Sunday 20 December 2020

How does your brain remember times and places. Research here.

 



Two studies, led by University of Texas Southwestern (UTSW) researchers, shed new light on how the brain encodes time and place into memories.  The findings, published recently in “PNAS” (Proceedings of the National Academy of Sciences – in the US) and “Science”, not only add to the body of fundamental research on memory, but could eventually provide the basis for new treatments to combat memory loss from conditions such as traumatic brain injury or Alzheimer's disease.

 

About a decade ago, a group of neurons known as "time cells" was discovered in rats.  These cells appear to play a unique role in recording when events take place, allowing the brain to correctly mark the order of what happens in an episodic memory.

 

Located in the brain's hippocampus, these cells show a characteristic activity pattern while the animals are encoding and recalling events, explains Bradley Lega, M.D., associate professor of neurological surgery at UTSW and senior author of the PNSD study.  By firing in a reproducible sequence, they allow the brain to organize when events happen, Lega says.  The timing of their firing is controlled by 5 Hz brain waves, called theta oscillations, in a process known as precession.

 

Lega investigated whether humans also have time cells by using a memory task that makes strong demands on time-related information.  Lega and his colleagues recruited volunteers from the Epilepsy Monitoring Unit at UT Southwestern's Peter O'Donnell Jr. Brain Institute, where epilepsy patients stay for several days before surgery to remove damaged parts of their brains that spark seizures.  Electrodes implanted in these patients' brains help their surgeons precisely identify the seizure foci, and also provide valuable information on the brain's inner workings, Lega says.

 

While recording electrical activity from the hippocampus in 27 volunteers' brains, the researchers had them do "free recall" tasks that involved reading a list of 12 words for 30 seconds, doing a short math problem to distract them from rehearsing the lists, and then recalling as many words from the list as possible for the next 30 seconds.  This task requires associating each word with a segment of time (the list it was on), which allowed Lega and his team to look for time cells.  What the team found was exciting:  Not only did they identify a robust population of time cells, but the firing of these cells predicted how well individuals were able to link words together in time (a phenomenon called temporal clustering).  Finally, these cells appear to exhibit phase precession in humans, as predicted.

 

"For years scientists have proposed that time cells are like the glue that holds together memories of events in our lives," according to Lega.  "This finding specifically supports that idea in an elegant way."

 

In the second study in “Science”, Brad Pfeiffer, Ph.D., assistant professor of neuroscience, led a team investigating place cells, a population of hippocampal cells in both animals and humans that records where events occur.  Researchers have long known that as animals travel a path they've been on before, neurons encoding different locations along the path will fire in sequence much like time cells fire in the order of temporal events, Pfeiffer explains.  In addition, while rats are actively exploring an environment, place cells are further organized into "mini-sequences" that represent a virtual sweep of locations ahead of the rat.  These radar-like sweeps happen roughly 8-10 times per second and are thought to be a brain mechanism for predicting immediately upcoming events or outcomes.

 

Prior to this study, it was known that when rats stopped running, place cells would often reactivate in long sequences that appeared to replay the rat's prior experience in the reverse.  While these "reverse replay" events were known to be important for memory formation, it was unclear how the hippocampus was able to produce such sequences.  Indeed, considerable work had indicated that experience should strengthen forward, "look ahead" sequences but weaken reverse replay events.

 

To determine how these backward and forward memories work together, Pfeiffer and his colleagues placed electrodes in the hippocampi of rats, then allowed them to explore two different places: a square arena and a long, straight track.  To encourage them to move through these spaces, they placed wells with chocolate milk at various places.  They then analysed the animals' place cell activity to see how it corresponded to their locations.

 

Particular neurons fired as the rats wandered through these spaces, encoding information on place.  These same neurons fired in the same sequence as the rats retraced their paths, and periodically fired in reverse as they completed different legs of their journeys.  However, taking a closer look at the data, the researchers found something new:  As the rats moved through these spaces, their neurons not only exhibited forward, predictive mini-sequences, but also backward, retrospective mini-sequences.  The forward and backward sequences alternated with each other, each taking only a few dozen milliseconds to complete.

