Botanical Name :Cassia nomame Family :FABACEAE or LEGUMINOSAE Pea Family Genus: Cassia Species:C. aldabrensis Kingdom:Plantae Order: Fabales Common Names : Cassia Nomame , Hama-cha, Kita; nomame herba; Mimosoides tea
Cassia nomame is native to China and originally produced in the south of the Changjiang river.
The species as a whole is widespread in the tropics of the Old World and has been recorded from the Americas, but this needs confirmation. The range of variation is wide but cannot be clearly linked to either geographic origins or the effect of a hybrid swarm. At present it is simply divided into seven unnamed groups.
* Group A = C. mimosoides L. var. telfairiana Hook. is from Mauritius and the Seychelles, with closely related plants in the Sudan and the Congo . Grows from 0 to 1 370 m in altitude.
* Group B is from the Congo, the Sudan, Mozambique, Malawi, Zambia, Angola and southern Africa. Grows at altitudes from 900 to 1 500 m.
* Group C is recorded only from Zanzibar, between sea level and 550 m.
* Group D only from north-western Kenya, between 1 680 and 1 740 m.
*Group E is from the Sudan, the Congo, Mozambique, Zimbabwe and the Transvaal, and is closely related to plants in Nigeria, C?te d’Ivoire, Mali and Madagascar between 470 and 1 550 m.
*Group F = var. glabriuscula Ghesq., and is widespread in tropical Africa from the Gambia to Nigeria and the Sudan and southwards to Angola and Natal; it is also found in Asia from India to Australia.
*Group G occurs in Sierra Leone, Liberia, the Congo, Eritrea, the Sudan, Mozambique, Zambia and Angola, and also in India between 0 and 2 110 m. It resembles C. capensis Thunb. var. humifusa Ghesq. (Brennan, 1967).C
An exceedingly variable, prostrate to erect legume up to 1.5 m high, usually annual, sometimes with stems becoming woody above ground level and enabling the plant to perenniate. Stems variable, usually puberulent with short curved hairs, sometimes more or less densely clothed with longer spreading hairs. Leaves linear to linear-oblong, more or less parallel-sided, 0.6 to 10 cm long, 0.4 to 1.5 cm . Gland usually at or near the top of the petiole, sessile, normally orbicular or nearly so, disk shaped when dry, 0.4 to 1 mm in diameter. Rachis glandular, serrate or crenate-crested along the upper side. Leaflets sessile, in 16 to 76 pairs, obliquely oblong to oblong-elliptic or linear-oblong, 2.5 to 8 (2 to 9) mm long, 0.5 to 1.25 (1.9) mm wide, acute or subacute and shortly mucronate, glabrous or nearly so. Midrib somewhat eccentric, lateral nerves obscure to prominent beneath. Inflorescence supra-axillary or sometimes axillary, one- to three-flowered. Pedicels 0.3 to 2.5 (3.0) cm long, usually shortly puberulent, sometimes spreading hairy. Petals yellow, obovate 4 to 13 mm long, 2 to 9 mm wide. Pods linear to linear-oblong, (sometimes 1.5 but usually 3.5 to 8 cm long); 3.5 mm wide, usually adpressed hairy. Seeds brown, more or less rhombic, 2 to 3 mm long, 1 to 2 mm wide
An extract of this herb is showing up in many weight loss and diet formulations. The claim is that Cassia nomame is a natural lipase inhibitor, which means it disrupts the digestive enzyme process to block fat from getting into the bloodstream. It also is said to have diuretic and stimulating properties. The most prevalent sources of information I have been able to find concerning this herb are those who have a financial interest in selling it. While it may well work, documentation is thin for the most part.
