Regarding ear equalization with in a Hyperbaric Oxygen Chamber| Eustachian Tube | |
|---|---|
 | |
| Anatomy of the human ear. | |
| The middle ear | |
| Latin | tuba auditiva; tuba auditoria; tuba auditivea |
| Gray's | subject #230 1042 |
| Precursor | first branchial pouch |
| MeSH | Eustachian+tube |
Babies’ Brains Process Words in an Adult Way“Babies are using the same brain mechanisms as adults to access the meaning of words from what is thought to be a mental ‘database’ of meanings, a database which is continually being updated right into adulthood,” says first author Katherine E. Travis of the Department of Neurosciences and the Multimodal Imaging Laboratory.
For the study, scientists used MRI and MEG (scan that measures magnetic fields emitted by neurons in the brain) to non-invasively analyze brain activity in infants, ages 12 to 18 months.
It was previously assumed that babies process words with a completely different learning mechanism, and it was believed that learning begins primitively—later evolving into the more “adult way” of learning. It has been difficult for scientists to figure out which areas of the brain are most involved in language learning because there is a lack information on how this process works in the developing brain.
Although lesions in two brain areas — Broca’s and Wernicke’s — have long been associated with loss of language skills in adults, these areas seem to have little impact on language development in early childhood. Some scientists have addressed this anomaly by theorizing that the right hemisphere and inferior frontal regions are vital for childhood language development, and that the other language areas of adulthood become dominant only when language development has matured.
Others have hypothesized that the plasticity of an infant’s brain allows other regions to take over the work of language-learning if the left frontotemporal regions become damaged at a young age.
During the first part of the experiment, the babies listened to words accompanied with sounds that have similar acoustic properties, but no meaning, to see if the infants could determine the difference between the two.
In the second part, the researchers wanted to see if the babies were able to understand the meaning of these words. For example, babies were shown pictures of familiar objects and then heard words that were either the correct or incorrect names for these objects: a picture of a ball followed by the spoken word ball, versus a picture of a ball followed by the spoken word dog.
It was determined through brain images that the infants could detect the mismatch between a picture and a word, as shown by the degree of brain activity. An incorrectly matched word triggered a classic brain response located in the same left frontotemporal areas known to process word meaning in the adult brain. The tests were then given to adults to confirm if the same mismatched picture/word combinations shown to babies would create larger responses in left frontotemporal areas.
“Our study shows that the neural machinery used by adults to understand words is already functional when words are first being learned,” said Eric Halgren, Ph.D., professor of radiology in the School of Medicine.
“This basic process seems to embody the process whereby words are understood, as well as the context for learning new words.”
The scientists believe the results could affect future studies. For example, the development of brain imaging tests could diagnose whether a baby has normal word understanding even before he or she can talk. This could allow early prediction for language disabilities or autism.
Crush Injuries and Hyperbaric Oxygen TreatmentWe therefore need to consider the two ways by which the crush injury treatment that incorporates the hyperbaric oxygen works. First, it is important to note that during the initial stages of injury perfusion is likely to be inadequate. At such a time, immediate use of the hyperbaric oxygen makes more sense as it would supplement the supply of oxygen. The second way that really makes the use of hyperbaric oxygen useful is that it increases the tissue oxygen tension to the sufficient levels. Increased tissue oxygen in the plasma keeps the tissues alive without the oxygen that is borne from hemoglobin.
When the tension of tissue oxygen is increased, the effects of hypoxia that were initially felt when there was oxygen deficiency is countered. The other advantage that results from crush injury hyperbaric oxygen is the reduction of blood flow by up to 20 percent. The oxygen increases the induction of vasoconstriction and this is what causes the reduction. This in the end reduces edema. The filtration of the fluid that comes from the capillary to the extracellular space is also maintained.
The same treatment regime ensures that there is mitigation of reperfusion. This in turn interrupts the toxic oxygen radicals and the cell membrane. But you may ask how is that possible? Well, it actually perturbs lipid peroxiadation of the cell membrane and prevents the sequestration of neutrophils on the post capillary venules.
The other benefit of crush injury treatment hyperbaric is that it assists in provision of the oxygenated environment. Superoxide dismutase, catalase, peroxidase and glulathione which are useful for detoxification of reactive oxygen species actually depend in such environment to thrive.
When the crush injuries present in their severe forms, you should not think twice. You would be safe if you can quickly make use of the hyperbaric oxygen intervention that is quite effective. It is the only sensible and best way through which you would be able to counteract the pathophysiological events that occur when you have encountered a crush injury. The intervention is the sure way through which you will reduce loss of the muscle functions, the metabolites that come with muscle injury, edema and even muscle necrosis. Of course, this treatment is to be used together with the usual surgical and medical interventions that are in place.
Discovery points to a common cause for multifaceted disease By Elaine Schmidt May 25, 2011For decades, autism researchers have faced a baffling riddle: how to unravel a disorder that leaves no known physical trace as it develops in the brain.