 

"While these animals were moving forward, their brains were constantly switching between expecting what would happen next and recalling what just happened, all within fraction-of-a-second timeframes," Pfeiffer says.

 

Pfeiffer and his team are currently studying what inputs these cells are receiving from other parts of the brain that cause them to act in these forward or reverse patterns.  In theory, he says, it might be possible to hijack this system to help the brain recall where an event happened with more fidelity.  Similarly, adds Lega, stimulation techniques might eventually be able to mimic the precise patterning of time cells to help people more accurately remember temporal sequences of events.  Further studies with "In the past few decades, there's been an explosion in new findings about memory," he adds.  "The distance between fundamental discoveries in animals and how they can help people is becoming much shorter now."


Why are HIIT workouts so good for you?

 


High-intensity interval training strengthens the heart even more than moderate exercise does.  Now researchers have found several answers to what makes hard workouts so effective.

"Our research on rats with heart failure shows that exercise reduces the severity of the disease, improves heart function, and increases work capacity.  And the intensity of the training is really importance to achieve this effect," says Thomas Stølen, a researcher at the Norwegian University of Science and Technology (NTNU).

 

Stølen and his colleague Morten Høydal are the main authors of a comprehensive study published in the “Journal of Molecular and Cellular Cardiology”.  The researchers went to great lengths to investigate what happens inside tiny heart muscle cells after regular exercise.

 

"We found that exercise improves important properties both in the way heart muscle cells handle calcium and in conducting electrical signals in the heart.  These improvements enable the heart to beat more vigorously and can counteract life-threatening heart rhythm disorders," says Stølen.

 

For a heart to be able to beat powerfully, regularly, and synchronously, a lot of functions have to work together.  Each time the heart beats, the sinus node (the heart's own pacemaker) sends out electrical impulses to the rest of the heart.  These electrical impulses are called action potentials.

 

All the heart muscle cells are enclosed by a membrane.  At rest, the electrical voltage on the inside of the cell membrane is negative compared to the voltage on the outside.  The difference between the voltage on the outside and the inside of the cell membrane is called the resting membrane potential.

 

When the action potentials reach the heart muscle cells, they need to overcome the resting membrane potential of each cell to depolarize the cell wall.  When this happens, calcium can flow into the cell through channels in the cell membrane.

 

Calcium initiates the actual contraction of the heart muscle cells.  When this process is complete, calcium is transported out of the cell or back to its storage site inside each heart muscle cell.  From there, the calcium is ready to contribute to a new contraction the next time an action potential comes rushing by.

 

If the heart's electrical conduction or calcium management system fails, the risk is that fewer heart muscle cells will contract, the contraction in each cell will be weak, and the electrical signals will become chaotic so that the heart chambers begin to flutter.

 

"All these processes are dysfunctional when someone has heart failure.  The action potentials last too long, the resting potential of the cells is too high, and the transport function of the calcium channels in the cell wall is disturbed.  Calcium then constantly leaks from its storage places inside every heart muscle cell," Stølen says.

 

Before Stølen gives us the rest of the good news, he notes, "Our results show that intensive training can completely or partially reverse all these dysfunctions."

 

Normally, the sinus node causes a human heart to beat between 50 and 80 beats every minute when at rest.  This is enough to supply all the organ systems and cells in the body with as much oxygen-rich blood as they need to function properly.

 

When we get up to take a walk, our heart automatically starts beating a little faster and pumping a little harder so that the blood supply is adapted to the increased level of activity.  The higher the intensity of the activity, the harder the heart has to work.

 

Exercise strengthens the heart so it can pump more blood out to the rest of the body with each beat.  Thus, the sinus node can take it a little easier, and well-trained people have a lower resting heart rate than people who have not done regular endurance training.

 

At the other end of the continuum are people with heart failure.  Here the pumping capacity of the heart is so weak that the organs no longer receive enough blood to maintain good functioning.  People with heart failure have a low tolerance for exercise and often get out of breath with minimal effort.

