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News on Health & Science

New Protein May Benefit Prostate Cancer Patients

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Men who have been diagnosed with prostate cancer and need to have a gland surgically removed may suffer some temporary nerve damage. Complications of this major nerve could lead to more health concerns, including the killing of healthy cells in the penis, as well as erectile dysfunction.

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However, researchers have discovered a protein that could speed up recovery of this complication. Using rats, the team of investigators administered sonic hedgehog, the beneficial protein, into the animals, using a gel that contains a high amount of nutrient.

The team of investigators discovered that the nerve regenerated twice as fast compared to if it healed on its own. This could lead to further research that may also help in treating peripheral nerves in the face that were damaged from certain types of cancer.

Successful studies may lead to improving male patients’ lives after surgery “because men are being diagnosed at a younger age and live longer due to improved cancer therapies,” said Carol Podlasek, assistant professor of urology at Northwestern University’s Feinburg School of Medicine.

These results may benefit prostate cancer patients for a more effective, natural treatment for the illness, as a recent report states. Other non-surgical procedures for these health complications have not been successful for the majority of experimental trial participants.

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“I have reduced the night trips to one in my seven-hour sleep period.” —Robert S., Montana

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Source :Better Health Research. July 19.2010

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Herbs & Plants

Ma Huang (Ephedra sinica)

Botanical Name: Ephedra sinica
Family: Ephedraceae
Genus: Ephedra
Kingdom: Plantae
Division: Gnetophyta
Class: Gnetopsida
Order: Ephedrales
Common Names: Ephedra, Ma Huang,Joint-pine, Jointfir, Mormon-tea or Brigham Tea.
The Chinese name is má huáng, which means “yellow hemp”. Ephedra is also sometimes called sea grape (from the French raisin de mer), although that is also a common name for Coccoloba uvifera.

Ephedra sinica Stapf. Engl.: Chinese ephedra, Chinese joint-fir. Suom.: efedra. Sven.: efedra. TCM: ma huang, cao ma huang

Habitat :These plants occur in dry climates over a wide area mainly in the northern hemisphere, across southern Europe, north Africa, southwest and central Asia, southwestern North America, and, in the southern hemisphere, in South America south to Patagonia.

Description: Ephedra is a shrublike plant found in desert regions throughout the world. It is distributed from northern China to Inner Mongolia. The dried green stems of the three Asian species (E. sinica, intermedia, equisetina) are the plant parts employed medicinally. The North American species of ephedra does not appear to contain the active ingredients of its Asian counterparts. The plants are 1.5 to 4 foot high. They typically grow on dry, rocky, or sandy slopes. The many slender, yellow green branches of ephedra have two very small leaf scales at each node. The mature, double seeded cones are visible in the fall.

click to see the pictures…..>…….(01).…….(1)..……...(2).………………….

Species
Ephedra alata Decne
Ephedra altissima Desf.
Ephedra americana Humb. & Bonpl. ex Willd.
Ephedra antisyphilitica Berl. ex C.A.Meyer – Clapweed, Erect Ephedra
Ephedra aspera Engelm. ex S.Wats. – Boundary Ephedra, Pitamoreal
Ephedra boelckei F.A.Roig
Ephedra californica S.Wats. – California Ephedra, California Jointfir
Ephedra campylopoda C. A. Mey.
Ephedra chilensis C. Presl
Ephedra ciliata Fisch. ex C. A. Mey.
Ephedra coryi E.L.Reed – Cory’s Ephedra
Ephedra cutleri Peebles – Navajo Ephedra, Cutler’s Ephedra, Cutler Mormon-tea, Cutler’s Jointfir
Ephedra dahurica Turcz.
Ephedra distachya L. – Joint-pine, Jointfir
Ephedra distachya L. subsp. distachya
Ephedra distachya subsp. helvetica (C.A.Meyer) Aschers. & Graebn.
Ephedra distachya L. subsp. monostachya (L.) Riedl
Ephedra equisetina Bunge – Ma huang
Ephedra fasciculata A.Nels. – Arizona Ephedra, Arizona Jointfir, Desert Mormon-tea Photo
Ephedra fedtschenkoae Pauls.
Ephedra foliata Boiss. ex C.A.Mey.
Ephedra fragilis Desf.
Ephedra fragilis subsp. campylopoda (C.A.Meyer) Aschers. & Graebn.
Ephedra frustillata Miers – Patagonian Ephedra
Ephedra funerea Coville & Morton – Death Valley Ephedra, Death Valley Jointfir
Ephedra gerardiana Wallich ex C.A.Meyer – Gerard’s Jointfir, Shan Ling Ma Huang
Ephedra holoptera Riedl
Ephedra intermedia Schrenk ex C.A.Meyer
Ephedra lepidosperma C.Y.Cheng

Ephedra distachyaEphedra likiangensis Florin
Ephedra lomatolepis Shrenk
Ephedra macedonica Kos.
Ephedra major Host
Ephedra major subsp. procera Fischer & C.A.Meyer
Ephedra minuta Florin
Ephedra monosperma C.A.Meyer
Ephedra multiflora Phil. ex Stapf
Ephedra nevadensis S.Wats. – Nevada Ephedra, Nevada Jointfir, Nevada Mormon-tea
Ephedra pachyclada Boiss.
Ephedra pedunculata Engelm. ex S.Wats. – Vine Ephedra, Vine Jointfir
Ephedra procera Fisch. & C. A. Mey.
Ephedra przewalskii Stapf
Ephedra przewalskii var. kaschgarica (B.Fedtsch. & Bobr.) C.Y.Cheng
Ephedra regeliana Florin – Xi Zi Ma Huang
Ephedra saxatilis (Stapf) Royle ex Florin
Ephedra sinica Stapf – Cao Ma Huang, Chinese ephedra
Ephedra strobilacea Bunge
Ephedra torreyana S.Wats. – Torrey’s Ephedra, Torrey’s Jointfir, Torrey’s Mormon-tea, Cañutillo
Ephedra trifurca Torrey ex S.Wats. – Longleaf Ephedra, Longleaf Jointfir, Longleaf Mormon-tea, Popotilla, Teposote
Ephedra viridis Coville – Green Ephedra, Green Mormon-tea

Active Compounds:
Ephedra’s active medicinal ingredients are the alkaloids ephedrine and pseudoephedrine. The stem contains 1-3% total alkaloids, with ephedrine accounting for 30-90% of this total, depending on the plant species employed. Both ephedrine and its synthetic counterparts stimulate the central nervous system, dilate the bronchial tubes, elevate blood pressure, and increase heart rate. Pseudoephedrine (the synthetic form) is a popular over-the-counter remedy for relief of nasal congestion.