Now a UCLA study is the first to reveal how the disorder makes its mark at the molecular level, resulting in an autistic brain that differs dramatically in structure from a healthy one. Published May 25 in the advance online edition of Nature, the findings provide new insight into how genes and proteins go awry in autism to alter the mind.
The discovery also identifies a new line of attack for researchers, who currently face a vast array of potential fronts for tackling the neurological disease and identifying its diverse causes.
"If you randomly pick 20 people with autism, the cause of each person's disease will be unique," said principal investigator Dr. Daniel Geschwind, the Gordon and Virginia MacDonald Distinguished Chair in Human Genetics and a professor of neurology and psychiatry at the David Geffen School of Medicine at UCLA. "Yet when we examined how genes and proteins interact in autistic people's brains, we saw well-defined shared patterns. This common thread could hold the key to pinpointing the disorder's origins."
The research team, led by Geschwind, included scientists from the University of Toronto and King's College London. They compared brain tissue samples obtained after death from 19 autism patients and 17 healthy volunteers. After profiling three brain areas previously linked to autism, the group zeroed in on the cerebral cortex, the most evolved part of the human brain.
The researchers focused on gene expression — how a gene's DNA sequence is copied into RNA, which directs the synthesis of cellular molecules called proteins. Each protein is assigned a specific task by the gene to perform in the cell.
By measuring gene-expression levels in the cerebral cortex, the team uncovered consistent differences in how genes in autistic and healthy brains encode information.
"We were surprised to see similar gene expression patterns in most of the autistic brains we studied," said first author Irina Voineagu, a UCLA postdoctoral fellow in neurology. "From a molecular perspective, half of these brains shared a common genetic signature. Given autism's numerous causes, this was an unexpected and exciting finding."
The researchers' next step was to identify the common patterns. To do this, they looked at the cerebral cortex's frontal lobe, which plays a role in judgment, creativity, emotions and speech, and at its temporal lobes, which regulate hearing, language and the processing and interpreting of sounds.
When the scientists compared the frontal and temporal lobes in the healthy brains, they saw that more than 500 genes were expressed at different levels in the two regions.
In the autistic brains, these differences were virtually non-existent.
"In a healthy brain, hundreds of genes behave differently from region to region, and the frontal and temporal lobes are easy to tell apart," Geschwind said. "We didn't see this in the autistic brain. Instead, the frontal lobe closely resembles the temporal lobe. Most of the features that normally distinguish the two regions had disappeared."
Two other clear-cut patterns emerged when the scientists compared the autistic and healthy brains. First, the autistic brain showed a drop in the levels of genes responsible for neuron function and communication. Second, the autistic brain displayed a jump in the levels of genes involved in immune function and inflammatory response.
"Several of the genes that cropped up in these shared patterns were previously linked to autism," said Geschwind. "By demonstrating that this pathology is passed from the genes to the RNA to the cellular proteins, we provide evidence that the common molecular changes in neuron function and communication are a cause, not an effect, of the disease."
The next step will be for the research team to expand its search for the genetic and related causes of autism to other regions of the brain.
Autism is a complex brain disorder that strikes in early childhood. The disease disrupts a child's ability to communicate and develop social relationships and is often accompanied by acute behavioral challenges. In the United States, autism spectrum disorders are diagnosed in one in 110 children — and one in 70 boys. Diagnoses have expanded tenfold in the last decade.
The study was funded by the National Institute of Mental Health, the Canadian Institutes of Health Research, and Genome Canada. Tissue samples were provided by the Autism Tissue Project, the Harvard Brain Bank and the Medical Research Council's London Brain Bank for Neurodegenerative Disease.
Geschwind's and Voineagu's co-authors included Jennifer Lowe, Yuan Tian, Steve Horvath, Jonathan Mill, Rita Cantor and Benjamin Blencowe of UCLA; Xinchen Wang of the University of Toronto; and Patrick Johnston of King's College London.
Encephalitis simply means brain inflammation. The inflammatory reaction not only damages tissue, but also the microcirculation - small arteries capillaries and particularly small veins. The damage to the blood supply is the main determinant of recovery because of oxygen transport limitation.
The result is that brain tissue can remain in suspended animation "not dead but sleeping" - simply because of the increased tissue water - edema - chronically preventing adequate oxygenation. The best analogy is a comparison with an electrical device.
Imagine coupling a transistor radio - which requires a 9-volt battery to a 6-volt battery - it simply will not work - even if the six-volt battery is capable of delivering thousands of amperes - like a submarine battery.
There is nowhere on the surface of this planet that breathing air the oxygen level (voltage) in plasma can exceed about 100 (mm Hg).
In a hyperbaric chamber breathing pure oxygen, the level can be increased to over 2000 (mm Hg). This simple and completely scientific explanation for the need for hyperbaric conditions is UNKNOWN to the overwhelming majority of physicians - hence oxygen is not properly used.
