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Herbs & Plants

Money Plant

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Botanical Name :  Epipremnum aureum
Family:Family: Araceae
Subfamily: Monsteroideae

Kingdom: Plantae
Order: Alismatales
Tribe: Monstereae
Genus: Epipremnum
Species: E. aureum

Synonyms: Epipremnum pinnatum, Pothos aureus, Scindapsus aureus, Raphidophora aurea.

Common Names: Pothos (once classified under the genus Pothos),Golden pothos, Silver Vine, Money Plant, Centipede tongavine, Devil’s Ivy and Solomon Islands‘ Ivy

Habitat : Native to southeastern Asia (Malaysia, Indonesia) and New Guinea. It is sometimes mistakenly labeled as a Philodendron in plant stores.

Description  :
It is a liana growing to 20 m tall, with stems up to 4 cm diameter, climbing by means of aerial roots which hook over tree branches. The leaves are evergreen, alternate, heart-shaped, entire on juvenile plants, but irregularly pinnatifid on mature plants, up to 100 cm long and 45 cm broad (juvenile leaves much smaller, typically under 20 cm long). The flowers are produced in a spathe up to 23 cm long.(Bloom Time: Rarely flowers)

CLICK TO  SEE.>…....(01)...(1)..…….(2).…....(3)..…...(4)..…...(5).……...(6).
This plant produces trailing stems when it climbs up trees and these take root when they reach the ground and grow along it. The leaves on these trailing stems grow up to 10cm long and are the ones normally seen on this plant when it is cultivated as a pot plant.

You may click to see more variety of money plant
Cultivation:-
It is a popular houseplant with numerous cultivars selected for leaves with white, yellow, or light green variegation. It is often used in decorative displays in shopping centers, offices, and other public locations largely because it is a very hardy plant that requires little care and is also attractively leafy. It is also efficient at removing indoor pollutants such as formaldehyde, xylene, and benzene A study found that this effect became less the higher the molecular weight of the polluting substance.

As a houseplant it can reach a height of two meters or more, given suitable support. For best results it requires medium indirect light; bright light is tolerated, but lengthy spells of direct sun will scorch the leaves. The plant prefers a temperature of between 17 to 30 °C (63 to 86 °F). Generally it only needs water when the soil begins to feel dry to the touch. For best results a liquid fertilizer can be added in spring, and they should be repotted every couple of years. However, this is a robust plant that can stand a very high degree of abuse. It will grow hydroponically quite readily.

Uses:
(1) Evergreen (2) Has showy flowers. (3)  Leaves colorful (4) Has showy fruit .
Because of its tolerance of low-light conditions, this easy-growing and hardy plant, E. aureum make excellent house plants in vases, pots and hanging baskets, allowing the stems to tumble down. Ideal as an indoor plant in greenhouse or conservatory in temperate regions. Its fabulous variegated foliage are used popularly for interiorscape in homes, offices, shopping malls and public places, as well as cut foliage to complement floral arrangement, while at the same time, cleansing the indoor air of pollutants.
Outdoors, Pothos is most suitable as a groundcover in garden beds and borders with its sprawling habit, or grown in above-ground planter or small to large containers raised on a pedestal for a cascading effect. Very suitable as a climbing vine on trellis, poles, fences, trees or wires. It can also be espaliered against the wall for landscapping or allowed to cascade down a wall for that something extra to spruce and beautify your garden.

The plant is listed as “toxic to cats, toxic to dogs” by the ASPCA, due to the presence of insoluble calcium oxalates. Care should be taken to ensure the plant is not consumed by house pets. Symptoms may include oral irritation, vomiting, and difficulty swallowing.

Popular E. aureum cultivars include:

•‘Golden Pothos’ – green waxy leaves, irregularly variegated with splashes and streaks of golden yellow and creamy white;
•‘Marble Queen’ – white to creamy leaves that are smooth and waxy, blotched and streaked with green and grey-green;
•‘Tricolor’ – green leaves marbled with deep yellow, cream and pale green;
•‘Jade Pothos’ – solid green leaves without variegation;
•‘Hawaiian Pothos’ – similar to ‘Golden Pothos’ in variegation, though the yellow is more striking and brilliant;
•‘Neon’ (or ‘Goldilocks’) – lime-green leaves without variegation, small and compact;
•‘Wilcoxii’ – with sharply-defined variegations of green and white;

Resources:
http://en.wikipedia.org/wiki/Epipremnum_aureum
http://www.mobot.org/gardinghelp/plantfinder/plant.asp?code=B594

Epipremnum aureum (Pothos) is both beautiful and useful!

