore. “Understanding the factors that came into play to lead to this outcome is really going to inform science.”
Out of the millions of children worldwide who are HIV-positive, the boy, now 9, is one of only three who have been identified by scientists as having the ability to stop the virus from resurging for an extended period of time.
Anthony Fauci, head of the National Institute of Allergy and Infectious Diseases, struck notes of both optimism and caution when speaking about him. Fauci described the child as being in “remission” rather than being cured. And while hoping the boy would never have an active infection in his lifetime, Fauci noted that HIV tends to hide in “funny places” and that it is “not entirely inconceivable” a small amount of the virus may remain in his body and start replicating again.
It is exciting to see this. It is encouraging to see a child going for such a long period of time without rebounding,” Fauci said. “But we don’t have the full answers to what this means yet.”
The first case of extended remission in a child was announced to great excitement in 2013. Startled researchers reported that a girl — who came to be known as the Mississippi baby — appeared to be “functionally cured” 23 months after stopping treatment. The celebration was premature, however: The virus returned shortly after that announcement, and the young girl had to be put back on medications. But her case brought to light the possibility of viral suppression in children and led to the funding of other research into the phenomenon.
The second case, reported in 2015, involved a French teen who underwent treatment from soon after birth to age 6 and whose blood continued to have undetectable levels of the virus for 12 years after stopping the drugs.
The South African boy came to the attention of researchers in 2008 through a larger study funded by the National Institutes of Health. It took place from 2005 to 2011 at hospitals near Johannesburg and Cape Town and involved nearly 400 HIV-positive babies.
Mark Cotton, a pediatric AIDS expert and one of the lead authors of the paper being presented Monday in Paris, explained that children were randomly put in one of three groups. One received the standard of care at the time, which was to start therapy only when the individual showed signs of becoming sick or evidence of a weakened immune system. The other two groups started treatment immediately after their HIV-positive status was confirmed, and stopped after 40 weeks or 96 weeks, respectively. The goal was to figure out whether early treatment was better than deferred treatment.
Cotton said the data appeared to show that children who had the virus rebound earlier had to go back on medication after a couple of weeks. But there was a huge surprise for subjects whose remission lasted longer, he said, with several children not needing to return for two or more years after 96 weeks of treatment.
For the 40-week treatment group, the average remission period was about 30 weeks; for the 96-week treatment group, it was about 70 weeks — although researchers caution that the results are still being analyzed and should be taken as very preliminary.
Yet the one boy is already considered a distinct outlier. Born to an HIV-positive mother, he was taken to one of the clinics in the study when he was about 8 weeks old. He began therapy when he had a relatively low viral load, and he took liquid antiretrovirals twice a day until he was about 48 weeks of age. By the time he was done treatment just before his first birthday, the viral load was undetectable, and year after year during follow-up visits, he continued to show no signs of an actively replicating virus.
One of the leading theories about how children in the study who had the longest remission might be different has to do with how their immune systems give them the power to suppress any rebound. Another factor may be that their very early treatment did not give the virus a chance to fully establish itself.
Healthdialogue.blogspot.com
https://www.washingtonpost.com/national/health-science/new-hope-for-hiv-cure-as-child-remains-virus-free-years-after-final-treatment/2017/07/23/6a4e41ac-6fd8-11e7-8839-ec48ec4cae25_story.html?utm_term=.9de945faebc0
A South African boy, believed to have been infected with HIV around the time of his birth, has remained free of the virus for 8½ years after early treatment — renewing hope among scientists that such outliers may hold clues to help end the decades-old epidemic.
The case study, described by researchers before a presentation Monday at an international AIDS conference in Paris, suggests a paradigm shift in the treatment of those infected. It establishes that HIV may be controllable in some way other than a daily and lifelong regimen of antiretroviral drugs.
“This is really the first step toward HIV remission and a cure,” said Deborah Persaud, a virologist at Johns Hopkins Children’s Center in Baltimore. “Understanding the factors that came into play to lead to this outcome is really going to inform science.”
Out of the millions of children worldwide who are HIV-positive, the boy, now 9, is one of only three who have been identified by scientists as having the ability to stop the virus from resurging for an extended period of time.
Anthony Fauci, head of the National Institute of Allergy and Infectious Diseases, struck notes of both optimism and caution when speaking about him. Fauci described the child as being in “remission” rather than being cured. And while hoping the boy would never have an active infection in his lifetime, Fauci noted that HIV tends to hide in “funny places” and that it is “not entirely inconceivable” a small amount of the virus may remain in his body and start replicating again.