 

In other words, increasing the pumping power to the heart is absolutely crucial for the quality of life and health of people with heart failure.

 

Many of the more than 100,000 Norwegians who live with heart failure have developed the condition after suffering a major heart attack:  just like the rats in Stølen and Høydal's study.

 

In the healthy rats, the heart pumped 75 percent of the blood with each contraction.  In rats with heart failure, this measure of pump capacity, called ejection fraction, was reduced to 20 per cent, Stølen says.

 

The ejection fraction increased to 35 percent after six to eight weeks with almost daily interval training sessions on a treadmill.  The rats did four-minute intervals at about 90 percent of their maximum capacity, quite similar to the 4 × 4 method that has been advocated by several research groups at NTNU for many years.

 

"The interval training also significantly improved the rats' conditioning.  After the training period, their fitness level was actually better than that of the untrained rats that hadn't had a heart attack," says Stølen.

 

Impaired calcium handling in a heart muscle cell not only causes the cell to contract with reduced force every time there is an action potential.  It also causes the calcium to accumulate inside the fluid-filled area of the cell (the cytosol) where each contraction begins.

 

The calcium stores inside the cells are only supposed to release calcium when the heart is preparing to beat.  Heart failure, however, causes a constant leakage of calcium out of these stores.  After each contraction, calcium needs to be efficiently transported back into the calcium stores, or out of the heart muscle cell, via specialized pumps.  In heart failure patients, these pumps work poorly.

 

When a lot of calcium builds up inside the cytosol, the heart muscle cells can initiate new contractions when they're actually supposed to be at rest.  An electrical gradient develops which causes the heart to send electrical signals when it shouldn't.  This can cause fibrillation in the heart chambers.  This ventricular fibrillation is fatal and a common cause of cardiac arrest.

 

"We found that interval training improves a number of mechanisms that allow calcium to be pumped out of the cells and stored more efficiently inside the cells. The leakage from the calcium stores inside the cells also stopped in the interval-trained rats," says Stølen.

 

The effect was clear when the researchers tried to induce ventricular fibrillation in the diseased rat hearts: they only succeeded at this in one of nine animals that had completed interval training.  By comparison, they had no problems inducing fibrillation in all the rats with heart failure who had not exercised.

 

So far, the research group had shown that exercise improves calcium management in diseased heart muscle cells in several ways.  The training also makes the electrical wiring system of the heart more functional.

 

In addition, they showed that exercise counteracted processes that cause the heart to become big and stiff.

 

Taken together, these improvements make each heartbeat more powerful and reduce the severity of heart failure.  The risk of dangerous ventricular fibrillation was also reduced.

 

But Stølen and team still lacked an answer to why exercise corrects slow action potentials and ensures that the heart muscle cells are able to take care of calcium in the right way.

 

Therefore, they investigated whether the training had altered the genetic activity inside the rat cells.  Thousands of different types of micro-molecules, called micro-RNA, probably control most of this activity through direct interaction with genes.

 

"It turned out that 55 of the micro-RNA variants we examined were altered in rats with heart failure compared to the healthy rats.  Interval training changed 18 of these back towards healthy levels.  Several of the relevant micro-molecules are known to play a role in both calcium management and the electrical conduction system of the heart, but the most interesting thing is that we discovered new micro-RNAs that can play an important role in heart failure," says Stølen.

 

This article has mostly considered the effects of high-intensity interval training.  But the study also includes a group of rats that trained more sedately.

 

The rats in this group ran the same distance and thus did as much total training work as the rats in the interval training group.  However, they had to exercise longer each time since they trained at a lower intensity.  Stolen notes that this form of training also resulted in several health improvements.

 

But, he emphasizes, the vast majority of improvements were greater with interval training.  "For example, we were able to induce cardiac fibrillation in five of eight rats after a period of moderate exercise, and their pumping capacity had only improved half as much as in the interval training group."

