Tuesday, 28 June 2016

Hair Loss During Pregnancy


Hair Scalp Anatomy

Hair Scalp Anatomy


View the latest health news and explore articles on fitness,t, nutrition, parenting, relationships, medicine, diseases and healthy living at CNN Health..


Hair Scalp Anatomy

Hair Scalp Anatomy

What Is A Maturing Hairline Is It A Sign Of Male Pattern Baldness

What Is A Maturing Hairline Is It A Sign Of Male Pattern Baldness


View the latest health news and explore articles on fitness,t, nutrition, parenting, relationships, medicine, diseases and healthy living at CNN Health..



Diclofenac sodium treatment sciatica


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Monday, 27 June 2016

Cold Tamil



Tennis elbow Lateral Epicondylitis



Tennis elbow(Lateral Epicondylitis)
tennis elbow is a very common clinical entity seen as a pain and tenderness in the common origin from the extensor group muscles from the forearm,usually due to a specific strain, overuse, or perhaps a direct bang.It's considered a cumulative trauma injury occurring over time from repeated utilisation of the muscles of the arm and forearm, resulting in small tears from the tendons (Tendonitis).The condition that's commonly associated with playing tennis along with other racket sports, though the injury may happen to almost anybody.
The tendinous origin of extensor carpi radialis brevis (ECRB) may be the area of most pathologic changes. Changes can be found at musculotendinous structures from the extensor carpi radialis longus, extensor carpi ulnaris and extensor digitorum communis. Overuse and repetitive trauma in this region causes fibrosis and micro tears within the involved tissues. Nirschl known the micro tears and also the vascular in development of the involved tissues as angiofibroblastic hyperplasia. A tear occurs in the teno-muscular junction, in the tendon, or in the teno-periosteal junction. The resulting inflammation produces exudate by which fibrin forms to heal the torn tissue.Repeated activity causes micro trauma, with subsequent granulation tissue formation around the underside of the tendon unit and also at the teno-periosteal junction. The granulation tissue formed seems to contain large number of free nerve endings, hence the pain sensation of the condition. The issue is that the granulation tissue doesn't progress quickly to some mature form, and thus healing fails to occur, almost a type of tendinous 'nonunion'.
Reason for tennis elbow
The most typical cause of Lateral Epicondylitis in tennis players is really a 'late' mechanically poor backhand, that places excess force over the extensor wad, that is, the elbow leads the arm. Other allies include incorrect grip size,string tension, poor racket dampening, and underlying weak muscles from the shoulder,elbow and arm.Tennis grips which are too small often exacerbate or cause tennis elbow. Normally a history of repetitive flexion-extension or pronation-supination activity and overuse is obtained (eg.,twisting a screwdriver, lifting heavy luggage using the palm down). Tightly gripping huge briefcase is a very common cause.Raking leaves, baseball, golfing, gardening, and bowling may also cause Lateral Epicondylitis. Less commonly,tendonitis is only a result of single acute injury.
Clinical Presentation
In the beginning, the athlete might be aware of only fatigue and spasm of dorsal forearm muscles associated with unaccustomed activity. They may note the start of aching lateral elbow pain after playing. Eventually the pain sensation may become so constant and severe in order to stop the athlete from further playing and also to interfere with activities of everyday living, such as carrying a briefcase, wringing wet clothes as well as holding a cup of tea. Grip becomes weak.Morning stiffness might be felt.
 Examination
-Point tenderness over or simply distal to the lateral humeral epicondyle (the bony attachment from the common extensor tendon) which provides rise to burning sensation when pressure is used.
Tenderness over muscles of dorsal forearm.
Pain with resisted wrist extension, finger extension and resisted radial deviation.
Pain with passive stretching of wrist extensors.
With traditional symptoms, there is apt to be considerable atrophy and weakness of extensor muscles and limitation of passive wrist flexion. Accessory movements from the elbow and superior radio-ulnar joint might be reduced in along term problem.
Special tests for tennis elboW
1)Cozen's test- The patient's elbow is stabilized through the examiner's thumb, which rests around the patient's lateral epicondyle. The individual is then asked to create a fist, pronate the forearm and radially deviate and extend the wrist as the examiner resists the motion. An optimistic sign is shown by sudden severe pain in the region of lateral epicondyle from the humerus.
2)Mill's test-While palpating the lateral epicondyle, the examiner pronates the patient's forearm, and flexes the wrist fully and extends the elbow. An optimistic test is shown by pain over the lateral epicondyle of humerus.
3)Maudsley's test- The examiner resists extension from the 3rd digit from the hand, stressing the extensor digitorum muscle and tendon. An optimistic test is shown by pain over the lateral epicondyle from the humerus.
Differential Diagnosis
Evaluation should note possible sensory paresthesias within the superficial radial nerve distribution to eliminate Radial tunnel syndrome.It's the most common cause of refractory lateral pain and coexists with Lateral Epicondylitis in 10% of the sufferers.
The cervical nerve roots ought to be examined to rule out cervical radiculopathy.
Other concerns that should be considered include bursitis from the bursa below the conjoined tendon, chronic irritation from the radiohumeral joint or capsule, radiocapitellar chondromalacia or arthritis, radial neck fracture, panner's disease, little league elbow and osteochondritis dissecans from the elbow.
 Investigations
X-rays aren't necessary. Rarely, magnetic resonance imaging (MRI) scans enables you to show changes in the tendon to begin of attachment to the bone. MRI typically shows fluid within the ECRB origin. There may also be a defect within this tissue. The use of the term "tear" to refer to this defect could be misleading. The word "tear" implies injury and also the need for repair--both of which are most likely inaccurate and inappropriate for this degenerative enthesopathy.
Conservative treatment of tennis elbow
Activity Modification
-In non-athletes, removal of activities that are painful is essential to improvement (eg., repetitive valve opening).
PRICE METHOD..