Biochemistry and pharmacology
The alkaloids ephedrine and pseudoephedrine are the active constituents of the plant. Pseudoephedrine is used in over-the-counter decongestants. Derivatives of ephedrine are used to treat low blood pressure, but alternatives with reduced cardiovascular risk have replaced it for treating asthma. Ephedrine is also considered a performance-enhancing drug and is prohibited in most competitive sports. Some species in the Ephedra genus have no alkaloid content; however, the most commonly used species, E. sinica, has a total alkaloid content of 1–3% by dry weight. Ephedrine constitutes 40–90% of the alkaloid content, with the remainder consisting of pseudoephedrine and the demethylated forms of each compound.

Medical uses:
Plants of the Ephedra genus, including E. sinica and others, have traditionally been used by indigenous people for a variety of medicinal purposes, including treatment of asthma, hay fever, and the common cold. They have also been proposed as a candidate for the Soma plant of Indo-Iranian religion. The alkaloids ephedrine and pseudoephedrine are active constituents of E. sinica and other members of the genus. These compounds are sympathomimetics with stimulant and decongestant qualities and are related chemically to the amphetamines. Ephedra nevadensis contains ephedrine in its roots, stems and branches. Ephedra distachya contains up to 3% ephedrine in the entire plant. Ephedra sinica contains approximately 2.2% ephedrine.

The stems of the ephedra plant can be brewed into a pungent, bitter, herb tea that dilates the bronchial vessels while stimulating the heart and central nervous system.

The active chemical components of ephedra, or ma huang, the alkaloids ephedrine and pseudo ephedrine, are found in over the counter allergy and cold medications as over-the-counter decongestants. . An internal review of FDA records between 1969 and September 2006 found 54 reports of deaths in children associated with decongestant medicines containing pseudoephedrine, phenylephrine or ephedrine, prompting the recent recall of these medications in children’s cold care products.

The phytochemical ephedrine possesses properties similar to adrenaline that serves a critical role in our system as a neurotransmitter and a modulator of our metabolic rate. This powerful stimulant action is the major reason why it is so dangerous when misused. Ephedra has fallen into disfavor because of its misuse in the west as a diet drug. A handful of people have died over the last few years prompting the FDA to ban its use.

Herbalists, however, use the whole plant which contains six other related alkaloids, one of which, pseudoephedrine, actually reduces the heart rate and lowers blood pressure. This plant has been used in China for thousands of years, yet no undesirable side-effects have been recorded from the proper administration of the whole plant. Mabey, Richard ,48 Those wishing to use the whole herb to treat allergies and asthma can still buy bulk ephedra from reputable whole herb sources such as Mountain Rose, however it is recommended that it be used under only under supervision of a qualified herbalist.

You may click for more knowledge :

Traditional Chinese Medicine

Ma Huang has a 5,000 year history of use in Chinese medicine as an asthma treatment and is traditionally prescribed in TCM as an effective treatment of hay fever, edema, arthritis, colds, asthma, bronchitis and hives.

Weight Loss Aid: Ephedrine suppresses the appetite and increases the metabolic rate of adipose tissue. Ephedrine activates the sympathetic nervous system, increasing the metabolic rate and increasing the amount of the food converted to heat (thermogenesis). This prevents the body from converting these foods to fat, thus helping in the control of weight gain by those who have low metabolism.

Ephedrine is often used in conjunction with methylxanthine sources such as coffee, tea, cola nut, and guarana. The methylxanthines enhances the thermogenic effect of ephedrine. Clinical studies have also shown that aspirin may be effective in increasing the thermogenic effect of ephedrine.


Side Effects:

The herb and its extracts are potentially addictive, and can disrupt regular heart rhythm, induce cardiac arrest, and raise blood pressure. They are very likely to make you sweat profusely, become irritable, nervous, nauseous and cause insomnia.

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.holisticonline.com/herbal-med/_herbs/h53.htm
http://en.wikipedia.org/wiki/Ephedra_sinica
http://www.anniesremedy.com/herb_detail298.php
http://en.wikipedia.org/wiki/Ephedra

Categories
Ailmemts & Remedies

SIDS (Sudden Infant Death Syndrome)

Definition:
Sudden infant death syndrome (SIDS) or crib death is a syndrome marked by the sudden death of an infant that is unexpected by history and remains unexplained after a thorough forensic autopsy and a detailed death scene investigation. The term cot death is often used in the United Kingdom, Ireland, Australia, India, South Africa and New Zealand.In USA the term SIDS  is widely spread and  many times  under educated parents  are very much panicky over SIDS and do overdoes  which  may causes harm to babies.

…………..CLICK & SEE THE PICTURES

Typically the infant is found dead after having been put to bed, and exhibits no signs of having suffered.The cause of death never identified is the actual SIDS  which is very rare in case of healthy babies.

 

SIDS is a diagnosis of exclusion. It should only be applied to an infant whose death is sudden and unexpected and remains unexplained after the performance of an adequate postmortem investigation including:

1.an autopsy;
2.investigation of the scene and circumstances of the death;
3.exploration of the medical history of the infant and family.

Australia and New Zealand are shifting to the term Sudden Unexplained Death in Infancy (SUDI) for professional, scientific and coronial clarity.

The term SUDI is now often used instead of  SIDS   because some coroners prefer to use the term ‘undetermined’ for a death previously considered to be SIDS. This change is causing diagnostic shift in the mortality data.

Causes:
SIDS is most likely to occur between 2 and 4 months of age, and 90% occur by 6 months of age. It occurs more often in winter months, with the peak in January. There is also a greater rate of SIDS among Native and African Americans.

The following have been linked to an increased risk of SIDS (as they call it):

*Babies who sleep on their stomachs (habitually)
*Babies who are around cigarette smoke while in the womb or after being born
*Babies who sleep in the same bed as their parents and the parents are tired to take proper care during sleep.
*Babies who have soft bedding in the crib
*Multiple birth babies (being a twin, triplet, etc.)
*Premature babies
*Babies who have a brother or sister who had SIDS
*Mothers who smoke or use illegal drugs
*Teen mothers
*Short time period between pregnancies
*Late or no prenatal care
*Situations of  extreme poverty

*Parents & baby sleep with animals inside the room (you may click to see how much carbon dioxide dogs exhale )

The dog’s respiratory system serves two purposes. First, it is the exchange mechanism by which the body’s carbon dioxide is replaced with oxygen. It is also a unique cooling system. Since dogs do not have sweat glands (except on their feet), they cannot perspire to lower their body’s temperature like humans do. To cool their body they must breathe harder (pant). By breathing faster, warm air is exchanged from the body for the cooler outside air. Additionally, moisture within the respiratory system evaporates, further cooling these surfaces. Therefore, the lungs function both to exchange carbon dioxide for oxygen and to cool the body.So,dogs need more oxygen than man.