It is exciting to see this. It is encouraging to see a child going for such a long period of time without rebounding,” Fauci said. “But we don’t have the full answers to what this means yet.”
The first case of extended remission in a child was announced to great excitement in 2013. Startled researchers reported that a girl — who came to be known as the Mississippi baby — appeared to be “functionally cured” 23 months after stopping treatment. The celebration was premature, however: The virus returned shortly after that announcement, and the young girl had to be put back on medications. But her case brought to light the possibility of viral suppression in children and led to the funding of other research into the phenomenon.
The second case, reported in 2015, involved a French teen who underwent treatment from soon after birth to age 6 and whose blood continued to have undetectable levels of the virus for 12 years after stopping the drugs.
The South African boy came to the attention of researchers in 2008 through a larger study funded by the National Institutes of Health. It took place from 2005 to 2011 at hospitals near Johannesburg and Cape Town and involved nearly 400 HIV-positive babies.
Mark Cotton, a pediatric AIDS expert and one of the lead authors of the paper being presented Monday in Paris, explained that children were randomly put in one of three groups. One received the standard of care at the time, which was to start therapy only when the individual showed signs of becoming sick or evidence of a weakened immune system. The other two groups started treatment immediately after their HIV-positive status was confirmed, and stopped after 40 weeks or 96 weeks, respectively. The goal was to figure out whether early treatment was better than deferred treatment.
Cotton said the data appeared to show that children who had the virus rebound earlier had to go back on medication after a couple of weeks. But there was a huge surprise for subjects whose remission lasted longer, he said, with several children not needing to return for two or more years after 96 weeks of treatment.
For the 40-week treatment group, the average remission period was about 30 weeks; for the 96-week treatment group, it was about 70 weeks — although researchers caution that the results are still being analyzed and should be taken as very preliminary.
Yet the one boy is already considered a distinct outlier. Born to an HIV-positive mother, he was taken to one of the clinics in the study when he was about 8 weeks old. He began therapy when he had a relatively low viral load, and he took liquid antiretrovirals twice a day until he was about 48 weeks of age. By the time he was done treatment just before his first birthday, the viral load was undetectable, and year after year during follow-up visits, he continued to show no signs of an actively replicating virus.
One of the leading theories about how children in the study who had the longest remission might be different has to do with how their immune systems give them the power to suppress any rebound. Another factor may be that their very early treatment did not give the virus a chance to fully establish itself.
Healthdialogue.blogspot.com
https://www.washingtonpost.com/national/health-science/new-hope-for-hiv-cure-as-child-remains-virus-free-years-after-final-treatment/2017/07/23/6a4e41ac-6fd8-11e7-8839-ec48ec4cae25_story.html?utm_term=.9de945faebc0
Saturday, 22 July 2017
10-year-old boy overeats due to rare genetic illness, weighs 88kg
- SOLA
Ten-year-old South African child, Caden Benjamin, cannot stop eating because of a rare genetic disorder he suffers from.
The disease leaves him with no option but to eat anything in sight, including rolls of toilet paper and dirt from the floor.
The rare condition is such that no matter how much he eats, he is never full.
Caden, from Standerton in South Africa’s Mpumalanga Province, was diagnosed with the disorder called Prader-Willi syndrome.
The condition means he has a constant desire to eat food, which can lead to dangerous weight gain, restricted growth and reduced muscle tone.
The 10-year-old currently weigh 88.9kg. Ideally, he should weigh between 18-40kg, doctors say.
His mother, Zola Benjamin, said: “At one point, Caden was eating toilet paper. He’d eat rolls of it. Actually, he’d eat any paper he would find in the house.
“If there’s nothing for him to eat, he’ll scrape together the dirt he finds on the floor and eat that.”
Prader-Willi syndrome is made worse by the fact that sufferers need less food than their peers because their bodies have less muscle and tend to burn fewer calories.
Zola added: “At three years old, he was 39.9kg and at that time, we didn’t know what was wrong with him.
“We went to a number of doctors and no one could tell us what was wrong and why he was gaining so much weight.”
Eventually, a doctor at the Steve Biko Academic Hospital in the city of Pretoria, in northern South Africa’s Gauteng Province, diagnosed Caden’s illness.
