Herbs & Plants

Shepherd’s Purse (Capsella bursa-pastoris)

Botanical Name ; Capsella bursa-pastoris
Family: Brassicaceae
Genus: Capsella
Species: C. bursa-pastoris
Kingdom: Plantae
Order: Brassicales

Synonyms :  Thlaspi bursa-pastoris. Bursa abscissa. Bursa druceana. Capsella concava.

Common Name ; Shepherd’s-purse

Habitat: is native to eastern Europe and Asia minor but is naturalized and considered a common weed in many parts of the world, especially in colder climates,including Britain, where it is regarded as an archaeophyte, North America and China but also in the Mediterranean and North Africa.  It grows in Arable land, gardens, waste places etc, it is a common weed of cultivated soil.

Shepherd’s-purse  is a small (up to 0.5m) annual and ruderal species, and a member of the Brassicaceae or mustard family. Capsella bursa-pastoris is closely related to the model organism Arabidopsis thaliana and is also used as a model organism due to the variety of genes expressed throughout its life cycle that can be compared to genes that are well studied in A. thaliana. Unlike most flowering plants, it flowers almost all year round. Like many other annual ruderals exploiting disturbed ground, C. bursa-pastoris reproduces entirely from seed, has a long soil seed bank, and short generation time and is capable of producing several generations each year.

Shepherd’s-purse plants grow from a rosette of lobed leaves at the base. From the base emerges a stem about 0.2 to 0.5 meters tall, which bears a few pointed leaves which partly grasp the stem. The flowers are white and small, in loose racemes, and produce seed pods which are heart-shaped.

Like a number of other plants in several plant families, its seeds contain a substance known as mucilage, a condition known as myxospermy. The adaptive value of myxospermy is unknown, although the fact that mucilage becomes sticky when wet has led some to propose that C. bursa-pastoris traps insects which then provide nutrients to the seedling, which would make it protocarnivorous.

Edible Uses :
Edible Parts: Leaves; Oil; Seed.
Edible Uses: Condiment; Oil.

Leaves – raw or cooked. The young leaves, used before the plant comes into flower, make a fine addition to salads. The leaves are a cress and cabbage substitute, becoming peppery with age. Leaves are usually available all year round, though they can also be dried for later use. The leaves contain about 2.9% protein, 0.2% fat, 3.4% carbohydrate, 1% ash. They are rich in iron, calcium and vitamin C. A zero moisture basis analysis is available. The young flowering shoots can be eaten raw or cooked. They are rather thin and fiddly but the taste is quite acceptable. They can be available at most times of the year. Seed – raw or cooked. It can be ground into a meal and used in soups etc. It is very fiddly to harvest and utilize, the seed is very small. The seed contains 35% of a fatty oil. This oil can be extracted and is edible. The seedpods can be used as a peppery seasoning for soups and stews. The fresh or dried root is a ginger substitute

Constituents: choline, acetylcholine and tyramine, saponins, mustard oil, flavonoids

Fumaric acid is one active substance that has been isolated.. Although Fumaric acid and its derivatives are used with success in many conditions there is no direct evidence that plant extract has been used with similar success.

Figures in grams (g) or miligrams (mg) per 100g of food.
Leaves (Dry weight)

*280 Calories per 100g
*Water : 0%
*Protein: 35.6g; Fat: 4.2g; Carbohydrate: 44.1g; Fibre: 10.2g; Ash: 16.1g;
*Minerals – Calcium: 1763mg; Phosphorus: 729mg; Iron: 40.7mg; Magnesium: 0mg; Sodium: 0mg; Potassium: 3939mg; Zinc: 0mg;
*Vitamins – A: 21949mg; Thiamine (B1): 2.12mg; Riboflavin (B2): 1.44mg; Niacin: 3.4mg; B6: 0mg; C: 305mg;

*Capsella bursa-pastoris
*Traditional Chinese

Medicinal Uses:
Common Uses: Abrasions/Cuts * Bladder Infection (UTI) Cystitis * Childbirth * Heart Tonics/Cordials * Menorrhagia *
Properties:  Antiscorbutic* Diuretic* Styptic* Astringent* Febrifuge* Refrigerant*
Parts Used: whole herb.

Shepherd’s purse is one of the important herbs to stop bleeding an effect due to the tyramine and other amines it contains. This property leads to its use is a number of condidtions such as heavy menstrual bleeding, nosebleeds, and as a post-partum herb. The herb is both a vasodilator, and also hastens coagulation and constrict blood vessels.

Shepherd’s purse contains a protein that acts in the same way in the body as the hormone oxytocin, constricting the smooth muscles that support and surround blood vessels, especially those in the uterus. Other chemicals in the herb may accelerate clotting. Still other compounds in the herb help the uterus contact, explaining the long-time use of the herb to help the womb return to normal size after childbirth. Mountain Rose Herbs (2008-07-09)

Herbally, it is primarily used to stop vaginal bleeding, an action which may be attributable to the common parasitic fungus found with it, which is related to the vasoconstrictor ergot.