NUMBER OF GENES LINKED TO HEIGHT REVEALED



The largest genome-wide association study (GWAS) to date, involving more than 300 institutions and more than 250,000 subjects, roughly doubles the number of known gene regions influencing height to more than 400. The study, from the international Genetic Investigation of Anthropometric Traits (GIANT) Consortium, provides a better glimpse at the biology of height and offers a model for investigating traits and diseases caused by many common gene changes acting together. Findings were published online October 5 by Nature Genetics

Height is almost completely determined by genetics, but our earlier studies were only able to explain about 10 percent of this genetic influence," says Joel Hirschhorn, MD, PhD, of Boston Children's Hospital and the Broad Institute of MIT and Harvard, leader of the GIANT Consortium and co-senior investigator on the study. "Now, by doubling the number of people in our study, we have a much more complete picture of how common genetic variants affect height -- how many of them there are and how much they contribute."
The GIANT investigators, numbering in the hundreds, shared and analyzed data from the genomes of 253,288 people. They checked about two million common genetic variants (those that showed up in at least 5 percent of their subjects). From this pool, they pinned down 697 (in 424 gene regions) as being related to height, the largest number to date associated with any trait or disease.
"We can now explain about 20 percent of the heritability of height, up from about 12 percent where we were before," says co-first author Tonu Esko, PhD, of Boston Children's Hospital, the Broad Institute and the University of Tartu (Estonia).
"The study also narrows down the genomic regions that contain a substantial proportion of remaining variation -- to be discovered with even larger sample sizes," adds co-senior investigator Peter Visscher, PhD, of the University of Queensland, Australia.
Greater size, greater power
Height is a model trait for understanding how human genetics works -- especially for traits produced by not one gene, but many. Height is easy to measure, and an estimated 80 percent of variation in height is genetic.
Previous large-scale genome-wide association studies (GWAS) have indicated that a large number of genes influence height, and suggested that the majority of heritability comes from common genetic variants, not rare ones. Because sample sizes have not been large enough to draw definitive conclusions, the GIANT team built the largest sample to date.
"When you double the sample size and increase your statistical power, you can make new discoveries," says Hirschhorn. "Our results prioritize many genes and pathways as important in skeletal growth during childhood. Without a highly collaborative model, there's no way we could get this work done."
The researchers believe their results answer critics of population-scale GWAS, who have argued that increasing the sample size yields diminishing returns or results that become meaningless.
"In 2007 we published the first paper that identified the first common height gene, and we have now identified nearly 700 genetic variants that are involved in determining height," says co-senior investigator Timothy Frayling, PhD, of the University of Exeter, U.K. "We believe that large genetic studies could yield similarly rich lists in a variety of other traits."
The biology of height
Many of the 697 height-related genetic variants were located near genes known to be involved in growth, but there were also plenty of surprises.
"There were some pathways that we knew were important, but had not come out in previous GWAS," says Hirschhorn, who is also an endocrinologist at Boston Children's. "Many of the genes we identified are likely to be important regulators of skeletal growth, but were not known to be involved until now. Some may also be responsible for unexplained syndromes of abnormal skeletal growth in children. As you increase the sample size, you get more biology."
For example, the mTOR gene is well known to be involved in cellular growth, but had not previously been connected with human skeletal growth. Other genes confirmed as important include genes involved in metabolism of collagen (a component of bone) and chondroitin sulfate (a component of cartilage), as well as networks of genes active in growth plates, the area of growing tissue near the ends of the long bones. Still other genes point to biology whose relationship with height isn't yet known.
Among GIANT's future goals is to look at variants that occur at lower than 5 percent frequency, and to look for variants in the non-protein-coding portions of genes.



Saturday, 25 June 2016

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NEW TECHNIQUE TO RESTORE BODYS INSULIN PRODUCING ABILITY



There is good news for patients suffering from type-one diabetes as they may soon be able to do away with their daily insulin dose to manage their blood-sugar levels.
Researchers have found that a peptide called caerulein can convert existing cells in the pancreas into those cells destroyed in type-one diabetes-insulin-producing beta cells.
“We have found a promising technique for type-one diabetics to restore the body’s ability to produce insulin,” said Fred Levine, a professor at Sanford-Burnham Medical Research Institute in the US.
“By introducing caerulein to the pancreas, we were able to generate new beta cells – the cells that produce insulin,” Levine added.
The study first examined how mice in which almost all beta cells were destroyed – similar to humans with type-one diabetes – responded to injections of caerulein.
In those mice, but not in normal mice, they found that caerulein caused existing alpha cells in the pancreas to differentiate into insulin-producing beta cells.
The research team then examined human pancreatic tissue from type-one diabetics, finding 
strong evidence that the same process induced by caerulein also occurred in the pancreases of those individuals.
Caerulein is a peptide originally discovered in the skin of Australian Blue Mountains tree frogs.
It stimulates gastric, biliary, and pancreatic secretions, and has been used in humans as a diagnostic tool in pancreatic diseases.
An estimated over 300 million people worldwide are living with type-one diabetes.
The study appeared in the journal Cell Death and Disease.

Neuropathy Over The Long Term


Today's post from livestrong.com (see link below) looks at the effects of neuropathy over the long term and although short and to the point, may help you understand what and why certain things are happening to you. It makes the point that ,"some types of peripheral neuropathy do not have a cure" when the truth is that, in fact very few types of neuropathy do have the potential for a cure but other than that, the information is accurate. Not happy reading for those living with nerve damage over several years but if you know what to look out for, you may be able to take steps to reduce the impact on your lives. Remember also, autonomic neuropathy is not a given by any means (you'll understand after reading the article).

Long-Term Effects of Peripheral Neuropathy 
Last Updated: Sep 22, 2015 | By Lia Stannard 

Overview

Peripheral neuropathy is a condition that affects the nerves outside of the brain or spinal cord. It can cause changes to sensation, movement and involuntary functions. Pressure on the nerves can cause peripheral neuropathy, as can certain conditions such as Charcot-Marie-Tooth disease, an inherited disorder. MedlinePlus, a website of the National Institutes of Health, points out that some types of peripheral neuropathy do not have a cure. The nerve damage from this condition can have lasting effects.


Reduced Feeling

Peripheral neuropathy affects three types of nerves: sensory, motor and autonomic. The sensory nerves relay information to the brain such as a change in temperature. When peripheral neuropathy damages the sensory nerves, patients can experience nerve pain, burning sensations or tingling. Some patients may have numbness that starts in the feet and moves up in the body. MayoClinic.com explains that with the numbness, patients can have reduced feeling in their limbs, which can affect their ability to sense changes. Problems can arise, such as in the case of a peripheral neuropathy patient who cannot feel pain in his feet and therefore does not notice a foot injury. If the injury goes untreated, an infection can develop.

Problems Moving

Since peripheral neuropathy can affect the motor nerves, patients may have a partial or total loss of movement and muscle control. For example, patients may experience paralysis of certain parts of the body such as the arms or legs. MedlinePlus points out that patients may fall from tripping over themselves. Peripheral neuropathy can cause muscle atrophy, in which patients lose some muscle tissue. Patients may have a lack of muscle control and dexterity, which can affect their ability to do tasks that require fine movements, such as writing with a pen. Damage to the autonomic nerves, which control the involuntary functions, can also impair movement. For example, patients can have dizziness when they stand up. 