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Healthy Tips

Progesterone Protects Brain Tissue As Well As Fetal Tissue

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Why do some females recover from brain injury much faster and more completely than males?

The answer may have far-reaching implications for the treatment of traumatic brain injury, stroke, and other neurological disorders.

Neuroscientist Dr. Donald G. Stein and his colleagues have been investigating this question and have discovered something remarkable — that the hormone progesterone confers profound neuroprotective effects that improve outcomes and reduce mortality following brain injuries.

Progesterone provides powerful neuroprotection to the fetus, particularly in late pregnancy, when it helps suppress neuronal excitation that can damage delicate new brain tissue. Dr. Stein and his colleagues have found that in addition to protecting the fetal brain, progesterone also protects and heals injured brain tissue.

Source: Life Extension Magazine November 2009

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Herbs & Plants

Abies religiosa

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Botanical Name: Abies religiosa
Family: Pinaceae
Genus: Abies
Species: A. religiosa
Kingdom: Plantae
Division: Pinophyta
Class: Pinopsida
Order: Pinales

Synonyms : Abies hirtella – (Kunth.)Lindl.,  Pinus religiosa – Kunth.
Common Names: Sacred fir, oyamel [Nahuatl], pinabete [Spanish].
Genus :  Abies

Habitat  : South-western N. America – Mexico .  Mountains of N.W. Mexico at elevations of 2400 – 3000 metres.

Description: An evergreen Tree growing to 40m at a fast rate.  It is hardy to zone 8. It is in leaf all year, and the seeds ripen from October to November. The flowers are monoecious (individual flowers are either male or female, but both sexes can be found on the same plant) and are  pollinated by Wind.

Trees to 40(-60) m tall and 200 cm dbh with a single, straight, round trunk and a pyramidal or conical crown  First-order branches long, slender, ascending, later becoming horizontal to pendant. Bark smooth, gray-white, becoming dark grey-brown, deeply fissured, breaking into small plates. Branchlets slender, red-brown to purple-red, irregularly grooved, glabrous or slightly pubescent, with circular leaf scars. Leaves spirally arranged, pectinate, slightly assurgent, (1-)1.5-3(-3.5) cm × 1.2-1.6 mm, linear, twisted at base, grooved above, stomata only on underside, in two white bands separated by a midrib; upper surface shiny dark green, lower surface lighter with whitish stomatal bands; 2 smallish marginal resin canals. Pollen cones lateral, ±pendulous, 10-15 mm long with red microsporophylls. Seed cones erect, lateral(-subterminal) on a short, often curved peduncle, ovoid-oblong to cylindrical, sometimes curved, obtuse, (8-)10-16 × 4-6 cm, violet-blue with yellow bracts, darkening with age to a purple-brown with brown bracts; rachis persistent, dark brown. Seed scales cuneate, a mid-cone measuring 2-3 × 3-3.5 cm, smooth, puberulent, outer margin rounded, entire. Bract scales spathulate, tapering, 3-3.5 cm long, exserted, reflexed. Seeds 10 × 5 mm, shiny brown with a cuneate brown wing 10-15 mm long (Farjon 1990).
CLICK &  SEE THE PICTURES

The plant prefers light (sandy), medium (loamy) and heavy (clay) soils and can grow in heavy clay soil. The plant
prefers acid and neutral soils. It can grow in full shade (deep woodland) semi-shade (light woodland) or no shade.
It requires moist soil.