Other Uses
Shepherd’s-purse is gathered from the wild or grown for food to supplement animal feed, for cosmetics, and for medicinal purposes. It is commonly used as food in Shanghai and the surrounding Jiangnan region as food, where they are stir-fried with rice cakes and other ingredients or as part of the filling in wontons. It is one of the ingredients of the symbolic dish consumed in the Japanese spring-time festival, Nanakusa-no-sekku.

Known Hazards :  Signs of toxicity are sedation, pupil enlargement and breathing difficulty. Avoid if on treatments for high blood pressure. Avoid with thyroid gland disorders or heart disease. Possible addictive sedative effects with other depressants (e.g. Alcohol). Avoid during pregnancy

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.


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Healthy Tips

How Mind Can Suppress Hunger Pangs

You might not be keeping a check on the amount of calories you’re consuming during a party, but your brain will, say Yale University researchers, who have identified a molecule that tells brain that the stomach is full – and signals it’s time to say no to a second piece of Delicious food and push back from the dining table. to see the picture
In a study on rodents, the researchers have discovered that one type of lipid produced in the gut, called N-acylphosphatidylethanolamines or NAPEs, rises after eating fatty foods.

The NAPEs enter the bloodstream and go straight to the brain, where they concentrate in a brain region that controls food intake and energy expenditure.

Led by Gerald I. Shulman, Yale professor of medicine and cellular & molecular physiology and a Howard Hughes Medical Institute investigator, the researchers suggested that the molecule may help regulate how much animals and people eat.

NAPEs are synthesized and secreted into the blood by the small intestine after fatty foods are eaten. The researchers found that mice and rats injected regularly with NAPEs ate less food and lost weight. In addition, treatment with NAPEs appeared to reduce the activity of “hunger” neurons in the brain while stimulating activity in neurons that are believed to play a role in reducing appetite.

In the last two decades, scientists have made great inroads toward understanding how the body communicates with the brain to control food intake. Till date, hormones such as leptin that act as regulators of this complex system have proved disappointing when tested as potential weight-loss treatments in humans.

The researchers are now planning to investigate how the new findings apply to humans.The team will first study non-human primates to determine if NAPE on centrations increase in a similar fashion after fat ingestion.

Then, Shulman said: “If chronic NAPE treatment is well tolerated and can cause weight loss by a reduction of food intake, we would have strong impetus to move forward with human NAPE trials.” The findings are published in the latest issue of the journal Cell.

Sources: The Times Of India

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Positive thinking

Fearlessness Can be Taught

The brain can produce antidepressants with the right signal, a finding that suggests that meditating, or going to your “happy place,” tru ly works, scientists reported .

Mice, who were forced to swim endlessly until they surrendered and just floated, waiting to drown, could be conditioned to regain their will to live when a tone they associated with safety was played.

The experiment suggests that there are good ways to teach people this skill, and points to new routes for developing better antidepressants, said Dr Eric Kandel of the Howard Hughes Medical Institute and Columbia University in New York, who led the research.

“The happy place works. This is like going to the country,” Kandel said in a telephone interview.

Writing in the journal Neuron, Kandel’s team said they used classical conditioning to train mice. They had already conditioned some mice to fear a neutral tone by playing the sound when they shocked the animals’ paws. After a while, the tone itself creates fear. “It scares the hell out of the animal,” Kandel said.

They decided to reverse the study — they played the tone when they were not shocking the mice. “It learned that the only time it was really safe is when the tone comes on,” Kandel said.

To make a mouse depressed, they used a method favored by drug companies called learned helplessness. “You put an animal into a pool of water and it can’t get out. It gives up and it stops swimming and it just floats,” Kandel said. “When you give the animal an antidepressant, it starts swimming again. When we played the tone, it started to swim again just as it did with the antidepressant.”

Further experiments showed the tone and an antidepressant drug worked synergistically, he said. When they looked at the brains of their mice, they saw using the conditioned “safety” tone activated a different pathway than the drugs did.

It affected dopamine, while antidepressants work on serotonin. Both are message-carrying molecules called neurotransmitters. The conditioning also affected a compound called brain-derived neurotrophic factor or BDNF —which helps nourish and encourages the growth of brain cells. The learned safety did not affect serotonin.
Mice conditioned by the “safety” tone also had more newborn brain cells in the dentate gyrus, a part of the brain linked with learning and depression.

When Kandel’s team used radiation to slow the birth of new cells in the dentate gyrus, the effects of learned safety and of antidepressants were blunted.

Kandel noted that antidepressant drugs appear to work, in part, by encouraging the growth of new brain cells — as does psychotherapy.

“Learning involves alterations in the brain and gene expression,” Kandel said. “Psychotherapy is only a form of learning.”

This shows how effective psychotherapy, meditation and other stress-reduction tools may be, and it could help in the design of new drugs, Kandel said. “This opens up new pathways that may profitable,” he said.