Weight Loss

Peripheral neuropathy patients may lose weight as a result of the autonomic nerve damage symptoms. MedlinePlus points out that peripheral neuropathy patients can lose more than 5 percent of their body weight. They may have nausea and vomiting after meals. The autonomic symptoms of peripheral neuropathy cause patients to feel full after eating a small amount of food, which can also affect weight. Motor nerve damage in the throat can affect patients' ability to swallow, which may cause them to eat less. 


Low Self-esteem

MedlinePlus explains that the symptoms of peripheral neuropathy can cause patients to have low self-esteem. For example, male peripheral neuropathy patients may feel self-conscious about impotency problems. Urinary incontinence, or urine leakage, is another embarrassing problem related to peripheral neuropathy that can affect self-esteem.




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Chemicals That Cause Neuropathy
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Side Effects of Neuropathy
Peripheral Neuropathy and Vitamin B12
Alternative Treatment for Peripheral Neuropathy
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Neuropathy Symptoms in the Feet
The Effects of Methyl B12 on Neuropathy
Neuropathy Pain Symptoms
Caffeine & Neuropathy
Vitamins for Peripheral Neuropathy
Vitamin & Mineral Supplements for Neuropathy
Arm Neuropathy Causes
Gluten & Peripheral Neuropathy
Fiber Neuropathy Symptoms

 
http://www.livestrong.com/article/161390-long-term-effects-of-peripheral-neuropathy/

Just a thought



Being in nature makes me perfectly happy, this kind of happiness that exists in unity and contentment. It is the place where the less I do, the more impact I have. The most effective, profound actions I can possibly take, are to listen, to watch, to feel, smell and be open. I don't have to prove anything to her. She doesn't care what achievements I have, how much or little I know, or what kind of jeans I have on. She doesn't know my sorrows or my joys, for they all melt together into the thin air of existence. It all is what it is. The duck floats. The Goose sits on her nest. The frog hops. The tree grows. The matrix is self sufficient.

Friday, 24 June 2016

The HIV Virus Itself Can Attack The Nervous System At An Early Stage


Today's post from the always reliable sciencedaily.com (see link below) reports something that will be of no surprise to people living with HIV across the world and that is that neuropathy very often appears from the early stages of infection. This gives proof to the theory that the virus itself attacks the nervous system. The accepted knowledge is that neuropathy in HIV is linked to older toxic HIV drugs and doctors are still continually surprised that people arrive in their surgeries with neuropathic symptoms, despite being on the most modern HIV medication combinations. The study mentioned here claims that the symptoms appear pre-medication treatment and generally disappear after treatment begins. However, there has to be some considerable doubt about this claim! Neuropathic symptoms don't disappear and nerve damage is, at the moment, generally irreversible. People living with HIV generally see a worsening of their symptoms over a period of time and end up on the treadmill of drugs designed to suppress the discomfort but not cure it. Perhaps the most relevant finding of the study is that after contracting HIV, many people will show signs of nerve damage, with all the symptoms that we're familiar with. The idea that this is linked to the older drug regimes is somewhat outdated but not totally incorrect and modern HIV drugs can cause nerve damage too. The problem is that it's clear that the HIV virus itself attacks nerve cells and especially mitochondria and although HIV medications (old or new) don't help, they're not exclusively responsible for neuropathy in HIV patients.


Neurologic symptoms common in early HIV infection
Much more extensive, though milder than previously thought
 

Date:June 13, 2016 Source:University of California - San Francisco

A team led by researchers from UCSF and Yale has found that half of people newly infected with HIV experience neurologic issues. These neurologic findings are generally not severe and usually resolve after participants started anti-retroviral therapy.

"We were surprised that neurologic findings were so pervasive in participants diagnosed with very recent HIV infection," said study lead author, Joanna Hellmuth, MD, MHS, clinical fellow in UCSF's Department of Neurology. "While the findings were mild, it is clear that HIV affects the nervous system within days of infection. Since the majority of these neurologic issues were resolved with treatment, our study reinforces recommendations that people at risk for HIV test often and start antiretroviral treatment immediately if they are infected."

The research will be published in the June 10, 2016, issue of Neurology, the medical journal of the American Academy of Neurology.

The team examined 139 participants in the RV254 Thai cohort who were recently infected with HIV. The time from infection to entry into the study ranged from 3 to 56 days with a median of 19 days. At this stage, participants would not test positive on the common antibody tests for HIV since they have not been infected long enough for a robust specific immune response to take place. Fifty-three percent had neurologic findings, with a third experiencing cognitive deficits, a quarter having motor issues, and nearly 20 percent experiencing neuropathy. Many experienced more than one symptom. One participant was diagnosed with Guillain-Barré Syndrome, the only severe case found in the cohort.

"In the early days of the epidemic in San Francisco, approximately 10 percent of patients with recent HIV infection presented with dramatic neurological disease. But that was likely due to patients coming in early because of the severity of symptoms they were experiencing. The Thai cohort has given us an opportunity to look at a broad range of newly infected patients, analyze their neurological functioning systematically and follow them over time. We are gaining deeper insights into the degree to which early HIV affects the nervous system," said study senior author, Serena Spudich, MD, Yale associate professor of neurology.

All participants were offered and commenced antiretroviral treatment at diagnosis. Ninety percent of the issues present at diagnosis were resolved after one month of treatment, but 9 percent of the participants had neurologic symptoms that were still not resolved six months after starting therapy. In addition, neurological symptoms were associated with higher levels of HIV found in participants' blood.

The study participants underwent extensive neurologic assessments. Self reported symptoms were correlated with objective neuropsychological testing. In addition, a quarter of participants opted to undergo a lumbar puncture and almost half of the patients agreed to undergo a MRI.

"This is one of the first comprehensive studies scrutinizing the involvement of the nervous system in early infection. Since we have been able to maintain the cohort for five years now, we will be able to study whether there are any persistent abnormalities that need to be addressed. Additionally, the ubiquity of symptoms in early infection found in this study reinforces the need for the brain to be considered as a compartment containing latent HIV as we design cure studies," said study co-author, Victor Valcour, MD, PhD, UCSF professor of neurology.

Story Source:

The above post is reprinted from materials provided by University of California - San Francisco. The original item was written by Jeff Sheehy. Note: Materials may be edited for content and length.

