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Natural Product Derived From Periwinkle Plant Reduces Inflammation

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A widely and safely used plant extract acts as a novel anti-inflammatory agent that may one day be used for the treatment of chronic obstructive pulmonary disease, or COPD, as well as other inflammatory conditions. There is an urgent need for new therapies for the treatment of chronic inflammatory diseases, such as COPD, otitis media (ear infection), and atherosclerosis (chronic inflammation in the walls of arteries), because the most effective and commonly used agents – steroids – often cause serious side effects, such as liver damage, which prevent long-term use.


Researchers at the University of Rochester Medical Center were the first to find that vinpocetine, a natural product derived from the periwinkle plant, acts as a potent anti-inflammatory agent when tested in a mouse model of lung inflammation, as well as several other types of human cells. Results of the study show that vinpocetine greatly reduces inflammation, and, unlike steroids, does not cause severe side effects.

“What is extremely exciting and promising about these findings is vinpocetine’s excellent safety profile,” said Chen Yan, a senior author of the study. “Previously, most drugs tested in this area have failed, not because of a lack of efficacy, but because of safety issues. We’re very encouraged by these results and believe vinpocetine has great potential for the treatment of COPD and other inflammatory diseases.”

Vinpocetine is a well-known natural product that was originally discovered nearly 30 years ago and is currently used as a dietary supplement for the prevention and treatment of cognitive disorders, such as stroke and memory loss, in Europe, Japan and China. The therapy has no evidence of toxicity or noticeable side effects in human patients. Scientists at the University of Rochester hope to reposition this compound as an anti-inflammatory agent for the treatment of COPD, and potentially other inflammatory conditions, such as asthma, otitis media, rheumatoid arthritis, atherosclerosis and psoriasis in the future.

While steroids successfully combat inflammation, patients often pay a high price when it comes to side effects. Steroids can cause liver damage, and can also suppress the immune system, increasing the likelihood of infections. With such a high risk profile, steroids are usually only used for a short period of time, which is problematic when treating chronic diseases.

“In managing chronic conditions such as COPD, it is crucial to have a therapy that can be used safely over the long term,” said Jian-Dong Li, a senior author of the study. “There is a great need for a drug like vinpocetine, because patients currently have no good options when it comes to long-term care.”

Vinpocetine decreases inflammation by targeting the activity of a specific enzyme, known as IKK. IKK is responsible for regulating inflammation, and does so through the activation of a key protein, nuclear-factor kappaB (NF-?B). By directly inhibiting IKK, vinpocetine is able to switch off NF-?B, which normally produces pro-inflammatory molecules that cause inflammation. Halting the activity of NF-?B ultimately reduces inflammation.

“Inflammation is a hallmark of a wide range of human diseases, so there is great potential for vinpocetine to be used for several indications,” said Bradford C. Berk, co-author of the study. “Given vinpocetine’s efficacy and solid safety profile, we believe there is great potential to bring this drug to market.”

Repositioning a therapy – taking a known compound that has been used safely in humans and testing it for a new application – can be an effective way to bring new therapies to market more quickly than starting the discovery process from scratch.

Inflammatory diseases are a major cause of illness worldwide. For example, chronic obstructive pulmonary disease is the fourth leading cause of death in the United States. In people with COPD, airflow is blocked due to chronic bronchitis or emphysema, making it increasingly difficult to breathe. Most COPD is caused by long-term smoking, although genetics may play a role as well. Approximately 13.5 million people in the United States are diagnosed with COPD each year, and in 2004 the annual cost of the disease was $37.2 billion.

Source: Elements4Health

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Ailmemts & Remedies



Emphysema is a type of chronic obstructive pulmonary disease (COPD) involving damage to the air sacs (alveoli) in the lungs. As a result, your body does not get the oxygen it needs. Emphysema makes it hard to catch your breath. You may also have a chronic cough and have trouble breathing during exercise.


The most common cause is cigarette smoking. If you smoke, quitting can help prevent you from getting the disease. If you already have emphysema, not smoking might keep it from getting worse.

It is  characterized by an abnormal, permanent enlargement of air spaces distal to the terminal bronchioles. The disease is coupled with the destruction of walls, but without obvious fibrosis.  It is often caused by exposure to toxic chemicals, including long-term exposure to tobacco smoke.

