Posts Tagged ‘medicine’

A 7-year-old boy complaining of jaw pain was found to have 526 teeth inside his mouth, according to the hospital in India where he was treated.

The boy was admitted last month in the southern city of Chennai because of swelling and pain near his molars in his lower right jaw.

When doctors scanned and x-rayed his mouth, they found a sac embedded in his lower jaw filled with “abnormal teeth,” Dr. Prathiba Ramani, the head of Oral and Maxillofacial Pathology at Saveetha Dental College and Hospital, told CNN.

While the surgery to remove the teeth took place last month, doctors needed time to individually examine each tooth before they could confirm their findings.

After discovering the sac, two surgeons removed it from the boy’s mouth. Then Ramani’s team took four to five hours to empty the sac to confirm its contents and discovered the hundreds of teeth.

“There were a total of 526 teeth ranging from 0.1 millimeters (.004 inches) to 15 millimeters (0.6 inches). Even the smallest piece had a crown, root and enamel coat indicating it was a tooth,” she said.

The boy was released three days after the surgery and is expected to make a full recovery, Ramani said.

Ramani said the boy was suffering from a very rare condition called compound composite odontoma. She said what caused the condition is unclear, but it could be genetic or it could be due to environmental factors like radiation.

The boy actually may have had the extra teeth for some time. His parents told doctors that they had noticed swelling in his jaw when he was as young as 3, but they couldn’t do much about it because he would not stay still or allow doctors to examine him.

Dr. P. Senthilnathan, head of the hospital’s Oral and Maxillofacial Surgery Department and one of two surgeons who operated on the boy, detailed the procedure to CNN.

“Under general anesthesia, we drilled into the jaw from the top,” he said. “We did not break the bone from the sides, meaning reconstruction surgery was not required. The sac was removed. You can think of it as a kind of balloon with small pieces inside.”

Dr. Senthilnathan said the discovery showed it was important to seek treatment for dental issues as early as possible.

Awareness about dental and oral health was improving, he said, though access in rural areas remained problematic.

“Earlier, things like not as many dentists, lack of education, poverty meant that there was not as much awareness. These problems are still there.

“You can see people in cities have better awareness but people who are in rural areas are not as educated or able to afford good dental health.”

In Ravindrath’s case, all has turned out well; the boy now has a healthy count of 21 teeth, Dr. Senthilnathan said.

Doctors find 526 teeth in boy’s mouth after he complains of jaw pain

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by Ed Cara

People who only occasionally fall down an internet rabbit hole on their smartphones late at night might be able to rest easier—at least according to the results of a new study in mice. Researchers found that short bursts of light exposure at night won’t necessarily disrupt your internal clock, including sleep habits.

The researchers used mice to study the circadian rhythm. In both mice and humans, the circadian rhythm is primarily controlled by the brain’s suprachiasmatic nucleus (SCN), a tiny region found in the hypothalamus. One crucial aspect of the SCN involves regulating our sleep/wake, or light/dark, cycle. It’s long been thought that any kind of light exposure our eyes take in affects the SCN, and thus, can affect our sleep.

“Light information comes into the SCN, and that’s what synchronizes all of the body’s clocks to the light/dark cycle,” said lead author Tiffany Schmidt, a neurogeneticist at Northwestern, in a release from the university. “This one master pacemaker makes sure everything is in sync.”

Schmidt and her team wanted to test this long-held theory that the SCN responds to any light exposure. So they bred mice that had light-sensitive nerve cells in the retina that were only capable of communicating with the SCN. Then they exposed these mice to light for short periods of time.

Because mice, unlike people, are nocturnal, the light should have made them want to fall asleep. But they instead just carried out on with their day, sleeping and waking as normal. Their body temperature, which fluctuates predictably before, during, and after sleep, also followed the same pattern seen in mice with normal circadian rhythms.

What this could mean, according to the authors, is that our brains respond to acute light—meaning brief exposures to light—through a different neural pathway than what’s used for long periods of light exposure, a pathway that doesn’t involve the SCN.

“If these two effects—acute and long-term light exposure—were driven through the same pathway, then every minor light exposure would run the risk of completely shifting our body’s circadian rhythms,” Schmidt said.

The findings will be published this week in the journal eLife.