Age is not a barrier to weight loss

 


Obese patients over the age of 60 can lose an equivalent amount of weight as younger people using only lifestyle changes, according to a new study from the University of Warwick and University Hospitals Coventry and Warwickshire (UHCW) NHS Trust that demonstrates that age is no barrier to losing weight.


The researchers hope that their findings will help to correct prevailing societal misconceptions about the effectiveness of weight loss programmes in older people, as well dispel myths about the potential benefits of older people trying to reduce their weight.


The findings are based on analysis of patient records from a hospital-based obesity service and are reported in the journal “Clinical Endocrinology”.

This retrospective study was conducted at the Warwickshire Institute for the Study of Diabetes, Endocrinology and Metabolism (WISDEM) at UHCW.  The researchers randomly selected 242 patients, who attended the WISDEM-based obesity service between 2005 and 2016, and compared two groups (those aged under 60 years and those aged between 60 and 78 years) for the weight loss that they achieved during their time within the service.


All patients had their body weight measured both before and after lifestyle interventions administered and coordinated within the WISDEM-based obesity service, and the percentage reduction in body weight calculated across both groups.  When compared, the two groups were equivalent statistically, with those aged 60 years and over on average reducing their body weight by 7.3% compared with a body weight reduction of 6.9% in those aged under 60 years.  Both groups spent a similar amount of time within the obesity service, on average 33.6 months for those 60 years and over, and 41.5 months for those younger than 60 years.


The hospital-based programme used only lifestyle-based changes tailored to each individual patient, focusing on dietary changes, psychological support, and encouragement of physical activity.  Most of the patients referred to the obesity service were morbidly obese with BMIs, typically over 40Kgm-2.

There are more than fifty co-morbidities of obesity that can be lessened as we lose weight, including diabetes, psychiatric conditions such as depression and anxiety, osteoarthritis, and other mechanical problems.  Obesity is also linked to increased mortality and poor wellbeing.


Lead author Dr Thomas Barber of Warwick Medical School at the University of Warwick said: "Weight loss is important at any age, but as we get older we're more likely to develop the weight-related co-morbidities of obesity.  Many of these are similar to the effects of aging, so you could argue that the relevance of weight loss becomes heightened as we get older, and this is something that we should embrace.”


"There are a number of reasons why people may discount weight loss in older people.  These include an 'ageist' perspective that weight-loss is not relevant to older people and misconceptions of reduced ability of older people to lose weight through dietary modification and increased exercise.  Older people may feel that hospital-based obesity services are not for them.  Service providers and policymakers should appreciate the importance of weight loss in older people with obesity, for the maintenance of health and wellbeing, and the facilitation of healthy ageing.  Furthermore, age per se should not contribute towards clinical decisions regarding the implementation of lifestyle management of older people.”


"Age should be no barrier to lifestyle management of obesity.  Rather than putting up barriers to older people accessing weight loss programmes, we should be proactively facilitating that process.  To do otherwise would risk further and unnecessary neglect of older people through societal ageist misconceptions."

Let's take a look at Schizophrenia

 

Schizophrenia is a chronic and severe mental disorder affecting 20 million people worldwide.

Schizophrenia is characterized by distortions in thinking, perception, emotions, language, sense of self and behaviour.  Common experiences include hallucinations (hearing voices or seeing things that are not there) and delusions (fixed, false beliefs).

Worldwide, schizophrenia is associated with considerable disability and may affect educational and occupational performance.

People with schizophrenia are 2-3 times more likely to die early than the general population.  This is often due to preventable physical diseases, such as cardiovascular disease, metabolic disease, and infections.

Stigma, discrimination, and violation of human rights of people with schizophrenia is common.

Schizophrenia is treatable.  Treatment with medicines and psychosocial support is effective.

Facilitation of assisted living, supported housing, and supported employment are effective management strategies for people with schizophrenia.

Schizophrenia is a psychosis, a type of mental illness characterized by distortions in thinking, perception, emotions, language, sense of self and behaviour.

Common experiences include:

·      hallucination: hearing, seeing, or feeling things that are not there.