Zola said: “Normally, he would start off the day by eating four slices of cheese toast and then an hour later, he would drink Coke and eat leftover food from the night before.
“Then at lunch, he’d eat two large pieces of chicken. He’d eat hourly for the rest of the day.”
His weight began to spiral out of control and doctors became worried for his health, so they put him on a diet.
Zola has been forced to lock all her kitchen cabinets and her fridge and hide all the food in the house to stop Caden from gorging.
She said: “He’s really battling. I feel so terrible, but the doctors said that if I want to see my son alive, then he has to go on a diet.
“Each and every day is a battle. I have to check up on him all day and night.”
Caden struggles to move around and to even breathe because he is so overweight.
He also suffers from depression because he is unable to live like a normal 10-year-old boy.
Zola said: “Sometimes, he’ll just break down in tears and tell me he wants to go and play with the other children outside.
“But he is unable to do that and there’s no way I can help him.”
Monday, 17 July 2017
Kogi State: 2017 Flag-off of Maternal, Newborn and Child Health Week
Kogi State Government has pledged its unalloyed commitment to totally eradicate maternal mortality rate in the state. Governor Yahaya Bello made the remark at the flag off for May/June round of Maternal, New Born and Child Health week today in Government House.
Governor Yahaya Bello who was represented by the Secretary to the State Government, Mrs. Arike Folashade said health is a priority in the New Direction agenda which no doubt has made the government to commit huge resources in the health sector to ensure quality health service is delivered to the people as one of the major focal points in the five thematic areas of the present administration.
According to him, the survival of these young children is so important to the government, describing the children as the future and representative of the next generation and encourage mothers to breast feed their children properly. He assured that the state government will not relent in its effort to ensure that it delivers on its promises to the people In the area of health.
He referred to the 10million Naira medical expense of an indigent from Idah Local Government Area that was offset recently by his administration out of his genuine love for the people to have access to adequate healthcare. The Governor called on all Local Government Administrators, Traditional Rulers and Religious Bodies to support the programme and sensitise their subjects on the need to maximise the opportunity presented by the government and to comply with the objectives of the programme to ensure its set goals are achieved.
In her remarks, the Governor's wife, Hajia Rashidat Bello advised mothers to take advantage of all the free health care services provided by the government, stressing that her office has advocated and initiated various mother and child health sensitisation and educative programmes to lower the risk of mortal mortality rates.
Earlier, the Commissioner for Health, Doctor Saka Audu said the present administration under the leadership of Governor Yahaya Bello has been very active in the delivery of health dividends to the people of the state, adding that under Bello Health Intervention program, Free Medical Outreach targeted towards over 50, 000 patients recorded a huge success, free paediatric drugs were distributed to health facilities and tens of Kogites were sponsored for advanced medical attention home and abroad.
Doctor Saka said the health week was targeted at supplementing children from 6 to 59 months with vitamin A, conduct Nutritional Screening, HIV counselling and Test services and immunise children (0 to 12 months) with prevalent vaccine as well as, provide long lasting insecticidal nets, ante-natal care, family planning services, birth registration and the promotion of selected key household practices such as breastfeeding, complementary feeding and hygiene.
He added that the Maternal Newborn and Child Health week which is a week long programme will deliver health dividends to women and children in the state saying that the state government has not failed in its effort to ensure quality health care service is delivered to citizens and encouraged mothers to administer Vitamin A supplementation to their children often as it has the capacity to reduce child mortality by 30 percent if given regularly.
Speaking, the State Chairman of the Nigeria Medical Association, Doctor Tijani Goodwin said the present government has recorded giant strides since its inception in the areas of construction and renovation of health structures, provision of drugs and free medical outreach and amongst others and pledged the readiness of the association to partner with the ministry of health to ensure Kogi state health care indices is improved and for the government actualise its objective in the health sector.
The Chairman, House Committee on Health, Doctor Friday Ali expressed appreciation to the Governor for his immense support to health programmes in the state, and enjoined mothers of reproductive age to avail themselves of the opportunity in order to benefit from the project.
Also speaking, the representative of the World Health Organisation, Doctor Ningi Nuhu while calling on mothers to come out to benefit from the programme, he noted that the organisation in a deliberate attempt connects to a large number of population in-order to bridge the gap in health related issues and expressed optimising that the first of the exercise will be a success and called for the cooperation of the people.
THE BENEFICIAL EFFECTS OF BANANA AS A SOURCE OF POTASSIUM AND MAGNESIUM.