Mice and their brains aren’t a perfect proxy for people, obviously. And even if the same general principle does apply to us, Schmidt and her team say there’s no clear lead on where these other pathways could exist in the brain. And there’s undoubtedly a point where being exposed to light late at night too long or too often can start to affect our internal clock—even if where that point lies is still a mystery right now. There needs to be a lot much research studying these questions and others.

What is clear, the authors cautioned, is that chronic nighttime light exposure, and the disruptions to our sleep it can cause, can be very bad for health. In other words, don’t use this study as an excuse to start regularly binge-watching Netflix till 4 a.m.

“Light at the wrong time of day is now recognized as a carcinogen,” Schmidt said. “We want people to feel alert while they are exposed to light without getting the health risks that are associated with shifted circadian rhythms, such as diabetes, depression and even cancer.”

https://gizmodo.com/checking-your-phone-at-night-wont-necessarily-throw-off-1836603924

Users of prosthetic limbs could soon be able to feel sensation on them, thanks to an “electronic skin” (e-skin) invented by researchers from the National University of Singapore (NUS).

The artificial nervous system can detect touch more than 1,000 times faster than the human equivalent and is the first e-skin in the world to do so, according to Assistant Professor Benjamin Tee from the Department of Materials Science and Engineering at the NUS Faculty of Engineering, who led the research.

Previously, damaged e-skins would lose their function due to their interlinked wiring system.

But if a corner of the Asynchronous Coded Electronic Skin (Aces) nervous system tears, the rest of the skin continues to have sensation, just like human skin, the researchers said.

This is because the Aces detects signals like the human nervous system and it comprises a network of sensors – each working independently – connected via a single electrical conductor.

The research team, which took 11/2 years to develop the sensor system, published its innovation in Science Robotics journal today.

“When you lose a limb and get fitted with a prosthetic that doesn’t feel, it’s almost like you’re always feeling numb and cannot control things very well,” said Prof Tee. “If we have a skin that can make prosthetics smarter, we can restore motor functions, productivity and general quality of life for these people.”

In human skin, receptors send information about touch to the brain, which enables humans to intuitively sense touch.

When the Aces is attached to a prosthetic hand, a neural implant must be inserted into the patient’s arm so that the brain can detect the sense of touch from the e-skin.

The team will work with prosthetics researchers abroad to conduct a clinical trial of the e-skin with a patient using an artificial hand.

The Aces has also been designed for robots. “Robots need to have a sense of touch to interact better with humans, but robots today still cannot feel objects very well,” said Prof Tee.

For instance, a search-and-rescue robot digging through rubble will need sensation to know that it has to push away rocks and concrete to rescue a trapped person.

E-skin such as the Aces can be commercialised for robots within a year or two, Prof Tee said, but it will take five to 10 years for prosthetics that sense touch to reach patients, to allow for clinical trials.

https://www.straitstimes.com/singapore/prosthetics-can-sense-touch-with-electronic-skin-invention


Kumar Alagramam. PhD, Case Western Reserve University

The ability to hear depends on proteins to reach the outer membrane of sensory cells in the inner ear. But in certain types of hereditary hearing loss, mutations in the protein prevent it from reaching these membranes. Using a zebrafish model, researchers at Case Western Reserve University School of Medicine have found that an anti-malarial drug called artemisinin may help prevent hearing loss associated with this genetic disorder.

In a recent study, published in the Proceedings of the National Academy of Sciences (PNAS), researchers found the classic anti-malarial drug can help sensory cells of the inner ear recognize and transport an essential protein to specialized membranes using established pathways within the cell.

The sensory cells of the inner ear are marked by hair-like projections on the surface, earning them the nickname “hair cells.” Hair cells convert sound and movement-induced vibrations into electrical signals that are conveyed through nerves and translated in the brain as information used for hearing and balance.

The mutant form of the protein–clarin1–render hair cells unable to recognize and transport them to membranes essential for hearing using typical pathways within the cell. Instead, most mutant clarin1 proteins gets trapped inside hair cells, where they are ineffective and detrimental to cell survival. Faulty clarin1 secretion can occur in people with Usher syndrome, a common genetic cause of hearing and vision loss.

The study found artemisinin restores inner ear sensory cell function—and thus hearing and balance—in zebrafish genetically engineered to have human versions of an essential hearing protein.

Senior author on the study, Kumar N. Alagramam, the Anthony J. Maniglia Chair for Research and Education and associate professor at Case Western Reserve University School of Medicine Department of Otolaryngology at University Hospitals Cleveland Medical Center, has been studying ways to get mutant clarin1 protein to reach cell membranes to improve hearing in people with Usher syndrome.