*Death due to long driving without taking care of baby much
*Stuffy room (oxygen level falls during night)
*Not bothering about baby’s consisting crying

SIDS affects boys more often than girls. While studies show that babies with the above risk factors are more likely to be affected, the impact or importance of each factor is not well-defined or understood.

In most cases if no specific cause can be found to explain the death, it’s defined as SIDS. Research has suggested that a number of different factors may be linked to SIDS. It’s believed that these factors don’t actually cause SIDS, but may make a baby more at risk. These factors include:

*allergies
*bacterial and viral infections
*unknown genetic conditions
*problems in the area of the brain that controls breathing
*irregular heartbeat
*accidental suffocation
*overheating

Symptoms:
There are no symptoms. Babies who die of SIDS  do not appear to suffer or struggle.

Risk  Factors:-
The cause of SIDS
is unknown. Although studies have identified risk factors for SIDS, such as putting infants to bed on their stomachs, there has been little understanding of the syndrome’s biological cause or potential causes. The frequency of SIDS appears to be a strong function of the infant’s sex, age and ethnicity, and the education and socio-economic-status of the infant’s parents.

According to a study published on November 1, 2006 in the Journal of the American Medical Association, babies who die of SIDS have abnormalities in the brain stem (the medulla oblongata), which helps control functions like breathing, blood pressure and arousal, and abnormalities in serotonin signaling. According to the National Institutes of Health, which funded the study, this finding is the strongest evidence to date that structural differences in a specific part of the brain may contribute to the risk of SIDS.

In a British study released May 29, 2008 researchers discovered that the common bacterial infections Staphylococcus aureus (staph) and Escherichia coli (E. coli) appear to be a risk factor in some cases of SIDS. Both bacteria were present at greater than usual concentrations in infants who died from SIDS. SIDS cases peak between eight and ten weeks after birth, which is also the time frame in which the antibodies that were passed along from mother to child are starting to disappear and babies have not yet made their own antibodies.

Listed below are several risk factors associated with increased probability of the syndrome based on information available prior to this recent study.

Prenatal risks:

*maternal nicotine use (tobacco or nicotine patch)
*inadequate prenatal care
*inadequate prenatal nutrition
*use of heroin, cocaine and other drugs
*subsequent births less than one year apart
*alcohol use
*infant being overweight
*mother being overweight
*Teen pregnancy (if the baby has a teen mother, it has a greater risk)
*infant’s sex (60% of SIDS cases occur in males)

Post-natal risks:

*mold (can cause bleeding lungs plus a variety of other uncommon conditions leading to a misdiagnosis and death). It is often misdiagnosed as a virus, flu, and/or asthma-like conditions.
*low birth weight (in the U.S. from 1995-1998 the rate for 1000-1499 g was 2.89/1000 and for 3500-3999 g it was 0.51/1000)
*exposure to tobacco smoke
*prone sleep position (lying on the stomach, see sleep positioning below)
*not breastfeeding
*elevated or reduced room temperature
*excess bedding, clothing, soft sleep surface and stuffed animals
*co-sleeping with parents or other siblings may increase risk for SIDS, but the mechanism remains unclear
*infant’s age (incidence rises from zero at birth, is highest from two to four months, and declines towards zero at one year)
*premature birth (increases risk of SIDS death by about 4 times.  In 1995-1998 the U.S. SIDS rate for 37–39 weeks of gestation was 0.73/1000; The SIDS rate for 28–31 weeks of gestation was 2.39/1000)
*anemia

Hypotheses:-

Mattress bugs
A 2004 study hypothesized that insects (called “bugs”) feeding on baby vomit and dust could be fatal for small children, creating “supertoxins” which spur the baby’s body into overreacting, leading to anaphylactic shock.

Brain disorder
A recently published research article showed evidence that cells in the brainstem fail to develop receptors for serotonin in the womb. This abnormality can continue postpartum until the end of the first year. This would account for there being few to no SIDS deaths after the first year of infancy and the reason the risk is greater for premature infants. Males have fewer serotonin receptors than females, perhaps contributing to the increased incidence of SIDS in the demographic.

In addition, a study done in 2006 showed that a possible cause of SIDS is because parents leave their infants in a position known as the Trendelenburg position.[28] This position can cause the brain stem to fall, and in a result, the brain becomes “crushed”. The proper position for an infant is either Fowler’s position or Sims’.

Air circulation with fan use

According to a study of nearly 500 babies published the October 2008 Archives of Pediatrics & Adolescent Medicine, using a fan to circulate air correlates with a lower risk of sudden infant death syndrome. Researchers took into account other risk factors and found that fan use was associated with a 72% lower risk of SIDS. Only 3% of the babies who died had a fan on in the room during their last sleep, the mothers reported. That compared to 12% of the babies who lived. Using a fan reduced risk most for babies in poor sleeping environments. Author De-Kun li said that “the baby’s sleeping environment really matters” and that “this seems to suggest that by improving room ventilation we can further reduce risk.”

However, Dr. John Olssen at East Carolina University has pointed out that this study had a number of methodological flaws, such selection and recall bias, low enrollment numbers, and dissimilar study groups. Olssen argues that although fan use is probably not harmful, it should not be recommended as a means to reduce the risk of SIDS.

Vitamin C
In the 1970s, high doses of vitamin C were touted as a preventive measure for SIDS, although the claim was controversial even then. Subsequent studies failed to support a preventive role for vitamin C in SIDS. To the contrary, a 2009 study found that high levels of vitamin C were strongly associated with SIDS, possibly through a pro-oxidant interaction with iron.

Toxic gases
In 1989, a controversial piece of research by UK Scientist Barry Richardson claimed that all cot deaths were the result of toxic nerve gases being produced through the action of fungus in mattresses on compounds of phosphorus, arsenic and antimony. These chemicals are frequently used to make mattresses fire-retardant.

Support for this hypothesis was based on the observation that the risk of cot death rises from one sibling to the next.[citation needed] Richardson claimed that parents are more likely to buy new bedding for their first child, and to re-use that bedding for later children. The more frequently used the bedding is, the more chance there will be that fungus has become resident in the material; thus, a higher chance of cot death. A paper by Peter Fleming and Peter Blair[39] references evidence from other studies that both supports and refutes the increasing occurrence of SIDS with mattress sharing and suggests that this is still inconclusive.