As it worsens, emphysema turns the spherical air sacs — clustered like bunches of grapes — into large, irregular pockets with gaping holes in their inner walls. This reduces the number of air sacs and keeps some of the oxygen entering your lungs from reaching your bloodstream. In addition, the elastic fibers that hold open the small airways leading to the air sacs are slowly destroyed, so that they collapse when you breathe out, not letting the air in your lungs escape.

Airway obstruction, another feature of COPD, contributes to emphysema. The combination of emphysema and obstructed airways makes breathing increasingly difficult. Treatment often slows, but doesn’t reverse, the process.

Emphysema is characterized by loss of elasticity (increased pulmonary compliance) of the lung tissue caused by destruction of structures feeding the alveoli, in some cases owing to the action of alpha 1-antitrypsin deficiency.

Emphysema can be classified into primary and secondary. However, it is more commonly classified by location.

Emphysema can be subdivided into panacinary and centroacinary (or panacinar and centriacinar, or centrilobular and panlobular).

Panacinary (or panlobular) emphysema is related to the destruction of alveoli, because of an inflammation or deficiency of alpha 1-antitrypsin. It is found more in young adults who do not have chronic bronchitis.

Centroacinary (or centrilobular) emphysema is due to destruction of terminal bronchioli muchosis, due to chronic bronchitis. This is found mostly in elderly people with a long history of smoking or extreme cases of passive smoking.
Other types include distal acinar and irregular.

A special type is congenital lobar emphysema (CLE).

Congenital lobar emphysema:-
CLE is results in overexpansion of a pulmonary lobe and resultant compression of the remaining lobes of the ipsilateral lung, and possibly also the contralateral lung. There is bronchial narrowing because of weakened or absent bronchial cartilage.

There may be congenital extrinsic compression, commonly by an abnormally large pulmonary artery. This causes malformation of bronchial cartilage, making them soft and collapsible.

CLE is potentially reversible, yet possibly life-threatening, causing respiratory distress in the neonate

Emphysema symptoms are mild to begin with but steadily get worse as the disease progresses. The main emphysema symptoms are:

*Shortness of breath
*Chest tightness
*Reduced capacity for physical activity
*Chronic coughing, which could also indicate chronic bronchitis
*Loss of appetite and weight
When to see a doctor

*You tire quickly, or you can’t easily do the things you used to do
*You can’t breathe well enough to tolerate even moderate exercise
*Your breathing difficulty worsens when you have a cold
*Your lips or fingernails are blue or gray, indicating low oxygen in your blood
*You frequently cough up yellow or greenish sputum
*You note that bending over to tie your shoes makes you short of breath
*You are losing weight.

These signs and symptoms don’t necessarily mean you have emphysema, but they do indicate that your lungs aren’t working properly and should be evaluated by your doctor as soon as possible.

The causes of emphysema include:

1.Smoking. Cigarette smoke is by far the most common cause of emphysema. There are more than 4,000 chemicals in tobacco smoke, including secondhand smoke. These chemical irritants slowly destroy the small peripheral airways, the elastic air sacs and their supporting elastic fibers.

2.Protein deficiency. Approximately 1 to 2 percent of people with emphysema have an inherited deficiency of a protein called AAt, which protects the elastic structures in the lungs. Without this protein, enzymes can cause progressive lung damage, eventually resulting in emphysema. If you’re a smoker with a lack of AAt, emphysema can begin in your 30s and 40s. The progression and severity of the disease are greatly accelerated by smoking.

Risk Factors:

Risk factors for emphysema include:

*Smoking. Emphysema is most likely to develop in cigarette smokers, but cigar and pipe smokers also are susceptible, and the risk for all types of smokers increases with the number of years and amount of tobacco smoked.

*Age. Although the lung damage that occurs in emphysema develops gradually, most people with tobacco-related emphysema begin to experience symptoms of the disease between the ages of 40 and 60.

*Exposure to secondhand smoke. Secondhand smoke, also known as passive or environmental tobacco smoke, is smoke that you inadvertently inhale from someone else’s cigarette, pipe or cigar. Being around secondhand smoke increases your risk of emphysema.

*Occupational exposure to fumes or dust. If you breathe fumes from certain chemicals or dust from grain, cotton, wood or mining products, you’re more likely to develop emphysema. This risk is even greater if you smoke.