“We knew mutant protein largely fails to reach the cell membrane, except patients with this mutation are born hearing,” Alagramam said. “This suggested to us that, somehow, at least a fraction of the mutant protein must get to cell membranes in the inner ear.”

Alagramam’s team searched for any unusual secretion pathways mutant clarin1 could take to get to hair cell membranes. “If we can understand how the human clarin1 mutant protein is transported to the membrane, then we can exploit that mechanism therapeutically,” Alagramam said.

For the PNAS study, Alagramam’s team created several new zebrafish models. They swapped the genes encoding zebrafish clarin1 with human versions—either normal clarin1, or clarin1 containing mutations found in humans with a type of Usher syndrome, which can lead to profound hearing loss.

“Using these ‘humanized’ fish models,” Alagramam said, “we were able to study the function of normal clarin1 and, more importantly, the functional consequences of its mutant counterpart. To our knowledge, this is the first time a human protein involved in hearing loss has been examined in this manner.”

Zebrafish offer several advantages to study hearing. Their larvae are transparent, making it easy to monitor inner ear cell shape and function. Their genes are also nearly identical to humans—particularly when it comes to genes that underlie hearing. Replacing zebrafish clarin1 with human clarin1 made an even more precise model.

The researchers found the unconventional cellular secretion pathway they were looking for by using florescent labels to track human clarin1 moving through zebrafish hair cells. The mutated clarin1 gets to the cell membrane using proteins and trafficking mechanisms within the cell, normally reserved for misfolded proteins “stuck” in certain cellular compartments.

“As far as we know, this is the first time a human mutant protein associated with hearing loss has been shown to be ‘escorted’ by the unconventional cellular secretion pathway,” Alagramam said. “This mechanism may shed light on the process underlying hearing loss associated with other mutant membrane proteins.”

The study showed the majority of mutant clarin1 gets trapped inside a network of tubules within the cell analogous to stairs and hallways helping proteins, including clarin1, get from place to place. Alagramam’s team surmised that liberating the mutant protein from this tubular network would be therapeutic and tested two drugs that target it: thapsigargin (an anti-cancer drug) and artemisinin (an anti-malarial drug).

The drugs did enable zebrafish larvae to liberate the trapped proteins and have higher clarin1 levels in the membrane; but artemisinin was the more effective of the two. Not only did the drug help mutant clarin1 to reach the membrane, hearing and balance functions were better preserved in zebrafish treated with the anti-malarial drug than untreated fish.

In zebrafish, survival depends on normal swim behavior, which in turn depends on balance and the ability to detect water movement, both of which are tied to hair cell function. Survival rates in zebrafish expressing the mutant clarin1 jumped from 5% to 45% after artemisinin treatment.

“Our report highlights the potential of artemisinin to mitigate both hearing and vision loss caused by clarin1 mutations,” Alagramam said. “This could be a re-purposable drug, with a safe profile, to treat Usher syndrome patients.”

Alagramam added that the unconventional secretion mechanism and the activation of that mechanism using artemisinin or similar drugs may also be relevant to other genetic disorders that involve mutant membrane proteins aggregating in the cell’s tubular network, including sensory and non-sensory disorders.

Gopal SR, et al. “Unconventional secretory pathway activation restores hair cell mechanotransduction in an USH3A model.” PNAS.

Drug to treat malaria could mitigate hereditary hearing loss

Vaccination against the human papilloma virus, which causes most cervical cancers, began over a decade ago.

A Lancet review of 65 studies covering 60 million people showed a fall in HPV cases and in pre-cancerous growths.

Over decades, this should translate into a significant fall, and possible eradication, of the cancer they said.

Jo’s Cervical Cancer Trust said the data should boost faith in the jab.

What is the human papilloma virus (HPV)?

HPV is the name for a common group of viruses; there are more than 100 types of HPV
Many women will be infected with HPV over the course of their lifetime, with no ill effect
Most cervical cancers are caused by infection from a high-risk HPV
Others cause conditions including genital warts and cancers of the head and neck
The vaccine, given as two injections to girls aged 12 and 13, protects against four types of HPV – 16 and 18, which are linked to more than 70% of cervical cancers – and six and 11, which
cause about 90% of genital warts
Girls who miss the HPV jab at school can still get it for free on the NHS up to the age of 25
It is also available privately, costing around £150 per dose
Boys aged 12-13 will also be offered the jab from September this year
The vaccine does not protect against all the types of HPV that can cause cervical cancer, so women still need to go for regular screening

There are 3,200 cases of cervical cancer and 850 deaths from the disease each year.