Dr. Jim Sprott recommends new parents either buy bedding free of the toxic compounds or to wrap the mattresses in a barrier film to prevent the escape of the gases. Sprott claims that no case of cot death has ever been traced back to a properly manufactured or wrapped mattress.

However, a final report of “The Expert Group to Investigate Cot Death Theories: Toxic Gas Hypothesis”, published in May 1998, concluded that “there was no evidence to substantiate the toxic gas hypothesis that antimony- and phosphorus-containing compounds used as fire retardants in PVC and other cot mattress materials are a cause of SIDS. Neither was there any evidence to believe that these chemicals could pose any other health risk to infants.”[41] The report also states that “in normal cot-like conditions it is not possible to generate toxic gas from antimony in mattresses” and “babies have also been found to die on wrapped mattresses.”

Contrary to media publicity, the 1998 UK Limerick Report did not disprove the toxic gas theory—as a highly qualified environmental scientist has stated in the New Zealand Medical Journal. In fact, the Limerick Committee’s experiments proved the fungal generation of toxic gases (forms of stibine and arsine) from cot mattress materials.

According to Dr. Sprott, as of 2006, the New Zealand government has not reported any SIDS deaths when babies have slept on mattresses wrapped according to his method. While the Limerick report claims that babies have been found to die on wrapped mattresses, Dr. Sprott argues that a chemical analysis of the bedding should be performed. He additionally claims that this part of the report was flawed:

In February 2000 Dr Peter Fleming (a co-author of the Limerick Report and principal author of the UK CESDI Report) conceded that the claim that three babies in the United Kingdom had died of cot death on polythene-covered mattresses could not be substantiated.[42]

Central respiratory pattern deficiency
There is ongoing research in the pediatric/neonatal community that has begun to associate apnea-like breathing cessations in animal models with unusual neural architecture or signal transduction in central pattern generator circuits including the pre-Bötzinger complex.[43]

Cervical spinal injury from birth trauma
During birth, if the infant’s head is traumatically turned side to side, upper cervical spinal injury can result. Difficulty breathing is a classic sign of upper spinal cord and brain-stem injury. When infants with undiagnosed upper cervical spinal cord injury are continually placed on their stomach for sleep, they are forced to turn their head to the side to breathe.

Genetics
There is a consistent 50% male excess in SIDS per 1000 live births of each sex. Given a 5% male excess birth rate (105 male to 100 female live births) there appear to be 3.15 male SIDS per 2 female SIDS for a male fraction of 0.61. This value of 61% in the U.S. is an average of 57% black male SIDS, 62.2% white male SIDS and 59.4% for all other races combined. Note that when multiracial parentage is involved, infant “race” is arbitrarily assigned to one category or the other; most often it is chosen by the mother. The X-linkage hypothesis for SIDS and the male excess in infant mortality have shown that the 50% male excess could be related to a dominant X-linked allele that occurs with a frequency of ? that is protective of transient cerebral anoxia. An unprotected XY male would occur with a frequency of ? and an unprotected XX female would occur with a frequency of 4?9. The ratio of ? to 4?9 is 1.5 to 1 which matches the observed male 50% excess rate of SIDS.

Although many authors have found autosomal and mitochondrial genetic risk factors for SIDS they cannot explain the male excess because such gene loci have the same frequencies for males and females. Supporting evidence for an X-linkage is found by examination of other causes of infant respiratory death, such as suffocation by inhalation of food and other foreign objects. Although food is prepared identically for male and female infants, there is a similar 50% male excess of death from such causes indicating that males are more susceptible to the cerebral anoxia created by such incidents in exactly the same proportion as found in SIDS.

The JAMA 2006 study which indicated that there was a relationship between fewer serotonin binding sites and SIDS noted that the boys “had significantly fewer serotonin binding sites than girls”, but the authors could not reproduce it in their 2010 paper. However, such neurological prematurity decreases with age, but the male fraction of approximately 0.61 persists each month throughout the first year of life. Furthermore, this cannot explain the identical male fraction of 0.61 in other respiratory mortality causes such as respiratory distress syndrome or suffocation from inhalation of food or foreign objects cited above, that also exists for all ages 1 to 14 years in the U.S. from 1979 to 2005.

Child abuse
Several instances of infanticide have been uncovered where the diagnosis was originally SIDS. This has led some researchers to estimate that 5% to 20% of SIDS deaths are infanticides. In 1997 The New York Times, covering a book called The Death of Innocents: A True Story of Murder, Medicine and High-Stakes Science, wrote:

The misdiagnosis of infanticide as SIDS “happens all over,” Ms. Talan, a medical reporter at Newsday, said. “A lot of doctors and police don’t know how to handle it. They don’t take it as seriously as they should.” As a result of the book’s revelations, people are starting to scrutinize possible cases of this “perfect crime,” which involves no physical evidence and no witnesses.

A former pediatrician, Roy Meadow, from the UK believes that many cases diagnosed as SIDS are really the result of child abuse on the part of a parent displaying Munchausen syndrome by proxy (a condition which he was first to describe, in 1977). During the 1990s and early 2000s, a number of mothers of multiple apparent SIDS victims were convicted of murder, to varying degrees on the basis of Meadow’s opinion. In 2003 a number of high-profile acquittals brought Meadow’s theories into disrepute. Several hundred murder convictions were reviewed, leading to several high-profile cases being re-opened and convictions overturned. Meadow was struck off in 2005.

The Royal Statistical Society issued a media release refuting the expert testimony in one UK case in which the conviction was subsequently overturned.

Nitrogen dioxide
A 2005 study by researchers at the University of California, San Diego found that “SIDS may be related to high levels of acute outdoor NO2 exposure during the last day of life.” While nitrogen dioxide (NO2) exposure may be one of many possible risk factors, it is not considered causal, and the report cautioned that further studies were needed to replicate the result.Animal sleeping in the same room where  parents  sleep with baby   is not administered.

Vaccination
According to the U.S. Centers for Disease Control and Prevention, several studies have failed to provide sufficient evidence of a causal link between vaccinations and SIDS. They state:

From 2 to 4 months old, babies begin their primary course of vaccinations. This is also the peak age for sudden infant death syndrome (SIDS). The timing of these two events has led some people to believe they might be related. However, studies have concluded that vaccines are not a risk factor for SIDS.