Sources: The Times Of India

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News on Health & Science

Slowing Down Life’s Clock

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Decades of research on aging are beginning to pay off, although it doesn’t mean that increasing longevity is a pill away, writes T.V. Jayan

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It’s been a decade and a half since Cynthia Kenyon genetically tweaked roundworms to expand their lifespan to twice the normal length. Science has not been able to uncork the fountain of youth yet, but the jump-start Kenyon and her colleagues at the University of California, San Francisco, gave to longevity research    by making the wrigglers, through the manipulation of a single gene, live for 40 days instead of 20  has helped resolve many mysteries surrounding the issue of ageing.

The latest in the list is the revelation that the ubiquitous molecule, insulin, comes in the way of a prolonged lifespan. Another independent study points to the benefits calorie restriction has on longevity by making nearly starved roundworms live 40 per cent longer than their well-fed peers.

Too much insulin ” a hormone that tells our cells to use sugar from the bloodstream, thus helping us to avoid metabolic complications that lead to diseases such as diabetes  in the brain may not be a good sign, said a team of researchers from the Howard Hughes Medical Institute in Boston.

By saying so, the researchers  led by endocrinologist Morris White  scientifically reinforced what every mother might tell her child: Eat a good diet and exercise; it will keep you healthy.

The researchers, who sought to understand the role of the insulin-signalling pathway in extending lifespan, found actually the opposite of what most scientists and clinicians believed. Because, according to White, most would find it difficult to accept the idea that insulin can reduce lifespan. This signalling pathway of insulin governs growth and metabolic processes in cells throughout the body.

Tests on lab mice showed that when both the copies of a gene responsible for insulin signalling called Irs2  were knocked off in the brain but retained in cells in other organs, the animals lived about six months longer than usual. This is nearly 18 per cent more than the animal  normal lifespan.

This even though the genetically modified mice were overweight and had higher blood insulin levels. To the scientist’s  surprise, they became more active with age and their glucose metabolism resembled that of younger mice. Besides, their brains showed higher levels of superoxide dismutase, an antioxidant enzyme that protects cells from damage caused by highly reactive chemicals called free radicals.

So diet, physical activity and lower weight keep one’s peripheral tissues sensitive to insulin. This reduces the amount and duration of insulin secretion required to keep glucose under control when one eats. This way, the brain is exposed to less insulin. And since insulin turns on Irs2, the lower the insulin, the lower the IRs2 activity, White observed. The findings were reported in the July 20 issue of the journal Science.

While White’s team pointed to a balanced diet and keeping fit as the recipe for a long life, Andrew Dillin of the Salk Institute of Biological Studies in the US   who had co-authored several papers on ageing with Kenyon  found a gene in roundworms that specifically links calorie restriction to longevity. Interestingly, an Indian scientist, Kalluri Subba Rao, arrived at a similar conclusion more than a decade ago by studying undernourished people and comparing them with those who ate a normal diet.

Dillin and his colleagues in a way cracked open the black box of how persistent hunger increases longevity. “After 72 years of not knowing how calorie restriction works, we finally have genetic evidence to unravel the underlying molecular programme required for increased longevity in response to calorie restriction,” he said.

What is significant about his work is that the gene they identified, pha-4, is independent of those involved in the insulin pathway, which has been the focus of most longevity research so far. The loss of only this gene       which encodes for the protein PHA-4  negated the lifespan-enhancing effects of calorie restriction in worms. So the scientists did the opposite  that is, overexpress the pha-4 gene in the worms. It worked, and the worms lived as much as 40 per cent longer.

Human beings, says Dillin, possess three genes similar to the pha-4 gene of worms, all belonging to what is called the Foxa family. These three genes play an important role in the development and later, the regulation, of glucagon — a pancreatic hormone that, unlike insulin, increases the blood sugar concentration and maintains the body’s energy balance, especially during fasting.

Subba Rao, an emeritus professor at the University of Hyderabad who in 1996 reported the benefits of diet restriction on ageing, agrees. Down-regulating glucose signalling has several positive effects, longevity being one of them.  The body is programmed to metabolise, say, one tonne of sugar over a lifetime. In how much time one does it is entirely up to that person,” said Subba Rao, coordinator of the university’s Centre for Research and Education in Ageing.

Concerted efforts over the last 15 years in the biology of ageing are paying off, although it doesn’t mean that increasing one’s lifespan is a pill away. But scientists are already taking the research to the next level: studying the proteins involved in the process. Examining the process of ageing from the protein perspective may lead to therapeutic methods of delaying ageing in the not-so-distant future, provided the scientists repeat in humans the feats they have achieved in worms and mice.

Last week, a team of researchers at the Scripps Research Institute in La Jolla, California, identified some 86 proteins whose abundance varied in mutant round worms as compared to normal ones. While 47 of the proteins were more abundant in worms that were genetically altered to live twice longer, another 39 were less abundant than in the controls. “Proteins are harder to study but they are closer to the enzymatic processes involved,” John Yates, who led the study, told KnowHow.

Enzymatic processes are the closest one can get when it comes to therapeutics as they are part of the bodys routine biochemical processes. It is for the same reason that many new-generation drugs today have enzymes as their key component.

Source: The Telegraph (Kolkata, India)