Neurologists have recognized the need for oxygen. Three of the most eminent neurologists/neurosurgeons of the 80's stated in relation to the ischemic penumbra.
"Presumably the critical parameter for tissue function is oxygen availability rather than blood flow." Using hyperbaric conditions allows a decoupling of blood flow and oxygen transport.
Astrup J, Siesjo BK, Symon L. "Thresholds in cerebral ischemia -the ischemic penumbra." Stroke 1981;12:723-725.
Therefore, if we are to discover if there is recoverable brain tissue we need to reoxygenate. Dr Richard Neubauer has used SPECT imaging to demonstrate this effect and the work is published e.g. Lancet March 3 1990.
Dr Philip James M.D.
Reprinted with Permission
Brain Injury and Recovery with Hyperbaric Oxygen
Hypoxia is a state of oxygen deficiency in the body, which is sufficient to cause an impairment of function. Hypoxia is caused by the reduction in partial pressure of oxygen, inadequate oxygen transport, or the inability of the tissues to use oxygen.
In brief, being drunk is kind of the same as being exposed to high altitude. In both cases, oxygen to your brain and muscles is reduced.
Hypoxic Hypoxia is a reduction in the amount of oxygen passing into the blood. It is caused by a reduction in oxygen pressure in the lungs, by a reduced gas exchange area, exposure to high altitude, or by lung disease. [This is the hypoxia that is a hazard to aviators.]
Pemic Hypoxia is defined as a reduction in the oxygen carrying capacity of the blood. It is caused by a reduction in the amount of hemoglobin in the blood or a reduced number of red blood cells. A reduction in the oxygen transport capacity of the blood occurs through blood donation, hemorrhage, or anemia. A reduction in the oxygen carrying capacity of the blood occurs through drugs, chemicals, or carbon monoxide. [This hypoxia usually experienced by smokers.]
Stagnant Hypoxia is an oxygen deficiency due to poor circulation of the blood or poor blood flow. Examples of this condition are high "G" forces, prolonged sitting in one position or hanging in a harness, cold temperatures, and positive pressure breathing. [This hypoxia usually experienced when sitting for hours in a boring class.]
Histotoxic Hypoxia is defined as the inability of the tissues to use oxygen. Examples are carbon monoxide and cyanide poisoning. Certain narcotics, chewing tobacco, and alcohol will prevent oxygen use by the tissues. [This hypoxia usually experienced after drinking too much.]
Dr James MD
Reprinted with Permission
Received Jul 30, 1997; accepted Sep 23, 1997.
Robert E. Weibel*, Vito Caserta*, David E. Benor
, and Geoffrey Evans*
Office of the General Counsel, United States Department of Health and Human Services, Rockville, Maryland.
MONDAY, Dec. 19 2009 (HealthDay News) -- New research with rats suggests that oxygen deprivation during birth could be a contributing cause of autism.
There's no easy way to test the oxygen-deprivation theory in humans, and the finding isn't likely to lead to better treatments in the near future. Still, the research gives scientists greater insight into how factors other than genetics may play a role in autism, said Fabrizio Strata, a neuroscience researcher at the University of California, San Francisco and co-author of the study.
Symptoms of autism, the most common condition in a group of developmental disorders known as autism spectrum disorders, can range from mild to severe. The disability usually strikes by age 3. It lasts a lifetime, and there is no cure, although some people with autism can learn to function well.
According to the U.S. Centers for Disease Control and Prevention
For reasons that aren't clear, autism seems to have become more common in recent years. One hotly debated theory suggests that vaccines are responsible, although some studies have failed to find a link.
Oxygen deprivation during birth is considered one possible cause because it can lead to brain damage
By boosting the level of nitrogen in the air, Strata and colleagues deprived rat pups of normal levels of oxygen for as long as 10 to 12 minutes during birth. When the rats grew older, they displayed symptoms similar to those found in autistic children. It took longer for the rats to respond to some sounds, for example, and the brain regions that handle sound were disrupted.
Why would a baby be oxygen-deprived in the first place? According to Strata, a complicated labor can cut off a newborn's oxygen supply, as can a twisted umbilical cord.
Andy Shih, chief science officer with the National Alliance for Autism Research, said the oxygen-deprivation study presents an "interesting hypothesis," although the research hasn't been confirmed in humans.
It's possible that future research could lead to changes in obstetric practices to minimize the chance that babies will go without oxygen, Shih said. But "we're far away from that at this point."
The study findings appear in the Dec. 19-24 issue of the Proceedings of the National Academy of Sciences.
SOURCES: Fabrizio Strata, Ph.D., Keck Center for Integrative Neuroscience, University of California, San Francisco; Andy Shih, Ph.D., chief science officer, National Alliance for Autism Research, Princeton, N.J.; Dec. 19-23, 2005, Proceedings of the National Academy of Sciences