·      delusion: fixed false beliefs or suspicions not shared by others in the person’s culture and that are firmly held even when there is evidence to the contrary.

·      abnormal behaviour: disorganised behaviour such as wandering aimlessly, mumbling, or laughing to self, strange appearance, self-neglect or appearing unkempt.

·      disorganised speech: incoherent or irrelevant speech; and/or

·      disturbances of emotions: marked apathy or disconnect between reported emotion and what is observed such as facial expression or body language.

Research has not identified one single factor as a cause.  It is thought that an interaction between genes and a range of environmental factors may cause schizophrenia.  Psychosocial factors may also contribute to schizophrenia.

It is estimated that more than 69% of people with schizophrenia are not receiving appropriate care.  Ninety per cent of people with untreated schizophrenia live in low- and middle- income countries.  Lack of access to mental health services is an important issue.  Furthermore, people with schizophrenia are less likely to seek care than the general population.

Schizophrenia is treatable. Treatment with medicines and psychosocial support is effective. However, most people with chronic schizophrenia lack access to treatment.

There is clear evidence that old-style mental hospitals are not effective in providing the treatment that people with mental disorders need and violate basic human rights of persons with mental disorders.  Efforts to transfer care from mental health institutions to the community need to be expanded and accelerated.  The engagement of family members and the wider community in providing support is especially important.

Programmes in several low- and middle- income countries (e.g., Ethiopia, Guinea-Bissau, India, Iran, Pakistan, and United Republic of Tanzania) have demonstrated the feasibility of providing care to people with severe mental illness through the primary health-care system by:

·       training primary healthcare personnel.

·      providing access to essential drugs.

·      supporting families in providing home care.

·      educating the public to decrease stigma and discrimination.

·      enhancing independent living skills through recovery-oriented psychosocial interventions (e.g., life skills training, social skills training) for people with schizophrenia and for their families and/or caregivers; and

·      facilitating independent living, if possible, or assisted living, supported housing, and supported employment for people with schizophrenia.  This can act as a base for people with schizophrenia to achieve recovery goals.  People affected by schizophrenia often face difficulty in obtaining or retaining normal employment or housing opportunities.

People with schizophrenia are prone to human rights violations both inside mental health institutions and in communities.  Stigma of the disorder is high.  This contributes to discrimination, which can in turn limit access to general health care, education, housing, and employment.

What is Gastritis?


 “Gastritis” is an inflammation of the stomach's lining.  It can be caused by smoking, drinking too much alcohol, long-term use of aspirin, or other nonsteroidal anti-inflammatory drugs such as ibuprofen or naproxen, infection with the bacterium “Helicobacter Pylori”, severe injury, or shock.  Sometimes gastritis is an autoimmune condition, in which the immune system mistakenly attacks the cells that line the stomach.

Symptoms of gastritis can include:

·      abdominal pain or discomfort

·      constant pain between the navel and lower ribs

·      nausea, sometimes with vomiting

·      poor appetite

·      belching, bloating, or a feeling of fullness in the abdomen that is made worse by eating

Serious gastritis can lead to erosion of the stomach lining, which can cause painful ulcers and black stools (a sign of bleeding in the stomach).  It can also cause anaemia, or too few red blood cells in circulation.  This can lead to fatigue and being short of breath with physical activity.

Your story of your symptoms and a physical examination may be all a doctor needs to diagnose gastritis.

A breath test may be needed to see if your stomach harbours Helicobacter Pylori.  Some people need a procedure called gastroscopy.  In this procedure, a doctor passes a flexible, lighted instrument down your throat and into your stomach.  With this instrument, he or she can inspect your stomach lining directly take a small tissue sample (biopsy) to be examined in the laboratory.

Treating gastritis begins with stopping or removing the cause, such as drinking too much alcohol or smoking.  If you take nonsteroidal anti-inflammatory drugs for arthritis or other pain, trying an alternative such as misoprostol may be important.

