Habitat: Fumaria officinalis occurs in Europe and America. Parts of Asia, Australia and South Africa. It grows on arable land and as a weed in gardens, usually on lighter soils. It is also found growing on old walls.
Fumaria officinalis is an herbaceous annual plant, which grows weakly erect and scrambling, with stalks about 10 to 50 cm long. Its pink 7 to 9 mm flowers appear from April to October in the northern hemis phere. They are two lipped and spurred, with sepals running a quarter the length of the petals. The fruit is an achene. It contains alkaloids, potassium salts, and tannins. It is also a major source of fumaric acid….CLICK & SEE THE PICTURES Cultivation:
Prefers a light well-drained soil in a sunny position. This plant can be a common weed in some gardens, self-sowing freely, though it is fairly easy to control by hand weeding[K]. The flowers are seldom visited by insects, but they are self-fertile and usually set every seed.
Seed – sow spring in situ. There is normally very little need to sow this seed, the plant normally self-sows freely and should manage quite nicely by itself.
The plant contains isoquinoline alkaloids protopine and allocryptopine. Both protopine and allocryptopine increased CYP1A1 and CYP1A2 mRNA levels in human hepatocyte cells. The use of products containing protopine and/or allocryptopine may be considered safe in terms of possible induction of CYP1A enzymes.
The leaves yield by expression a juice which has medicinal properties. An extract, prepared by evaporating the expressed juice, or a decoction of the leaves, throws out upon its surface a copious saline efflorescence. Fumaric acid was early identified as present, and its isomerism with maleic acid was established later. The alkaloid Fumarine has been believed to be identical with corydaline, but it differs both in formula and in its reaction to sulphuric and nitric acids. It occurs in colourless, tasteless crystals, freely soluble in chloroform, less so in benzine, still less so in alcohol and ether, sparingly soluble in water.
Edible Uses: ……Curdling agent.
The fresh or dried herb can be added to sour plant milks. A few sprays are added to each litre of liquid and left until the liquid has soured thickly. The sprays are then removed. It gives a tangy taste to the milk, acts as a preservative and prevents the rancid taste that can accompany soured milk.
A weak tonic, slightly diaphoretic, diuretic, and aperient; valuable in all visceral obstructions, particularly those of the liver, in scorbutic affections, and in troublesome eruptive diseases, even those of the leprous order. A decoction makes a curative lotion for milk-crust on the scalp of an infant. Physicians and writers from Dioscorides to Chaucer, and from the fourteenth century to Cullen and to modern times value its purifying power. The Japanese make a tonic from it. Cows and sheep eat it, and the latter are said to derive great benefit from it. The leaves, in decoction or extract, may be used in almost any doses. The inspissated juice has also been employed, also a syrup, powder, cataplasm, distilled water, and several tinctures.
French and German physicians still preferit to most other medicines as a purifier of the blood; while sometimes the dried leaves are smoked in the manner of tobacco, for disorders of the head. Dr. Cullen, among its good effects in cutaneous disorders, mentions the following:
‘There is a disorder of the skin, which, though not attended with any alarming symptoms of danger to the life of the patient, is thought to place the empire of beauty in great jeopardy; the complaint is frequently brought on by neglecting to use a parasol, and may be known by sandy spots, vulgarly known as freckles, scattered over the face. Now, be it known to all whom it may concern, that the infusion of the leaves of the abovedescribed plant is said to be an excellent specific for removing these freckles and clearing the skin; and ought, we think, to be chiefly employed by those who have previously removed those moral blemishes which deform the mind, or degrade the dignity of a reasonable and an immortal being.’
The herb has a stimulant action on the liver and gallbladder and is chiefly used to treat skin conditions such as eczema, dermatitis and exanthema. Its action is probably due to a general cleansing mediated via the kidneys and liver. It is also diuretic and mildly laxative. Taken over a long period, it helps to cure depression. Also used internally for biliary colic and migraine with digestive disturbances. Externally used for conjunctivitis.
Other Uses: Dye & Baby care;
A yellow dye is obtained from the flowers. A decoction makes a curative lotion for ‘milk-crust’ on the scalps of babies.
Caution:It was traditionally thought to be good for the eyes, and to remove skin blemishes. In modern times herbalists use it to treat skin diseases, and conjunctivitis; as well as to cleanse the kidneys. However, Howard (1987) warns that fumitory is poisonous and should only be used “under the direction of a medical herbalist.
Disclaimer : The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplement, it is always advisable to consult with your own health care provider.
Fragile X syndrome is a genetic condition involving changes in part of the X chromosome. It is the most common form of inherited mental retardation in males and a significant cause of mental retardation in females.
Fragile X is a family of genetic conditions, which can impact individuals and families in various ways. These genetic conditions are related in that they are all caused by gene changes in the same gene, called the FMR1 gene.
Boys are usually more severely affected as they have only one X chromosome (they carry one X and one Y chromosome). Girls have a second X chromosome, which can to some extent make up for problems with the faulty one and so they may have only mild disabilities. They may also be carriers of the condition – that is, they are not affected themselves but can pass the condition on to their children.