Inner ear damage
Records of hearing tests (oto-acoustic emissions, OAEs) administered to certain infants show that those who later died of SIDS had differences in the pattern of these tests compared with normal babies. To be specific the OAE signal to noise ratio was reduced in the right ear in the SIDS babies (Rubens DD et al. Early Human Development 84, 225-9 (2008)). It should be noted this was a small study (n=31 cases and 31 controls), had serious limitations (several significant factors were not controlled), and has been criticised from various perspectives. The authors’ suggestion for the cause of SIDS is that the deaths are caused by disturbances in respiratory control (other than suffocation). The vestibular apparatus of the inner ear has been shown to play an important role in respiratory control during sleep. It is speculated that this inner ear damage could be linked to SIDS. It is speculated that the damage occurs during delivery, particularly when prolonged contractions create greater blood pressure in the placenta. The right ear is directly in the “line of fire” for blood entering the fetus from the placenta, and thus could be most susceptible to damage. If the findings are relevant, it may be possible to take corrective measures. Researchers are beginning animal studies to explore the connection.

Differential diagnosis
Some conditions that may be undiagnosed and thus could be alternative diagnoses to SIDS include:

*medium-chain acyl-coenzyme A dehydrogenase deficiency (MCAD deficiency)
*infant botulism.
*long QT syndrome (accounting for less than 2% of cases)
*infections with the bacterium Helicobacter pylori
*shaken baby syndrome and other forms of child abuse.
*overlying

For example an infant with MCAD deficiency could have died by “classical SIDS” if found swaddled and prone with head covered in an overheated room where parents were smoking. Genes of susceptibility to MCAD and Long QT syndrome do not protect an infant from dying of classical SIDS. Therefore presence of a susceptibility gene, such as for MCAD, means the infant may have died either from SIDS or from MCAD deficiency. It is impossible for the pathologist to distinguish between them.

Sleeping on the back has been recommended by (among others) the American Academy of Pediatrics (starting in 1992) to avoid SIDS, with the catchphrases “Back To Bed” and “Back to Sleep”. The incidence of SIDS has fallen sharply in a number of countries in which the back to bed recommendation has been widely adopted, such as the U.S. and New Zealand. However, the absolute incidence of SIDS prior to the Back to Sleep Campaign was already dropping in the U.S., from 1.511 per 1000 in 1979 to 1.301 per 1000 in 1991.

Among the theories supporting the Back to Sleep recommendation is the idea that small infants with little or no control of their heads may, while face down, inhale their exhaled breath (high in carbon dioxide) or smother themselves on their bedding—the brain-stem anomaly research (above) suggests that babies with that particular genetic makeup do not react “normally” by moving away from the pooled CO2, and thus smother. Another theory is that babies sleep more soundly when placed on their stomachs, and are unable to rouse themselves when they have an incidence of sleep apnea, which is thought to be common in infants.

Hospital neonatal-intensive-care-unit (NICU) staff commonly place preterm newborns on their stomach, although they advise parents to place their infants on their backs after going home from the hospital.

Breastfeeding
A 2003 study published in Pediatrics, which investigated racial disparities in infant mortality in Chicago, found that previously or currently breastfeeding infants in the study had ? the rate of SIDS compared with non-breastfed infants, but that “it became nonsignificant in the multivariate model that included the other environmental factors”. These results are consistent with most published reports and suggest that other factors associated with breastfeeding, rather than breastfeeding itself, are protective.” However, a more recent study shows that breast feeding reduces the risk of SIDS by approximately 50% at all infant ages.

Secondhand smoke reduction

According to the U.S. Surgeon General’s Report, secondhand smoke is connected to SIDS. Infants who die from SIDS tend to have higher concentrations of nicotine and cotinine (a biological marker for secondhand smoke exposure) in their body fluids than those who die from other causes. Parents who smoke can significantly reduce their children’s risk of SIDS by either quitting or smoking only outside and leaving their house completely smoke-free.

The maternal pregnancy smoking rate decreased by 38% between 1990 and 2002.

Bedding
Product safety experts advise against using pillows, sleep positioners, bumper pads, stuffed animals, or fluffy bedding in the crib and recommend instead dressing the child warmly and keeping the crib “naked.”

Blankets should not be placed over an infant’s head. It has been recommended that infants should be covered only up to their chest with their arms exposed. This reduces the chance of the infant shifting the blanket over his or her head.

Sleep sacks
In colder environments where bedding is required to maintain a baby’s body temperature, the use of a “baby sleep bag” or “sleep sack” is becoming more popular. This is a soft bag with holes for the baby’s arms and head. A zipper allows the bag to be closed around the baby. A study published in the European Journal of Pediatrics in August 1998 has shown the protective effects of a sleep sack as reducing the incidence of turning from back to front during sleep, reinforcing putting a baby to sleep on its back for placement into the sleep sack and preventing bedding from coming up over the face which leads to increased temperature and carbon dioxide rebreathing. They conclude in their study “The use of a sleeping-sack should be particularly promoted for infants with a low birth weight.” The American Academy of Pediatrics also recommends them as a type of bedding that warms the baby without covering its head. The use of swaddling clothes, a traditional form of infant restraint which leaves only the head uncovered, is controversial.

Pacifiers
According to a 2005 meta-analysis, most studies favor pacifier use. According to the American Academy of Pediatrics, pacifier use seems to reduce the risk of SIDS, although the mechanism by which this happens is unclear. SIDS experts and policy makers haven’t recommended the use of pacifiers to reduce the risk of SIDS because of several problems associated with pacifier use, like increased risk of otitis, gastrointestinal infections and oral colonization with Candida species. A 2005 study indicated that use of a pacifier is associated with up to a 90% reduction in the risk of SIDS depending on the ambient factors, and it reduced the effect of other risk factors. It has been speculated that the raised surface of the pacifier holds the infant’s face away from the mattress, reducing the risk of suffocation. If a postmortem investigation does not occur or is insufficient, a suffocated baby may be misdiagnosed with SIDS.

Bumper pads
Bumper pads may be a contributing factor in SIDS deaths and should be removed. Health Canada, the Canadian government’s health department, issued an advisory[92] recommending against the use of bumper pads, stating:

The presence of bumper pads in a crib may also be a contributing factor for Sudden Infant Death Syndrome (SIDS). These products may reduce the flow of oxygen rich air to the infant in the crib. Furthermore, proposed theories indicate that the rebreathing of carbon dioxide plays a role in the occurrence of SIDS.

Concerns regarding recommendations
Dr. Rafael Pelayo from Stanford University and a number of other pediatric sleep researchers in the U.S. have stated that they believe that the American Academy of Pediatrics’ recommendations regarding cosleeping and pacifier use may have unintended consequences. They have stated that the SIDS prevention strategy of the American Academy of Pediatrics which keeps infants at a low arousal threshold and reduces the time in quiet sleep may be unhealthy for children. They state that slow wave sleep is the most restorative form of sleep and limiting this sleep in the first 12 months of life may have unintended consequences to both the sleep and the infant.