*Exposure to indoor and outdoor pollution. Breathing indoor pollutants, such as fumes from heating fuel, as well as outdoor pollutants — car exhaust, for instance — increases your risk of emphysema.

*HIV infection. Smokers living with HIV are at greater risk of emphysema than are smokers who don’t have HIV infection.

*Connective tissue disorders. Some conditions that affect connective tissue — the fibers that provide the framework and support for your body — are associated with emphysema. These conditions include cutis laxa, a rare disease that causes premature aging, and Marfan syndrome, a disorder that affects many different organs, especially the heart, eyes, skeleton and lungs.

Emphysema can increase the severity of other chronic conditions, such as diabetes and heart failure. If you have emphysema, air pollution or a respiratory infection can lead to an acute COPD exacerbation, with extreme shortness of breath and dangerously low oxygen levels. You may need admission to an intensive care unit and temporary support from an artificial breathing machine (ventilator) until the infection clears.

In normal breathing, air is drawn in through the bronchi and into the alveoli, which are tiny sacs surrounded by capillaries. Alveoli absorb oxygen and then transfer it into the blood. When toxicants, such as cigarette smoke, are breathed into the lungs, the harmful particles become trapped in the alveoli, causing a localized inflammatory response. Chemicals released during the inflammatory response (e.g., elastase) can eventually cause the alveolar septum to disintegrate. This condition, known as septal rupture, leads to significant deformation of the lung architecture. These deformations result in a large decrease of alveoli surface area used for gas exchange. This results in a decreased Transfer Factor of the Lung for Carbon Monoxide (TLCO). To accommodate the decreased surface area, thoracic cage expansion (barrel chest) and diaphragm contraction (flattening) take place. Expiration increasingly depends on the thoracic cage and abdominal muscle action, particularly in the end expiratory phase. Due to decreased ventilation, the ability to exude carbon dioxide is significantly impaired. In the more serious cases, oxygen uptake is also impaired.

As the alveoli continue to break down, hyperventilation is unable to compensate for the progressively shrinking surface area, and the body is not able to maintain high enough oxygen levels in the blood. The body’s last resort is vasoconstricting appropriate vessels. This leads to pulmonary hypertension, which places increased strain on the right side of the heart, the side responsible for pumping deoxygenated blood to the lungs. The heart muscle thickens in order to pump more blood. This condition is often accompanied by the appearance of jugular venous distension. Eventually, as the heart continues to fail, it becomes larger and blood backs up in the liver.

Patients with alpha 1-antitrypsin deficiency (A1AD) are more likely to suffer from emphysema. A1AD allows inflammatory enzymes (such as elastase) to destroy the alveolar tissue. Most A1AD patients do not develop clinically significant emphysema, but smoking and severely decreased A1AT levels (10-15%) can cause emphysema at a young age. The type of emphysema caused by A1AD is known as panacinar emphysema (involving the entire acinus) as opposed to centrilobular emphysema, which is caused by smoking. Panacinar emphysema typically affects the lower lungs, while centrilobular emphysema affects the upper lungs. A1AD causes about 2% of all emphysema. Smokers with A1AD are at the greatest risk for emphysema. Mild emphysema can often develop into a severe case over a short period of time (1–2 weeks).

Severe emphysemaWhile A1AD provides some insight into the pathogenesis of the disease, hereditary A1AT deficiency only accounts for a small proportion of the disease. Studies for the better part of the past century have focused mainly upon the putative role of leukocyte elastase (also neutrophil elastase), a serine protease found in neutrophils, as a primary contributor to the connective tissue damage seen in the disease. This hypothesis, a result of the observation that neutrophil elastase is the primary substrate for A1AT, and A1AT is the primary inhibitor of neutrophil elastase, together have been known as the “protease-antiprotease” theory, implicating neutrophils as an important mediator of the disease. However, more recent studies have brought into light the possibility that one of the many other numerous proteases, especially matrix metalloproteases might be equally or more relevant than neutrophil elastase in the development of non-hereditary emphysema.

The better part of the past few decades of research into the pathogenesis of emphysema involved animal experiments where various proteases were instilled into the trachea of various species of animals. These animals developed connective tissue damage, which was taken as support for the protease-antiprotease theory. However, just because these substances can destroy connective tissue in the lung, as anyone would be able to predict, doesn’t establish causality. More recent experiments have focused on more technologically advanced approaches, such as ones involving genetic manipulation. One particular development with respect to our understanding of the disease involves the production of protease “knock-out” animals, which are genetically deficient in one or more proteases, and the assessment of whether they would be less susceptible to the development of the disease. Often individuals who are unfortunate enough to contract this disease have a very short life expectancy, often 0–3 years at most.

Prognosis and treatment

Emphysema is an irreversible degenerative condition. The most important measure to slow its progression is for the patient to stop smoking and avoid all exposure to cigarette smoke and lung irritants. Pulmonary rehabilitation can be very helpful to optimize the patient’s quality of life and teach the patient how to actively manage his or her care. Patients with emphysema and chronic bronchitis can do more for themselves than patients with any other disabling disease.

Emphysema is also treated by supporting the breathing with anticholinergics, bronchodilators, steroid medication (inhaled or oral), and supplemental oxygen as required. Treating the patient’s other conditions including gastric reflux and allergies may improve lung function. Supplemental oxygen used as prescribed (usually more than 20 hours per day) is the only non-surgical treatment which has been shown to prolong life in emphysema patients. There are lightweight portable oxygen systems which allow patients increased mobility. Patients can fly, cruise, and work while using supplemental oxygen. Other medications are being researched, and herbal organic remedies are being offered by companies.

Lung volume reduction surgery (LVRS) can improve the quality of life for certain carefully selected patients. It can be done by different methods, some of which are minimally invasive. In July 2006 a new treatment, placing tiny valves in passages leading to diseased lung areas, was announced to have good results, but 7% of patients suffered partial lung collapse. The only known “cure” for emphysema is lung transplant, but few patients are strong enough physically to survive the surgery. The combination of a patient’s age, oxygen deprivation and the side-effects of the medications used to treat emphysema cause damage to the kidneys, heart and other organs. Transplants also require the patient to take an anti-rejection drug regimen which suppresses the immune system, and so can lead to microbial infection of the patient. Patients who think they may have contracted the disease are recommended to seek medical attention as soon as possible.

A study published by the European Respiratory Journal suggests that tretinoin (an anti-acne drug commercially available as Retin-A) derived from vitamin A can reverse the effects of emphysema in mice by returning elasticity (and regenerating lung tissue through gene mediation) to the alveoli.

While vitamin A consumption is not known to be an effective treatment or prevention for the disease, this research could in the future lead to a cure. A follow-up study done in 2006 found inconclusive results (“no definitive clinical benefits”) using Vitamin A (retinoic acid) in treatment of emphysema in humans and stated that further research is needed to reach conclusions on this treatment… & see

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Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.


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Diagnonistic Test

Pulmonary Function Tests

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Alternative Names: PFTs; Spirometry; Spirogram; Lung function tests
Definition:Pulmonary function tests are a group of tests that measure how well the lungs take in and release air and how well they move oxygen into the blood. These tests can tell your doctor what quantity of air you breathe with each breath, how efficiently you move air in and out of your lungs.
Pulmonary Function Testing has been a major step forward in assessing the functional status of the lungs as it relates to :

1.How much air volume can be moved in and out of the lungs
2.How fast the air in the lungs can be moved in and out
3.How stiff are the lungs and chest wall – a question about compliance
4.The diffusion characteristics of the membrane through which the gas moves (determined by special tests)
5.How the lungs respond to chest physical therapy procedures

Pulmonary Function Tests are used for the following reasons :

1.Screening for the presence of obstructive and restrictive diseases

2.Evaluating the patient prior to surgery – this is especially true of patients who :
a. are older than 60-65 years of age
b. are known to have pulmonary disease
c. are obese (as in pathologically obese)
d. have a history of smoking, cough or wheezing
e. will be under anesthesia for a lengthy period of time
f. are undergoing an abdominal or a thoracic operation

: A vital capacity is an important preoperative assessment tool. Significant reductions in vital capacity (less than 20 cc/Kg of ideal body weight) indicates that the patient is at a higher risk for postoperative respiratory complications. This is because vital capacity reflects the patient’s ability to take a deep breath, to cough, and to clear the airways of excess secretions.

3.Evaluating the patient’s condition for weaning from a ventilator. If the patient on a ventilator can demonstrate a vital capacity (VC) of 10 – 15 ml/Kg of body weight, it is generally thought that there is enough ventilatory reserve to permit (try) weaning and extubation.

4.Documenting the progression of pulmonary disease – restrictive or obstructive

5.Documenting the effectiveness of therapeutic intervention

How do you prepare for the test?
Do not eat a heavy meal before the test. Do not smoke for 4 – 6 hours before the test. You’ll get specific instructions if you need to stop using bronchodilators or inhaler medications. You may have to breathe in medication before the test.

No other preparation is necessary.

How the Test Will Feel ?
Since the test involves some forced breathing and rapid breathing, you may have some temporary shortness of breath or light-headedness. You breathe through a tight-fitting mouthpiece, and you’ll have nose clips.

What happens when the test is performed?
This testing is done in a special laboratory. During the test, you are instructed to breathe in and out through a tube that is connected to various machines.

A test called spirometry measures how forcefully you are able to inhale and exhale when you are trying to take as large a breath as possible. The lab technicians encourage you to give this test your best effort, because you can make the test result abnormal just by not trying hard.

A separate test to measure your lung volume (size) is done in one of two ways. One way is to have you inhale a small carefully measured amount of a specific gas (such as helium) that is not absorbed into your bloodstream. This gas mixes with the air in your lungs before you breathe it out again. The air and helium that you breathe out is tested to see how much the helium was diluted by the air in your lungs, and a calculation can reveal how much air your lungs were holding in the first place.

The other way to measure lung volume is with a test called plethysmography. In this test, you sit inside an airtight cubicle that looks like a phone booth, and you breathe in and out through a pipe in the wall. The air pressure inside the box changes with your breathing because your chest expands and contracts while you breathe. This pressure change can be measured and used to calculate the amount of air you are breathing.

Your lungs’ efficiency at delivering oxygen and other gases to your bloodstream is known as your diffusion capacity. To measure this, you breathe in a small quantity of carbon monoxide (too small a quantity to do you any harm), and the amount you breathe out is measured. Your ability to absorb carbon monoxide into the blood is representative of your ability to absorb other gases, such as oxygen.

Some patients have variations of these tests-for example, with inhaler medicines given partway through a test to see if the results improve, or with a test being done during exercise. Some patients also have their oxygen level measured in the pulmonary function lab (see “Oxygen saturation test,” page 29).

Why the Test is Performed  ?

Pulmonary function tests are done to:
*Diagnose certain types of lung disease (especially asthma, bronchitis, and emphysema)
*Find the cause of shortness of breath
*Measure whether exposure to contaminants at work affects lung function
It also can be done to:

*Assess the effect of medication
*Measure progress in disease treatment
*Spirometry measures airflow. By measuring how much air you exhale, and how quickly, spirometry can evaluate a broad range of lung diseases.

Lung volume measures the amount of air in the lungs without forcibly blowing out. Some lung diseases (such as emphysema and chronic bronchitis) can make the lungs contain too much air. Other lung diseases (such as fibrosis of the lungs and asbestosis) make the lungs scarred and smaller so that they contain too little air.

Testing the diffusion capacity (also called the DLCO) allows the doctor to estimate how well the lungs move oxygen from the air into the bloodstream.

Risk Factors:
The risk is minimal for most people. There is a small risk of collapsed lung in people with a certain type of lung disease. The test should not be given to a person who has experienced a recent heart attack, or who has certain other types of heart disease.

Must you do anything special after the test is over?

Normal Results:
Normal values are based upon your age, height, ethnicity, and sex. Normal results are expressed as a percentage. A value is usually considered abnormal if it is less than 80% of your predicted value.

Normal value ranges may vary slightly among different laboratories. Talk to your doctor about the meaning of your specific test results.

What Abnormal Results Mean:
Abnormal results usually mean that you may have some chest or lung disease.

Your cooperation while performing the test is crucial in order to get accurate results. A poor seal around the mouthpiece of the spirometer can give poor results that can’t be interpreted. Do not smoke before the test.

How long is it before the result of the test is known?
Your doctor will receive a copy of your test results within a few days and can review them with you then.


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