Potassium is a mineral that is essential for heart health, especially blood pressure control.
Yet despite its importance, most people are not getting enough potassium in their diet
Bananas are a great dietary source of potassium. One medium-sized banana (118 grams) contains 9% of the RDI.
A potassium-rich diet can help lower blood pressure, and people who eat plenty of potassium have up to a 27% lower risk of heart disease
Furthermore, bananas contain a decent amount of magnesium, which is also important for heart health.
Bananas Contain Powerful Antioxidants
Fruits and vegetables are excellent sources of dietary antioxidants, and bananas are no exception.
They contain several types of potent antioxidants, including dopamine and catechins
These antioxidants have been linked to many health benefits, such as a reduced risk of heart disease and degenerative diseases.
However, it is a common misunderstanding that the dopamine from bananas acts as a feel-good chemical in the brain.
In reality, dopamine from bananas does not cross the blood-brain barrier. It simply acts as a strong antioxidant instead of altering hormones or mood.
Bananas May Help You Feel More Full
Resistant starch is a type of indigestible carbohydrate found in unripe bananas, which functions sort of like soluble fiber in the body.
As a rule of thumb, you can estimate that the greener the banana is, the higher the amount of resistant starch it contains.
On the other hand, ripe (yellow) bananas contain lower amounts of resistant starch and total fiber, but proportionally higher amounts of soluble fiber.
Both pectin and resistant starch have been shown to have appetite-reducing effects and increase the feeling of fullness after meals.
Tuesday, 4 July 2017
*Working at night may* *interfere with DNA repair*
Night shift work has been associated with a variety of adverse health effects. New research adds to these, suggesting that the body’s ability to repair DNA damage may be inhibited by night shifts.
Working at night has been associated with a wide range of negative health effects, including cognitive impairment, metabolic disorders, and breast cancer.
Additionally, some studies have indicated that night shifts may increase a person’s risk of developing lung cancer and cardiovascular disease.
Now, new research examines how night shifts influence the body’s ability to repair its DNA. The first author of the study is Dr. Parveen Bhatti, of the Fred Hutchinson Cancer Research Center in Seattle, Washington.
The findings were published in the journal Occupational & Environmental Medicine.
Building on previous research
In a previous study, Dr. Bhatti and colleagues showed that sleeping during the day correlated with lower levels of 8-hydroxydeoxyguanosine (8-OH-dG), which is a chemical released as a byproduct by the body when it works to repair its own DNA.
The authors were therefore led to believe that these low levels of 8-OH-dG found in the urine may indicate the body’s impaired ability to repair its cellular damage.
They also hypothesized that the reduced levels of urinary 8-OH-dG may be due to the fact that our bodies produce less melatonin during day sleep compared with night sleep.
To further explore this idea, Dr. Bhatti and colleagues set out to examine whether night work also correlates with reduced urinary levels of 8-OH-dG.
The authors explain the motivation for their new research, saying, “If excretion of 8-OH-dG during night work among these subjects is also decreased relative to night sleep, it would provide additional support for our hypothesis that reduced melatonin among shift workers is associated with decreased oxidative DNA damage repair capacity.”
Night shifts may inhibit DNA repair
Dr. Bhatti and colleagues selected 50 shift workers from the 223 included in their former research.
These shift workers had the widest gap between their levels of circulating melatonin when they were working at night and when they engaged in normal night sleep.
The levels of circulating melatonin were assessed by measuring 6-sulfatoxymelatonin levels in the urine.
To measure 8-OH-dG levels, Dr. Bhatti and colleagues used “high-performance liquid chromatography with electrochemical detection.” They then used mixed effects models to compare night work 8-OH-dG levels with night sleep 8-OH-dG levels.
The study found that melatonin levels were drastically lower during night work than during night sleep.
The researchers also adjusted for possible confounders, such as alcohol use and shorter sleep duration during the day before the night shift. After the adjustments, 8-OH-dG levels were 80 percent lower than the levels recorded during night sleep.
“Our results,” write the authors, “indicate that, relative to night sleep, reduced melatonin production among shift workers during night work is associated with significantly reduced urinary excretion of 8-OH-dG.”
Dr. Bhatti and colleagues also explain what these results mean, saying, “This likely reflects a reduced capacity to repair oxidative DNA damage due to insufficient levels of melatonin and may result in cells harboring higher levels of DNA damage.”