Journal Reference:
Joanna Hellmuth, James L.K. Fletcher, Victor Valcour, Eugène Kroon, Jintanat Ananworanich, Jintana Intasan, Sukalaya Lerdlum, Jared Narvid, Mantana Pothisri, Isabel Allen, Shelly J. Krebs, Bonnie Slike, Peeriya Prueksakaew, Linda L. Jagodzinski, Suwanna Puttamaswin, Nittaya Phanuphak, Serena Spudich. Neurologic signs and symptoms frequently manifest in acute HIV infection. Neurology, 2016; 10.1212/WNL.0000000000002837 DOI: 10.1212/WNL.0000000000002837


https://www.sciencedaily.com/releases/2016/06/160613105753.htm

WHY YOUR BRAIN MAKES YOU REACH FOR JUNK FOOD


Will that be a pizza for you or will you go for a salad? Choosing what you eat is not simply a matter of taste, conclude scientists in a new study at the Montreal Neurological Institute and Hospital of McGill University and the McGill University Health Centre. As you glance over a menu or peruse the shelves in a supermarket, your brain is making decisions based more on a food's caloric content.
The study, published in Psychological Science, is based on brain scans of healthy participants who were asked to examine pictures of various foods. Participants rated which foods they would like to consume and were asked to estimate the calorie content of each food. Surprisingly, they were poor at accurately judging the number of calories in the various foods, but their choices and their willingness to pay still centered on those foods with higher caloric content.
"Earlier studies found that children and adults tend to choose high-calorie food" says Dr. Alain Dagher, neurologist at the Montreal Neurological Institute and Hospital and lead author of the study. "The easy availability and low cost of high-calorie food has been blamed for the rise in obesity. Their consumption is largely governed by the anticipated effects of these foods, which are likely learned through experience. Our study sought to determine how people's awareness of caloric content influenced the brain areas known to be implicated in evaluating food options. We found that brain activity tracked the true caloric content of foods."
Decisions about food consumption and caloric density are linked to a part of the brain called the ventromedial prefrontal cortex, an area that encodes the value of stimuli and predicts immediate consumption.
Understanding the reasons for people's food choices could help to control the factors that lead to obesity, a condition affecting 1 in 4 Canadian adults and 1 in 10 children. Obesity is linked to many health problems including high blood pressure, heart disease and type 2 diabetes. Treating Canadians who have these problems costs billions of tax health dollars.
This work was funded by the Canadian Institutes of Health Research.


Breathing Exercises



Breathing exercise and ventilator training are fundamental intervention for that prevention or comprehensive management of impairment associated with acute or chronic pulmonary disorders. Breathing Workouts are commonly incorporated into the general pulmonary rehabilitation program of patients with acute or chronic pulmonary disorders. Breathing workouts are designed to restrain the muscles of respiration and improve or redistribute ventilation, decrease the work of breathing, and enhance the gas exchange and oxygenation. Active flexibility exercises, to the shoulders and trunk also help expand the chest area, facilitate deep breathing, and frequently stimulate the cough reflex. After heart surgery, pneumonia or injuries involving fractured ribs, it's not uncommon for lung ability to be impaired. To recuperate and maintain proper breathing, physiotherapy breathing exercises might be implemented. Techniques like "huffing," a controlled type of coughing, and use of the incentive spirometer, a self-administered breathing device, are types of standard therapeutic exercises. Based on MayoClinic.com, people who have acute asthma or cystic fibrosis could also benefit from pulmonary rehabilitation exercises.
Aim for Breathing Exercises
To mobilize secretions.
To show effective coughing and take away secretions.
To teach relaxation.
To show breathing control.
To show postural awareness.
To mobilize thorax and shoulder girdle.
Enhance the strength,endurance,and coordination from the muscle of ventilation.
Prevent postoperative pulmonary complications.
Indications for Breathing Exercises
Acute or chronic lung disease.
Chronic obstructive lung disease.
Pneumonia.
Atelectasis.
Pulmonary embolism.
Acute respiratory distress.
Pain within the thoracic or abdominal area due to surgery or trauma.
Airway obstruction secondary to bronchospasm or retained secretions.
Deficit within the central nervous system that lead to muscle weakness.
High spinal-cord injury.
Acute, chronic, or progressive myopathic or neuropathy diseases.
Severe orthopedic abnormalities, for example scoliosis and kyphosis, that affect respiratory function.
Stress management and relaxation procedures.


Types for Breathing Exercises..


DIAPHARAGMATIC BREATHING


Lateral costal expansion
Posterior basal expansion
PURSED LIP BREATHING
PREVENTING AND RELIEVING Instances of DYSPNEA
POSITIVE EXPIRATORY PRESSURE BREATHING
RESPIRATORY RESISTANCE TRAINIG
GLOSSOPHARYNGEAL BREATHING
Goals of Breathing Exercises
Improve ventilation.
Increase the potency of the cough mechanism.
Prevent pulmonary impairments.
Improve the strength, endurance, and coordination of respiratory muscles.
Maintain or improve chest and thoracic spine mobility.
Correct inefficient or abnormal breathing patterns.
Promote relaxation.
Teach the individual how to deal with shortness of breath attacks.
Improve a patient’s overall functional capacity.

Words To Help You Understand Neuropathy Better


Today's short post from pain.com (see link below) is a useful one for both newcomers to neuropathy and those who have been living with it for some time. There are very few diseases with as much associated vocabulary as neuropathy! You can guarantee that whatever words your doctor uses at your diagnosis, there are 10 or more alternatives. more or less describing the same thing, that you will hear of or read about during the following months and years. It's a disease that prefers to use 10 scientific terms when actually one or two will do. This makes it a minefield for patients, who think they've finally got a handle on their condition, only to find that they've still got a whole new lexicon of descriptive words to learn. That comes from the fact that there are over 100 sorts and over 100 causes of neuropathy and each comes with its own descriptive vocabulary. This article at least tries to narrow it down to a few key words but even then, I find myself thinking, 'Why haven't they included this one or that one?' I also had to admit...'dermatomes' is a new one for me too. It's like being back at school again but at least articles like this try to help navigate the obstacle course.

Neuropathy: 10 Terms to Know
Pain.com May 2016
 
Neuropathy, simply put, is pain from nerve damage. Here are ten terms you should know about the condition.

Peripheral nervous system: the system of nerves outside the central nervous system (which is made up of the brain and spinal cord). The peripheral nervous system sends signals from the central nervous system to the rest of your body.

Peripheral neuropathy:
damage to these nerves, which leads to pain, numbness, weakness, and burning or tingling sensations in the limbs, hands, and feet. It can be caused by genetics, toxin exposure, traumatic injury, infection, or metabolic conditions.

Diabetic neuropathy: nerve damage that occurs specifically as a result of complications from undiagnosed or untreated diabetes.

Sensory nerves: nerves that perceive sensations on the skin, such as heat, cold, pain, vibrations, or physical contact.