However the genetics of fragile X are actually more complicated as some people only have a small change called a premutation in the FMR1 gene. While they don’t usually have problems from this , it makes the gene unstable and can develop into a full mutation when passed on to the next generation.
Fragile X affects about one in 3,600 men and one in 4,000 to 6,000 women of all races and ethnic groups. It shows an X-linked recessive pattern of inheritance and changes in the gene can become more serious as it’s passed from parent to child (especially when it is passed from a woman who carries it to her child).
Some people with a permutation of FMR1 may have no, or minimal, fragile X symptoms. But those with full mutation, where larger changes in the gene exist, demonstrate more severe signs of the condition.
Despite being carriers, some men aren’t affected (even though they have no normal copy of their X chromosome). But men who have the full mutation are almost always affected.
In women with the full mutation, a third have a below-normal IQ, a third have a borderline-normal IQ and the remaining third have a normal IQ
Fragile X includes:
fragile X syndrome (FXS), the most common cause of inherited mental impairment. This impairment can range from learning disabilities to more severe cognitive or intellectual disabilities. (Sometimes referred to as mental retardation.) FXS is the most common known cause of autism or “autistic-like” behaviors. Symptoms also can include characteristic physical and behavioral features and delays in speech and language development.
fragile X-associated primary ovarian insufficiency (FXPOI), a problem with ovarian function which can lead to infertility and early menopause in some female gene carriers.
Some gene carriers do not exhibit any of these features. To learn more about carriers click here.
Fragile X can be passed on in a family by individuals who have no apparent signs of this genetic condition. In some families a number of family members appear to be affected, whereas in other families a newly diagnosed individual may be the first family member to exhibit symptoms.
Since 1984, The National Fragile X Foundation (NFXF) has been helping individuals with Fragile X, their families, and the professionals who work with them. As research into Fragile X continues, our understanding of who it affects and how it affects them will grow. The NFXF is committed to: 1) supporting and funding all efforts that will increase awareness, 2) improving education, 3) advancing research toward improved treatments and an ultimate cure, and 4) keeping the Fragile X community always well-informed about the progress of these efforts.
Understanding Fragile X: A short, independent film produced by Image Union at station wttw11 in Chicago. (26 min.)
The main problem in fragile X is intellectual impairment. This can range from very minor, so that the person has a normal IQ and shows no sign of fragile X, to severe learning difficulties. How badly someone is affected depends on the degree of change in the gene. Click to see the picture
*Large body size
*Large forehead or ears with a prominent jaw
*Large testicles (macro-orchidism) after the beginning of puberty
*Tendency to avoid eye contact
Family members who have fewer repeats in the FMR1 gene may not have mental retardation, but may have other problems. Women with less severe changes may have premature menopause or difficulty becoming pregnant. Both men and women may have problems with tremors and poor coordination.
Fragile X syndrome is a genetic disorder caused by mutation of the FMR1 gene on the X-chromosome. Mutation at that site is found in 1 out of about every 2000 males and 1 out of about every 259 females. (Incidence of the disorder itself is about 1 in every 3600 males and 1 in 4000–6000 females.)
Normally, the FMR1 gene contains between 6–55 (29 in Robbins–Kumar pathology textbooks) repeats of the CGG codon (trinucleotide repeats). In people with the fragile X syndrome, the FMR1 allele has over 230–4000 repeats of this codon.
Expansion of the CGG repeating codon to such a degree results in a methylation of that portion of the DNA, effectively silencing the expression of the FMR1 protein.
This methylation of the FMR1 locus in chromosome band Xq27.3 is believed to result in constriction of the X chromosome which appears ‘fragile’ under the microscope at that point, a phenomenon that gave the syndrome its name.
Mutation of the FMR1 gene leads to the transcriptional silencing of the fragile X-mental retardation protein, FMRP. In normal individuals, FMRP is believed to regulate a substantial population of mRNA: FMRP plays important roles in learning and memory, and also appears to be involved in development of axons, formation of synapses, and the wiring and development of neural circuits
Complications vary depending on the type and severity of symptoms.
*Recurrent infections in children
Fragile X syndrome is an X-linked dominant condition with variable expressivity and possibly reduced penetrance.
Because males normally have only one copy of the X-chromosome, those males with significant trinucleotide expansion at the FMR1 locus are symptomatic. They are intellectually disabled and may show various physical features of the fragile X syndrome.
Females have two X-chromosomes and thus have an increased probability of having a working FMR1 allele. Females carrying one X-chromosome with an expanded FMR1 gene can have some signs and symptoms of the disorder or be normal. Although the extra X-chromosome can serve as a backup, only one X-chromosome is active in each cell due to X-inactivation.
Males with the fragile X cannot transmit it to any of their sons (since males contribute a Y-chromosome, not an X, to their male offspring), but will transmit the premutation to all of their daughters, as males contribute their X to all of their daughters. Males never transmit their full mutation (males with full mutations in their blood have premutations in their sperm), and expansion to full mutations never occurs through paternal transmission.