Furthermore, the authors note that a so-called NER molecular pathway is believed to play a key role in DNA damage repair – and some studies have indicated that the production of melatonin enhances the activity of NER genes.
Limitations of the study include the observational nature of the research, meaning that no conclusions could be drawn on cause and effect. Additionally, the population sample was limited to Caucasian healthcare workers, so it is difficult to generalize the findings to a wider population.
Source: MNT
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E-mail us via healthdialogue1@gmail.com
Like our Facebook page on web.facebook.com/healthdialogue
Night shift work has been associated with a variety of adverse health effects. New research adds to these, suggesting that the body’s ability to repair DNA damage may be inhibited by night shifts.
Working at night has been associated with a wide range of negative health effects, including cognitive impairment, metabolic disorders, and breast cancer.
Additionally, some studies have indicated that night shifts may increase a person’s risk of developing lung cancer and cardiovascular disease.
Now, new research examines how night shifts influence the body’s ability to repair its DNA. The first author of the study is Dr. Parveen Bhatti, of the Fred Hutchinson Cancer Research Center in Seattle, Washington.
The findings were published in the journal Occupational & Environmental Medicine.
Building on previous research
In a previous study, Dr. Bhatti and colleagues showed that sleeping during the day correlated with lower levels of 8-hydroxydeoxyguanosine (8-OH-dG), which is a chemical released as a byproduct by the body when it works to repair its own DNA.
The authors were therefore led to believe that these low levels of 8-OH-dG found in the urine may indicate the body’s impaired ability to repair its cellular damage.
They also hypothesized that the reduced levels of urinary 8-OH-dG may be due to the fact that our bodies produce less melatonin during day sleep compared with night sleep.
To further explore this idea, Dr. Bhatti and colleagues set out to examine whether night work also correlates with reduced urinary levels of 8-OH-dG.
The authors explain the motivation for their new research, saying, “If excretion of 8-OH-dG during night work among these subjects is also decreased relative to night sleep, it would provide additional support for our hypothesis that reduced melatonin among shift workers is associated with decreased oxidative DNA damage repair capacity.”
Night shifts may inhibit DNA repair
Dr. Bhatti and colleagues selected 50 shift workers from the 223 included in their former research.
These shift workers had the widest gap between their levels of circulating melatonin when they were working at night and when they engaged in normal night sleep.
The levels of circulating melatonin were assessed by measuring 6-sulfatoxymelatonin levels in the urine.
To measure 8-OH-dG levels, Dr. Bhatti and colleagues used “high-performance liquid chromatography with electrochemical detection.” They then used mixed effects models to compare night work 8-OH-dG levels with night sleep 8-OH-dG levels.
The study found that melatonin levels were drastically lower during night work than during night sleep.
The researchers also adjusted for possible confounders, such as alcohol use and shorter sleep duration during the day before the night shift. After the adjustments, 8-OH-dG levels were 80 percent lower than the levels recorded during night sleep.
“Our results,” write the authors, “indicate that, relative to night sleep, reduced melatonin production among shift workers during night work is associated with significantly reduced urinary excretion of 8-OH-dG.”
Dr. Bhatti and colleagues also explain what these results mean, saying, “This likely reflects a reduced capacity to repair oxidative DNA damage due to insufficient levels of melatonin and may result in cells harboring higher levels of DNA damage.”
Furthermore, the authors note that a so-called NER molecular pathway is believed to play a key role in DNA damage repair – and some studies have indicated that the production of melatonin enhances the activity of NER genes.
Limitations of the study include the observational nature of the research, meaning that no conclusions could be drawn on cause and effect. Additionally, the population sample was limited to Caucasian healthcare workers, so it is difficult to generalize the findings to a wider population.
Source: MNT
For more information; advert placements; submission of articles, et cetera:
E-mail us via healthdialogue1@gmail.com
Like our Facebook page on web.facebook.com/healthdialogue
Monday, 24 April 2017
Scientists step closer to finding cause of multiple sclerosis
Written by Catharine Paddock PhD
As they find out more about the cell biology of multiple sclerosis , scientists are gradually unraveling the mysteries of the disease , although the exact causes are still unclear . Now , a new study continues this progress with a significant discovery about a new cellular mechanism . It suggests that high levels of the protein Rab 32 disrupt key communications involving mitochondria . The disruption causes these "cellular batteries " to misbehave , leading to the toxic effects seen in the brain cells of people with multiple sclerosis
The new study is the work of researchers from the University of Exeter in the United Kingdom and the University of Alberta in Canada. They report their findings in the Journal of Neuroinflammation.