If you think that certain foods make your symptoms worse, keep a food diary and track what you eat against your symptoms.  If you see connections between certain foods and symptoms, don't eat the offending foods for a while and see if your gastritis improves.  Problem foods tend to be those that are fatty, spicy, or very acidic, like coffee, orange juice, tomato juice, and colas.

A common treatment for gastritis is taking medication to decrease stomach acid. Several classes of medication can do this:

·      over-the-counter antacids

·      over-the-counter or prescription H2 blockers (also known as acid reducers) such as Tagamet, Zantac, Pepcid, and their generic equivalents

·      and proton pump inhibitors such as omeprazole (Prilosec), esomeprazole (Nexium), lansoprazole (Prevacid), and pantoprazole (Protonix).

Proton pump inhibitors are the strongest acid blockers but are usually more expensive.

If your test for Helicobacter pylori is positive, a two-week course of "triple therapy" may stop the infection and improve your symptoms. Triple therapy includes a proton-pump inhibitor plus two different antibiotics, amoxicillin and clarithromycin.

Friday 4 December 2020

Are you risking eye damage by not visiting the Optician? Research here.

 


Experts suggest, once you reach age 65, you need comprehensive, dilated eye exams every one or two years, and more often if you have eye problems.  But doctors say the pandemic is keeping some people from getting eye care.

It is reported that some people are delaying treatment, trying to avoid crowds or health facilities like hospitals.  They're not getting their eye pressure checked, and they're not using their eye medication.

Vision loss usually occurs gradually and painlessly, and most people don't notice until after the damage has been done.  Putting off eye care increases the risk for undetected or uncontrolled eye conditions, eye damage, and vision loss, especially from glaucoma.

With delayed eye care, doctors are seeing more severe cases of glaucoma and more people coming to the hospital emergency room with advanced vision loss.

Delayed eye care also allows other eye problems to go unchecked.  The following eye conditions have few or minor symptoms at first and may only be detected by eye exams.

An Eye Stroke:  Like the heart or brain, the eye can suffer damage from obstruction of a blood vessel.  One type of eye stroke occurs when blood flow leaving the retina (the light-sensing component in the back of the eye) is disrupted.  It can cause temporary or permanent vision loss.  People with high blood pressure, diabetes, glaucoma, and cardiovascular disease are at greater risk for this condition.

Diabetic Retinopathy:  Diabetes can cause blood vessels in the retina to become "leaky," leading to temporary vision loss.  Sometimes the blood will clear on its own.  If it doesn't, you may need surgery.  If the old blood or new blood vessels block the drain in your eye, you can get increased eye pressure and glaucoma.

Age Related Macular Degeneration:  This condition gradually destroys the macula, the retina's central portion. It's the part of the eye that provides central vision needed for seeing objects clearly.

Symptoms and Intervention

You may not be able to tell if an eye condition has developed or is progressing unless it's advanced and you experience symptoms, which can include

·      blind spots in your peripheral or central vision

·      severe pain in the eye or forehead

·      severe light sensitivity

·      blurred or reduced vision

·      temporary vision loss

·      headache along with vision change

·      eye redness

·      halos around lights

·      spots or cobwebs in your field of vision.

 

Check your vision in one eye at a time. If you have symptoms in only one eye, that's a sign of a problem.  But don't wait until symptoms occur to see your doctor; keep scheduled eye appointments.  Your doctor can dilate (widen) your pupils and look into the back of each eye to examine the health of the retina and optic nerve.  Your eye care team can also check your eye pressure, make sure your eye muscles are functioning properly, and check for vision changes.

If necessary, the doctor can prescribe medicines, give injections, or perform procedures to halt disease progression.  If eye disease advances, medications will need to be adjusted.  In some cases, you may need surgery.

Re Covid worries, by talking to your eye care team, you'll find out about precautions the office is taking to ensure your safety;  such as disinfecting equipment, wearing masks, screening patients for COVID before arrival, limiting waiting room times, limiting the number of people in waiting rooms and keeping them six feet apart, and offering hybrid visits.