Cultivation :
Prefers a good moist but not water-logged soil. Grows well in heavy clay soils. Plants are very shade tolerant,
especially when young, but growth is slower in dense shade. Intolerant of atmospheric pollution. Prefers slightly
acid conditions down to a pH of about 5. Prefers growing on a north-facing slope. Requires a sheltered position,
trees are susceptible to wind damage. Trees are tender in most parts of Britain, they tolerate temperatures down to
about -5 to -10°c. There are trees in Kent and Hampshire that are 12 metres tall. Grows best in the Perthshire
valleys of Scotland and other areas with cool wet summers. Growth from young trees has proved to be very vigorous in

Britain, 60cm in its first year has been recorded and 70 cm in its third year from seed. New growth takes place mainly between July and October. Trees should be planted into their permanent positions when they are quite small, between 30 and 90cm in height. Larger trees will check badly and hardly put on any growth for several years.

This also badly affects root development and wind resistance. Plants are strongly outbreeding, self-fertilized seed
usually grows poorly. They hybridize freely with other members of this genus.

Propagation
Seed – sow early February in a greenhouse or outdoors in March. Germination is often poor, usually taking about
6 – 8 weeks . Stratification is said to produce a more even germination so it is probably best to sow the seed in a cold frame as soon as it is ripe in the autumn . The seed remains viable for up to 5 years if it is well store. When large enough to handle, prick the seedlings out into individual pots and grow them on for at least their first winter in pots. Plant them out into their permanent positions in late spring or early summer, after the last expected frosts. Alternatively, if you have sufficient seed, it is possible to sow in an outdoor seedbed. One report says that it is best to grow the seedlings on in the shade at a density of about 550 plants per square metre whilst another report says that they are best grown on in a sunny position

Medicinal Uses:

Balsamic: A healing and soothing agent

Other Uses
Paint; Wood.

An oleo-resin is obtained from the tree (probably from the trunk). It is balsamic and is used in medicines and in paints . Wood – light, soft, not very durable. Used for pulp, construction, furniture etc.

Disclaimer:The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplements, it is always advisable to consult with your own health care provider.

Resources:
http://www.pfaf.org/database/plants.php?Abies+religiosa
http://www.ubcbotanicalgarden.org/potd/2009/03/abies_religiosa_and_danaus_plexippus.php
http://www.conifers.org/pi/ab/religiosa.htm

https://en.wikipedia.org/wiki/Abies_religiosa

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Ailmemts & Remedies

Pulmonary Embolism

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Definition:-
Pulmonary embolism (PE) is a blockage of the main artery of the lung or one of its branches by a substance that has travelled from elsewhere in the body through the bloodstream (embolism). Usually this is due to embolism of a thrombus (blood clot) from the deep veins in the legs, a process termed venous thromboembolism. A small proportion is due to the embolization of air, fat or amniotic fluid. The obstruction of the blood flow through the lungs and the resultant pressure on the right ventricle of the heart leads to the symptoms and signs of PE. The risk of PE is increased in various situations, such as cancer and prolonged bed rest..

You may click to see more pictures of Pulmonary Embolism
Pulmonary embolism is a condition that occurs when one or more arteries in your lungs become blocked. In most cases, pulmonary embolism is caused by blood clots that travel to your lungs from another part of your body — most commonly, your legs.

Symptoms:-
Symptoms of PE are sudden-onset dyspnea (shortness of breath), tachypnea (rapid breathing), chest pain of a “pleuritic” nature (worsened by breathing), cough and hemoptysis (coughing up blood). More severe cases can include signs such as cyanosis (blue discoloration, usually of the lips and fingers), collapse, and circulatory instability. About 15% of all cases of sudden death are attributable to PE.

On physical examination, a pleural rub may be audible by stethoscope over affected areas of the lung. Strain on the right ventricle may be detected as a left parasternal heave, a loud pulmonary component of the second heart sound, raised jugular venous pressure, and more rarely leg swelling.

A fever though usually low grade is present in 14% of people with pulmonary embolism.

Symptoms of pulmonary embolism include difficulty breathing, chest pain on inspiration, and palpitations. Clinical signs include low blood oxygen saturation and cyanosis, rapid breathing, and a rapid heart rate. Severe cases of PE can lead to collapse, abnormally low blood pressure, and sudden death.