Co-author Paul Eggleton, an immunologist and professor at the University of Exeter Medical School, says that multiple sclerosis can have a "devastating impact on people's lives," and yet, unfortunately, the present situation is that "all medicine can offer is treatment and therapy for the symptoms."
Multiple sclerosis (MS) is a disease in which the immune system mistakenly attacks tissue of the
central nervous system - which comprises the brain, spinal cord, and optic nerve.
As the disease progresses, it destroys more and more of the fatty myelin sheath that insulates and protects the nerve fibers that send electrical messages in the central nervous system.
This destruction can lead to brain damage, vision impairment, pain, altered sensation, extreme
fatigue , problems with movement, and other symptoms.
In earlier work, the team behind the new study was the first to provide an explanation for the role of defective mitochondria in MS through clinical and laboratory experiments.
In their new investigation, the researchers study a protein called Rab32, which is known to be involved in certain mitochondrial processes.
They found that levels of Rab32 are much higher in the brains of people with MS and hardly detectable in brains of people without the disease.
They also discovered that the presence of Rab32 coincides with disruption to a communication system that causes mitochondria to malfunction, causing toxic effects in the brain cells of people with MS.
The disruption is caused by a cell compartment called the endoplasmic reticulum (ER) being too close to the mitochondria.
The ER produces, processes , and transports many compounds that are used inside and outside the cell.
Study may lead to new MS treatments that target Rab 32
The researchers note that one of the functions of the ER is to store calcium, and if the distance between the ER and mitochondria is too short, it disrupts the communication between the mitochondria and the calcium supply.
Calcium uptake into mitochondria is already known to be critical to cell functioning.
Written by Catharine Paddock PhD
As they find out more about the cell biology of multiple sclerosis , scientists are gradually unraveling the mysteries of the disease , although the exact causes are still unclear . Now , a new study continues this progress with a significant discovery about a new cellular mechanism . It suggests that high levels of the protein Rab 32 disrupt key communications involving mitochondria . The disruption causes these "cellular batteries " to misbehave , leading to the toxic effects seen in the brain cells of people with multiple sclerosis
The new study is the work of researchers from the University of Exeter in the United Kingdom and the University of Alberta in Canada. They report their findings in the Journal of Neuroinflammation.
Co-author Paul Eggleton, an immunologist and professor at the University of Exeter Medical School, says that multiple sclerosis can have a "devastating impact on people's lives," and yet, unfortunately, the present situation is that "all medicine can offer is treatment and therapy for the symptoms."
Multiple sclerosis (MS) is a disease in which the immune system mistakenly attacks tissue of the
central nervous system - which comprises the brain, spinal cord, and optic nerve.
As the disease progresses, it destroys more and more of the fatty myelin sheath that insulates and protects the nerve fibers that send electrical messages in the central nervous system.
This destruction can lead to brain damage, vision impairment, pain, altered sensation, extreme
fatigue , problems with movement, and other symptoms.
In earlier work, the team behind the new study was the first to provide an explanation for the role of defective mitochondria in MS through clinical and laboratory experiments.
In their new investigation, the researchers study a protein called Rab32, which is known to be involved in certain mitochondrial processes.
They found that levels of Rab32 are much higher in the brains of people with MS and hardly detectable in brains of people without the disease.
They also discovered that the presence of Rab32 coincides with disruption to a communication system that causes mitochondria to malfunction, causing toxic effects in the brain cells of people with MS.
The disruption is caused by a cell compartment called the endoplasmic reticulum (ER) being too close to the mitochondria.
The ER produces, processes , and transports many compounds that are used inside and outside the cell.
Study may lead to new MS treatments that target Rab 32
The researchers note that one of the functions of the ER is to store calcium, and if the distance between the ER and mitochondria is too short, it disrupts the communication between the mitochondria and the calcium supply.
Calcium uptake into mitochondria is already known to be critical to cell functioning.
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THE BENEFICIAL EFFECTS OF BANANA AS A SOURCE OF POTASSIUM AND MAGNESIUM. Potassium is a mineral that is essential for heart health, e...
-
Kogi State: 2017 Flag-off of Maternal, Newborn and Child Health Week Kogi State Government has pledged its unalloyed commitment to total...