Motor nerves: control the movement of muscles

Autonomic nerves: control automatic bodily functions like digestion, bladder function, heartbeat, and blood pressure.

Dermatomes: connect peripheral nerves to the spinal cord; because the dermatomes coordinate with certain areas of the body, the symptoms can be used to trace which nerves are damaged.

Mononeuropathy: damage to a single nerve.

Multiple mononeuropathy: damage to two or more nerves that affect different areas of the body.

Polyneuropathy: damage that affects many nerves.

If you are experiencing symptoms such as muscle weakness, tingling or numbness, burning or shooting pains in the limbs, loss of control over muscles or bowel and bladder function, consult your doctor for tests.


References:
http://www.mayoclinic.org/diseases-conditions/peripheral-neuropathy/basics/definition/con-20019948
http://www.medicinenet.com/peripheral_neuropathy/article.htm
http://www.webmd.com/brain/understanding-peripheral-neuropathy-basics
http://www.diabetes.org/living-with-diabetes/complications/neuropathy/


http://pain.com/archives/2016/05/04-neuropathy-10-terms/

Relief Therapeutics To Develop New Neuropathy Treatment


Today's post from pharmaceutical-technology.com (see link below) looks at the news that pharma company, Merck has agreed to allow Relief Therapeutics to develop and commercialise a new drug to combat neuropathy. However, in contrast to others, this drug will not combat the pain and discomfort of neuropathy alone but is aimed at regenerating and stimulating nerve health and growth. The drug is called atexakin alfa and it's a human recombinant version of interleukin-6. Basically, that means that it's a bio-active protein that enables cell culture in studies to be carried out with as little contamination as possible. it's essentially a sort of stem cell therapy. It has been found that atexakin alfa induces a regrowth of nerve cells and as such has obvious potential where nerve damage occurs. This may all seem gobbledegook to you but it's evidence of progress in tackling nerve damage itself and not just the effects of nerve damage, which is what most treatments currently do. That's research moving in a different direction and suggests that our neuropathic damage may be able to be repaired in the future.


Relief gets rights from Merck to develop atexakin alfa for peripheral neuropathies treatment
8 September 2015

Swiss start-up company Relief Therapeutics has entered an in-licensing agreement from Merck Serono to secure exclusive rights to develop and commercialise atexakin alfa, a human recombinant version of interleukin-6.

In preclinical studies, atexakin alfa has been shown to induce the re-growth of nerves and re-establish normal nerve conduction and sensory perception in various relevant animal models of neuropathies.

Initially discovered at the Weizmann institute (IL), atexakin alfa was first tested as a potential treatment for thrombocytopenia in chemotherapy-treated cancer patients, allowing the delineation of its safety and pharmacodynamic profiles.
"This agreement constitutes a great opportunity to develop the first disease modifying treatment that has the potential to significantly reduce the burden of neuropathies to patients, care givers and society."

As part of the deal, Relief Therapeutics will be responsible for development of atexakin alfa to treat neuropathies.

Based on positive preclinical, toxicological and clinical data, Relief will engage in clinical development to evaluate the therapeutic efficacy of atexakin alfa in diabetic patients suffering from neuropathy.

The company noted that atexakin alfa has the potential of relieving pain, as well as non-pain symptoms associated with neuropathies by restoring normal innervation in the periphery.

Relief Therapeutics co-founder Dr Gael Hédou said: "This agreement constitutes a great opportunity to develop the first disease modifying treatment that has the potential to significantly reduce the burden of neuropathies to patients, care givers and society."

Peripheral neuropathies are a group of conditions characterised by degeneration of peripheral motor, sensory, or autonomic nerves, which causes a wide variety of symptoms and signs ranging from intractable pain, numbness and tingling to potentially impairment of strength, balance and coordination.

Neuropathies develop as a result of toxic, inflammatory, infectious, genetic, neoplastic, and metabolic diseases.

http://www.pharmaceutical-technology.com/news/newsrelief-rights-merck-develop-atexakin-alfa-peripheral-neuropathies-treatment-4665940

Thursday, 23 June 2016

Strategies For Living With Neuropathy Vid


In today's video from beatingneuropathy.tv (see link below) Dr. John Hayes gives some very useful advice for people living with neuropathy, chronic pain and other related diseases. He stresses the importance of having a strategic plan for getting the best out of your situation and that involves considerable input on your part, especially relating to lifestyle. Worth a watch.


Episode 49: Do YOU have a REAL Neuropathy and ChronicPain Treatment Strategy?
 
Posted by John Hayes Jr Friday, March 7th, 2014

Do YOU have a REAL Neuropathy and Chronic Pain Treatment Strategy? Has anyone ever suggested an organized and focused treatment plan? Well in this video Dr John Hayes Jr talks real about what you must know to make informed care choices and Neuropathy treatment decisions!





 http://beatingneuropathy.tv/2014/03/episode-49-do-you-have-a-real-neuropathy-chronicpain-treatment-strategy/

HIGH DENSITY SOUND WAVES MAY AID REGENERATIVE MEDICINE


Researchers at the University of Washington have developed a way to use sound to create cellular scaffolding for tissue engineering, a unique approach that could help overcome one of regenerative medicine's significant obstacles. The researchers will present their technique at the 168th meeting of the Acoustical Society of America (ASA), held October 27-31, 2014, at the Indianapolis Marriott Downtown Hotel.
The development of the new technique started with somewhat of a serendipitous discovery. The University of Washington team had been studying boiling histotripsy -- a technique that uses millisecond-long bursts of high-intensity ultrasound waves to break apart tissue -- as a method to eliminate cancerous tumors by liquefying them with ultrasound waves. After the sound waves destroy the tumors, the body should eliminate them as cellular waste. When the researchers examined these 'decellularized' tissues, however, they were surprised by what the boiling left intact.
"In some of our experiments, we discovered that some of the stromal tissue and vasculature was being left behind," said Yak-Nam Wang, a senior engineer at the University of Washington's Applied Physics Laboratory. "So we had the idea about using this to decellularize tissues for tissue engineering and regenerative medicine."
The structure that remains after decellularizing tissues is known as the extracellular matrix, a fibrous network that provides a scaffold for cells to grow upon. Most other methods for decellularizing tissues and organs involve chemical and enzymatic treatments that can cause damage to the tissues and fibers and takes multiple days. Histrostipsy, on the other hand, offers the possibility of fast decellularization of tissue with minimal damage to the matrix.
"In tissue engineering, one of the holy grails is to develop biomimetic structures so that you can replace tissues with native tissue," Wang said. Stripping away cells from already developed tissue could provide a good candidate for these structures, since the extracellular matrix already acts as the cellular framework for tissue systems, Wang said.
Due to its bare composition, the matrix also induces only a relatively weak immune response from the host. The matrix could then theoretically be fed with stem cells or cells from the same person to effectively re-grow an organ.
"The other thought is that maybe you could just implant the extracellular matrix and then the body itself would self-seed the tissues, if it's just a small patch of tissue that you're replacing," Wang said. "You won't have any immune issues, and because you have this biomimetic scaffold that's closer to the native tissue, healing would be better, and the body would recognize it as normal tissue."
Wang is currently investigating decellularization of kidney and liver tissue from large animals. Future work involves increasing the size of the decellularized tissues and assessing their in-vivo regenerative efficacy.