According to a 1998 study by British researchers that compared back sleeping infants to stomach sleeping infants there were developmental differences at 6 months of age between the two groups. At 6 months of age the stomach sleeping infants had higher gross motor scores, social skills scores, and total development skills scores than the back sleeping infants. The differences were apparent at the 5% statistical significant level. But, at 18 months the differences were no longer apparent. The researchers deemed the lower development scores of back sleeping infants at 6 months of age to be transient and stated that they do not believe the back sleeping recommendations should be changed. Other scientists have stated that the conclusion that the negative effects of back sleep at 18 months of age is transient is based upon very little evidence and that no long-term randomized trials have been completed.

Other side effects of the back sleeping position include increased rates of shoulder retraction, positional plagiocephaly, and positional torticollis.[96] Some scientists dispute that plagiocephaly is a negative side effect. Dr. Peter Fleming, who is co-author of the study that deemed delays at 6 months of age to be transient, has stated that he does not think plagiocephaly is a negative side effect of back sleep. In an interview with the Guardian Dr. Fleming stated “I do not think it is a medical problem—it is more of a cosmetic one. Mothers may feel it is a syndrome and a problem when it really is nonsense.”[97] A research study on children with plagiocephaly found that 26% had mild to severe psychomotor delay. This study also showed that 10% of infants with plagiocephaly had mild to severe mental development delay.

Because of the delays caused by back sleep some medical professionals have suggested that the “normal” ages at which children had previously attained developmental milestones should be pushed back. This would enable medical professionals to consider “normal” children who previously were considered developmentally delayed.

Additional studies have reported that the following negative conditions are associated with the back sleep position: increase in sleep apnea, decrease in sleep duration, strabismus, social skills delays, deformational plagiocephaly, and temporomandibular jaw difficulties. In addition, the following are symptoms that are associated with sleep apnea: growth abnormalities, failure to thrive syndrome in infants, neurocognitive abnormalities, daytime sleepiness, emotional problems, decrease in memory, decrease in learning, and a delay in nonverbal skills. The conditions associated with deformational plagiocephaly include visual impairments, cerebral dysfunction, delays in psychomotor development and decreases in mental functioning. The conditions associated with gross motor milestone delays include speech and language disorders. In addition, it has been hypothesized that delays in motor skills can have a negative impact on the development of social skills. In addition, other studies have reported that the prone position prevents subluxation of the hips, increases psychomotor development, prevents scoliosis, lessens the risk of gastroesophageal reflux, decreases infant screaming periods, causes less fatigue in infants, and increases the relief of infant colic. In addition, prior to the “Back to Sleep” campaign many babies self-treated their own torticollis by turning their heads from one side to the other while sleeping in the prone position. Supine sleeping infants cannot self-treat their own torticollis.

Epidemiology
SIDS was reported  responsible for 0.543 deaths per 1,000 live births in the U.S. in 2005. It is responsible for far fewer deaths than congenital disorders and disorders related to short gestation, though it is the leading cause of death in healthy infants after one month of age.Actual death due to pure  SIDS  is perhaps one in million today.

SIDS deaths in the U.S. decreased from 4,895 in 1992 to 2,247 in 2004 But, during a similar time period, 1989 to 2004, SIDS being listed as the cause of death for sudden infant death (SID) decreased from 80% to 55%. According to Dr. John Kattwinkel, chairman of the Center for Disease Control (CDC) Special Task Force on SIDS “A lot of us are concerned that the rate (of SIDS) isn’t decreasing significantly, but that a lot of it is just code shifting”.

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:
http://hcd2.bupa.co.uk/fact_sheets/html/sids.html
http://en.wikipedia.org/wiki/Sudden_infant_death_syndrome
http://www.nlm.nih.gov/medlineplus/ency/article/001566.htm
*Simon C, Everitt H, Kendrick T. Oxford Handbook of General Practice. 2nd ed. Oxford: Oxford University Press, 2007:906

*Sudden unexpected death in infancy: a multi-agency protocol for care and investigation. Royal College of Pathologists and Royal College of Paediatrics and Child Health. 2004. www.rcpch.ac.uk

*Cot death facts & figures. Foundation for the Study of Infant Deaths. 2006. www.fsid.org.uk

*What is cot death? Foundation for the Study of Infant Deaths. www.fsid.org.uk, accessed 9 July 2008

*FAQ – current topics. Foundation for the Study of Infant Deaths. www.fsid.org.uk, accessed 9 July 2008

*Thach B. Tragic and sudden death: potential and proven mechanisms causing sudden infant death syndrome. EMBO J 2008; 9:114-118. www.nature.com

*Reduce the risk of cot death – an easy guide. Department of Health, 2007. www.dh.gov.uk

*Department of Health. The Pregnancy Book. 2007:119-127. www.dh.gov.uk, accessed 2 January 2009

*Anderson ME, Johnson DC, Batal HA. Sudden infant death syndrome and prenatal maternal smoking: rising attributed risk in the Back to Sleep era. BMC Med 2005; 3:4. www.biomedcentral.com

*Looking after your baby. Foundation for the Study of Infant Deaths. www.fsid.org.uk, accessed 11 July 2008

*New dummy advice for parents. Foundation for the Study of Infant Deaths. www.fsid.org.uk, accessed 11 July 2008

*Breastfeeding reduces the risk of cot death. Foundation for the Study of Infant Deaths. www.fsid.org.uk, accessed 11 July 2008

*Keep an eye on your baby’s room temperature. Foundation for the Study of Infant Deaths. www.fsid.org.uk, accessed 11 July 2008

*If you are bereaved. Foundation for the Study of Infant Deaths. www.fsid.org.uk, accessed 11 July 2008

*Care of the next infant (CONI). Foundation for the Study of Infant Deaths. www.fsid.org.uk, accessed 11 July 2008

*UNICEF UK statement on dummy use, sudden infant death syndrome and breastfeeding. UNICEF. www.babyfriendly.org.uk, accessed 8 December 2008

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Herbs & Plants

Cabbage Tree (Cordyline australis)

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Botanical Name : Cordyline australis
Family: Laxmanniaceae
Genus: Cordyline
Kingdom: Plantae
Order: Asparagales
Species: C. australis
Synonyms :  Dracaena australis. Forst.f.