Females carrying one copy of the fragile X can transmit it to their sons or daughters; in this case each child has a 50% chance of inheriting the fragile X. Sons who receive the fragile X are at high risk of intellectual disability. Daughters who receive the fragile X may appear normal or they may be intellectually disabled, usually to a lesser degree than boys with the syndrome. The transmission of fragile X often increases with each passing generation. This seemingly anomalous pattern of inheritance is referred to as the Sherman paradox.
Fragile X syndrome was originally diagnosed by culturing cells in a folate deficient medium and then assessing the cultures for X-chromosome breakage by cytogenetic analysis of the long arm of the X-chromosome. This technique proved unreliable for both diagnosis and carrier testing.
The fragile X abnormality is now directly determined by analysis of the number of CGG repeats and their methylation status using restriction endonuclease digestion and Southern blot analysis.
Not everyone with fragile X syndrome has the same signs and symptoms. Even affected people in the same family don’t show the same symptoms. The signs and symptoms fall into six categories:
*Intelligence and learning
*Social and emotional
*Speech and language
*Disorders commonly associated or sharing features with Fragile X
Autism and Fragile X syndrome:
Fragile X syndrome can cause a child to have autism or an Autism Spectrum Disorder (ASD) though not all children with fragile X syndrome have autism or an ASD.
For 2% to 6% of all children diagnosed with autism, the cause is the Fragile X gene mutation. Approximately one-third of all children diagnosed with fragile X syndrome also have some degree of autism. Fragile X syndrome is the most common known single gene cause of autism.
From Dr. Randi Hagerman’s statement to the United States House of Representatives Subcommittee on Health and Environment: “…Fragile X represents a portal through which we hope to view and treat a wide variety of other disorders of brain development and function. All children with autism…should be tested for Fragile X.”
Genetic mouse models of Fragile X syndrome have also been shown to have autistic-like behaviors
As yet there are no specific treatments or a cure for fragile X, but emotional and educational support for children and their families are vital to help them reach their best potential.
Most affected children have delayed speech and language development and specialised help from a speech and language therapist is vital. Behavioural therapy may help children and their families to cope with problems such as hyperactivity and impulsivity, and sometimes medication is tried. Behavioural therapy may also help those children who have problems developing relationships to develop social skills and to cope with stressful situations.
Some children cope in mainstream schools, sometimes with some extra help, while others need to go to a school which can provide for their special educational needs.
The outcome depends on the extent of intellectual impairment that is present as well as emotional and social skills.
Genetic counseling may help both existing and prospective parents with a family history of Fragile X syndrome, or a family history of other symptoms such as tremor. Genetic testing can help determine the level of risk in these families.
Recent studies have focused on a number of critical areas. The role of FMRP’s RNA partners, many of which have now been validated through in vitro assays, is of primary importance. Also being examined is the function the various domains of FMRP, an RNA-binding protein, which is still relatively unknown. One hypothesis is that many symptoms are caused by unchecked activation of mGluR5, a metabotropic glutamate receptor, which was found in a 2007 study to contribute significantly to the pathogenesis of the disease; this suggests that mGluR5 blockers could be used to treat fragile X syndrome
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.
From a swollen thumb to a bruise to food poisoning, good old grandma has often had a single remedy: a dash of turmeric. Indian researchers have now found that this dietary supplement plays a positive role in taming cancers too.
The ubiquitous spice of the typical Indian kitchen has of late been a subject of much curiosity among medical researchers because of its well-known wound healing and anti-inflammatory properties.
Researchers stumbled upon the anti-cancer potential of curcumin, the active ingredient of turmeric, recently. Since then, a number of research groups all over the world have been engaged in animal studies to prove curcumin’s efficacy.
Reported in the latest issue of Carcinogenesis, the work by a team of Indian medical scientists led by Girish Maru of the Advanced Centre for Treatment, Research and Education in Cancer (ACTREC), Mumbai, is one of first studies on the subject.
More importantly, the Mumbai scientists were able to unravel the exact mechanism behind curcumin’s action. They found that curcumin not only inhibits the enzymes that directly help a cancer-causing agent to damage the DNA but also increases the availability of yet another set of enzymes that helps the body fight the carcinogenic compound.
For their studies the ACTREC researchers used the carcinogen benzo[a]pyrene (B[a]P), a compound commonly found in cigarette smoke and wood smoke and that is implicated in lung cancer. They fed mice with curcumin for 16 days. Then the animals were given a relatively high quantity of B[a]P enough to induce DNA damage that can lead to tumour growth.
Subsequent studies on how the carcinogen interacted with various sets of enzymes inside the animals gave interesting results. The mice fed with curcumin had much depleted levels of cancer-promoting enzymes compared with the control group. Also, they showed higher levels of friendly enzymes such as glutathione S-transferase, indicating increased detoxification of B[a]P.
But is the quantity of turmeric, which one consumes through food, enough to have a protective effect against cancers? Scientists do not think so.
Though very potent, the levels of curcumin in turmeric are as low as 0.01 per cent. Moreover, curcumin uptake by the human body is relatively low. However, scientists are trying to increase curcumin uptake by the human body. For instance, they have already found that adding one part of piperine, the compound responsible for black pepper’s pungency, to 20 parts of curcumin can increase the uptake by several hundred-fold.