Benjamin Franklin Neuropathy Sufferer Who Knew!


Today's post from thefoodrealityblog.wordpress.com (see link below) is one that may surprise you. We're always looking for neuropathy 'role models' and they're about as public and easy to find as hen's teeth. Who knew then that a good role model (at least in terms of the history of the disease) comes from 250 years ago! This article talks about Benjamin Franklin and his struggles with gout, which was basically the accepted term for diabetic neuropathy. We know what he went through and it's interesting to see how his diet directly affected his nervous system - problem is that his diet is not so very far removed from what many people eat today. Irrespective of what the cause of your neuropathy is, the symptoms would have been the same as you suffer today - nevertheless, might be worth having a look at your dietary habits  - diabetes can strike, no matter how many other illnesses you have!


Benjamin Franklin, The Father of Diabetic Neuropathy
This entry was posted on July 26, 2015 by C Katt Krespach,

Like most of us, Benjamin Franklin was health conscious in his early adult life. Writing under the pen name of Poor Richard, he offered such health-conscious phrases as, no pain, no gain. But, healthy living just cannot be listed as one of his accomplishments worthy of following.

His alter ego Poor Richard, had repeatedly preached moderation in his Almanack, and for the most part Franklin seemed to follow Poor Richard’s advice—at least into middle age. But sometime during his years as the foreign liaison to France, his diet became grossly indulgent and so began his parry with diabetic neuropathy.

“For most of his adult life, Ben Franklin suffered from Gout (a symptom of Type 2 Diabetes, and a co-creator of Diabetic Neuropathy) This painful nerve disease is often caused by indulgent eating and moderate to heavy alcohol consumption coupled with dehydration.

The Standard American Diet (S.A.D.)


“Franklin enjoyed red meats and rich foods, and often indulged in them. A good meal for him might have included hors d’oeuvres, beef, mutton, veal, fish, cheeses, butter, pastries, bonbons, and other sweets.”(1)

Doesn’t this diet sound remarkably similar to our own, filled with processed meats, pizza, dining out at restaurants, chips, fried food… etc? And let’s not forget the beer and wine.

“Particularly telling are the notes of the Duc de Croÿ, who visited him in France in 1779, while he was recovering from a severe gout attack. He wrote that Franklin ate only one meal each day, but that it included “large slices of cold meat,” and that he washed down his foods with “two or three bumpers of good wine.” (1)

He was an overweight male, leading an indulgent life of rich food and alcohol consumption without much exercise, similar to people today who are suffering from the symptoms of Type 2 Diabetes.
What is Gout (Diabetic Neuropathy)?

“Gout is caused when there is too much uric acid in the blood. Uric acid is a waste product in the body and is normally excreted through urine. Buildup of uric acid results in needlelike crystals forming in the joints, soft tissues, and organs.

“The most common sign of gout is a nighttime attack of swelling, tenderness, redness, and sharp pain in your big toe . You can also get gout attacks in your foot, ankle, or knees, or other joints. The attacks can last a few days or many weeks before the pain goes away. Another attack may not happen for months or years.

“8.3 million people in the U.S. have gout. This number is growing because of an aging population, the rise in obesity, increasing numbers of people who also have other conditions such as heart disease, kidney disease, and/or diabetes.” (3)



A new study, reported in the journal Rheumatology, revealed there were 32,741 hospital admissions of gout sufferers in England – a 7.2 per cent annual increase – between 1999 and 2009. “We have shown that hospital admissions for gout are increasing significantly over time,” said Dr Philip Robinson of the University of Queensland, who led the study – one of the world’s largest. “We are seeing this trend in all countries that have reported figures. Why is gout increasing? The prevalence of obesity is increasing worldwide due to people taking in too many calories and not exercising.” (4)
Causes of Gout and Diabetic Neuropathy
Vitamin deficiencies in the diet
Exposure to toxins and heavy metals, such as lead, mercury, or pesticides
Type 1 or type 2 diabetes
Moderate alcohol consumption coupled with dehydration 


Treatment and Management
Hydration is the best form of medicine. Being fully hydrated will move the uric crystals out of the body and keep them from building up in the nerve centers.
Drinking dandelion root tea will bring down blood sugar levels which will help the body process food into cell energy instead of creating uric acid crystals as a byproduct of poor energy metabolism in the cell membrane.
Lifestyle changes are important in preventing attacks and managing the condition. Measures include adding raw vegitables to each meal, limiting or eliminating processed foods, and removing alcohol.

Sources
http://www.amphilsoc.org/sites/default/files/proceedings/1520203.pdf
http://www.webmd.com/arthritis/tc/gout-topic-overview
http://umm.edu/health/medical/reports/articles/gout
http://www.independent.co.uk/life-style/health-and-families/health-news/gout-disease-of-kings-is-on-the-way-back-8191044.html
https://lahey.org/Departments_and_Locations/Departments/Rheumatology/Ebsco_Content/Health_Info_-_Gout.aspx?chunkiid=11627
Additional Research

W.S.C. Copeman, A Short History of the Gout and the Rheumatic Diseases (Berkeley: University of California Press, 1964).

G. Cheyne, An Essay of the True Nature and Due Method of Treating the Gout, 6th ed. (London: Strahan, 1824), 72.

W. E. Kittredge and R. Downs, “The Role of Gout in the Formation of Urinary Calculi,” Journal of Urology 67 (1952).

https://thefoodrealityblog.wordpress.com/2015/07/26/benjamin-franklin-the-father-of-diabetic-neuropathy-2/

Neuropathy And Electro Stimulation Part 2


Today's post from absolutept.com (see link below) is the second of 4 looking at the qualities and effectiveness of EMS or Tens units in helping reduce neuropathic symptoms. Not all experts are fans of TENS systems, or believe that electro-stimulation is beneficial to neuropathy patients but as with so many of these things in the neuropathy world; they work for many people and bring relief, so deserve to be taken seriously. The problem may be that to get treatment in this area, many people have to go to private clinics and pay outside their normal insurance and that immediately raises the spectre of rampant commercialism and leads people to suspect they're going to be ripped off. This blog doesn't normally advertise but when someone provides useful and fact based information, which is of benefit to everyone considering their treatment options, then there is no objection to highlighting a medical facility. That's the case here. Chad Reilly (sports physical therapist) provides such a comprehensive analysis of EMS/TENS that patients may wish to take it further, either with him or their local TENS provider. Definitely worth reading if you want to know more about how it all works. All four sections appear within these four days.
 