Habitat :New Zealand. Forest margins and open places. Abundant near swamps. North, South and Stewart Islands.Woodland Garden Sunny Edge; Dappled Shade;

A quote from Philip Simpson sums up the wide range of habitats the cabbage tree occupied in early New Zealand, and how much its abundance and distinctive form shaped the impression travellers received of the country:

“In primeval New Zealand cabbage trees occupied a range of habitats, anywhere open, moist, fertile and warm enough for them to establish and mature: with forest; around the rocky coast; in lowland swamps, around the lakes and along the lower rivers; and perched on isolated rocks. Approaching the land from the sea would have reminded a Polynesian traveller of home, and for a European traveller, conjured up images of the tropical Pacific”.

Cordyline australis occurs from North Cape to the very south of the South Island, where it becomes less and less common, until it reaches its southernmost natural limits at Sandy Point (46° 30′ S), west of Invercargill near Oreti Beach. It is absent from much of Fiordland, probably because there is no suitable habitat, and is unknown on the subantarctic islands to the south of New Zealand, probably because it is too cold. It occurs on some offshore islands—Poor Knights, Stewart and the Chathams—but was probably introduced by M?ori. In the Stewart Island region, it is rare, growing only on certain islands, headlands and former settlement sites where it may have been introduced by muttonbird collectors, while on the Chatham Islands it is also largely “a notable absentee”.

Generally a lowland species, it grows from sea level to about 1000 metres (3300 ft), reaching its upper limits on the volcanoes of the central North Island, where eruptions have created open spaces for it to exploit, and in the foothills of the Southern Alps in the South Island, where deforestation may have played a part in giving it room to grow. C. australis in the central North Island has evolved a much sturdier form called t? manu “with branches bearing broad, straight upright leaves.” This form resembles that found in the far south of the South Island, suggesting that they are both adapted to cold conditions.

Cordyline australis is a light-demanding pioneer species, and seedlings die when overtopped by other trees. To grow well, young plants require open space so they are not shaded out by other vegetation. Another requirement is water during the seedling stage. Although adult trees can store water and are drought resistant, seedlings need a good supply of water to survive. This stops the species from growing in sand dunes unless there are wet depressions present, and from hillsides unless there is a seepage area. The fertility of the soil is another factor—settlers in Canterbury used the presence of the species to situate their homesteads and gardens. The fallen leaves of the tree also help to raise the fertility of the soil when they break down. Another factor is temperature, especially the degree of frost. Young trees are killed by frost, and even old trees can be cut back. This is why C. australis is absent from upland areas and from very frosty inland areas.

Early European explorers of New Zealand described “jungles of cabbage trees” along the banks of streams and rivers, in huge swamps and lowland valleys. Few examples of this former abundance survive today—such areas were the first to be cleared by farmers looking for flat land and fertile soil. In modern New Zealand, Cabbage trees usually grow as isolated individuals rather than as parts of a healthy ecosystem.

Description:
An evergreen Tree growing   up to 20 metres (66 ft) tall with a stout trunk and sword-like leaves, which are clustered at the tips of the branches and can be up to 1 metre (3 ft) long. With its tall, straight trunk and dense, rounded heads, C. australis is a characteristic feature of the New Zealand landscape. Its fruit is a favourite food source for the New Zealand pigeon and other native birds. It is common over a wide latitudinal range from the far north of the North Island at 34° 25’S to the south of the South Island at 46° 30’S. Absent from much of Fiordland, it was probably introduced by M?ori to the Chatham Islands at 44° 00’S and to Stewart Island at 46° 50’S. It grows in a broad range of habitats, including forest margins, river banks and open places, and is abundant near swamps. The largest known tree with a single trunk is growing at Pakawau, Golden Bay. It is estimated to be 400 or 500 years old, and stands 17 metres (56 ft) tall with a circumference of 9 metres (30 ft) at the base. Known to M?ori as T? k?uka, the tree was used as a source of food, particularly in the South Island, where it was cultivated in areas where other crops would not grow. It provided durable fibre for textiles, anchor ropes, fishing lines, baskets, waterproof rain capes and cloaks, and sandals. It is also grown as an ornamental tree in Northern.

Hemisphere countries with mild maritime climates, including the warmer parts of Britain, where its common names include Torquay palm. Hardy and fast growing, C. australis is widely planted in New Zealand gardens, parks and streets, and numerous cultivars are available. The tree can also be found in large numbers in island restoration projects such as Tiritiri Matangi Island, where it was among the first seedling trees to be planted.

It is hardy to zone 8 and is not frost tender. It is in leaf 12-Jan It is in flower from Aug to September. The flowers are hermaphrodite (have both male and female organs) Before it flowers, it has a slender unbranched stem. After the first flowering, it divides to form a much-branched crown with tufts of leaves at the tips of the branches. Each branch may fork after producing a flowering stem. The pale to dark grey bark is corky, persistent and fissured, and feels spongy to the touch.

The long narrow leaves are sword-shaped, erect, dark to light green, 40 to 100 cm (15–40 in) long and 3 to 7 cm (12–28 in) wide at the base, with numerous parallel veins. The leaves grow in crowded clusters at the ends of the branches, and may droop slightly at the tips and bend down from the bases when old. They are thick and have an indistinct midrib. The fine nerves are more or less equal and parallel. The upper and lower leaf surfaces are similar.
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In spring and early summer, sweetly perfumed flowers are produced in large, dense panicles (flower spikes) 60 to 100 cm (2–3 ft) long, bearing well-spaced to somewhat crowded, almost sessile to sessile flowers and axes. The flowers are crowded along the ultimate branches of the panicles. The bracts which protect the developing flowers often have a distinct pink tinge before the flowers open. In south Canterbury and North Otago the bracts are green.

The individual flowers are 5 to 6 mm (about 0.2 in) in diameter, the tepals are free almost to the base, and reflexed. The stamens are about the same length as the tepals. The stigmas are short and trifid. The fruit is a white berry 5 to 7 mm (2–3 in) in diameter which is greedily eaten by birds. The nectar attracts great numbers of insects to the flowers.

Large, peg-like rhizomes, covered with soft, purplish bark, up to 3 metres (10 ft) long in old plants, grow vertically down beneath the ground. They serve to anchor the plant and to store fructose in the form of fructan. When young, the rhizomes are mostly fleshy and are made up of thin-walled storage cells. They grow from a layer called the secondary thickening meristem.