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
Botanical Name : Schinziophyton rautanenii Family: Euphorbiaceae Subfamily: Crotonoideae Tribe: Ricinodendreae Genus: Schinziophyton Hutch. ex Radcl.-Sm. Species: S. rautanenii Kingdom: Plantae Order: Malpighiales
Common Names:Mongongo nut, Feather weight tree, Manketti Tree
Habitat :The Schinziophyton rautanenii is distributed widely throughout southern Africa. There are several distinct belts of distribution, the largest of which reaches from northern Namibia into northern Botswana, south-western Zambia and western Zimbabwe. Another belt is found in eastern Malawi, and yet another in eastern Mozambique.
The manketti tree prefers hot and dry climates with low amounts of rain. It also prefers to grow in wooded hills and sand dunes.
Its habitat is dotted with trees and does not receive enough rain to be considered a prairie. The countries that lie in this biome are Mauritania, Guinea, Liberia, Ethiopia, Sudan, Chad, Mali, Niger and Uganda.
Schinziophyton rautanenii is a deciduous tree.It has a large, straight trunk with stubby and contorted branches and a large spreading crown. It has an upright manner of growth and is about 49 to 66 feet (15 to 20) meters tall. The leaves are a distinctive hand shape and are compound. The leaflet is a wide lance to an egg shape. They are composed of seven leaflets that are carried on hairy stalks that are up to 6 inches (15 cm) in length. The leaves are about 6 inches (15 cm) long and both sides are dark green in color. They are covered in fine hairs and are arranged alternately on branches.
The flowers are somewhat oval in shape, and are about 1 1/4 inch (3.5 cm) long, 3/4 inch (2.5 cm) wide, and are about 1/2 inch (10 mm) in diameter. They flower in early summer. The whitish flowers are carried in slender loose spays.
Leaves alternate, digitately compound, consisting of 5-7 leathery segments usually hairless below and with grey wooly hairs above. There are usually 1 or 2 black glands on the upper side of each leaf-stalk.
Flowers whitish or yellow, dioecious, in loose rusty sprays. Male flowers in long rusty sprays, female shorter in length.
Fruit ovoid, waxy and brown in colour; weighing 7-10 g with a thick leathery skin, fleshy, dry, spongy pulp 2-5 mm thick, shell tough 3-7 mm thick.
Seeds 1 or 2 in the fruit.
The taproot on the tree goes down until it reaches water. In this case, it is long because it is located in the savanna. The lateral root is very small.
So popular are the fruit and nuts of the mongongo tree that they have even been described as a “staple diet” in some areas, most notably amongst the San bushmen of northern Botswana and Namibia. Archaeological evidence has shown that they have been consumed amongst San communities for over 7,000 years. Their popularity stems in part from their flavour, and in part from the fact that they store well, and remain edible for much of the year.
The fruit is edible and can be eaten fresh, dried or cooked and have a pleasant taste likened to that of plums. The fruit retains its flavour even when dry.
Dry fruits are first steamed to soften the skins. After peeling, the fruits are then cooked in water until the maroon-coloured flesh separates from the hard inner nuts. The pulp is eaten, and the nuts are saved to be roasted later. Alternatively, nuts are collected from elephant dung; the hard nut survives intact through the digestive process and the elephant does the hard work of collecting the nuts. During roasting of the nuts, direct contact with the fire is avoided, using sand to distribute the heat evenly. Once dry, the outer shell cracks easily, revealing the nut, encased within a soft, inner shell. The nuts are either eaten straight, or pounded as ingredients in other dishes.
. The fruit is normally skinned after steaming in a pot with little water, then boiled in fresh water to separate the nuts. The fruit is used in making aromatic soups and sweet porridge, they can be dried and consumed as sweetmeats. During roasting direct contact of seeds with the fire coals is avoided by roasting in a sand heap. Fruit carbohydrate content is between 65-77%, fibre 2.5-3%, crude protein 6-9% and Ca levels are 85-100 mg/ 100 g. In the abscence of moisture fruits can remain edible for up to 8 months if left on ground where they fall.
The fruit pulp is fermented to give a refreshing potent beer, distilled for alcohol.