Electric Stimulation and Neuropathy (Part 2)
Chad's Physical Therapy Blog - Chad Reilly

Diabetic peripheral neuropathy. Effectiveness of electrotherapy and amitriptyline for symptomatic relief. Diabetes Care. 1998 Aug;21(8):1322-5. Kumar D, Alvaro MS, Julka IS, Marshall HJ.

From the study:
Abstract


OBJECTIVE:
To evaluate the efficacy of combining electrotherapy with amitriptyline for the management of chronic painful peripheral neuropathy in patients with type 2 diabetes.


RESEARCH DESIGN AND METHODS:
Patients (n = 26) with peripheral neuropathy were treated with amitriptyline. After 4 weeks, those patients (n = 23) who failed to respond to amitriptyline or who only had partial relief were randomized between a sham treatment group (control) or an electrotherapy group. Transcutaneous electrotherapy was given for 12 weeks by a portable unit (H-wave machine) that generated a biphasic exponentially decaying waveform (pulse width 4 ms, 25-35 V, > or = 2 Hz). The degree of pain and discomfort was graded on a scale of 0-5. An analog scale was used to record the overall change in symptoms.


RESULTS:

Amitriptyline produced some degree of symptomatic relief in 15 (60%) of the 26 patients by the 4th week; pain scores decreased from 3.8 +/- 0.1 to 2.9 +/- 0.2 (P and lt; 0.1) and the overall reduction in pain was 26 +/- 5% on an analog scale. In the amitriptyline plus sham treatment group (n = 9), pain scores declined from 2.8 +/- 0.3 to 1.9 +/- 0.5 (P < 0.03) and the overall reduction in pain was 55 +/- 12%, suggesting a procedure-related placebo effect. In the group receiving combined electrotherapy and amitriptyline (n = 14), symptomatic improvement occurred in 12 (85%) patients. Five (36%) of the patients in this group became asymptomatic. Pain scores declined from 3.2 +/- 0.2 to 1.4 +/- 0.4 (P and lt; 0.01) and the overall reduction in pain was 66 +/- 10%. The degree of reduction in pain scores and the incremental relief (above the amitriptyline effect) were significantly greater (P and lt; 0.03) with electrotherapy as compared with sham treatment. The outcomes indicate a substantial beneficial effect of electrotherapy over and above any placebo influence.


CONCLUSIONS:
Our clinical observations suggest that transcutaneous electrotherapy is effective in reducing the pain associated with peripheral neuropathy. This form of therapy may be a useful adjunctive modality when it is combined with a pharmacological agent, such as amitriptyline, to augment symptomatic relief.

My Comments:

This study was conducted by the same authors of the one I reviewed in my prior blog with a focus on decreasing the pain in those with painful neuropathy. Electric stimulation parameters were identical as the prior study…

Parameters:
Waveform: biphasic exponentially decaying
Duty Cycle: continuous (I think)

Pulse Duration: 400 uS
Intensity: 35 mA (max)
Rate: user adjustable from 2-70 Hz
Treatment Length: 30 minutes
Training Frequency: Daily
Training Length: 4 weeks
Electrodes: 4 electrodes; 2 placed on the distal quadriceps, 1 on the neck of the fibula and 1 centered gastrocnemius muscle (size not given)

…but what was different was the combination of electric stimulation with the drug amitriptyline. As noted in the abstract above the electric stimulation led to considerably greater pain reduction than the amitriptyline by itself. The drug seems to have helped as well, as there was an average pain reduction in the electric stim/drug group of 66% with 36% of these subjects became completely asymptomatic in 4 weeks. In the prior study average pain reduction of the electric stimulation (only) group was 52% with 17% becoming completely asymptomatic, so the drug and electric stimulation interaction appears to be complimentary. My first question after reading this study is; what would another 4 weeks of electric stimulation do?

http://absolutept.com/electric-stimulation-and-neuropathy-part-2/

The Pain Perception Problem


Today's post from theconversation.edu.au (see link below) is a fascinating look at how pain works and how doctors approach it. The relationship between nerve damage and the brain for instance is extremely complex but long held ideas about how pain signals are transmitted may well be less true than previously thought. This is especially applicable to many neuropathy patients where it has often been thought that the wrong signals are being transmitted from nerve to brain. Well worth a  read.



Pain really is in the mind, but not in the way you think
7 August 2012 by Lorimer Moseley
Professor of Clinical Neurosciences and Chair in Physiotherapy at University of South Australia

Everybody hurts, but not everybody keeps hurting. The unlucky few who do end up on a downward spiral of economic, social and physical disadvantage.
While we don’t know why some people don’t recover from an acute episode of pain, we do know that it’s not because their injury was worse in the first place. We also know that it’s not because they have a personality problem. Finally, we do know that, on the whole, treatments for chronic pain are not particularly successful.

This sobering reality draws up some interesting reflections on pain itself. What is pain? Is it simply a symptom of tissue damage or is it something more complex? One way to approach this second question is to determine whether it’s possible to have one without the other – tissue damage without pain or pain without tissue damage.

And you can answer that one yourself – ever noticed a bruise that you have absolutely no recollection of getting? If you answered yes, then you have sustained tissue damage without pain. Ever taken a shower at the end of a long day in the sun and found the normally pleasantly warm water, painfully hot? That’s not the shower injuring you – it’s just activating sensitised receptors in your skin.

Such questions and their answers are of great interest to pain scientists because they remind us that pain is not simply a measure of tissue damage.

What is pain?

The International Association for the Study of Pain defines pain as an experience. Pain is usually triggered by messages that are sent from the tissues of the body when those tissues are presented with something potentially dangerous.

The neurones that carry those messages are called nociceptors, or danger receptors. We call the system that detects and transmits noxious events “nociception”. Critically, nociception is neither sufficient nor necessary for pain. But most of the time, pain is associated with some nociception.

The exact amount or type of pain depends on many things. One way to understand this is to consider that once a danger message arrives at the brain, it has to answer a very important question: “How dangerous is this really?” In order to respond, the brain draws on every piece of credible information – previous exposure, cultural influences, knowledge, other sensory cues – the list is endless.