‘Real-world’ evidence
The review covered studies in 14 high-income countries, including the UK. They looked at HPV rates, plus cases of genital warts and pre-cancerous cells in the cervix called CIN.

It found that when rates were compared before vaccination started and eight years after:

Cases of HPV 16 and 18 were down 83% in girls aged 15-19 – 66% in women 20-24
Genital warts cases fell 67% in girls 15-19 – 54% in women 20-24
Pre-cancerous growths were down by 51% in girls 15-19 – 31% in women 20-24
It also showed people who were not vaccinated benefited. Cases of genital warts in boys aged 15-19 fell by almost 50%, and also significantly in women over 30.

Rates fell more in countries where a wider age group was vaccinated and where coverage was higher.

Public Health England principal scientist Dr David Mesher said: “We are seeing reductions in HPV strains and in cervical disease as well, so there is every suggestion there will be reductions in cervical cancers too.”

Prof Marc Brisson, from Laval University, Canada, who led the review, said: “We will see reductions in women aged 20-30 within the next 10 years.”

He said cervical cancer elimination – defined as fewer than four cases per 100,000 – “might be possible if sufficiently high vaccination coverage can be achieved and maintained”.

Jo’s Cervical Cancer Trust said the findings “clearly showed” the impact of HPV vaccination.

“This study furthers the growing evidence to counteract those who don’t believe that this vaccine works, which is now extremely encouraging,” said chief executive Robert Music.

“We sincerely hope this will boost public faith in the HPV vaccine, so that more lives can be saved and we get closer to a world where cervical cancer is a thing of the past.”

https://www.bbc.com/news/health-48758730?utm_source=Nature+Briefing&utm_campaign=5a6f57394e-briefing-dy-20190627&utm_medium=email&utm_term=0_c9dfd39373-5a6f57394e-44039353

“Focusing our resources on the combination of these three interventions can have a huge potential impact on cardiovascular health through 2040,” said lead author Goodarz Danaei, associate professor of global health at Harvard Chan School.

Researchers used global data from multiple studies and estimates from the World Health Organization in making their calculations.

They estimated that scaling up treatment of high blood pressure to 70% of the world’s population could extend the lives of 39.4 million people. Cutting sodium intake by 30% could stave off another 40 million deaths and could also help decrease high blood pressure, a major risk factor for CVD. And eliminating trans fat could prevent 14.8 million early deaths.

More than half of all delayed deaths, and two-thirds of deaths delayed before age 70, are projected to be among men, who have the highest numbers of noncommunicable disease deaths globally, researchers found. Regions expected to benefit most from the interventions include East Asia, the Pacific, and South Asia, as well as countries in sub-Saharan Africa.

The authors said that a variety of programs and policies would be necessary to reduce premature CVD-related deaths. One important strategy would be to increase the use of blood pressure medications, many of which are safe and affordable.

The researchers acknowledged that scaling up the three interventions would be a “huge challenge,” requiring countries to commit additional resources to boost health care capacity and quality. But they added that previous analyses have shown that the interventions are achievable and affordable. For example, a Kaiser Permanente program in Northern California increased control of hypertension to 90% among thousands of the health system’s patients between 2001 and 2013, using strategies such as improved treatment protocols, patient-friendly services, and healthcare information systems that facilitate tracking people with hypertension. Similar approaches have been adapted and tested in some low- and middle-income countries, leading to notable improvements in hypertension treatment and control, the authors said.

“These are realistic goals that have been shown to be attainable on smaller scales,” said Danaei. “We need the commitment to scale up the programs to achieve them globally.”

Doctors have newly outlined a type of dementia that could be more common than Alzheimer’s among the oldest adults, according to a report published Tuesday in the journal Brain.

The disease, called LATE, may often mirror the symptoms of Alzheimer’s disease, though it affects the brain differently and develops more slowly than Alzheimer’s. Doctors say the two are frequently found together, and in those cases may lead to a steeper cognitive decline than either by itself.

In developing its report, the international team of authors is hoping to spur research — and, perhaps one day, treatments — for a disease that tends to affect people over 80 and “has an expanding but under-recognized impact on public health,” according to the paper.