Nutritional value:- Per 100 grams shelled nuts:
*57 g fat:
*24 g protein
*193 mg calcium
*527 mg magnesium
*4 mg zinc
*2.8 mg copper
*565 mg vitamin E (and tocopherol)
The roots are used as a remedy for stomach pains and diarrhea, the nuts tied around the ankles are said to relieve leg pains.
The oil from the nuts has also been traditionally used as a body rub in the dry winter months, to clean and moisten the skin, while the hard, outer nut-shells are popular as divining “bones”. The wood, being both strong and light, makes excellent fishing floats, toys, insulating material and drawing boards. More recently, it has been used to make dart-boards and packing cases.
The plant has potential use in desert encroachment prevention and sand dune stabilization. Its hardiness makes it ideal for arid land reclamation. Erosion control: S. rautanenii roots protect sandy soils from wind and water erosion.
Fruit enjoyed by both cattle and game. Fruit pulp and the seed meal which is very rich in protein was fed to cattle up to 1962, however this feed is suspected to cause a discolouration of beef. Elephants feed on the bark.
Truncheon-cuttings used for fencing around homes in southern Angola. In some places the tree is highly held culturally and venerable.
Offers shade in hot areas e.g. in the Kalahari desert.
Known Hazards: : Toxicological results suggest a tenous link between oil use and goitre.
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
Yellow fever (also called yellow jack, black vomit or sometimes American Plague) is an acute viral disease. It is an important cause of hemorrhagic illness in many African and South American countries despite existence of an effective vaccine. The yellow refers to the jaundice symptoms that affect some patients.It is a viral infection transmitted by mosquitoes.
Yellow fever is a viral hemorrhagic fever caused by the yellow fever virus. The yellow fever virus is a single-stranded enveloped virus that belongs to the flavivirus group. The disease can result in mild symptoms or severe illness and death (mortality rate 5-70%). Yellow fever derives its name from the yellowing of the skin and whites of the eyes (jaundice) that occur in some people infected with the virus. Jaundice is caused by the presence of bile pigment (bilirubin) in the bloodstream and results from damage to liver cells (hepatocytes) during severe infection.…click & see
The yellow fever virus infects mainly monkeys and humans: monkeys are the animal reservoir. Infection is transmitted from human to human, monkey to monkey, monkey to human, and human to monkey by daytime-biting mosquitos. Several species of Aedes and Haemoagogus mosquitos can serve as vectors, transmitting the virus during a blood meal.
Three types of transmission cycles exist for yellow fever: sylvatic (jungle), intermediate and urban. Although all three transmission cycles occur in Africa, only sylvatic and urban transmission cycles occur in South America.
* Occurs in monkeys infected by wild mosquitos in tropical rainforests
* Infected monkeys pass the virus to mosquitos during feeding
* Infected wild mosquitos bite humans entering the rainforest (accidental infection)
Intermediate yellow fever (monkey to human; human to monkey)
* Small-scale epidemics that occur in humid or semi-humid grasslands of Africa
* Separate villages experience simultaneous infections transmitted by semi-domestic mosquitos that infect both monkey and human hosts
* Most common type of outbreak in Africa
Urban yellow fever (human to human)
* Large epidemics occurring when the virus is introduced into high human population areas by migrants
* Domestic mosquitos of one species (Aedes aegypti) transmit the virus from person to person
* Monkeys are not involved in transmission
* Outbreaks spread from one source to cover a wide area
Yellow fever has been a source of several devastating epidemics. Yellow fever epidemics broke out in the 1700s in Italy, France, Spain, and England. 300,000 people are believed to have died from yellow fever in Spain during the 19th century. French soldiers were attacked by yellow fever during the 1802 Haitian Revolution; more than half of the army perished from the disease. Outbreaks followed by thousands of deaths occurred periodically in other Western Hemisphere locations until research, which included human volunteers (some of whom died), led to an understanding of the method of transmission to humans (primarily by mosquitos) and development of a vaccine and other preventive efforts in the early 20th century.