How might all these things modulate pain? The favourite theory among pain scientists relies on the complexity of the human brain. We can think about pain as a conscious experience that emerges in response to activity in a particular network of brain cells that are spread across the brain. We can call the network a “neurotag” and we can call the brain cells that make up the neurotag “member brain cells”.

Each of the member brain cells in the pain neurotag are also member brain cells of other neurotags. If we have the phrase “slipped disc” in our brain for instance, it has to be held by a network of brain cells (we can call this the “slipped disc” neurotag). And it’s highly likely that there are some brain cells that are members of both the slipped disc neurotag and the back pain neurotag. This means that if we activate the slipped disc neurotag, we slightly increase the likelihood of activating the back pain neurotag.

Using this model, thinking that we have a slipped disc has the potential to increase back pain. But what if this piece of knowledge we have stored is inaccurate, just like our notion of a slipped disc? A disc is so firmly attached to its vertebrae that it can never, ever slip. Despite this, we have the language, and the pictures to go with it, and both strongly suggest it can.
When the brain is using this inaccurate information to evaluate how much danger one’s back is in, we can predict with confidence that, if all other things were equal, thinking you have a slipped disc and picturing one of those horrible clinical models of a slipped disc will increase your back pain.

Self-perpetuating pain

This is where our understanding of pain itself becomes part of a vicious cycle. We know that as pain persists the nociception system becomes more sensitive. What this means is that the spinal cord sends danger messages to the brain at a rate that overestimates the true danger level.

This is a normal adaption to persistent firing of spinal nociceptors. Because pain is (wrongly) interpreted to be a measure of tissue damage, the brain has no option but to presume that the tissues are becoming more damaged. So when pain persists, we automatically assume that tissue damage persists.

On the basis of what we now know about the changing nervous system, this presumption is often wrong. The piece of knowledge that’s turning up the pain neurotag is actually being reinforced by itself! I think it goes like this: “more pain = more damage = more danger = more pain” and so on and so forth.
The idea that an inaccurate understanding of chronic pain increases chronic pain begs the question – what happens if we correct that inaccurate piece of knowledge?

We’ve been researching the answer to this for over a decade, and here’s some of what we’ve found:

(i) Pain and disability reduce, not by much and not very quickly but they do;
(ii) Activity-based treatments have better effects;
(iii) Flare-ups reduce in their frequency and magnitude;
(iv) Long-term outcomes of activity-based treatments are vast improvements.

There’s compelling evidence that reconceptualising pain according to its underlying biology is a good thing to do. But it’s not easy. Our research group is continually looking for better ways of doing this, and we’re not the only ones. The idea of explaining pain has taken off in pain management programs and outpatients departments the world over.

Clinicians need to rethink too

What we know about how pain works is not just relevant to how we teach it to patients, we need to base our clinical decisions on it. This means abandoning Rene Descartes famous model of 1654. His drawing depicts a man with his foot in the fire and a “pain receptor” activating an hydraulic system that rings a bell in his head. (ed:see image at the top of this article) Of course no one believes we have hydraulics making this happen, but the idea of an electrical circuit turning on the pain centre is still at the heart of many clinical practices across professional and geographic boundaries.

The type of thinking captured in Descartes' model has led to some amazing advances in clinical medicine. But the evidence against it is now almost as compelling as that against the world being flat.

Of course, those sailors who never leave the harbour might hang on to the idea of a flat world. And, in the same way, there are probably clinicians who hang on to the idea of pain equalling tissue damage. I suspect they either don’t see complex or chronic pain patients, or, when they do, they presume that those patients are somehow faulty or psychologically fragile, or, tragically, are lying.
Perhaps they can continue to practice without ever leaving the harbour. The problems I want to solve clearly exist on the open seas.

http://theconversation.edu.au/pain-really-is-in-the-mind-but-not-in-the-way-you-think-1151

Wednesday, 22 June 2016

IMAGES OF NEARLY INVISIBLE MOUSE


Researchers at the RIKEN Quantitative Biology Center in Japan, together with collaborators from the University of Tokyo, have developed a method that combines tissue decolorization and light-sheet fluorescent microscopy to take extremely detailed images of the interior of individual organs and even entire organisms. The work, published in Cell, opens new possibilities for understanding the way life works--the ultimate dream of systems biology--by allowing scientists to make tissues and whole organisms transparent and then image them at extremely precise, single-cell resolution.
To achieve this feat, the researchers, led by Hiroki Ueda, began with a method called CUBIC (Clear, Unobstructed Brain Imaging Cocktails and Computational Analysis), which they had previously used to image whole brains. Though brain tissue is lipid-rich, and thus susceptible to many clearance methods, other parts of the body contain many molecular subunits known as chromophores, which absorb light. One chromophore, heme, which forms part of hemoglobin, is present in most tissues of the body and blocks light. The group decided to focus on this issue and discovered, in a surprise finding, that the aminoalcohols included in the CUBIC reagent could elute the heme from the hemoglobin and by doing so make other organs dramatically more transparent.
Using the method, they took images of mouse brains, hearts, lungs, kidneys, and livers, and then went on to attempt the method on infant and adult mice, and found that in all cases they could get clear tissues. They used the technique of light-sheet fluorescent microscopy, which involves taking "slices" of tissues without having to actually cut into it, to gain 3D images of the organs. To test the practicability of the method, they examined the pancreases of diabetic and non-diabetic mice, and found clear differences in the isles of Langerhans, the structures in the pancreas that produce insulin.
Although these methods could not be used in living organisms, since they require the tissues to be fixed using reagents, they could, according to Kazuki Tainaka, the first author of the paper, be very useful for gaining new understanding of the 3D structure of organs and how certain genes are expressed in various tissues. He said, "We were very surprised that the entire body of infant and adult mice could be made nearly transparent by a direct transcardial CUBIC perfusion coupled with a two-week clearing protocol. It allowed us to see cellular networks inside tissues, which is one of the fundamental challenges in biology and medicine."
According to Hiroki Ueda, who led the research team, "This new method could be used for 3D pathology, anatomical studies, and immunohistochemistry of entire organisms. For example, it could be used to study how embryos develop or how cancer and autoimmune diseases develop at the cellular level, leading to a deeper understanding of such diseases and perhaps to new therapeutic strategies. It could lead to the achievement of one of our great dreams, organism-level systems biology based on whole-body imaging at single-cell resolution."
Though it is an important finding, more work lies ahead. In the future, the group plans to make improvements to the microscopy method to allow for the rapid imaging of whole bodies of adult mice or larger samples such as human brains, and to apply this technology to further our understanding of autoimmune and psychiatric diseases.