Cultivation:
Prefers a good sandy loam rich in humus[1]. Succeeds in full sun or light shade. A very wind hardy plant, tolerating maritime exposure. A very ornamental plant[1], it is not very cold-hardy, tolerating short-lived lows down to about -10°c. It only succeeds outdoors in the milder areas of Britain. It grows very well in Cornwall where it often self-sows. A form with purplish leaves is hardier than the type and succeeds outdoors in Gloucestershire. The flowers have a delicious sweet scent that pervades the air to a considerable distance. Mice often kill young plants by eating out the pith of the stem[

Cordyline australis is one of the most widely cultivated New Zealand native trees, very popular as an ornamental tree in Europe, Great Britain and the United States. Hardy forms from the coldest areas of the southern or inland South Island tolerate Northern Hemisphere conditions best, while North Island forms are much more tender. It is easily grown from fresh seed — seedlings often spontaneously appear in gardens from bird-dispersed seed — and can be grown very easily from shoot, stem and even trunk cuttings. It does well in pots and tubs.

It is also widely planted in western Europe and the Northwest coast of the United States.It is particularly popular in Britain, where it is thought to resemble a palm tree. Cabbage trees are so common in the south of England that they are called Torquay palms, and are used in tourist posters promoting South Devon as the English Riviera. Some plants grow well as far north as western coast of Scotland where the Gulf Stream tempers the climate, including the village of Plockton. It is occasionally mis-named Cornish palm, Dracaena palm, Torbay palm or Manx palm in the British Isles due to its extensive use in Torbay and as the official symbol of that area under its alternative identity, the English Riviera. It also grows in Spain, Italy and Japan.Even though the natural distribution of C. australis ranges from a subtropical 34° S to a mid-latitude 46°S, and despite its ultimately tropical origins, it also grows at about five degrees from the Arctic Circle in Masfjorden, Norway, latitude 61ºN, in a microclimate protected from arctic winds and moderated by the Gulf Stream.

Propagation  :

Seed – pre-soak for about 10 minutes in warm water and sow in late winter to early spring in a warm greenhouse. The seed usually germinates in 1 – 3 months at 25°c. There is usually a good percentage germination. Prick out the seedlings into individual pots as soon as they are large enough to handle and grow them on in the greenhouse for at least their first winter. Plant out in late spring after the last expected frosts and give the plants some protection in their first winter outdoors. Stem cuttings – cut off the main stem just below the head and then saw off 5cm thick blocks of stem and place them 3cm deep in pure peat in a heated frame. Keep them moist until they are rooting well, then pot them up into individual pots. Plant out in late spring after the last expected frosts. Suckers. These are best removed in early spring and planted out in situ. Protect the division from wind and cold weather and do not allow the soil to become dry until the plant is established. Divisions can also be potted up and grown on until established, planting them out in the summer.


Edible Uses:

Root – baked. It can also be brewed into an intoxicating drink. Pith of the trunk – dried and steamed until soft. Sweet and starchy, it is used to make porridge or a sweet drink. The root and stems are rich in fructose, the yields compare favourably with sugar beet (Beta vulgaris altissima). Edible shoots – a cabbage substitute. The leaves are very fibrous even when young, we would not fancy eating them.

Medicinal Uses:
The Maori used various parts of Cordyline australis to treat injuries and illnesses, either boiled up into a drink or pounded into a paste. The koata, the growing tip of the plant, was eaten raw as a blood tonic or cleanser. Juice from the leaves was used for cuts, cracks and sores. An infusion of the leaves was taken internally for diarrhoea and used externally for bathing cuts. The leaves were rubbed until soft and applied either directly or as an ointment to cuts, skin cracks and cracked or sore hands. The young shoot was eaten by nursing mothers and given to children for colic. The liquid from boiled shoots was taken for other stomach pains. Cordyline australis contains an agent with anti-inflammatory properties, cinchophen, and the seeds are high in linoleic acid, one of the essential fatty acids.

Other Uses:
The leaves contain saponins, but not in commercial quantities. The leaves contain a strong fibre, used for making paper, twine, cloth, baskets, thatching, rain capes etc. The whole leaves would be used for some of these applications. When used for making paper, the leaves are harvested in summer, they are scraped to remove the outer skin and are then soaked in water for 24 hours prior to cooking.

When used for making paper, the leaves are harvested in summer, they are scraped to remove the outer skin and are then soaked in water for 24 hours prior to cooking.

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/user/Plant.aspx?LatinName=Cordyline australis
http://en.wikipedia.org/wiki/Cordyline_australis

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News on Health & Science

Wheat,Rye & Barley Triggers Gut Disease

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The precise cause of the immune reaction that leads to coeliac disease has been discovered.

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Foods like cake are off-limit to coeliacs

Three key substances in the gluten found in wheat, rye and barley trigger the digestive condition, UK and Australian researchers say.

This gives a potential new target for developing treatments and even a vaccine, they believe.

Coeliac disease is caused by an intolerance to gluten found in foods like bread, pasta and biscuits.

It is thought to affect around 1 in every 100 people in the UK, particularly women.

The link between gluten and coeliac disease was first established 60 years ago but scientists have struggled to pinpoint the precise component in gluten that triggers it.

The research, published in the journal, Science Translational Medicine, studied 200 patients with coeliac disease attending clinics in Oxford and Melbourne.

The volunteers were asked to eat bread, rye muffins or boiled barley. Six days later they had blood samples taken to measure their immune response to thousands of different gluten fragments, or peptides.

The tests identified 90 peptides that caused some level of immune reaction, but three were found to be particularly toxic.

Professor Bob Anderson, head of the Walter and Eliza Hall Institute of Medical Research in Melbourne, Australia, said: “These three components account for the majority of the immune response to gluten that is observed in people with coeliac disease.”

Coeliac disease can be managed with a gluten-free diet but this is often a challenge for patients. Nearly half still have damage to their intestines five years after starting a gluten-free diet.

Professor Anderson said one potential new therapy is already being developed, using immunotherapy to expose people with coeliac disease to tiny amounts of the three toxic peptides.

Early results of the trial are expected in the next few months.

Sarah Sleet, Chief Executive of the charity Coeliac UK, said the new finding could potentially help lead to a vaccine against coeliac disease but far more research was needed.

She said: “It’s an important piece of the jigsaw but a lot of further work remains so nobody should be expecting a practical solution in their surgery within the next 10 years.”

The symptoms of coeliac disease vary from person to person and can range from very mild to severe.

Possible symptoms include diarrhoea, nausea and vomiting, recurrent stomach pain, tiredness, headaches, weight loss and mouth ulcers.

Some symptoms may be mistaken as irritable bowel syndrome or wheat intolerance.

COELIAC DISEASE
*Continue reading the main story Coeliac disease is an autoimmune disease
*Gluten found in wheat, barley and rye triggers an immune reaction in people with coeliac disease
*This damages the lining of the small intestine
*Other parts of the body may be affected
Source: Coeliac UK

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