Despite the costly and sacrificial breakthrough research by Cuban physician Carlos Finlay, American physician Walter Reed, and many others over 100 years ago, unvaccinated populations in many developing nations in Africa and Central and South America continue to be at risk. As of 2001, the World Health Organization (WHO) estimates that yellow fever causes 200,000 illnesses and 30,000 deaths every year in unvaccinated populations.
Yellow fever is caused by a small virus that is spread by the bite of mosquitoes. This disease is common in South America and in sub-Saharan Africa.
Anyone can get yellow fever, but the elderly have a higher risk of severe infection. If a person is bitten by an infected mosquito, symptoms usually develop 3 – 6 days later.
Yellow fever has three stages:
1.Early stage: Headache, muscle aches, fever, loss of appetite, vomiting, and jaundice are common. After approximately 3 – 4 days, often symptoms go away briefly (remission).
2.Period of remission: After 3 – 4 days, fever and other symptoms go away. Most people will recover at this stage, but others may move onto the third, most dangerous stage (intoxication stage) within 24 hours.
3.Period of intoxication: Multi-organ dysfunction occurs. This includes liver and kidney failure, bleeding disorders/hemorrhage, and brain dysfunction including delirium, seizures, coma, shock, and death.
Although viral replication begins in cells at the site of the mosquito bite, symptoms of infection are not usually noted for a period of three to six days when the acute phase of infection presents. Acute yellow fever infection is characterized by high fever, muscle pain, backache, headache, shivers, loss of appetite, nausea and/or vomiting. Most people infected improve after three to four days.
However, within 24 hours of the disappearance of symptoms, up to 15% of those infected enter a toxic phase during which fever resumes, and the yellow fever virus quickly spreads to the kidneys, lymph nodes, spleen, bone marrow and liver. Liver invasion of one of the last stages to occur: as the liver is increasingly damaged, patients develop jaundice as bilirubin is released from damaged liver cells, experience abdominal pain and vomiting, and develop coagulopathies (inability of the blood to clot) characterized by bleeding from the mouth, nose, eyes and stomach, and presence of blood in vomit and stool. Up to 50% of people who enter the toxic phase die within two weeks of infection.
Yellow fever may be difficult to diagnose, especially during the early stages, and may be confused with malaria, typhoid, other hemorrhagic fevers (dengue, Rift Valley, Venezuelan, Bolivian, Argentine, Lassa, Crimean-Congo, Marburg and Ebola), rickettsial infection, leptospirosis, viral hepatitis, other causes of liver failure and toxic hepatitis (e.g. carbon-tetrachloride poisoning).
Exams and Tests
A person with advanced yellow fever may show signs of liver failure, renal failure, and shock.
If you have symptoms of yellow fever, tell your doctor if you have traveled to areas where the disease is known to thrive. Blood tests can confirm the diagnosis.
There is no specific treatment for yellow fever. Treatment for symptoms can include:
*Blood products for severe bleeding
*Dialysis for kidney failure
*Fluids through a vein (intravenous fluids)
The treatment for yellow fever is supportive: control of fever, fluids to treat dehydration, and intensive support related to organ damage.
The World Health Organization estimates 200,000 cases of yellow fever per year with approximately 30,000 deaths.
Yellow fever ranges in severity. Severe infections with internal bleeding and fever (hemorrhagic fever) are deadly in up to half of cases.
Historical reports have claimed a mortality rate of between 1 in 17 (5.8%) and 1 in 3 (33%). CDC has claimed that case-fatality rates from severe disease range from 15% to more than 50%. The WHO factsheet on yellow fever, updated in 2001, states that 15% of patients enter a “toxic phase” and that half of that number die within ten to fourteen days, with the other half recovering
If you will be traveling to an area where yellow fever is common:
*Sleep in screened housing
*Use mosquito repellents
*Wear clothing that fully covers your body
*There is an effective vaccine against yellow fever. Ask your doctor at least 10 – 14 days before traveling if you should be *vaccinated against yellow fever.