Pulmonary embolism occurs when a clump of material, most often a blood clot, gets wedged into an artery in your lungs. These blood clots most commonly originate in the deep veins of your legs, but they can also come from other parts of your body. This condition is known as deep vein thrombosis (DVT).

Occasionally, other substances can form blockages within the blood vessels inside your lungs. Examples include:

*Fat from within the marrow of a broken bone
*Part of a tumor
*Air bubbles

It’s rare to experience a solitary pulmonary embolism. In most cases, multiple clots are involved. The lung tissue served by each blocked artery is robbed of fuel and may die. This makes it more difficult for your lungs to provide oxygen to the rest of your body.

Because pulmonary embolism almost always occurs in conjunction with deep vein thrombosis, some doctors refer to the two conditions together as venous thromboembolism (VTE).

Causes:-

In 9 out of 10 cases, pulmonary embolism (PE) begins as a blood clot in the deep veins of the leg (a condition known as deep vein thrombosis). The clot breaks free from the vein and travels through the bloodstream to the lungs, where it can block an artery.Click to see to learn more

Diagnosis:-
The diagnosis of PE is based primarily on validated clinical criteria combined with selective testing because the typical clinical presentation (shortness of breath, chest pain) cannot be definitively differentiated from other causes of chest pain and shortness of breath. The decision to do medical imaging is usually based on clinical grounds, i.e. the medical history, symptoms and findings on physical examination, followed by an assessment of clinical probability.

The most commonly used method to predict clinical probability, the Wells score, is a clinical prediction rule, whose use is complicated by multiple versions being available. In 1995, Wells et al. initially developed a prediction rule (based on a literature search) to predict the likelihood of PE, based on clinical criteria. The prediction rule was revised in 1998 This prediction rule was further revised when simplified during a validation by Wells et al. in 2000. In the 2000 publication, Wells proposed two different scoring systems using cutoffs of 2 or 4 with the same prediction rule. In 2001, Wells published results using the more conservative cutoff of 2 to create three categories. An additional version, the “modified extended version”, using the more recent cutoff of 2 but including findings from Wells’s initial studies were proposed. Most recently, a further study reverted to Wells’s earlier use of a cutoff of 4 points to create only two categories.

There are additional prediction rules for PE, such as the Geneva rule. More importantly, the use of any rule is associated with reduction in recurrent thromboembolism.

The Wells score:
*Clinically suspected DVT – 3.0 points
*Alternative diagnosis is less likely than PE – 3.0 points
*Tachycardia – 1.5 points
*Immobilization/surgery in previous four weeks – 1.5 points
*History of DVT or PE – 1.5 points
*Hemoptysis – 1.0 points
*Malignancy (treatment for within 6 months, palliative) – 1.0 points

Traditional interpretation

*Score >6.0 – High (probability 59% based on pooled data)
*Score 2.0 to 6.0 – Moderate (probability 29% based on pooled data)
*Score <2.0 – Low (probability 15% based on pooled data)

Alternate interpretation.
:-
*Score > 4 – PE likely. Consider diagnostic imaging.
*Score 4 or less – PE unlikely. Consider D-dimer to rule out PE.

Blood tests:-
In low/moderate suspicion of PE, a normal D-dimer level (shown in a blood test) is enough to exclude the possibility of thrombotic PE.

When a PE is being suspected, a number of blood tests are done, in order to exclude important secondary causes of PE. This includes a full blood count, clotting status (PT, APTT, TT), and some screening tests (erythrocyte sedimentation rate, renal function, liver enzymes, electrolytes). If one of these is abnormal, further investigations might be warranted.

Non-invasive imaging:-
CT pulmonary angiography (CTPA) is a pulmonary angiogram obtained using computed tomography (CT) with radiocontrast rather than right heart catheterization. Its advantages are clinical equivalence, its non-invasive nature, its greater availability to patients, and the possibility of identifying other lung disorders from the differential diagnosis in case there is no pulmonary embolism. Assessing the accuracy of CT pulmonary angiography is hindered by the rapid changes in the number of rows of detectors available in multidetector CT (MDCT) machines.[14] A study with a mixture of 4 slice and 16 slice scanners reported a sensitivity of 83% and a specificity of 96%. This study noted that additional testing is necessary when the clinical probability is inconsistent with the imaging results.[15] CTPA is non-inferior to VQ scanning, and identifies more emboli (without necessarily improving the outcome) compared to VQ scanning

Ventilation/perfusion scan (or V/Q scan or lung scintigraphy), which shows that some areas of the lung are being ventilated but not perfused with blood (due to obstruction by a clot). This type of examination is used less often because of the more widespread availability of CT technology, however, it may be useful in patients who have an allergy to iodinated contrast or in pregnancy due to lower radiation exposure than CT

Ventilation/perfusion scan (or V/Q scan or lung scintigraphy), which shows that some areas of the lung are being ventilated but not perfused with blood (due to obstruction by a clot). This type of examination is used less often because of the more widespread availability of CT technology, however, it may be useful in patients who have an allergy to iodinated contrast or in pregnancy due to lower radiation exposure than CT.

Low probability diagnostic tests/non-diagnostic tests:-

Tests that are frequently done that are not sensitive for PE, but can be diagnostic.

*Chest X-rays are often done on patients with shortness of breath to help rule-out other causes, such as congestive heart failure and rib fracture. Chest X-rays in PE are rarely normal,[18] but usually lack signs that suggest the diagnosis of PE (e.g. Westermark sign, Hampton’s hump).

*Ultrasonography of the legs, also known as leg doppler, in search of deep venous thrombosis (DVT). The presence of DVT, as shown on ultrasonography of the legs, is in itself enough to warrant anticoagulation, without requiring the V/Q or spiral CT scans (because of the strong association between DVT and PE). This may be valid approach in pregnancy, in which the other modalities would increase the risk of birth defects in the unborn child. However, a negative scan does not rule out PE, and low-radiation dose scanning may be required if the mother is deemed at high risk of having pulmonary embolism.

Electrocardiogram findings:-
Electrocardiogram of a patient with pulmonary embolism showing sinus tachycardia of approximately 150 beats per minute and right bundle branch block.An electrocardiogram (ECG) is routinely done on patients with chest pain to quickly diagnose myocardial infarctions (heart attacks). An ECG may show signs of right heart strain or acute cor pulmonale in cases of large PEs – the classic signs are a large S wave in lead I, a large Q wave in lead III and an inverted T wave in lead III (“S1Q3T3”). This is occasionally (up to 20%) present, but may also occur in other acute lung conditions and has therefore limited diagnostic value. The most commonly seen signs in the ECG is sinus tachycardia, right axis deviation and right bundle branch block. Sinus tachycardia was however still only found in 8 – 69% of people with PE.

Echocardiography findings:-
In massive and submassive PE, dysfunction of the right side of the heart can be seen on echocardiography, an indication that the pulmonary artery is severely obstructed and the heart is unable to match the pressure. Some studies  suggest that this finding may be an indication for thrombolysis. Not every patient with a (suspected) pulmonary embolism requires an echocardiogram, but elevations in cardiac troponins or brain natriuretic peptide may indicate heart strain and warrant an echocardiogram.

The specific appearance of the right ventricle on echocardiography is referred to as the McConnell sign. This is the finding of akinesia of the mid-free wall but normal motion of the apex. This phenomenon has a 77% sensitivity and a 94% specificity for the diagnosis of acute pulmonary embolism.

Combining tests into algorithms:-
Recent recommendations for a diagnostic algorithm have been published by the PIOPED investigators; however, these recommendations do not reflect research using 64 slice MDCT.[12] These investigators recommended:

*Low clinical probability. If negative D-dimer, PE is excluded. If positive D-dimer, obtain MDCT and based treatment on results.

*Moderate clinical probability. If negative D-dimer, PE is excluded. However, the authors were not concerned that a negative MDCT with negative D-dimer in this setting has an 5% probability of being false. Presumably, the 5% error rate will fall as 64 slice MDCT is more commonly used. If positive D-dimer, obtain MDCT and based treatment on results.

*High clinical probability. Proceed to MDCT. If positive, treat, if negative, additional tests are needed to exclude PE.

Pulmonary Embolism Rule-out Criteria:-
The Pulmonary Embolism Rule-out Criteria, or PERC rule, helps assess patients in whom pulmonary embolism is suspected, but unlikely. Unlike the Wells Score and Geneva score, which are clinical prediction rules intended to risk stratify patients with suspected PE, the PERC rule is designed to rule-out risk of PE in patients when the physician has already stratified them into a low-risk category.

Patients in this low risk category without any of these criteria may undergo no further diagnostic testing for PE: Hypoxia – Sa02 <95%, unilateral leg swelling, hemoptysis, prior DVT or PE, recent surgery or trauma, age >50, hormone use, tachycardia. The rationale behind this decision is that further testing (specifically CT angiogram of the chest) may cause more harm (from radiation exposure and contrast dye) than the risk of PE.[24] The PERC rule has a sensitivity of 97.4% and specificity of 21.9% with a false negative rate of 1.0% (16/1666).

Treatment:-
In most cases, anticoagulant therapy is the mainstay of treatment. Acutely, supportive treatments, such as oxygen or analgesia, are often required.

Anticoagulation:-
In most cases, anticoagulant therapy is the mainstay of treatment. Heparin, low molecular weight heparins (such as enoxaparin and dalteparin), or fondaparinux is administered initially, while warfarin, acenocoumarol, or phenprocoumon therapy is commenced (this may take several days, usually while the patient is in hospital). It however may be possible to treat low risk patients as outpatients. An ongoing study is looking into the safety of this practice. Warfarin therapy often requires frequent dose adjustment and monitoring of the INR. In PE, INRs between 2.0 and 3.0 are generally considered ideal. If another episode of PE occurs under warfarin treatment, the INR window may be increased to e.g. 2.5-3.5 (unless there are contraindications) or anticoagulation may be changed to a different anticoagulant e.g. low molecular weight heparin. In patients with an underlying malignancy, therapy with a course of low molecular weight heparin may be favored over warfarin based on the results of the CLOT trial. Similarly, pregnant women are often maintained on low molecular weight heparin to avoid the known teratogenic effects of warfarin, especially in the early stages of pregnancy. People are usually admitted to hospital in the early stages of treatment, and tend to remain under inpatient care until INR has reached therapeutic levels. Increasingly, low-risk cases are managed on an outpatient basis in a fashion already common in the treatment of DVT.

Warfarin therapy is usually continued for 3–6 months, or “lifelong” if there have been previous DVTs or PEs, or none of the usual risk factors is present. An abnormal D-dimer level at the end of treatment might signal the need for continued treatment among patients with a first unprovoked pulmonary embolus.

Thrombolysis:-
Massive PE causing hemodynamic instability (shock and/or hypotension, defined as a systolic blood pressure <90 mmHg or a pressure drop of 40 mmHg for>15 min if not caused by new-onset arrhythmia, hypovolemia or sepsis) is an indication for thrombolysis, the enzymatic destruction of the clot with medication. It is the best available medical treatment in this situation and is supported by clinical guidelines.

The use of thrombolysis in non-massive PEs is still debated. The aim of the therapy is to dissolve the clot, but there is an attendant risk of bleeding or stroke. The main indication for thrombolysis is in submassive PE where right ventricular dysfunction can be demonstrated on echocardiography, and the presence of visible thrombus in the atrium.

Surgical management:-
Surgical management of acute pulmonary embolism (pulmonary thrombectomy) is uncommon and has largely been abandoned because of poor long-term outcomes. However, recently, it has gone through a resurgence with the revision of the surgical technique and is thought to benefit selected patients

Chronic pulmonary embolism leading to pulmonary hypertension (known as chronic thromboembolic hypertension) is treated with a surgical procedure known as a pulmonary thromboendarterectomy.

Inferior vena cava filter:-
If anticoagulant therapy is contraindicated and/or ineffective, or to prevent new emboli from entering the pulmonary artery and combining with an existing blockage, an inferior vena cava filter may be implanted.

Prognosis:-
Mortality from untreated PE is said to be 26%. This figure comes from a trial published in 1960 by Barrit and Jordan,[38] which compared anticoagulation against placebo for the management of PE. Barritt and Jordan performed their study in the Bristol Royal Infirmary in 1957. This study is the only placebo controlled trial ever to examine the place of anticoagulants in the treatment of PE, the results of which were so convincing that the trial has never been repeated as to do so would be considered unethical. That said, the reported mortality rate of 26% in the placebo group is probably an overstatement, given that the technology of the day may have detected only severe PEs.

Prognosis depends on the amount of lung that is affected and on the co-existence of other medical conditions; chronic embolisation to the lung can lead to pulmonary hypertension. After a massive PE, the embolus must be resolved somehow if the patient is to survive. In thrombotic PE, the blood clot may be broken down by fibrinolysis, or it may be organized and recanalized so that a new channel forms through the clot. Blood flow is restored most rapidly in the first day or two after a PE. Improvement slows thereafter, and some defects may remain permanently. There is controversy over whether or not small subsegmental PEs need to be treated at all[40] and some evidence exists that patients with subsegmental PEs may do well without treatment.

Predicting mortality:-
The PESI and Geneva prediction rules can estimate mortality and so may guide selection of patients who can be considered for outpatient therapy.

Underlying causes:-
After a first PE, the search for secondary causes is usually brief. Only when a second PE occurs, and especially when this happens while still under anticoagulant therapy, a further search for underlying conditions is undertaken. This will include testing (“thrombophilia screen”) for Factor V Leiden mutation, antiphospholipid antibodies, protein C and S and antithrombin levels, and later prothrombin mutation, MTHFR mutation, Factor VIII concentration and rarer inherited coagulation abnormalities.

Epidemiology:-

Risk factors:-
The most common sources of embolism are proximal leg deep venous thrombosis (DVTs) or pelvic vein thromboses. Any risk factor for DVT also increases the risk that the venous clot will dislodge and migrate to the lung circulation, which happens in up to 15% of all DVTs. The conditions are generally regarded as a continuum termed venous thromboembolism (VTE).

The development of thrombosis is classically due to a group of causes named Virchow’s triad (alterations in blood flow, factors in the vessel wall and factors affecting the properties of the blood). Often, more than one risk factor is present.

*Alterations in blood flow: immobilization (after surgery, injury or long-distance air travel), pregnancy (also procoagulant), obesity (also procoagulant)

*Factors in the vessel wall: of limited direct relevance in VTE

*Factors affecting the properties of the blood (procoagulant state):

*Oestrogen-containing hormonal contraception
*Genetic thrombophilia (factor V Leiden, prothrombin mutation G20210A, protein C deficiency, protein S deficiency, antithrombin deficiency, hyperhomocysteinemia and plasminogen/fibrinolysis disorders).
*Acquired thrombophilia (antiphospholipid syndrome, nephrotic syndrome, paroxysmal nocturnal hemoglobinuria)

Prognosis:-
Once anticoagulation is stopped, the risk of a fatal pulmonary embolism is 0.5% per year

Prevention:-
If you are in hospital for surgery or because of illness, your doctor will suggest some leg exercises you can do, to ensure you keep your legs moving. You will be encouraged to drink plenty of fluids (or may have fluids via a drip if you are unable to drink).

If you are having major surgery, you may be given injections of heparin before your surgery to reduce your risk of getting a DVT or pulmonary embolism. You may also be given elastic compression stockings to wear or a device called an intermittent compression pump to keep the blood flowing through your legs.

*Compression stockings (also called TED or thrombo-embolic deterrent stockings) are usually worn to help maintain circulation and reduce the risk of blood clots forming in the veins of your legs. They come in different sizes and will be checked by nursing staff every day to make sure that they’re the correct size and fit for you. You might be asked to wear them after you have had surgery.

*Intermittent compression pumps help to dissolve blood clots by compressing the calf and/or thigh muscles of your leg. They are usually used straight before or during surgery.

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.

Resources:-

Researchers May Have Found an Efficient Way to Detect Pulmonary Embolisms


http://en.wikipedia.org/wiki/Pulmonary_embolism
http://www.mayoclinic.com/health/pulmonary-embolism/DS00429/DSECTION=causes

http://hcd2.bupa.co.uk/fact_sheets/html/Pulmonary_embolism.html

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New Remedies for Swine Flu

Honeybee venom and vitamin C may protect you against swine flu, suggest Indian researchers.

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Have no access to the H1N1 flu vaccine because of its being produced by a handful of global pharmaceutical biggies? Not to worry. Try honeybee venom or a good amount of vitamin C.

That’s the word from some Indian scientists. A caveat here. These ideas put forward by independent research groups are “hypotheses” rather than findings that have emerged from rigorous scientific experiments. But they stem from the basic premise that a nudge prepares the immune system better in the eventuality of a fatal viral attack.

A team of pharmacologists at Manipal University in Karnataka proposed the idea of using honeybee venom to shore up the human immune system in its fight against the swine flu virus. Their paper, which appears in the latest issue of the journal Medical Hypotheses, suggests honeybee venom therapy as a first-line strategy to quickly vaccinate the population in the event of a widespread H1N1 flu outbreak. It can provide passive as well as active immunisation against the infection, they argue.
……..-Nishi_tribalhoneybee stinging
“Many tribal communities use the sting of a honeybee as an antidote to colds and coughs,” says Rajeev Singla, lead author of the study. Singla, who teaches at the Shri Gopichand College of Pharmacy in Baghpet, Uttar Pradesh, says that bee venom’s anti inflammatory and immune-boosting properties are already well documented in modern science.

Even if the substance offers limited protection against swine flu, it is worth investigating as it is effective against several symptoms associated with the infection such as pneumonia and oedema, they say.

The second study, by researchers at the department of experimental medicine and biotechnology at the Post Graduate Institute of Medical Education and Research (PGI), Chandigarh, suggests that vitamin C can serve as a vaccine to control a H1N1 flu pandemic.

The study, scheduled to appear in the January 2010 issue of the journal Nutrition, builds upon past research to establish the efficacy of vitamin C in preventing common flu, an idea first proposed in the 1970s by Nobel Prize-winning American scientist Linus Pauling. Swine flu may be caused by a different influenza virus, but most of the symptoms associated with it are similar to those of the common cold.

The scientists explain that the viruses — there are nearly 100 of them — that cause flu enter the human body through the nasal route and attach themselves to a protein to get entry to the respiratory tract cells. Once there, the virus pushes its genetic material into the genome of the host cell. The virus thus takes over the host cell’s multiplication mechanism for its own proliferation.

But the PGI scientists think that it is possible to jeopardise the virus’s plan for replication, if adequate quantities of vitamin C are delivered to the cells in the respiratory tract.

The mixing of the flu viral genome with that of the human host cell will happen only when the latter is at a particular phase of the cell division cycle. But, Dibyajyoti Banerjee, lead author of the PGI study, says it possible to stop the infected cell from proceeding to that phase, if a high amount of vitamin C is present in the cell.“This restricts the viral genome integration in the human body,” Banerjee told KnowHow.

Delivering a high dose of vitamin C to the respiratory tract, however, is a challenge. It’s tough because no matter how big the dosage, very little of it reaches the respiratory tract, if delivered orally. That’s because of the digestion of the vitamin by the human digestive system.

To overcome this difficulty, the Chandigarh scientists propose a strategy of administering vitamin C through a combination of nasal and oral routes. “The combination of oral and inhalational delivery of vitamin C is important for attainment of high concentrations of it in the respiratory tract,” says Banerjee. The group is planning further studies to prove that this strategy will actually work, he adds.

Shahid Jameel, head of virology research at the International Centre for Genetic Engineering and Biotechnology, New Delhi, says it is possible to ward off many viral infections, including swine flu, by boosting general immunity. That’s because viruses depend entirely on the host for their multiplication.

As a result of co-evolution of the host and the virus, both have developed mechanisms to protect themselves.

“Just like we have immunity, viruses have ways to evade immunity. Eventually, this evolutionary tug of war leads to a virus that can infect, but not cause disease,” says Jameel.

That would be an ideal situation as the infection then cannot spread to others, he concludes.

You may click & see:->
*Bee venom therapy
*Apitoxin
*Stinger
*Hornet stings
*Characteristics of common wasps and bees
*Schmidt Sting Pain Index

Source: The Telegraph (Kolkata, India)

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