“We’re really overhauling the concept of what dementia is,” said lead author Dr. Peter Nelson, director of neuropathology at the University of Kentucky Medical Center.

Still, the disease itself didn’t come out of the blue. The evidence has been building for years, including reports of patients who didn’t quite fit the mold for known types of dementia such as Alzheimer’s.

“There isn’t going to be one single disease that is causing all forms of dementia,” said Sandra Weintraub, a professor of psychiatry, behavioral sciences and neurology at Northwestern University Feinberg School of Medicine. She was not involved in the new paper.

Weintraub said researchers have been well aware of the “heterogeneity of dementia,” but figuring out precisely why each type can look so different has been a challenge. Why do some people lose memory first, while others lose language or have personality changes? Why do some develop dementia earlier in life, while others develop it later?

Experts say this heterogeneity has complicated dementia research, including Alzheimer’s, because it hasn’t always been clear what the root cause was — and thus, if doctors were treating the right thing.

What is it?

The acronym LATE stands for limbic-predominant age-related TDP-43 encephalopathy. The full name refers to the area in the brain most likely to be affected, as well as the protein at the center of it all.

“These age-related dementia diseases are frequently associated with proteinaceous glop,” Nelson said. “But different proteins can contribute to the glop.”

In Alzheimer’s, you’ll find one set of glops. In Lewy body dementia, another glop.

And in LATE, the glop is a protein called TDP-43. Doctors aren’t sure why the protein is found in a modified, misfolded form in a disease like LATE.

“TDP-43 likes certain parts of the brain that the Alzheimer’s pathology is less enamored of,” explained Weintraub, who is also a member of Northwestern’s Mesulam Center for Cognitive Neurology and Alzheimer’s Disease.

“This is an area that’s going to be really huge in the future. What are the individual vulnerabilities that cause the proteins to go to particular regions of the brain?” she said. “It’s not just what the protein abnormality is, but where it is.”

More than a decade ago, doctors first linked the TDP protein to amyotrophic lateral sclerosis, otherwise known as ALS or Lou Gehrig’s disease. It was also linked to another type of dementia, called frontotemporal lobar degeneration.

LATE “is a disease that’s 100 times more common than either of those, and nobody knows about it,” said Nelson.

The new paper estimates, based on autopsy studies, that between 20 and 50% of people over 80 will have brain changes associated with LATE. And that prevalence increases with age.

Experts say nailing down these numbers — as well as finding better ways to detect and research the disease — is what they hope comes out of consensus statements like the new paper, which gives scientists a common language to discuss it, according to Nelson.

“People have, in their own separate bailiwicks, found different parts of the elephant,” he said. “But this is the first place where everybody gets together and says, ‘This is the whole elephant.’ ”

What this could mean for Alzheimer’s

The new guidelines could have an impact on Alzheimer’s research, as well. For one, experts say some high-profile drug trials may have suffered as a result of some patients having unidentified LATE — and thus not responding to treatment.

In fact, Nelson’s colleagues recently saw that firsthand: a patient, now deceased, who was part of an Alzheimer’s drug trial but developed dementia anyway.

“So, the clinical trial was a failure for Alzheimer’s disease,” Nelson said, “but it turns out he didn’t have Alzheimer’s disease. He had LATE.”

Nina Silverberg, director of the Alzheimer’s Disease Research Centers Program at the National Institute on Aging, said she suspects examples like this are not the majority — in part because people in clinical trials tend to be on the younger end of the spectrum.

“I’m sure it plays some part, but maybe not as much as one might think at first,” said Silverberg, who co-chaired the working group that led to the new paper.

Advances in testing had already shown that some patients in these trials lacked “the telltale signs of Alzheimer’s,” she said.

In some cases, perhaps it was LATE — “and it’s certainly possible that there are other, as yet undiscovered, pathologies that people may have,” she added.

“We could go back and screen all the people that had failed their Alzheimer’s disease therapies,” Nelson said. “But what we really need to do is go forward and try to get these people out of the Alzheimer’s clinical trials — and instead get them into their own clinical trials.”

Silverberg describes the new paper as “a roadmap” for research that could change as we come to discover more about the disease. And researchers can’t do it without a large, diverse group of patients, she added.

“It’s probably going to take years and research participants to help us understand all of that,” she said.

https://www.cnn.com/2019/04/30/health/dementia-late-alzheimers-study/index.html