In 1937, Max Theiler, working at the Rockefeller Foundation, developed a safe and highly efficacious vaccine for yellow fever that gives a ten-year or more immunity from the virus. The vaccine consists of a live, but attenuated, virus called 17D. The 17D vaccine has been used commercially since the 1950s. The mechanisms of attenuation and immunogenicity for the 17D strain are not known. However, this vaccine is very safe, with few adverse reactions having been reported and millions of doses administered, and highly effective with over 90% of vaccinees developing a measurable immune response after the first dose.
Although the vaccine is considered safe, there are risks involved. The majority of adverse reactions to the 17D vaccine result from allergic reaction to the eggs in which the vaccine is grown. Persons with a known egg allergy should discuss this with their physician prior to vaccination. In addition, there is a small risk of neurologic disease and encephalitis, particularly in individuals with compromised immune systems and very young children. The 17D vaccine is contraindicated in infants, pregnant women, and anyone with a diminished immune capacity, including those taking immunosuppressant drugs.
According to the travel clinic at the University of Utah Hospital, the vaccine presents an increased risk of adverse reaction in adults aged 60 and older, with the risk increasing again after age 65, and again after age 70. The reaction is capable of producing multiple organ failure and should be evaluated carefully by a qualified health professional before being administered to the elderly.
Finally, there is a very small risk of more severe yellow fever-like disease associated with the vaccine. This reaction occurs in 1~3 vaccinees per million doses administered. This reaction, called YEL-AVD, causes a fairly severe disease closely resembling yellow fever caused by virulent strains of the virus. The risk factor/s for YEL-AVD are not known, although it has been suggested that it may be genetic. The 2`-5` oligoadenylate synthetase (OAS) component of the innate immune response has been shown to be particularly important in protection from Flavivirus infection. In at least one case of YEL-AVD, the patient was found to have an allelic mutation in a single nucleotide polymorphism (SNP) of the OAS gene. People most at risk of contracting the virus should be vaccinated. Woodcutters working in tropical areas should be particularly targeted for vaccination. Insecticides, protective clothing, and screening of houses are helpful, but not always sufficient for mosquito control; people should always use an insecticide spray while in certain areas. In affected areas, mosquito control methods have proven effective in decreasing the number of cases.
Recent studies have noted the increase in the number of areas affected by a number of mosquito-borne viral infections and have called for further research and funding for vaccines
In the hamster model of yellow fever, early administration of the antiviral ribavirin is an effective early treatment of many pathological features of the disease. Ribavirin treatment during the first five days after virus infection improved survival rates, reduced tissue damage in target organs (liver and spleen), prevented hepatocellular steatosis, and normalized alanine aminotransferase (a liver damage marker) levels. The results of this study suggest that ribavirin may be effective in the early treatment of yellow fever, and that its mechanism of action in reducing liver pathology in yellow fever virus infection may be similar to that observed with ribavirin in the treatment of hepatitis C, a virus related to yellow fever. Because ribavirin had failed to improve survival in a virulent primate (rhesus) model of yellow fever infection, it had been previously discounted as a possible therapy.
In 2007, the World Community Grid launched a project whereby computer modelling of the yellow fever virus (and related viruses), thousands of small molecules are screened for their potential anti-viral properties in fighting yellow fever. This is the first project to utilize computer simulations in seeking out medicines to directly attack the virus once a person is infected. This is a distributed process project similar to SETI@Home where the general public downloads the World Community Grid agent and the program (along with thousands of other users) screens thousands of molecules while their computer would be otherwise idle. If the user needs to use the computer the program sleeps. There are several different projects running, including a similar one screening for anti-AIDS drugs. The project covering yellow fever is called “Discovering Dengue Drugs – Together.” The software and information about the project can be found at: World Community Grid web site
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: